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Mitos da nutrição
 

Mitos da nutrição

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    Mitos da nutrição Mitos da nutrição Presentation Transcript

    • MITOS EM NUTRIÇÃOPedro Carrera Bastos
    • RECOMENDAÇÕES NUTRICIONAIS
    • PIRÂMIDEAMERICANA USDA, 1992
    • NOVA RODA PORTUGUESACereais e 4 a 11 doses derivados, tubérculosHortaliças 3 a 5 dosesFruta 3 a 5 dosesLácteos 2 a 3 dosesCarnes, peixe e ovos 1,5 a 4,5 dosesLeguminosas 1 a 2 dosesGorduras e óleos 1 a 3 doses Instituto do Consumidor, 2003
    • HARVARD SCHOOL OF PUBLIC HEALTH, 2005 http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/pyramid/
    • PIRÂMIDE VEGETARIANA
    • PIRÂMIDE MEDITERRÂNICA
    • PIRÂMIDE LATINO-AMERICANA
    • VÁRIAS DIETAS
    • LENDAS Battle Creek S. Graham J.H. KelloggM. Bircher-Benner W. Arbuthnot-Lane D. Burkitt
    • DINHEIRO
    • COMO CHEGAR A CONCLUSÕES
    • CAUSA/EFEITO EpidemiologiaCordain L. Dietary implications for the development of acne: a shifting paradigm. In: U.S. Dermatology Review II 2006, (Ed.,Bedlow, J). Touch Briefings Publications, London, 2006.
    • Estudos com Humanos: Estudos Metabólicos de curto prazo RCTs CAUSA/EFEITO Estudos com Animais Epidemiologia Estudos In vitroCordain L. Dietary implications for the development of acne: a shifting paradigm. In: U.S. Dermatology Review II 2006, (Ed.,Bedlow, J). Touch Briefings Publications, London, 2006.
    • RECOMENDAÇÕES BASEADAS EM LENDAS E EPIDEMIOLOGIA
    • CONTROVÉRSIAS
    • COLESTEROL DIETÉTICO < 300 MG/DIA Dietary Guidelines for Americans, USDA, 2005
    • ALIMENTO (100 G) COLESTEROL (MG) Queijo de Azeitão 88 Nata 33% gordura 97 Costoleta de Porco (gorda) grelhada 111 Peito de vitela estufado 121 Camarão Cozido 198 Mexilhão cozido 360 Fígado de vitela grelhado 387 Ovo cozido 408Tabela de Composição dos Alimentos. Centro de Segurança Alimentar e Nutrição. Instituto nacional de Saúde Dr. Ricardo Jorge, 2006
    • EFEITOS NO CURTO PRAZOINCREMENTO DE 100 MG/D DE COLESTEROL DIETÉTICO AUMENTOU: ü  CT: 2.2 mg/dl ü  C- HDL: 0.3 mg/dl 30 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
    • US NATIONAL HEALTH AND NUTRITIONAL SURVEY (1984–1994)34 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
    • CHOLESTEROL SYNTHESIS, TRANSPORT, & EXCRETION / 225 ENTEROHEPATIC CIRCULATION HEPATIC PORTAL VEIN Diet (0.4 g/d) C CE GALL BLADDER Synthesis – – Bile acids (total pool, 3–5 g) BILE DUCT Unesterified cholesterol CE pool C ACAT CE Bile C C acids HL VLDL C TG Chylomicron CE TG ILEUM ,C CE E LDL C (apo B-100, E) TG LIVER receptor CE 8 –9 9 % 9 LDL C TG CE LRP receptor CE C TG CE CE TG C CE TP C Bile acids TG TG CE AT A-I (0.6 g/d) (0.4 g/d) CE LC CE IDL C C HDL Feces (VLDL remnant) Chylomicron remnant LPL C LDL (apo B-100, E) C receptor EXTRAHEPATIC C Synthesis TISSUES CE Murray R, et al. Harper’s Illustrated Biochemistry 26th Edition. McGraw-Hill, 2003Figure 26–6. Transport of cholesterol between the tissues in humans. (C, unesterified cholesterol; CE, cho-
    • 24, 25]. Other cholesterol-containing foods, such as dairy fed for 4 weeks with a 1-month washout period in between.products, also contain high concentrations of saturated fat, The participants were classified as insulin sensitive (n=65), Curr Atheroscler Rep (2010) 12:377–383which is a confounder for dietary cholesterol effects. This DOI 10.1007/s11883-010-0130-7 insulin resistant (n=75), and obese insulin resistant (OIR,might be the reason why controversial results exist n=58). Insulin-resistant and insulin-sensitive individuals hadregarding the effects of dairy products on CHD risk [26]. significant increases in LDL-C of 7.8% and 3.3%, respec- Clinical trials conducted in children [27], younger adults tively, after consuming 4 eggs per day, whereas OIR Revisiting Dietary Cholesterol Recommendations: LDL-C at any intake level.[24, 25], and the elderly [28, 29] have clearly demonstrated individuals had no changes inthat although dietary cholesterol provided by eggs signifi- Does the Evidence Support a LimitHDL-C was significantly increased for all groups In contrast, of 300 mg/d?cantly increases LDL-C in one third of the population, those even after the consumption of only 2 eggs per day. Theseindividuals considered hyper-responders to & a cholesterol Maria Luz Fernandez Mariana Calle studies suggest that dietary management of OIR individualschallenge exhibit increases in both LDL-C and HDL-C, with need not include restrictions on eggs.Table 2 Changes in LDL-C, HDL-C, LDL size, and HDL size as a response to dietary cholesterol provided by eggs in various populations Published online: 4 August 2010 # Springer Science+Business Media, LLC 2010Population Duration Additional dietary cholesterol LDL-C HDL-C LDL-C/HDL-C ratio LDL size HDL sizeChildren (n=54) [27] 4 Abstract The mg/d wk 518 perceived association between Increase Introduction No change dietary cho- Increase Increase ND lesterol (DC) and risk for coronary heart disease (CHD) hasWomen (n=51) [25] 4 resulted in recommendations of no more than 300 mg/d for Increase wk 640 mg/d Increase The AmericanNo change Heart Association (AHA)Increase recommends ND noMen (n=28) [32••] 12 healthy 640 mg/d the United States. These change Increase 300 Decrease wk persons in No dietary more than mg/d of dietary cholesterolIncrease healthy (DC) for Increase recommendations proposed in the 1960s had little scientificMen/women (n=42) [34] 12 wk 215 mg/d No change Increaseto prevent change risk for coronary heart disease persons No increased Increase Increase evidence other than the known association between (CHD) [1]. These recommendations are mostly based onMen/women (n=34) [28] 4 saturated640 and cholesterol and animal studies where Increase wk fat mg/d Increase No change Increase Increase the presence of both saturated fat and cholesterol in manyMen/women (n=56) [35•] 12 wk 250 mg/d No normal foods and onDecrease cholesterol was fed in amounts far exceeding change Increase data derived from animal studies where ND ND intakes. In contrast, European countries, Asian countries, supraphysiologic doses of cholesterol, ranging from theMen/women (n=45) [33•] 12 and Canada do not have an upper limit for DC. change No changeof 1,000 mg to 20,000 mg/d for humans, were wk 400 mg/d No Further, equivalent No change ND ND current epidemiologic data have clearly demonstrated that fed in order to produce atherosclerosis [2].HDL-C high-density lipoprotein increasing concentrations of DC arelipoprotein cholesterol; ND not determined. that many other countries do not cholesterol; LDL-C low-density not correlated with It is important to note increased risk for CHD. Clinical studies have shown that have the same guidelines for DC. Canada [3••], Korea [4•], even if DC may increase plasma low-density lipoprotein New Zealand [5], and India [6], for example, do not set an (LDL) cholesterol in certain individuals (hyper-responders), upper limit for DC, focusing instead on controlling the this is always accompanied by increases in high-density intake of saturated fat and trans fat, which are the major lipoprotein (HDL) cholesterol, so the LDL/HDL cholesterol determinants of blood cholesterol concentrations. Similarly, ratio is maintained. More importantly, DC reduces circu- the European guidelines on cardiovascular disease preven- lating levels of small, dense LDL particles, a well-defined tion have the following recommendations regarding healthy risk factor for CHD. This article presents recent evidence food choices: “consume a wide variety of foods, adjust from human studies documenting the lack of effect of DC energy intake to maintain a healthy weight, encourage on CHD risk, suggesting that guidelines for DC should be consumption of fruits and vegetables, replace saturated fat revisited. with mono or polyunsaturated fatty acids and reduce salt intake” [7]. In contrast to US policies, Europeans have no Keywords Dietary cholesterol . LDL cholesterol . dietary guidelines for DC [7]. A summary of the dietary
    • LDL PEQUENAS E DENSAS ü  sdLDL: ü  Tamanho da partícula < 25.5nm ü  Densidade > 1.04g/ml ü  Aumenta significativamente o risco de DCV ü  TG elevados e HDL-C baixo é um bom preditor de sdLDL Griffin BA. Proc Nutr Soc 1999;58:163-69
    • Cordain, 2009FLUXO DE LDL PARA A INTIMA É > PARA LDL PEQUENAS E DENSASUMA VEZ NA INTIMA, LDL PEQUENAS E DENSAS SÃO SUSCEPTÍVEIS DE SOFREROXIDAÇÃO41
    • •  1. Célulasespumosas
    • 214 Esrey et al.TABLE 3. Cox regression estimates of the effect of dietary intake measured at baseline on coronary heart disease death among3925 men and women 30 to 59 years of age after 12.4 years foIIow-up in the North American Lipid Research Clinics PrevalenceFoIIow-Up Study Model 3 Model 1 Modei 2 (adjusted for age, sex, (adjusted for age, sex, (adjusted for age, sex, energy intake, serum lipids, energy intake) energy intake, serum lipids”) and other risk factorsb)Variable Estimate RR (95% CI) Estimate RR (95% CI) Estimate RR (95% CI)% Fat Total 0.044" 1.04 (1.01-1.08) 0.043" 1.04 (1.01-1.08) 0.043 1.04 (l.Ol-1.08) Saturated 0.104” 1.11 (1.04-1.18) 0.095" 1.10 (1.03-1.17) 0.103" 1.11 (1.04-1.18) Monounsaturated 0.095" 1.10 (1.03-1.17) 0.094 l 1.10 (1.03-1.18) 0.080 1.08 (1.01-1.16) Polyunsaturated -0.040 0.96 (0.88-1.05) -0.027 0.97 (0.89-1.07) -0.014 0.99 (0.90-1.08)% Carbohydrate -0.034" 0.97 (0.94-0.99) -0.040" 0.96 (0.93-0.99) -0.036 0.96 (0.94-0.99)% Protein 0.020 1.02 (0.97-1.08) 0.013 1.01 (0.96-1.07) 0.011 1.01 (0.95-1.07)% Alcohol + alcohol’ -0.019 0.98 (0.92-1.05) 0.001 1.00 (0.94-1.06) 0.0001 1.00 (0.95-1.07)Cholesterol (10 mg) per 5000 kJ 0.004 1.00 (0.99-1.02) 0.006 1.01 (0.99-1.02) 0.004 1.00 (0.99-1.02)?Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins. bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m*), and glucoseintolerance (present/absent). ‘p < 0.05.
    • ?Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins. bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m*), and glucoseintolerance (present/absent). ‘p < 0.05. “p < 0.01. RR = Relative risk for coronary heart disease mortality, defined as exp(@, associated with a I+unit increase in the dietary variable; 95% CI = 95% confidenceinterval, defined as exp@ 2 1.96 SE)(z, - q), where SE is the standard error of /3, and 7, and Q represent the two levels of the dietary variable beingcompared; % =percentage of total energy provided by the dietary variable.(total cholesterol and HDL) were added to the regression model and none approached statistical significance. The magnitude and direc-(model 2), the estimated relative risks for the dietary variables re- tion of some estimates changed between the three models evaluated,mained stable. The magnitudes of these relationships were also unaf- but within a small range. When a quadratic alcohol term was includedfected by the addition of other known coronary risk factors (model 3). in the Cox model, percentage of energy intake as alcohol was signifi- cantly associated with risk of coronary disease death within this older Among the older age group, no relationships between dietary fat or age group.its fatty acid components, carbohydrate, or protein, and coronary heart None of the dietary components examined were significantly associ-disease death were identified (Table 4). The estimares of the regression ated with total mortality within either the young or the older agecoefficients were al1 smaller than those among the younger age group groups.TABLE 4. Cox regression estimates of the effect of dietary intake measured at baseline on coronary heart disease death among621 men and women 60 to 79 years of age after 12.4 years follow-up in the North American Lipid Research Clinics PrevalenceFollow-Up Study Model 3 Model 1 Model 2 (adjusted for age, sex, (adjusted for age, sex, (adjusted for age, sex, energy intake, serum lipids, energy intake) energy intake, serum lipids”) and other risk factorsb)Variable Estimate RR (95% CI) Estimate RR (95% CI) Estimate RR (95% CI)% Fat Total -0.0004 1.00 (0.96-1.04) -0.002 1.00 (0.96-1.04) -0.011 0.99 (0.95-1.03) Saturated -0.031 0.97 (0.89-1.05) -0.026 0.97 (0.90-1.06) -0.038 0.96 (0.88-1.05) Monounsaturated 0.025 1.03 (0.95-1.11) 0.019 1.02 (0.94-l. 11) -0.005 1.00 (0.91-1.08) Polyunsaturated 0.006 1.01 (0.91-1.11) -0.004 1.00 (0.90-l. 10) -0.004 1.00 (0.90-1.10)% Carbohydrate 0.004 1.00 (0.97-1.04) 0.003 1.00 (0.97-1.04) 0.016 1.02 (0.98-1.05)% Protein 0.017 1.02 (0.94-l. 10) 0.015 1.02 (0.94-1.10) 0.0002 1.00 (0.93-1.08)% Alcohol + alcohol’ -0.114" 0.89 (0.84-0.94) -0.116** 0.89 (0.83-0.95) -0.124” 0.88 (0.83-0.95)Cholesterol (10 mg) per 5000 kJ 0.011 1.01 (0.99-1.03) 0.011 1.01 (0.99-1.03) 0.006 1.01 (0.98-1.03)“Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins. bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m’), and glucoseintolerance foresent/absent).
    • 37,851 H seguidos por 8 anos 80.082 M seguidas por 14 anosBaseado em Hu Fb, et al. JAMA. 1999;281:1387-1394 e adaptado por Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
    • Egg consumption and coronary heart disease 925 Table 3. Coronary heart disease incidence according to egg consumption categories in the Japan Public Health Center-based prospective study (Hazard ratios (HR) and 95 % CI) , 1 d/week 1 – 2 d/week 3 – 4 d/week Almost daily Egg consumption. . . HR 95 % CI HR 95 % CI HR 95 % CI HR 95 % CI Trend P Subjects at risk* (n) 10 491 20 802 31 182 28 260 Person-years 96 748 213 907 323 856 292 858 CHD incidence Cases† (n) 64 110 147 141 Men (%) 72 84 76 81 Incidence (per 1000 person-years) 0·66 0·51 0·45 0·48 Age and sex-adjusted HR 1·28 0·95, 1·72 1·11 0·86, 1·42 1·01 0·80, 1·27 1 – 0·11 Multivariate-adjusted HR‡ 1·19 0·86, 1·64 1·00 0·77, 1·30 1·00 0·79, 1·26 1 – 0·45 * Total number of subjects was 90 735. † Subtotal of subjects was 462. ‡ Multivariate Cox analysis adjusted for age, sex, BMI, hypertension, diabetes, use of cholesterol-lowering drugs, smoking (never, ex-, and current smoker), alcohol drinking (six categories), whether or not intended to avoid cholesterol-rich diets, consumption frequencies of meat, fish, vegetables, fruits, and cohort effects.P¼0·45), analyses excluding those who were taking compared with those with total cholesterol concentrationcholesterol-lowering drugs or those with total cholesterol con- ,1800 mg/l; trend P¼0·0018).centration $ 2200 mg/l (trend P¼0·72), analyses using quan-titative variables (cholesterol and systolic blood pressure) in Discussion
    • 266 CG Scrafford et al.Table 2 Egg consumption and mortality from CHD in NHANES III mortality follow-up Egg consumption ,1 egg EO/week $1 to ,7 egg EO/week $7 egg EO/weekMen Deaths from CHD (person-years) 53 (17 597) 106 (34 060) 39 (7877) Egg EO per week (range) 0?27 (0–0?7) 1?93 (1–6?5) 7?54 (7–49?7) HR HR 95 % CI HR 95 % CI Model 1 1?00 1?44 0?89, 2?33 1?60 0?94, 2?72 Model 2 1?00 1?34 0?82, 2?18 1?25 0?70, 2?22 Model 3 1?00 1?26 0?79, 2?00 1?13 0?61, 2?11 Model 4 1?00 1?38 0?85, 2?24 1?38 0?84, 2?26Women Deaths from CHD (person-years) 72 (28 626) 74 (35 871) 22 (5770) Egg EO per week (range) 0?24 (0–0?7) 1?79 (1–6?3) 7?41 (7–35?5) HR HR 95 % CI HR 95 % CI Model 1 1?00 1?06 0?71, 1?57 0?96 0?38, 2?46 Model 2 1?00 1?12 0?71, 1?75 0?81 0?27, 2?47 Model 3 1?00 1?12 0?66, 1?89 0?92 0?27, 3?11 Model 4 1?00 1?06 0?67, 1?68 0?78 0?26, 2?30NHANES III, Third National Health and Nutrition Examination Survey 1988–1994; EO, eating occasion; HR, hazard ratio; WHR, waist-to-hip ratio.Model 1: Age and energy.Model 2: Age, energy, marital status, educational status, race/ethnicity, smoking status, BMI, WHR, hypertension, diabetes.Model 3: Age, energy, marital status, educational status, race/ethnicity, smoking status, BMI, WHR, diabetes, hypertension and dietary variables.Model 4: Men – age, energy, marital status, race/ethnicity, BMI, diabetes, hypertension and alcohol intake.Model 4: Women – age, energy, marital status, educational status, race/ethnicity, WHR, diabetes, hypertension and vitamin E.Table 3 Egg consumption and mortality from stroke in NHANES III mortality follow-up
    • NUTRITION MYTHS
    • REDUZIR GORDURA DIETÉTICA DIMINUI RISCO DE DCV
    • “DIMINUIR GORDURA REDUZ O RISCO CARDIOVASCULAR”
    • lly twelve volunteers composite samples taken from each menu once during the s unable to complete study for both the stabilization diet and intervention diets.en complete physical The results for the seven composite samples were averagedwithin -10 to +20 per- to find the actual composition of the diets. No alcohol was in- tropolitan Life Insur-values from the 1983 TABLE 1r chronic disease was Composition of HNS*27 Diets, Proximal Analysis a on was not an exclu- Low-fat diets High-fat dietscruited tended to have (% of total calories) e for men in this age Target Target nsumption, and evi- Measured value Measured valuesionary. Macronutrient energyeers were confined to distribution Protein 15.9 16.0 15.7 16.0 tern Human Nutrition Fat 22.2 20.0 38.7 40.0 or the duration of the Carbohydrate 61.9 64.0 45.7 44.0 onfines of the Nutri- Cholesterol content sed outings, they had (mean, mg/day) -- 360 -- 360 cept that provided by Fatty acid energy distribution rotocol was, of neces- Saturated 6.4 5 10.6 10 was monitored, por- Monounsaturated 9.2 10 15.5 20 required to consume Polyunsaturated 6.6 5 12.6 10heir meals. (A rubber P/S ratio 1.0 1.0 1.2 1.0 ood was scraped from ap/s, polyunsaturated/saturated; HNS-2 7 diet. Nelson GJ, Schmidt PC, Kelley DS. Lipids. 1995 Nov;30(11):969-76
    • dicated an increase in the plasma very low density lipopro- factory because the conditions of this experiment were ca n (VLDL) level and a decrease in both the plasma HDL and fully controlled and the statistical power of the protocol wDL levels. Thus, the total cholesterol level remained con- excellent. nt because the increase in plasma VLDL cholesterol com- (ii) The average cholesterol level in the subjects was consated for the reduction in HDL-cholesterol and LDL-cho- siderably below that in the European and American popu terol. Because of individual variations, the standard devia- tions used to develop the Keys et aL (5) and Hegsted et al. TABLE 6 High- and Low-Fat Diets, Blood Cholesterol, Triglycerides, and Lipoprotein Values Total HDL- LDL- cholesterol Triglycerides cholesterol cholesterol Period Diet mean + SD mean _+ SD mean • SD mean • SD Entry A d libitum 176.3 + 33.1 85.8 + 28.4 46.3 _+ 14.0 112.8 • 26.8 Stabilization High-fat 172.5 + 30.3 75.3 • 46.4 44.8 • 11.6 112.6 • 21.9 Intervention Low-fat 173.2 _+27.3 91.5 • 38.0 40.5 • 12.4 114.5 • 21.3 Intervention High-fat 176.9 _+ 32.9 66.4 • 41.7 43.2 + 13.4 119.5 _+24.3 Paired t-test, Pvalues a 0.425 0.002 0.258 0.238 ~lhe t-test compares only the values at the end of the high- or low-fat diets with the values obtained at the end of the stabi- lization period, study day 20. Groups A and B values were taken at study day 70 and day 120, depending on the leg of the intervention diet for the each group; HDL, high density lipoprotein; LDL, low density lipoprotein. Lipids, Vol. 30, no. 11 (19 Nelson GJ, Schmidt PC, Kelley DS. Lipids. 1995 Nov;30(11):969-76
    • ENTRE 1968-1978, NA GRONELÂNDIA ü  Nenhum caso de morte por DAC ü  Nenhum caso de enfarte agudo do miocardio (População = 2,600) Bang HO, Dyerberg J. Adv Nutr Res 1980 3:1-22.
    • ALIMENTOS VEGETAIS / ANIMAIS EM 13 SOCIEDADES PRIMITIVAS! Cordain L et al. Eur J Clin Nutr 2002; 56 (suppl 1):S42-S52. !
    • misnomer. The countries around the Mediterranean basin have differe differ in the amount of total fat, olive oil, type of meat andamount of total fat, olivemilk vs. cheese;intake; differ in the wine intake; oil, type of meat and wine frui the rates of coronary heart disease and cancer, with the lower death ra the rates of coronary heart disease and cancer, with the lower death rates andof Greece (the diet e Greece. Extensive studies on the traditional diet longer life be The Greece. Extensive studies on So Special about the ofGreece (the high intake of fruits, vegetables (particularly wildt Mediterranean Diets: What Is the traditional diet ofDiet of Greece? before 1960) indicate Greeks consists of a diet 1 of sourdough bread rather than pasta; more olive oil and olives; less m The Scientific Evidence of Greeks consists of a high intake of fruits, vegetables (particularly wild plants), nuts and cer and moderate amounts of wine, more so than other Mediterranean coun diet of Crete shows a number of protective substances, such as s of sourdough bread rather than pasta; more olive oil and olives; less(EFA), high amounts of fiber, antioxid Artemis P. Simopoulos2 (n-6):(n-3) essential fatty acids milk but more cheese polyphenols from olive oil), vitamins E and C, some of which have been and Center for Genetics, Nutrition and Health, Washington, DCthan othercancer, including cancer ofcountries. Analyses of th The moderate amounts of wine, more so Mediterranean the breast. These findings should serve intervention trials that will test the effect of specific dietary patterns in t diet of Crete shows a diet,” implying that all Mediterranean people with cancer. J. diet, is131:as selenium, glutathione ABSTRACT The term “Mediterranean number of protective substances, sucha 3065S–3073S, 2001. have the same Nutr. (n-6):(n-3) countries around the Mediterranean basin have different diets, religions andWORDS: Their antioxidants (especially resv misnomer. The essential fatty acids (EFA), high amounts of fiber, diets KEY cultures. diet of Crete (n-3) fatty acids c wild plants c a c c differ in the amount of total fat, olive oil, type of meat and wine intake; milk vs. cheese; fruits and vegetables; and polyphenols from olive oil), vitamins E and C, some of which have been shown to be assoc the rates of coronary heart disease and cancer, with the lower death rates and longer life expectancy occurring in The health of thedietary pattern the population in general individual and intake and cancer, including the traditionalvegetables (particularly wild These indicate that the should serve as aa strong incenti of Greeks consists of a high intake of fruits, of the breast. plants),is thefindings Greece. Extensive studies on cancer diet of Greece (the diet before 1960) and cereals mostly in the form genetics and number of diet” is a m nuts result of interactions between intervention trials that will testoil and olives; less of specificofdietarypattern of the an in the prevention but in facb of sourdough bread rather than pasta; more olive the effect milk but environmentalmore fish; less meat; more cheese; factors. Nutrition is major importance (1– patterns environmental factor of and moderate amounts of wine, more so than other Mediterranean countries. Analyses the dietary 4). Our genetic profile has not changed and m surprising Downloaded from jn.nutrition.org by on September 27, 2006 withofcancer. a number of protective substances, such as selenium, glutathione, a balanced ratio energy expenditure and phys- and diets. diet Crete shows J. Nutr. 131: 3065S–3073S, 2001. our food supply and in over the past 10,000 y, whereasofmajor changes have taken place in sin have d (n-6):(n-3) essential fatty acids (EFA), high amounts of fiber, antioxidants (especially resveratrol from wine and ical activity (5–17). Today industrialized societies are charac- polyphenols from olive oil), vitamins E and C, some of which have been shown to be associated with lower risk of Muslims d cancer, including cancer of the breast. These findings should serve as a strong incentivefollowing: 1) an increase in energy intake and terized by the for the initiation of drinks, wh KEY WORDS: diet of Crete (n-3) fatty acids wild plants intervention trials that will test the effect of specific dietary patterns in the prevention and management of patientsan c c c decrease in energy expenditure; 2) c increase in saturated fat, antioxidants canc c eat meat o with cancer. J. Nutr. 131: 3065S–3073S, 2001. (n-6) fatty acids and trans fatty acids and a decrease in (n-3) on. Althou fatty acid intake; 3) a decrease in complex carbohydrates and usually con KEY WORDS: diet of Crete (n-3) fatty acids wild plants antioxidants c cancer c (n-6) fattyin cereal grains and a decrease in fiber intake; 4) an increase acids (14.0 –18.0 The health of the individual and the population infruit andand calcium intakeand 5) a decreasehealth anti- general intake; (5–17). Furthermore, the ratio of intake and in protein, status. Ther c c c c vegetable Crete have oxidantis the the result of of the individual and the betweengeneral intakeisand a numberisof fattythe term 16.74:1, whereas during evolutionThere is n is result of interactions population number of diet” a misnomer. There(n-3) just acidsMediterranean diet The health interactions between genetics and a in genetics and health (n-6) to status. Therefore, not diet” is a misnomer. is “Mediterranean oneFig. 1). 1930 (19). as low a de Nutrition not changed but in fact manyit Mediterranean 1, butwhich not environmental factors. Nutrition is an major importance (1– 4). Our profile has was 2–1:1 (Tableenvironmental factors.genetic environmental an environmental factor of diets (18), the in isfact many Mediterran is factor of Recent investigations of dietary patterns and health United Na was 11.3–1 surprising becausestatus of the countries surrounding the ba- the countries along the Mediterranean Mediterranean basinmajor importancey,(1– 4). Our genetic profile hasdifferentchanged majorandsurprisingthem in both dietary countrie over the past 10,000 whereas major changes have taken sin have not clearly indicate religions, economic differences among because the cultural traditions ;10.6 in 1 place in our food supply and in energy expenditure and phys-over ical activity (5–17). Today industrialized societies are charac- changes have pork or drink wine and other alcoholic the past 10,000 y, whereas major Muslims do not eat taken and diets. Diets are influenced by religious habits, that is, sin have different religions, ec almost thr United Staplacedecrease in energy expenditure; 2) an increase inenergy expenditureWednesdays and Fridays but andwine, and so Diets are influence in our food supply and in saturated fat, eat meat on terized by the following: 1) an increase in energy intake and drinks, whereasand phys- populations usually do not Greek Orthodox drink diets. 1 Presented as part of the 11th Annual Research Conference on Diet, Nutrition and Cancer held in Washington, DC, July 16 –17, 2001. This conference was the traditio tries Studyical activity (5–17). Today industrialized on. Although Greece and the (n-6) fatty acids and trans fatty acids and a decrease in (n-3) societies are charac- Mediterranean countries are fatty acid intake; 3) a decrease in complex carbohydrates and Muslims do not eat pork or d sponsored by the American Institute for Cancer Research and was supported by the California Dried Plum Board, The Campbell Soup Company, General Mills, vascular di usually considered to be areas of medium-high death rates (United Stterized by thean increase in cereal1) an increase in (14.0 –18.0 per 1000 inhabitants), death rates on the island of fiber intake; 4) following: grains and a decrease in energy intake and Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. Guest drinks, whereas Greek Orthod editors for this symposium publication were Ritva R. Butrum and Helen A. goslavia, Ja fruit and vegetable intake; and 5) a decrease in protein, anti- Norman, American Institute for Cancer Research, Washington, DC.decrease in energy expenditure; 2)the ratio of 1930 (19). No other area in the Mediterranean basin has had Wednesdays and oxidant and calcium intake (5–17). Furthermore, an increase Cretein saturated fat, continuously since before have been below this level eat meat on 2 To whom correspondence should be addressed. E-mail: cgnh@bellatlantic.net order of 5- the field w(n-6) fatty acidsacids isIETÉTICA: during evolutionENERGIA TrateinCrete, according to data compiled by the (n-6) to (n-3) fatty GORDURA D and16.74:1, whereas 37% DA aasdecrease as (n-3) it was 2–1:1 (Table 1, Fig. 1).trans fatty acids and low a death OTAL CONSUMIDA Although Greece and th on. United Nations in their demographic yearbook for 1948. Nutritional Sciences. Itfatty status of intake; 3) the dietary Mediterranean basin was 11.3–13.7 per0022-3166/01 $3.00 © beforeusually IIforand acid the countries surrounding the patterns complex carbohydratesinhabitants 2001 American Society considered to be area Recent investigations ofa decrease inand health 1000 and World Warfiber clearly indicate major differences among in cereal grains;10.6 ina decrease Cancer and heart disease in the per 1000 inhabitan intake; 4) an increase them in both dietary almost three times as(19). indeaths proportionally caused and 1946 –1948 many (14.0 –18.0 3065Sfruit and vegetable intake; and 5) a decrease in protein,Greece before 1960.Crete have been below this l anti- United States as in Crete (19). The diet of Crete represents the traditional diet of The Seven Coun-oxidant and calcium intake (5–17). Furthermore, was theratio establish credible data on cardio- tries Study the first to of 1 Presented as part of the 11th Annual Research Conference on Diet, Nutrition and Cancer held in Washington, DC, July 16 –17, 2001. This conference was sponsored by the American Institute for Cancer Research and was supported by 1930 (19). No other area in th(n-6) to (n-3) fatty acids is 16.74:1, whereas during evolution in contrasting populations vascular disease prevalence rates the California Dried Plum Board, The Campbell Soup Company, General Mills, goslavia, Japan and Greece), with differences low a death rate as Crete, acc as found on the (United States, Finland, The Netherlands, Italy, former Yu- Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. Guestit was 2–1:1 (Table 1, Fig. 1). editors for this symposium publication were Ritva R. Butrum and Helen A. United Nations in their demo Norman, American Institute for Cancer Research, Washington, DC. 2 To whom correspondence should be addressed. order of 5- to 10-fold in coronary heart disease (20). In 1958,
    • n’s Health Initiative Randomized ControlledHealth Initiative Randomized Controlledcation TrialTrial epidemiologic studies and some trials have linked diet with car-dification Multiple Context diovascular disease (CVD) prevention, but long-term intervention data are needed. Linda Objective To test the hypothesis thatsome trials have linked diet with car- diet be low in Context Multiple epidemiologic studies andstudies and intervention, intended to with car- Context Multiple epidemiologic a dietary some trials have linkedHsia, MD; fat and high in vegetables, fruits, but long-term intervention data are needed. D; diovascular disease (CVD) prevention, and grains to long-term intervention data are CVD risk. . diovascular disease (CVD) prevention, but reduce cancer, would reduce needed.L.arcia L. D; Design, Setting, To test the hypothesis that a dietary intervention, trial of 48 835low in Objective and Participants Randomized controlled intended Objective To test the hypothesis that a dietary intervention, intended to be low in to be post- s; H. Lewis H. menopausal women aged 50 tograins to reduce cancer, would reduce would reduce CVD risk. fat and highand high in vegetables, fruits, and grains to reduce cancer, CVD risk. fat in vegetables, fruits, and 79 years, of diverse backgrounds and ethnicities, who PhD; , PhDDesign,Design, Setting, and Participants Randomized controlled trial ofWomenpost- Croix participated in the Women’s Health Initiative controlled trial of 48 835 Trial. 48 835 were ; Setting, and Participants Randomized Dietary Modification post- menopausal women aged 50 to 79 years, of diverse541 [40%])and ethnicities, whogroup (29 294 L. menopausal to an aged 50 to 79(19 backgroundsbackgrounds orman L. randomly assignedwomeninterventionDietary Modification Trial. Womenand ethnicities, who years, of diverse or comparison s, MD; ;L. [60%]) participated in the Women’s(19 541 [40%]) orDietary Modification were Women were participated in the Women’s Health Initiative in a free-living setting. Study enrollment occurred between Trial. and 1998 in randomly assigned to an intervention Health Initiative comparison group (291993 294 40 US clinical centers; mean follow-up in this 541 [40%]) or8.1 years. in group (29 294 randomly assigned to an intervention (19 analysis was comparison Karen L. [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998MD; .ysiw 40 US clinical centers; mean follow-up in Study enrollment occurred between 1993 and 1998 in [60%]) in a free-living setting.D; , MD; Intervention Intensive behavior this analysis this in group and individual sessions de- was 8.1 years. modification analysis was 8.1 years. 40 US clinical centers; mean follow-up inPhD; M. signed to reduce total fat intake to 20% of calories and increase intakes of vegetables/ inda Intervention Intensive behavior modification in group and individual sessions de-Perri, PhD;fruits toInterventionand grains behavior modification inintakescomparison group received signed to5 servings/d intake to 20% of calories and increase group of vegetables/ sessions de- reduce total fat Intensive to at least 6 servings/d. The and individual D; L. oss fruits to 5 servings/d and grains to at intake servings/d. The comparison group received of vegetables/ signed to reduce total fat least 6 to 20% of calories and increase intakes diet-related education materials. bins, MD; diet-related education materials. fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received RISCO 0% 5% 10% 15% 20% 25% DAC Total DCV RELATIVO E. nda G. E. Main Outcome Measures Fatal and nonfatal coronary heart disease (CHD), fatal (CHD), fatal GloriaG. Main Outcome Measures Fatal and nonfatal coronary heart disease Linda diet-related education materials. PhD;ns, MD; ;Linda G.nonfatal stroke, andand CVD (composite of CHD and stroke). disease (CHD), fatal z, PhD and nonfatal Outcome Measures Fatal and nonfatal coronary heart and Main stroke, CVD (composite of CHD and stroke). Stevens, PhD; Resultsand nonfatal stroke, and CVD (composite of CHD and stroke). intake Results By year 6, mean fat intakeintake decreased byenergy intake in the inter- in the inter- By year 6, mean fat decreased by 8.2% of 8.2% of energy DrPH; PH; aurizioouise R. ventionvs(3.3%),comparisonmean fatwith fat; increases occurred inof energy veg- in monoun- vention the comparison group, with small decreases in saturated (2.9%), monoun- saturated Results By year 6, group, intake decreased by 8.2% vs the and polyunsaturated (1.5%) small decreases in saturated (2.9%), the inter- intakes of intake tolins, DrPH;se ;R. D saturated (3.3%),the comparison group, with small decreases in saturated (2.9%), monoun- vention vs and polyunsaturated (1.5%) fat; increases occurred in intakes of veg- ; Annlouiseetables/fruits (1.1(3.3%), and grains grains (0.5 serving/d). Low-density lipoprotein cholesterol etables/fruits (1.1 servings/d) R. (0.5 serving/d). Low-density lipoprotein cholesterolenry R. levels, diastolic blood pressure, and factor VIIc levels(1.5%) fat; increases occurred in intakes of veg- saturated servings/d) polyunsaturated were significantly reduced by 3.55 and and ord,; MD; y R. PhD mg/dL, 0.31 mm Hg, and 4.29%, respectively; levels serving/d). Low-density lipoprotein cholesterol etables/fruits (1.1 servings/d) and grains (0.5 levels were lipoprotein cho- levels, diastolic blood pressure, and factor VIIcof high-densitysignificantly reduced by 3.55 D; ; Henry mg/dL, triglycerides,Hg,blood 4.29%, respectively; levels of in the intervention hD R. lesterol, levels, mm glucose, and insulin did not significantly differ high-density lipoprotein 3.55 0.31 diastolic and pressure, and factor VIIc levels were significantly reduced by cho-unner, PhD;vs comparison groups. mm numbers who developed CHD, stroke, of high-density lipoprotein cho- ski, MD; ette; MD lesterol,mg/dL, 0.31 The Hg, and BV, et al. JAMA. 2006 Febsignificantly differ in the intervention Howard 4.29%, respectively; levels and triglycerides, glucose, and insulin did not 8;295(6):655-66CVD (annual- , MD; , vs comparison groups. 1000glucose, and insulin(0.88%) 1357 (0.86%)differ in the intervention hlebowski MD; lesterol, triglycerides, (0.63%), 434 (0.28%), and significantly in the in- ized incidence rates) were did not The numbersand 2088 developed CHD, stroke,and CVD (annual- tervention and 1549 (0.65%), 642 (0.27%), who developed the comparison group. CVD (annual- in CHD, stroke, and vs comparison groups. The numbers who
    • RISCO RELATIVO25% EM MULHERES QUE TINHAM DCV20%15% RISCO 0% 5% 10% 15% 20% 25% DAC Total DCV RELATIVO10%5%0% DAC Total DCV Howard BV, et al. JAMA. 2006 Feb 8;295(6):655-66
    • DIMINUIÇÃO DA GORDURA TOTAL DE 35% PARA 32.3% AUMENTO DO RÁCIO PUFA/ SAFA EM 100%Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.
    • ÁCIDOS GORDOS SATURADOSUSDA, AHA: < 10% DO TOTAL CALÓRICO Dietary Guidelines for Americans, USDA, 2010
    • Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55
    • SAFA EM ALGUNS ALIMENTOS Alimento AG Saturados AG AG AG AG (100 g) (g) Laúrico Mirístico Palmitico Esteárico 12:0 14:0 16:0 18:0 Manteiga 51 3 7 2 10 Óleo de 86,5 44,6 16,8 8,2 2,8 Coco Cacau 8,07 0 0,02 3,69 4,25 Óleo de 49,3 0,1 1 43,496 4,3 palma Leite gordo 1,865 0,077 0,297 0,829 0,36567 Fonte: USDA food database
    • Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55
    • Based on Evolutionary, Historical, Dietary Fat Quality and Coronary HeartGlobal, and Modern ed Theory Disease Prevention: A Unifi PerspectivesChristopher E.on Evolutionary, Historical, Based Ramsden, MD Global, and Modern PerspectivesKeturah R. Faurot, PA, MPHPedro ChristopherFaurot, PA, MPH Carrera-Bastos, MD Keturah R. E. Ramsden, BALoren Pedro Carrera-Bastos, BA Cordain, PhD Loren Cordain, PhDMichel De De Lorgeril, MD, PhD PhD Michel Lorgeril, MD,Laurence S. Sperling, MD Laurence S. Sperling, MD Corresponding authorCorresponding author Christopher E. Ramsden, MD Department of Physical Medicine and Rehabilitation, Program onChristopher E. Ramsden,University of North Carolina–Chapel Hill School Integrative Medicine, MDDepartment Medicine, CB# 7200, Chapel Hill, and Rehabilitation, Program on of of Physical Medicine NC 27599, USA. E-mail: cramsden@med.unc.eduIntegrative Current Treatment Options in Cardiovascular Medicine 2009, 11:289–301Hill School Medicine, University of North Carolina–Chapelof Medicine, CB# 7200, Chapel Hill, NC 27599, USA. Current Medicine Group LLC ISSN 1092-8464 Copyright © 2009 by Current Medicine Group LLCE-mail: cramsden@med.unc.eduCurrent Treatmentstatement in Cardiovascular Medicine 2009, 11:289–301 Opinion OptionsCurrent Medicine and growing body of evidence indicates that dietary fatty acids regulate A large Group LLC ISSN 1092-8464Copyright © 2009 by Current Medicine in the pathogenesis of coronary heart disease crucial metabolic processes involved Group LLC (CHD). Despite this evidence, optimal dietary fatty acid intakes for CHD preven- tion remain unclear. Significant gaps in the modern nutrition literature and contra- dictions in its interpretation have precluded broad consensus. These shortcomingsOpinion statement can be addressed through the incorporation of evolutionary, historical, and global perspectives. The objective of this review is to propose a unified theory of optimal A large and growing bodyCHD evidence indicates that dietary fatty acids regulate dietary fatty acid intake for of prevention that integrates critical insights from evolutionary, historical, global, and modern perspectives. This broad approach may crucial metabolic processesmethods to characterize optimal fatty acid intakes. coronary heart disease be more likely than previous involved in the pathogenesis of (CHD). Despite this evidence, optimal dietary fatty acid intakes for CHD preven- tion remain unclear. Significant gaps in the modern nutrition literature and contra- Introduction dictions Coronaryinterpretation have precluded broad consensus. Thesewith increasing dura- in its heart disease (CHD) incidence and mor- resident inhabitants, especially shortcomings can be addressed through the incorporation tion of residence [5–7]. tality reflect complex interactions between genetic of evolutionary, historical, and global susceptibilities and environmental factors. Although For instance, CHD is historically far more common in perspectives. CHD susceptibility genesthis review is to the United States unified theory of men of Japa- several The objective of have been identified propose a than in Japan [4]. Among optimal dietary fattyrather lines genetics is the main driver environ- nese ancestry,highestriskCaliforniain[8,9]. These differences ment acid intake for CHD prevention Hawaii,integrates is lowest Japan, intermediate in [1], several than of evidence indicate that of CHD that and CHD in critical insights from evolutionary, historical, global,CHD incidence and appear to reflect This broad of traditional Japanese risk [2]. Globally, age-adjusted and modern perspectives. the replacement approach may be moremortality vary as previous factors arepopulations cultural traditions with Western acid [8]. Indeed, Japa- likely than much as 10-fold across sensitive to nese Americans who maintained habits intakes. and [3,4]. CHD incidence and risk methods to characterize optimal fatty traditional customs lifestyle changes. When immigrants from traditionally habits had a CHD risk similar to that of their counterparts low-risk regions adopt the habits of high-risk popula- residing in Japan, whereas those who adopted Western cul- tions, their CHD incidence rises to approach that of ture had a three- to fivefold excess in CHD prevalence [8]. Introduction
    • CHINA RURAL: < 5% EUA: 11-12% CRS: 4-18%KITAVA: 17% MAASAI: 30-35% TOKELAU: 40%
    • A meta-analysis of prospective epidemiologicstudies showed that there is no significantevidence for concluding that dietarysaturated fat is associated with anincreased risk of CHD or CVD.
    • NUTRITION MYTHS
    • ÓLEOS VEGETAIS RICOS EM ÓMEGA-6 DIMINUEM O RISCO DE DCV
    • with omega-6 PUFAs on follow that decreasing omega-6 levels will do the same.re present for each trial, Indeed, the evidence considered here suggests that it would es and the observationalcing saturated fatty acid have the opposite AHA Science Advisory PUFA intakes effect. Higher omega-6 ars, white bread, white can inhibit the conversion of ␣-linolenic acid to eicosa-As reduces CHD risk. On pentaenoic Fatty 79 but and Risk for Cardiovascular Disease Omega-6 acid, Acids such conversion is already quite A Science Advisory From the American Heart Association Nutrition a-6 PUFAs used in the low,80 and whether additional Nutrition, Physical would have Subcommittee of the Council on small changes Activity, and ies, and nonhuman pri- net effects on Council on Cardiovascular other benefits of on Metabolism; CHD risk after the Nursing; and Council LA Epidemiology and Prevention eductions in CHD risk consumption are taken into account is not clear. The focus William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, MD, DrPH, FAHA;PUFA intakes of 10% to on Eric Rimm, ScD, FAHA; Penny Kris-Etherton, PhD, FAHA; Lawrence L. Rudel, PhD, FAHA; ratios, rather than on levels of intake of each type of Lawrence J. Appel, MD, MPH, FAHA; Marguerite M. Engler, PhD, FAHA; lower intakes, with no PUFA, has many B. Engler, PhD, FAHA; Frank Sacks, MD, FAHA Mary conceptual and biological limitations. 81nts. A large body of literature suggests that higher intakes of Conclusions omega-6 (or n-6) polyunsaturated fatty acids (PUFAs) reduce risk for coronary heart disease (CHD). However, for levels,5 may have physiological sequelae.6 – 8 LA comes primarily from vegetable oils (eg, corn, sunflower, safflower, soy). The average US intake of LA, according to National s of Omega-6 This advisory was undertaken to summarize the current the reasons outlined below, some individuals and groups have recommended substantial reductions in omega-6 PUFA in- Health and Nutrition Examination Survey 2001 to 2002 data for adults Ն19 years of age, is 14.8 g/d.9 On the basis of ands evidence on the consumption of omega-6 PUFAs, partic- take.1– 4 The purpose of this advisory is to review evidence on the relationship between omega-6 PUFAs and the risk of average intake of 2000 kcal/d, LA intake is 6.7% of energy. AA (Ϸ0.15 g/d) is consumed preformed in meat, eggs, and ega-6 PUFAs tradition- ularly LA, and CHD risk. Aggregate data from randomized CHD and cardiovascular disease. some fish. of essential fatty acid trials,PUFAs are characterized by the presence of at least Arguments for reduced LAandlong-term the Omega-6 case-control and cohort studies,PUFAs intakes are based on Omega-6 PUFAs Omega-6 and Inflammation ngly seeking to define animal thedouble bonds, with the first bond at(LA), an assumptionthatbecause CHD has an inflammatory is the 2 carbon-carbon carbon from feeding experiments indicate andthat the omega-6 fatty acid, AA, com- methyl terminus. Linoleic acid the sixth ponent 10 because the consumption k for chronic disease, of primaryleastomega-6 PUFA. LA (18:2 omega-6),energy from synthesisintakes shouldofreduce tissue AA at dietary 5% to 10% be synthe- substrate forreducing LA of a variety PUFAs 18-carbon fatty acid with 2 double bonds the cannot of is molecules, the omega-6 proinflammatoryof Medicine’s Food and reduces established for healthyCHD relative content, which lower the risk the inflammatory evidence, the risk of adults, estimates de- and therefore should reduce for The The potential sized by humans, and although firm minimum requirements have not been to lower intakes. CHD. dataReference Intake Report also suggest thathospitalized patients receiv- appear istofrom human studies, regarding this line rived from studies in infants and higher intakes derived primarily be safe and may ing total parenteral nutrition suggest that an LA intake of of reasoning examined below.67 defines an adequate be LA can be more and elongated to form(as part of a low–saturated-fat,proin- tion, even desaturated beneficial other eicosanoids (20-carbon AA metabolites). Some are of Ϸ0.5% to 2% of energy is likely to suffice. After consump- AA is the substrate for the production of a wide varietyd 12 g/d for women (5% low-cholesterol the metabolically␥important flammatory, vasoconstrictive, and/or proaggregatory, such as acids. The latter is converted to diet). In summary, the , AHA supports anHow- omega-6 PUFAs such as ␥-linolenic and dihomo- -linolenic prostaglandin E thromboxane A , and leukotriene B . 2 2 4f age, approximately the omega-6 PUFA intake of at least 5% to 10% and epoxyeicosatrienoic acids. omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the substrate for a wide array of reactive oxygenated metabolites. prostacyclin, lipoxin A , 4 of energy in ever, others are antiinflammatory/antiaggregatory, such as 11 12 the Dietary Reference the context focusesother on this fattylifestyle AA by a cytochrome P450recommen- PUFA, this advisory of primarily AHA acid, Because LA accounts for 85% to 90% of the dietary omega-6 from and dietary epoxygenase. Epoxyeicosa- Epoxyeicosatrienoic acids are fatty acid epoxides producedry Guidelines for Amer- dations. To reduce omega-6 PUFA also have important vasodilatortheir via recognizing that dietary AA, which can affect tissue AA trienoic acids intakes from propertiesacronutrient distribution current Heart Associationwouldeffort to avoid any actual or potential conflicts of interest that may arise than oftooutside The American levels makes every be more likely to increase as a result an relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group areparticular energy source decrease risk for CHD. showing all such relationships that might be perceived as real or potential conflicts required to complete and submit a Disclosure Questionnaire of interest. This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 6, 2008. A copy of the statement is available at http://www.americanheart.org/presenter.jhtml?identifierϭ3003999 by selecting either the “topic list” link or the “chronological Downloaded from circ.ahajournals.org by on July 26, 2010 list” link (No. LS-1966). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.americanheart.org/presenter.jhtml?identifierϭ3023366. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
    • Simopoulos AP, Cleland LG (eds): Omega–6/Omega–3 Essential Fatty Acid Ratio: The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 81–91 Omega–6/Omega–3 Fatty Acid Ratio: The Israeli Paradox Gal Dubnov, Elliot M. Berry Department of Human Nutrition and Metabolism, Hebrew University, Hadassah Medical School, Jerusalem, Israelü  ÓLEO MAIS CONSUMIDO: ÓLEO DE SOJA While the amount of fat is very important in terms of public health in dealing with the current epidemic of obesity, an equally significant issue is theü  R ÁCIO P/S = 0,9 – 1,2 type of fat consumed. As polyunsaturated fatty acids (PUFA) have long been shown to possess cholesterol-lowering effects [1], increasing their consumption has been promoted in the management of coronary artery disease (CAD) [2].ü  Á L : 10% E CIDO INOLEICO recommendations followed bothOTAL IÁRIA These T DA NERGIA experimental and population based studies that showed decreasing rates of CAD in countries with increasing D polyunsaturated/saturated fat (P/S) ratios over the past years. The dietary habits in Israel appear to be as recommended: low in totalü  % LA : 25% NO ADIPÓCITO in total fat and in saturated fat, while high in hypolipidemic omega–6 calories, fatty acids (␻6) as compared with other western countries [3, 4]. Unexpectedly, the rates of modern-world illnesses are about the same as they are in the USA and RÁCIO N-6/N-3 > 20/1 Europe [3, 5, 6]. The reason for this is not clear. Recent evidence suggests that a high intake of omega–6 fatty acids may prove harmful [2, 7–9]: these fatty acids may elevate the risk of hyperinsulinemia and its associated metabolic dis- orders, atherogenesis, and cancer. Another group of PUFA, the omega–3 fatty PREVALÊNCIA DE DAC É COMPARÁVEL À DE acids (␻3), have demonstrated cardioprotection in observational [10–15] and intervention studies for both secondary [16–18] and primary [18] prevention. An example for this is shown in figure 1: an Indo-Mediterranean diet, rich in OUTROS PAÍSES OCIDENTAIS the plant-derived omega–3 fatty acid alpha-linolenic acid, markedly decreased the risk for a cardiac event among both those with established coronary artery disease, or those only with risk factors [18]. A recent meta-analysis showed that both dietary and non-dietary sources are equally beneficial [19], and the health benefits of plant- derived or fish- derived omega–3 fatty acids now seem to have a sound basis [20]. As the omega–6 and omega–3 fatty acids compete for
    • non-fatal myocardial infarction (MI) + CHD death.n-6 specific PUFA trials non significantly increased the risk of non-fatal MI + CHD death by 13% (risk ratio (RR) 1·13; 95% CI 0·84, 1·53; P=0·427)
    • has reported the effects of tissue levels does reduce the risk for CHD,77,78 it does not tein with omega-6 PUFAs on follow that decreasing omega-6 levels will do the same.ons are present for each trial, Indeed, the evidence considered Advisory AHA Science here suggests that it would studies and the observationalreplacing saturated fatty acid have the opposite effect. Higher omega-6 PUFA intakes Omega-6 Fatty Acids and Risk ␣-linolenic acid to eicosa- can inhibit the conversion of for Cardiovascular Disease sugars, white bread, white A Science Advisory 79 From the American Heart Association NutritionPUFAs reduces CHD risk. On pentaenoic acid,the Council on Nutrition, Physicalalready quite Subcommittee of but such conversion is Activity, andomega-6 PUFAs used in the low,80 and whether on Cardiovascular Nursing; andwould have Metabolism; Council additional small changes Council on Epidemiology and Prevention studies, and nonhuman pri- net effects on CHD risk after the other benefits of LA w, reductions in CHD risk consumption are taken into account is not MD, DrPH, FAHA; William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, clear. The focus Eric Rimm, ScD, FAHA; Penny Kris-Etherton, PhD, FAHA; Lawrence L. Rudel, PhD, FAHA;ga-6 PUFA intakes of 10% to on ratios, rather thanMPH, FAHA; Marguerite M. Engler, PhD, FAHA; Lawrence J. Appel, MD, on levels of intake of each type of Mary B. Engler, PhD, FAHA; Frank Sacks, MD, FAHAwith lower intakes, with no PUFA, has many conceptual and biological limitations.81 events. A large body of literature suggests that higher intakes of omega-6 (or n-6) polyunsaturated fatty acids (PUFAs) levels,5 may have physiological sequelae.6 – 8 LA comes primarily from vegetable oils (eg, corn, sunflower, safflower, reduce risk for coronary heart disease (CHD). However, forConclusions the reasons outlined below, some individuals and groups have soy). The average US intake of LA, according to National Health and Nutrition Examination Survey 2001 to 2002 datatakes of Omega-6 This advisory was undertaken to summarize the current recommended substantial reductions in omega-6 PUFA in- for adults Ն19 years of age, is 14.8 g/d.9 On the basis of an take.1– 4 The purpose of this advisory is to review evidence on average intake of 2000 kcal/d, LA intake is 6.7% of energy.Acids evidence on the consumption of omega-6 PUFAs, partic- the relationship between omega-6 PUFAs and the risk of AA (Ϸ0.15 g/d) is consumed preformed in meat, eggs, and CHD and cardiovascular disease. some fish. r omega-6 PUFAs tradition- ularly LA, and CHD risk. Aggregate data from randomized Omega-6 PUFAs Omega-6 PUFAs and Inflammation Omega-6 PUFAs arecase-control and least trials, characterized by the presence of at cohort studies, andintakes are based on the long-term tion of essential fatty acid 2 carbon-carbon double bonds, with the first bond at the sixth Arguments for reduced LA assumption that because CHD has an inflammatory com- reasingly seeking to define carbon from the methyl terminus. Linoleic acid (LA), an indicate that the consumption the animal feeding experiments ponent and because the omega-6 fatty acid, AA, is 10 18-carbon fatty acid with 2 double bonds (18:2 omega-6), is substrate for the synthesis of a variety of proinflammatorye risk for chronic disease, the primary at least 5% to cannot be synthe- energy from omega-6 PUFAs AA of dietary omega-6 PUFA. LA 10% of molecules, reducing LA intakes should reduce tissue sized by humans, and although firm minimum requirements content, which should reduce the inflammatory potential ute of Medicine’s Food and have reduces thefor healthy adults, estimates de- not been established risk of CHD relative to lower intakes. CHD. The evidence, and therefore lower the risk for The data rived from studies in infants and hospitalized patients receiv-tary Reference Intake Report also suggest that higher intakes reasoning is examined below. and may line ing total parenteral nutrition suggest that an LA intake of derived primarily from human studies, regarding this of appear to be safe ents,67 defines an adequate be even more beneficial (as partis of(20-carbon AA metabolites). Some are proin- Ϸ0.5% to 2% of energy is likely to suffice. After consump- tion, LA can be desaturated and elongated to form other eicosanoids a low–saturated-fat, AA the substrate for the production of a wide variety of acids.low-cholesterol metabolically In summary, the thromboxane A , and leukotriene anHow- The latter is converted to the diet). important prostaglandin E , AHA supports B . omega-6 PUFAs such as ␥-linolenic and dihomo-␥-linolenic flammatory, vasoconstrictive, and/or proaggregatory, such asen and 12 g/d for women (5% 2 2 4ars of age, approximately the omega-6 PUFA intake of at least others are antiinflammatory/antiaggregatory,in as omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the substrate for a wide array of reactive oxygenated metabolites. ever, 5% to 10% of energy such prostacyclin, lipoxin A , and epoxyeicosatrienoic acids. 4 11 12 Both the Dietary Reference the context of other AHA lifestyle and dietaryfatty acid epoxides produced Because LA accounts for 85% to 90% of the dietary omega-6 PUFA, this advisory focuses primarily on this fatty acid, Epoxyeicosatrienoic acids are recommen- from AA by a cytochrome P450 epoxygenase. Epoxyeicosa-Dietary Guidelines for Amer- dations. To reduce omega-6 PUFA intakes vasodilator properties recognizing that dietary AA, which can affect tissue AA trienoic acids also have importantfrom their via e macronutrient distribution current levels would be more likely to increase than to The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outsideor a particular energy source decrease risk for CHD. relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest. This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 6, 2008. A copy of the Downloaded from circ.ahajournals.org by on July 26, 2010 statement is available at http://www.americanheart.org/presenter.jhtml?identifierϭ3003999 by selecting either the “topic list” link or the “chronological list” link (No. LS-1966). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com. Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.americanheart.org/presenter.jhtml?identifierϭ3023366. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express
    • LYON HEART STUDY Okuyama H, Ichikawa Y, Sun Y, Hamazaki T, Lands WE. World Rev Nutr Diet. 2007;96:83-103.85
    • NUTRITION MYTHS
    • e-Book
    • As pessoas com Diabetes terão que ter uma alimentação MITO 1 completamente diferente das pessoas sem doença. • É errado pensar-se que as pessoas com Diabetes terão que ter uma arroz, As pessoas com Diabetes devem evitar comerMITO 2 As pessoas com Diabetes devem ou pão. massa, batata evitar comer arroz, MITO 2 alimentação diferente das outras pessoas. A alimentação de um Diabético deve reger-se pelosmassa, batatade pão. alimentação princípios ou uma saudável, devendo, por isso, ser equilibrada, diversificada e completa.• Estes Contudo, tal como grandes fornecedores de hidratos de carbono alimentos são para a população em geral, pode ser benéfica a • Estes alimentos são grandes fornecedores de hidratos de carbono (HC), os nutrientes que mais influenciam os níveisglicemia após osapós as adopçãonutrientes que mais influenciam ostais como:de glicemia (HC), os de alguns princípios básicos, níveis de distribuir as refeições. No entanto, equilibrada por várias refeições, comem açúcar,açúcar, alimentos de forma ao contrário dos alimentos intervalos refeições. No entanto, aocontrário dos alimentos ricosricos em regulares e não contêm HC de absorção lenta, permitindo do dia (em estes alimentos omitindo refeições; beber água ao longo um melhor estes alimentosaglicemia aoHC dedo dia. média 1,5l contêm longo absorção lenta, permitindo um melhor controlo da 2l por dia); limitar o consumo de fritos e molhos gordos, controlo da preferênciaaooutras confecções culinárias, como os grelhados, dando glicemia a longo do dia. os cozidos, os estufados e os assados com pouca gordura. • A sua ingestão é indispensável, pois devem fornecer a maior parte da• A sua energia que o nosso organismo necessita, cerca de 45aamaior parte ingestão é indispensável, pois devem fornecer 60% dasda calorias totais por dia. energia que o nosso organismo necessita, cerca de 45 a 60% das calorias totais por dia. • Desta forma, estes alimentos devem fazer parte de todas as refeições
    • IG E INSULINA!Last AR, Wilson SA. Low-Carbohydrate Diet. Am Fam Physician 2006;73:1942-8
    • ÍNDICE GLICÉMICO E CARGA GLICÉMICA Alimento IG Dose Hidratos   CG CarbonoAbóbora 75 80  grs 6  grs 4Beterraba 64 80  grs 7  grs 4Cenoura 47 80  grs 6  grs 3Batata  com  pel 60 150  grs 30  grs 18Batata  no  forno 85 150  grs 30  grs 27Batata  frita   85 150  grs 29  grs 22congeladaPuré  de  Batata 74 150  grs 20  grs 15Batata  Doce 61 150  grs 28  grs 17Mandioca 70 150  grs 57  grs 40Inhame 37 150  grs 36  grs 13 Foster-Powell K, Holt SH, Brand-Miller JC. Am J Clin Nutr. 2002 Jul;76(1):5-56.
    • ÍNDICE GLICÉMICO E CARGA GLICÉMICA Alimento IG Dose Hidratos   CG CarbonoPão  branco 70 60  grs 30  grs 21Barra  francesa 62 70  grs 42  grs 26Pão  centeio 50 60  grs 24  grs 12Cheerios 74 30  grs 20  grs 15Chocapic 84 30  grs 25  grs 21CornFlakes 92 30  grs 26  grs 24Golden  Grahams 71 30  grs 25  grs 18Special  K 84 30  grs 24  grs 20Bran  Flakes 74 30  grs 16  grs 13Cream  Crackers 65 25  grs 17  grs 11Alpen  Muesli 55 30  grs 19  grs 10 Foster-Powell K, Holt SH, Brand-Miller JC. Am J Clin Nutr. 2002 Jul;76(1):5-56.
    • ÍNDICE GLICÉMICO E CARGA GLICÉMICA Alimento IG Dose HC CGArroz  branco  Uncle  Ben’s  10  min 68 150  grs 37  grs 25Arroz  branco 56 150  grs 41  grs 23Arroz  branco  BasmaP 58 150  grs 38  grs 22Arroz  integral 55 150  grs 33  grs 18Millet 71 150  grs 36  grs 25Bulgur 48 150  grs 26  grs 12Esparguete  de  milho 78 180  grs 42  grs 32FeRucine  com  ovo 40 180  grs 46  grs 18Gnocchi 68 180  grs 48  grs 33Linguini 46 180  grs 48  grs 22Macarroni 47 180  grs 48  grs 23Ravioli 40 180  grs 42  grs 32SpagheV,  cozido  5  min   38 180  grs 48  grs 18SpagheV,  cozido  20  min   61 180  grs 44  grs 27Esparguete  integral 37 180  grs 42  grs 16 Foster-Powell K, Holt SH, Brand-Miller JC. Am J Clin Nutr. 2002 Jul;76(1):5-56.
    • • Ingerir diariamente 4 a 11 porções de cereais, derivados• Ingerir diariamente 4 a 11 porções de cereais, derivados e tubérculos segundo as recomendações da Roda dos Alimentos. Estas po segundo as recomendações da Roda dos Alimentos. Estas porções devem ser distribuídas por 5 a 7 refeições. 5 a 7 refeições. ser distribuídas por  1 Porção de Cereais e derivados, tubérculos  1 Porção de Cereais representa: e derivados, tubérculos  1 pão (50g) Nota: pesar os representa:  1 fatia fina de broa (70g) alimentos poderá  médio (125g)  1 e ½ batata – tamanho 1 pão (50g) ser uma boa forma de compreender as  5 colheres de sopa de cereais de  1 fatia fina de broa (70g) pequeno-almoço (35g) porções.  e e (35g)  6 bolachas Maria/água 1 sal ½ batata – tamanho médio (125g) s  2 colheres de sopa de arroz/massa crus (35g) d  5 colheres de sopa de cereais de  4 colheres de sopa de arroz/massa cozinhados (110g) pequeno-almoço (35g)  6 bolachas Maria/água e sal (35g)  2 colheres de sopa de arroz/massa crus (35g) O número de porções recomendado depende das necessidades energéticas  crianças de 1 a anos devem guiar-se pelos limites inferiores individuais. As 4 colheres3de sopa de arroz/massa e os homens activos e os rapazes adolescentes pelos limites superiores; a restante população (110g) cozinhados deve orientar-se pelos valores intermédios. O número de porções recomendado depende das ne individuais. As crianças de 1 a 3 anos devem guiar-se e os homens activos e os rapazes adolescentes pel
    • IG E INSULINA!Last AR, Wilson SA. Low-Carbohydrate Diet. Am Fam Physician 2006;73:1942-8
    • HIPERINSULINEMIA à RESISTÊNCIA À INSULINA Rizza RA, et al. Diabetologia. 1985 Feb;28(2):70-5 Del Prato S, et al. Diabetologia. 1994 Oct;37(10):1025-35. Flores-Riveros JR, McLenithan JC, Ezaki O, Lane MD. Proc Natl Acad Sci 1993;90:512–6.
    • Zammit et al. J Nutr 2001;131:2074-77.
    • " !Resistência à Insulina é a primeira alteração metabólica da Síndrome Metabólica! ! " " "Ludwig D.JAMA 2002;287:2414–2423. " "
    • Alguns homens apresentamalterações metabólicas com perímetroda cintura entre 94-102 cm* Propensão genética parainsulinorresistência ACSM, 2005 Para diagnosticar Síndrome Metabólico: Apresentar, pelo menos, 3 sintomas
    • Cordain, 2009FLUXO DE LDL PARA A INTIMA É > PARA LDL PEQUENAS E DENSASUMA VEZ NA INTIMA, LDL PEQUENAS E DENSAS SÃO SUSCEPTÍVEIS DE SOFREROXIDAÇÃO99
    • LDL PEQUENAS E DENSAS 80 r = -0.95 60 P< 0.001% Pessoas com > % sdLDL 40 20 0 % Gord 0 10 20 30 40 50 % CHO 75 65 55 45 35 Krauss RM. J Nutr 2001;131:340s-43s Griffin BA. Proc Nutr Soc 1999;58:163-69
    • British Journal of Nutrition (2001), 86, 557–568 DOI: 10.1079/BJN2001427q Nutrition Society 2001 Effect of a low-glycaemic index –low-fat–high protein diet on the atherogenic metabolic risk profile of abdominally obese men Jean G. Dumesnil1,2*, Jacques Turgeon1,2,3, Angelo Tremblay2,5, Paul Poirier1,2, Marcel Gilbert1,2, Louise Gagnon1,2, Sylvie St-Pierre2,5, Caroline Garneau1,3, Isabelle Lemieux1,4, Agnes Pascot1,4, ` 4 1,4 Jean Bergeron and Jean-Pierre Despres ´ 1 ´ ´ Quebec Heart Institute, Laval Hospital Research Center, Quebec, Canada 2 ´ Faculty of Medicine, Laval University, Quebec, Canada 3 ´ Faculty of Pharmacy, Laval University, Quebec, Canada 4 ´ Lipid Research Center, CHUQ Research Center, Quebec, Canada 5 ´ Division of Kinesiology, Department of Preventive and Social Medicine, Laval University, Quebec, Canada (Received 29 October 1999 – Revised 14 May 2001 – Accepted 28 May 2001) It has been suggested that the current dietary recommendations (low-fat–high-carbohydrate diet) may promote the intake of sugar and highly refined starches which could have adverse effects on the metabolic risk profile. We have investigated the short-term (6-d) nutritional and metabolic effects of an ad libitum low-glycaemic index–low-fat–high-protein diet (prepared according to the Montignac method) compared with the American Heart Association (AHA) phase I diet consumed ad libitum as well as with a pair-fed session consisting of the same daily energy intake as the former but with the same macronutrient composition as the AHA phase I diet. Twelve overweight men (BMI 33:0 (SD 3:5) kg/m2) without other diseases were involved in three experimental conditions with a minimal washout period of 2 weeks separating each intervention. By protocol design, the first two conditions were administered randomly whereas the pair-fed session had to be administered last. During the ad
    • British Journal of Nutrition (2001), 86, 557–568 INSULINA! q Nutrition Society 2001Dieta clássica Dieta low GI Dieta clássicaad libitum ad libitum hipocalórica Effect of a low-glycaemic index atherogenic metabolic risk pr Jean G. Dumesnil1,2*, Jacques Turgeon1,2,3, An Louise Gagnon1,2, Sylvie St-Pierre2,5, Caroline Jean Bergeron4 and 1 ´ Quebec Heart Institute, Laval Hos 2 Faculty of Medicine, Lav 3 Faculty of Pharmacy, Lav 4 Lipid Research Center, CHUQ 5 Division of Kinesiology, Department of Preventive (Received 29 October 1999 – Revise It has been suggested that the current dietary may promote the intake of sugar and highly refi metabolic risk profile. We have investigated the an ad libitum low-glycaemic index–low-fat–hi method) compared with the American Heart As well as with a pair-fed session consisting of the same macronutrient composition as the AHA (SD 3:5) kg/m2) without other diseases were invo washout period of 2 weeks separating each inte were administered randomly whereas the pair-f libitum version of the AHA diet, subjects consu 28 % increase in plasma triacylglycerol levels ( a 10 % reduction in plasma HDL-cholesterol co P,0:01) which contributed to a significant incr this lipid index being commonly used to assess t glycaemic index–low-fat–high-protein diet c decrease (P,0:001) in total energy intake whic
    • British Journal of Nutrition (2001), 86, 557–568 q Nutrition Society 2001 DISLIPIDEMIA! Effect of a low-glycaemic index atherogenic metabolic risk pr Jean G. Dumesnil1,2*, Jacques Turgeon1,2,3, An Louise Gagnon1,2, Sylvie St-Pierre2,5, Caroline Jean Bergeron4 and 1 ´ Quebec Heart Institute, Laval Hos 2 Faculty of Medicine, Lav 3 Faculty of Pharmacy, Lav 4 Lipid Research Center, CHUQ 5 Division of Kinesiology, Department of Preventive (Received 29 October 1999 – Revise It has been suggested that the current dietary may promote the intake of sugar and highly refi metabolic risk profile. We have investigated the an ad libitum low-glycaemic index–low-fat–hi method) compared with the American Heart As well as with a pair-fed session consisting of the same macronutrient composition as the AHA (SD 3:5) kg/m2) without other diseases were invo washout period of 2 weeks separating each inte were administered randomly whereas the pair-f libitum version of the AHA diet, subjects consu 28 % increase in plasma triacylglycerol levels ( (a), apolipoprotein B (b) and LDL size (c) before (A) and after (B) each of the three a 10 % reduction in plasma HDL-cholesterol co dietary regimens. P,0:01) which contributed to, apolipoprotein B (e) and LDL size (f) in response to the three dietary regimens. Standard errors are a significant incr this lipid index being commonly used to assess t values were significantly different from baseline, P , 0:05: a,bMean responses to diets glycaemic index–low-fat–high-protein diet c with unlike lettersFor details of diets and procedures, see p. 558–559. decrease (P,0:001) in total energy intake whic
    • diet (LoGIX; 40 6 0.3 units) or a high-GI diet (HiGIX; 80 6 0.6 cessfully im units). Body composition (measured by using dual-energy X-ray have shown absorptiometry and computed tomography), insulin sensitivity IR (6–9). In (measured with a hyperinsulinemic euglycemic clamp with alter insul 2 [6,6- H2]-glucose), and oral glucose–induced insulin and incretin humans (10 hormone secretion were examined. prove these Results: Both groups lost equal amounts of body weight (28.8 6 certain nut 0.9%) and adiposity and showed similar improvements in peripheral centrations tissue (+76.2 6 14.9%) and hepatic insulin sensitivity (+27.1 6 index diet 0.05). However, oral glucose–induced insulin secre- whereas aA low–glycemic 7.1%) (all P ,combined with exercise reduces insulinresistance, postprandial hyperinsulinemia, and glucose-dependent peripheral tion was reduced only in the LoGIX group (6.59 6 0.86 nmol in the1–4insulinotropic polypeptide responses in 6 0.67 nmol in the poststudy, P , play a crit prestudy compared with 4.70 obese, prediabetic humans interventioThomas PJ Solomon, Jacob 0.05), which was Marc D Cook, Julianne to the suppressedSangeeta R Kashyap, M Haus, Karen R Kelly, a change related Filion, Michael Rocco, postprandialRichard M Watanabe, Hope response and John P Kirwan Barkoukis, of glucose-dependent insulinotropic polypeptide. When The con much attenABSTRACT corrected for changes in b that preserving b exposure, in these at-risk insulin is cell glucose cell function changes in populations secretion were attenuated a critical factor in the prevention of became signifi-Background: The optimal lifestyle intervention that reverses dia- in the LoGIX group but T2D onset (2). Therefore, 1betes risk factors is not known. therapeutic management of such individuals should consider all From theObjective: We examined the effect of a low–glycemicin the HiGIX group. cantly elevated index (GI) processes involved in maintaining glucose homeostasis. Downloaded from www.ajcn.org at Lund University Conclusions: Although lifestyle-induced weight Prevention Program Outcomes JMH, KRK,diet and exercise intervention on glucose metabolism and insulin Although the recent Diabetes loss improves in-secretion in obese, prediabetic individuals. Study underlined the large effect that intensive lifestyle in- Medicine (M sulin resistance in prediabetic individuals, postprandialofhyperinsu- in troenterologyDesign: Twenty-two participants [mean 6 SEM age: 66 6 1 y; tervention can have on the prevention diabetes onset 2body mass index (in kg/m ): 34.4 6 0.8] underwent a 12-wk linemia is reduced only when a low-GI diet (3),consumed. Inby which lifestyle partments ofexercise-training intervention (1 h/d for 5 d/wk at ’85% of max- overweight individuals is the mechanisms contrast, intervention prevents the development of glucose intolerance are a high-GI diet impairs pancreatic b cell andExercise training interventions can suc- Western Resimum heart rate) while randomly assigned to receive either a low-GI not fully understood. intestinal K cell functiondiet (LoGIX; 40 6 0.3 units) or a high-GI diet (HiGIX; 80 6 0.6 despite significant weight loss. These findingstolerance (4, 5),the impor- cessfully improve glucose highlight and several groupsunits). Body composition (measured by using dual-energy X-ray have shown that exercise can reverse peripheral tissue and hepatic tive Medicinabsorptiometry and computedtant role of insulin sensitivity tomography), the gut in mediating the effectshas been shown that exercise training can nia, Los Ang IR (6–9). In addition, it of a low-GI diet on type(measured with a hyperinsulinemic euglycemic clamp with 2 diabetes risk reduction.alter insulin secretion and improvehas also been shown to im- 2 Supporte[6,6-2H2]-glucose), and oral glucose–induced insulin and incretin b cell function in Am J Clin Nutr 2010;92:1359–68.obese humans (10–13). Caloric restrictionhormone secretion were examined. prove these components of glucose tolerance (8, 14). However, AG12834; toResults: Both groups lost equal amounts of body weight (28.8 60.9%) and adiposity and showed similar improvements in peripheral certain nutrients (high-fat feeding) and elevated glycemic con- (Cleveland, centrations can induce IR and impair b cell function (15–17),tissue (+76.2 6 14.9%) and hepatic insulin sensitivity (+27.1 6 whereas a high-carbohydrate and high-fiber diet can improve 1UL1RR024
    • Richard M Watanabe, Hope Barkoukis, and John P KirwanABSTRACT that preserving b cell function in these at-risk populations isBackground: The optimal lifestyle intervention that reverses dia- a critical factor in the prevention of T2D onset (2). Therefore,betes risk factors is not known. therapeutic management of such individuals should consider all Downloaded from www.ajcn.org at Lund University Libraries on May 5, 2011Objective: We examined the effect of a low–glycemic index (GI) processes involved in maintaining glucose homeostasis.diet and exercise intervention on glucose metabolism and insulin Although the recent Diabetes Prevention Program Outcomessecretion in obese, prediabetic individuals. Study underlined the large effect that intensive lifestyle in-Design: Twenty-two participants [mean 6 SEM age: 66 6 1 y; tervention can have on the prevention of diabetes onset inbody mass index (in kg/m2): 34.4 6 0.8] underwent a 12-wkexercise-training intervention (1 h/d for 5 d/wk at ’85% of max- SÓ HOUVE overweight individuals (3), the mechanisms by which lifestyle intervention prevents the development of glucose intolerance areimum heart rate) while randomly assigned to receive either a low-GIdiet (LoGIX; 40 6 0.3 units) or a high-GI diet (HiGIX; 80 6 0.6 MELHORIA DA not fully understood. Exercise training interventions can suc- cessfully improve glucose tolerance (4, 5), and several groupsunits). Body composition (measured by using dual-energy X-rayabsorptiometry and computed tomography), insulin sensitivity INSULINA have shown that exercise can reverse peripheral tissue and hepatic IR (6–9). In addition, it has been shown that exercise training can(measured with a hyperinsulinemic euglycemic clamp with[6,6-2H2]-glucose), and oral glucose–induced insulin and incretin POSTPRANDIAL alter insulin secretion and improve b cell function in obese humans (10–13). Caloric restriction has also been shown to im-hormone secretion were examined.Results: Both groups lost equal amounts of body weight (28.8 6 NO GRUPO DE prove these components of glucose tolerance (8, 14). However, certain nutrients (high-fat feeding) and elevated glycemic con-0.9%) and adiposity and showed similar improvements in peripheraltissue (+76.2 6 14.9%) and hepatic insulin sensitivity (+27.1 67.1%) (all P , 0.05). However, oral glucose–induced insulin secre- IG centrations can induce IR and impair b cell function (15–17), BAIXO whereas a high-carbohydrate and high-fiber diet can improve peripheral insulin sensitivity (18). Thus, dietary composition maytion was reduced only in the LoGIX group (6.59 6 0.86 nmol in the play a critical role in determining the ultimate success of suchprestudy compared with 4.70 6 0.67 nmol in the poststudy, P , interventions.0.05), which was a change related to the suppressed postprandial The concept of a dietary glycemic index (GI) has receivedresponse of glucose-dependent insulinotropic polypeptide. When much attention: the consumption of high-GI diets may increasecorrected for changes in b cell glucose exposure, changes in insulinsecretion were attenuated in the LoGIX group but became signifi- 1cantly elevated in the HiGIX group. From the Department of Pathobiology, Lerner Research Institute (TPJS, JMH, KRK, MDC, JF, and JPK), and the Departments of CardiovascularConclusions: Although lifestyle-induced weight loss improves in- Medicine (MC), Endocrinology, Diabetes, and Metabolism (SRK), and Gas-sulin resistance in prediabetic individuals, postprandial hyperinsu- troenterology/Hepatology (JPK), Cleveland Clinic, Cleveland, OH; the De-linemia is reduced only when a low-GI diet is consumed. In contrast, partments of Physiology (JMH and JPK) and Nutrition (KRK and JPK), Casea high-GI diet impairs pancreatic b cell and intestinal K cell function Western Reserve University, Cleveland, OH; and the Department of Preven-despite significant weight loss. These findings highlight the impor- tive Medicine, Physiology, and Biophysics, University of Southern Califor-tant role of the gut in mediating the effects of a low-GI diet on type nia, Los Angeles, CA (RMW). 22 diabetes risk reduction. Am J Clin Nutr 2010;92:1359–68. Supported by the National Institutes of Health (NIH) (grants RO1 AG12834; to JPK) and the NIH National Center for Research Resources (Cleveland, OH) (Clinical and Translational Science Award
    • APD 1 Can a Low–Glycemic Index D In normal subjects, mixed based on low– glycemic index fo Need for Insulin in Gestation Clinical Care/Education/Nutrition/Psychosocial Research O R I G I N A L A R T I C L E to a reduction in postprandial g A low– glycemic index diet is effective as a treatment for individuals with (6). We have previously demons Mellitus? in Gestational Diabetes en shown to improve pregnancy outcomes when used from the first trimester. normal pregnant women that a di Can a Low–Glycemic Index Diet Reduce the ndex diet is commonly advised as treatment for women with gestational on low– glycemic index foods w Need for Insulin GDM). However, the efficacy of this advice and associated pregnancy out- tainable and resulted in more f een systematically examined. The purpose of this study was to determine fetal outcomes (7). The aim of th Mellitus? A randomized trial g a low– glycemic index diet for women with GDM could reduce the number was to examine whether a low– g g insulin without compromise of pregnancy outcomes. A randomized trial index diet used as MNT for wom SIGN AND METHODS — , MD1 PETER PETOCZ, PHDseen over a PETERsource of GDM could resistance to a reduced R OBERT OSES, M G. MG. with P insulin use both PHD 2 result in ROBERT BARKER, APDMD1 OSES All womenENNIE C. GDM 2ILLER, PHD3 12-monthETOCZ,anxiety and of during pregnancy 1 ered for inclusion inBARKER, APD1 (nJϭ 63) BRAND-M MEGAN the study. Women MEAGAN WINTER, APD1 were randomly assigned to treatment change. 3 M EGAN JENNIE C. normal subjects, mixedof obstetric an In BRAND-MILLER, meals w– glycemic index diet or a conventional high-fiber (and higher glycemic on compromise lead PHD MEAGAN WINTER, APD1 based low– glycemic index foods outcomes. to a reduction in postprandial glycemia OBJECTIVE — A low– glycemic index diet is effective as a treatment for individuals with(6). We have previously demonstrated in normal pregnant women that a diet based diabetes and has been shown to improve pregnancy outcomes when used from the first trimester. the 31 women randomly assigned to a low– glycemic index diet, 9 (29%) glycemic index foods was sus- A low– glycemic index diet is commonly advised as treatment for women with gestational on low– REDUZIU AS NECESSIDADES DE RESEARCHfor The study w DESIGN AND diabetes mellitus (GDM). However, the efficacy of this advice and associated pregnancy out-Of the women randomly assigned to a higher– glycemic index diet, a signifi- outcomes (7). Theinaim of this study tainable and resulted more favorable OBJECTIVE — A low– glycemic index diet is effective asINSULINA individuals wit comes have not been systematically examined. The purpose of this study was to determinefetal a treatment whether prescribing a low– glycemic index diet for women with GDM could reduce the number ϭ METHODS — ortion, 19 of 32 (59%), met the criteria to commence insulin treatment (Pwas to examine whether a low– glycemic diabetes and has been shown to improve pregnancy outcomes when used from the first trimeste of women requiring insulin without compromise of pregnancy outcomes. SEM AFECTAR NEGATIVAMENTE A MÃE E O of Wollongon A low– glycemic index diet is commonly advised as treatment for women with gestationa index diet used as MNT for women with 9 of these 19 women were able to avoid insulin use by changing to a low– could result in a reduced need for GDM ducted in the city t. Key obstetric were considered forAND METHODS not significantly seen over aassigned to insulin use during pregnancy with no RESEARCH DESIGN and fetal outcomesinwere — Women (n ϭ 63)GDM randomly 12-month All women with different. South Wales, Australia, a coastal c period inclusion the study. FETO were diabetes mellitus (GDM). However, the efficacy of this advice and associated pregnancy out receive either a low– glycemic index diet or a conventional high-fiber (and higher glycemic compromise of obstetric and fetal index) diet. a population of ϳ280,000 peop outcomes. comes have not been systematically examined. The purpose of this study was to determin S — Using a low– glycemic index diet for women with GDM effectively ated about 50 miles south of Sydn needing toRESULTS —prescribingcompromise a higher– indexor fetal a9 signifi- RESEARCH DESIGN ANDreduce the numbe whether Of the 31 women randomly assigned ofa obstetric index diet, outcomes. with GDM could use insulin, with no a low– glycemic glycemic index diet, (29%) required insulin. Of the women randomly assigned to to low– glycemic diet for women Australasian Diabetes in Pregnan of women requiring(59%), met ablecriteria to insulin use by changing to aof ϭ METHODSoutcomes. recommends that a cantly higher proportion, 19 of 32 insulin without compromise (P pregnancy — The study was con- 0.023). However, 9 of these 19 women were the to avoid commence insulin treatment ety (ADIPS) low– ducted in the city of Wollongong, New Diabetes Care 32:996–1000, 2009 Wales, Australia, a coastal city with glycemic index diet. Key obstetric and fetal outcomes were not significantly different. South nant ϳ280,000 people women should be tested fo RESEARCH Using a low– glycemic index diet for women with GDM— All women 50 ofUnlessof Sydney.situ- earlier, wom CONCLUSIONS — DESIGN AND METHODS effectively ated about with GDM seen over a 12-mont a population (8).miles south indicated The halved the number needing to use insulin, with no compromise of obstetric or fetal outcomes. iabetes mellitus (GDM)considered for inclusion in the study. Women (n ϭDiabetes in Pregnancy Soci- assigned t period were is distribution and ideally on the resultsAustralasian 63) were randomly of
    • 3 Reprints not availa cently, Atkins-type very-low-carbohydrate diets have rapidly AD in popularitySee corresponding editorial onFeldman, RISK ment of Medicine, Chil page 949. Cara B Ebbeling, Michael M Leidig, Kelly BLIBITUM Linda G although low-fatHenry remain the cor- David S E-mail: david.l grown Sinclair, LOW-GLYCEMIC LOADdiets A AND CVDand 02115. Ludwig (2), Seger-Shippee, DIET nerstone of conventional treatment based on clinical practice Received August 18, TABLE 3Effects of an ad libitum low-glycemic load diet on cardiovascular ABSTRACT Study outcomes1 recommendations (3, 4).that carbohydrate-restricted diets may have significantly greater Background: The optimal nutritional approach for the prevention of Whereas a few studies have suggested Accepted for publica benefits than do low-fat diets in reducing CVD risk (5, 6), there 1–3disease risk factors in obese young adults cardiovascular disease among obese persons 976 remains a topic of in- Group widespread concern regarding the safety and long-term effi- U is Am J Clin Nutr 2005;81:976 – 82. Printed in P2 tense controversy. Available approaches range from conventional cacy of severe carbohydrate restriction (7, 8). Experimental diet Conventional dietCara B Ebbeling,very-low-carbohydrate diets. B Sinclair, Linda G Seger-Shippee, Henry A Feldman,diet, containing unrestricted low-fat to Michael M Leidig, Kelly A low-glycemic load (GL) and David S Ludwig Objective: The aim of this pilot study was to evaluate 11) efficacy Variable (n ҃ the amounts of carbohydrate from low-glycemic index Time foods, (n ҃ 12) Group (GI) of an ad libitum low-glycemic load diet, without strict limitation on represents an% alternative to low-fat diets on the one hand and toABSTRACT Weight % that carbohydrate-restricted diets may have significantly greater carbohydrate intake, as an alternative to a conventional low-fat diet. 0.18 0.001 Interim3 Ҁ8.4 (Ҁ11.4, ofBackground: TheA randomized controlled trial compared 2 dietary treat- optimal nutritional approach for the prevention Ҁ5.3) benefits than do (Ҁ10.7, Ҁ4.9) in reducing CVD risk (5, 6), there the low- Ҁ7.8 carbohydrate diets on the other. The GI is defined as low-fat diets Design: Ҁ7.8 (Ҁ13.0, Ҁ2.2) is widespread concern under the blood glucose response curve after 12 mo obese persons remains a topic of in- incremental area Ҁ0.7) Ҁ6.1 (Ҁ11.2, regarding the safety and long-term effi-cardiovascular disease among adults (n ҃ 23) over 12 mo. The experimental ments in obese young consumption of 50 g of available carbohydrate from 0.06 food, a test Total cholesteroltense controversy. Available approaches range from conventional 0.90 treatment emphasized ad libitum consumption of low-glycemic- cacy of severe carbohydrate restriction (7, 8). divided by (Ҁ9.2, 5.5) Interim Ҁ9.9 (Ҁ16.7, Ҁ2.5) Ҁ2.1 the area under the curve after consumption of 50 g oflow-fat toindex foods, with 45–50% of energy from carbohydrates and 30 – A low-glycemic load (GL) diet, (ie, glucose or unrestricted(9). very-low-carbohydrate diets. carbohydrate from 3.5) containing white bread) 12 mo Ҁ8.5 (Ҁ17.4, 1.5) Ҁ6.2 (Ҁ15.0, a reference foodObjective: The aimfat. this pilot study was to evaluate restricted in energy of The conventional treatment was the efficacy 35% fromLDL cholesterol amounts of carbohydrate fromproduct of 0.85 amount of carbohydrate The GL is the arithmetic low-glycemic index (GI)0.17 the foods, Downloaded from www.ajcn.org at Lund University Libraries on Maof an ad libitum low-glycemic load diet, (30% of energy),(Ҁ18.6,on60% of (250 –500 kcal/d deficit) and fat without strict limitation 1.4) represents an alternative to low-fatthus describes one overalland to of Interim Ҁ9.1 with 55– consumed and the GI (10) and diets on the the hand effects Ҁ2.6 (Ҁ12.3, 8.2)carbohydrate intake, as an alternative tocompared changes in study outcomes carbohydrate. We a conventional low-fat diet. energy from 12 mo Ҁ9.7 (Ҁ21.6, 3.9) low- carbohydrate and sourcethe carbohydrateGI postprandialas the both quantity diets on of other. The on is defined glycemia Ҁ7.4 (Ҁ19.1, 6.0)Design: A randomized controlled trial compared 2 dietary data and ex- by repeated-measures analysis of log-transformed treat- HDL cholesterol incremental area under has been inversely0.41 (11). Risk of CVD the blood glucose response curve after or associated with dietary GI 0.08ments in obese youngresults as mean percentage change. (Ҁ6.0, 11.3) consumption of (Ҁ8.1, 8.2)but not all (16) epidemiologicastudies. More- pressed the Interim(n ҃ 23) over 12 mo. The experimental adults 2.3 GL inҀ0.3 50 g of available carbohydrate from test food, some (12–15)treatment Results: Bodyad libitum consumption of low-glycemic- emphasized weight decreased significantly 12.2 (2.9, 22.3) 12 mo over a 6-mo intensive divided by the area under theshort-term intervention studies have de- over, whereas several curve after consumption of 50 g of 1.1 (Ҁ6.9, 9.8)index foods, with 45–50% ofthe experimental and conventional 30 – groups intervention in both energy from carbohydrates and diet Triacylglycerols carbohydrate from a reference food (ie, glucoseon white bread)in over- scribed beneficial effects of low-GI diets or blood lipids (9). 0.96 0.001 (Ҁ8.4% andInterim respectively) was remained below baseline The GL is the arithmetic productthe capacity for fibrinolysis in diabetic Ҁ7.8%, treatment and restricted (Ҁ44.6, Ҁ24.7) at35% from fat. The conventional Ҁ35.4 in energy weight adults (17–20) and Ҁ7.1 (Ҁ19.8, 7.6) on of the amount of carbohydrate 12 mo deficit) mo fat (30% of energy), with 55– 60% of diet(250 –500 kcal/d (Ҁ7.8%and Ҁ6.1%, respectively).Ҁ37.2experimental consumed Ҁ19.1 (Ҁ32.2, Ҁ3.6) thus efficacy ofthe overall effects of 12 and The (Ҁ47.7, Ҁ24.5) patients (21, 22),(10)long-term describes low-GL diets in reducing and the GI the and PAI-1 0.78 0.11energy from carbohydrate.significantly greater mean study outcomes tria- quantity and source of carbohydrate on postprandial glycemia group showed a We compared changes in decline in plasma both CVD risk has not previously been evaluated (23). cylglycerols Interim Ҁ58.3 (Ҁ74.7, Ҁ31.3) The30.4 (Ҁ19.2, 110.4)study was to evaluate the efficacy ofby repeated-measures than did the conventional diet data and ex- and Risk of CVD has been inversely associated with dietary GI or an analysis of log-transformed group (Ҁ37.2% (11). aim of this pilot Ҁ19.1%, respectively; P ҃ 0.005). MeanҀ39.0 (Ҁ70.2, 24.9) 12 mo plasminogen activator 33.1 (Ҁ32.9, 164.3) experimental ad libitum low-GL diet. We hypothesized that thepressed the results as meanblood pressure Systolic percentage change. GL in some (12–15) but not all (16) epidemiologic studies. More- 0.78 0.81 inhibitor 1 concentrations decreased (Ҁ39.0%) in the experimental experimental diet would have a more beneficial effect on CVDResults: Body weightInterim decreased significantly over a 6-mo (Ҁ5.9, 4.2) Ҁ0.9 intensive over, whereas several 4.4) Ҁ0.5 (Ҁ5.3, short-term intervention studies have de- diet group but increased (33.1%) in the conventional diet group (P ҃ risk factors than would a conventional, energy-restricted, low-fatintervention in both the experimental and conventionalbloodgroups and diet pressure, scribed beneficial effects of low-GI diets on blood lipids in over- 0.004). Changes in cholesterol concentrations,0.2 (Ҁ4.7, 5.3) 12 mo diet over a(Ҁ4.1, 5.5) 0.6 12-mo intervention.(Ҁ8.4% and Ҁ7.8%, respectively)differremained below baseline at Diastolic blood and significantly between the groups.weight adults (17–20) and on the capacity for fibrinolysis in diabetic insulin sensitivity did notpressure 0.84 0.7212 mo (Ҁ7.8% and Ҁ6.1%, libitum low-glycemic load diet may be more Interim respectively). The experimental diet Conclusion: An ad Ҁ2.0 (Ҁ7.2, 3.4) patients (21, 22), the long-term efficacy of low-GL diets in reducing 0.3 (Ҁ4.8, 5.6) SUBJECTS AND METHODSgroup showed a significantly greater mean decline in plasma tria- diet in 12 mo Ҁ0.3 (Ҁ6.2, 6.0) efficacious than a conventional, energy-restricted, low-fat CVD risk has1.4 (Ҁ4.4, 7.6) been evaluated (23). not previouslycylglycerols than did the sensitivity indexrisk. group (Ҁ37.2% and Insulin conventional diet reducing cardiovascular disease 0.32 Am J Clin Nutr 2005;81: TheScreening and enrollment to evaluate the efficacy of an aim of this pilot study was 0.001Ҁ19.1%, 976 – 82. Interim 0.005). Mean plasminogen (1.5, 11.5) respectively; P ҃ 6.4 activator experimentalprotocol10.7)low-GL diet.the institutional review board at 5.8 (1.1, The 8.7 (2.3, 15.5) approved by We hypothesized that the ad libitum was 12 mo 10.4 (3.6, 17.6)inhibitor 1 concentrations decreased (Ҁ39.0%) in the experimental experimental diet would have a more written informed on CVDwas Children’s Hospital Boston, and beneficial effect consentdiet groupKEY WORDS MeanObesity,in log-transformed variable(P ҃and 12 mo factors than wouldpercentage changeenergy-restricted, low-fat95% co but increased (33.1%) in the conventional diet glycemic 6 1 change glycemic index, group at load, di- (b), retransformed to a conventional, [100% ҂ (exp(b) Ҁ1)], with be- risk obtained from each subject. Inclusion criteria included: age0.004). Changes in Repeated-measures ANOVAdiet, used to account for within-subject correlations.35 y, body mass index (BMI; in kg/m2) Œ27, body cholesterol concentrations, blood pressure, and etary composition, weight-reducing was cholesterol, triacylglyc- over a 12-mo intervention. diet tween 18 and
    • fuels. Blood glucose and free fatty a previ- week of energy restriction in acids ing weight dietarya diet focused onquintile of glycemic load had double the pliance with loss, energy restriction gly- ous study.18 are reduced in the postabsorptive phase The difference in REE is too small to cemicphysiological mechanisms relat- greater developing heart disease, after The load reduction produced risk of increasingly difficult over time. controlling for potentially confound- Effects of a Low–Glycemic Load Diet following a high– vs low–glycemic in- account for any significant change in dex meal, andcomposition over the shortsuf- body this reduction can be term. improvements in several important car- ing dietary composition to REE during ing factors. However, these effects have diovascular disease–related may diabe- weight loss remain speculative but and not previously been examined in inter- on Resting Energy Expenditure and ficient in For example, 80 trigger releasethan magnitude to kcal/d over 10 weeks (5600 kcal) would amount to less of 1 kg of body weight. Thus, our study tes mellitus–relatedfree fatty acids thanweightstudies. diet found that dur- involve altered availability of metabolic ventional fuels. Blood glucose and end points ing a are reduced in the postabsorptive phase loss, a We focused on gly- cemic load reduction produced greater Heart Disease Risk Factors does not support claims that popular di- fore and After 10% Weight Loss by Dietary Treatment Group ets can cause rapid weight loss by induc- following a high– vs low–glycemic in- dex meal, and this reduction can be suf- improvements in several important car- diovascular disease–related and diabe- During Weight Loss ing major shifts in Mean (SE)Fat Diet Group (n = 17) energy metabolism. ficient in magnitude to trigger release of Low–Glycemic Load Diet Group (n = 22) tes mellitus–related end points than a Table 5. Cardiovascular Disease Risk Factors Before and After 10% Weight Loss by Dietary Treatment Group Mark A. Pereira, PhD Context Weight loss elicits physiological adaptations relating to energy intake and % Change %Mean (SE) Change Posttreatment Janis Swain, MS, Baseline (Adjusted) RD expenditure that antagonize ongoing weight loss. Posttreatment17) (Adjusted)Low–Glycemic Load Diet Group (n = 22) P Value* Low-Fat Diet Group (n = 1.10 (0.13) –15.8 (5.13) Goldfine, MD Allison B. 1.50 (0.18) Objective To test whether dietary composition affects the physiological adapta- 0.97 (0.11) –33.9 (4.51) .01 Nader Rifai, PhD Baseline tions to% Change weight loss, as assessed by resting energy expenditure. % Change 102.3 (8.11) 16.2 (5.24) 78.3 (8.40) Posttreatment 72.4 (7.19) (Adjusted) (4.63) –3.5 Baseline .01 Posttreatment (Adjusted) P Value* David S. Ludwig, MD, PhD Design, Study, and Participants A randomized parallel-design study of 39 over- 44.1 (2.41) score–8.1 (3.49) HOMA 1.45 (0.20) 46.9 (3.20) 1.10 (0.13) 42.2 (2.14) –15.8 (5.13)young1.50 (0.18) .87 0.9740 years who received an energy-restricted weight or obese (3.09) –8.9 adults aged 18 to (0.11) –33.9 (4.51) .01 T Triglycerides, mg/dL† 92.4 (9.47) 102.3 (8.11) diet, 16.2 (5.24) 78.3 (8.40) 72.4 (7.19) –3.5 (4.63) .01 104.6 (9.73)HDL-C, mg/dL† –15.0 (4.12) POOR LONG(9.75) EFFICACY(2.41) either low–glycemic load or low-fat. Participants were studied in the.87 HE 138.7 -(3.61) 49.4 TERM 115.9 (8.63) –8.1 –16.1 (3.65) (3.20) .84 42.2 (2.14) 44.1 (3.49) General Clini- 46.9 Brigham and Women’s Hospital and the Children’s Hos- –8.9 (3.09) cal Research Centers of the 0.13 (0.04) LDL-C, mg/dL† (13.61) –5.1 of conventional obesity 104.6 (9.73) 0.28 (0.06) 124.3 (9.86) treat- (0.03) Boston, Mass, before and after 10% weight loss. The (3.65) was conducted from 0.10 pital, –15.0 –47.7 (11.94) (9.75) .03115.9 (8.63) (4.12) 138.7 –16.1 study .84 ment has promoted the notion January–5.12001, to May 6,(0.06) 104.6 (2.35)C-reactive protein, (1.32) –3.1 mg/dL 0.19 (0.06) 110.4 (2.55) 102.3 (2.06) 4, (13.61) (1.16) 2003..07 0.10 (0.03) 0.13 (0.04) –6.4 0.28 –47.7 (11.94) .03 Systolic BP, mm Hg of a body107.5 (2.90) point,1,2(2.35) weight set 104.6 –3.1 (1.32) 110.4 (2.55) 102.3 (2.06) –6.4 (1.16) .07 66.2 (1.80) –2.5 (1.61) 64.2 Main Outcome Measures Resting energy expenditure measured in the fasting state more recently termed settling point. Ac- (1.58) –2.5calorimetry,69.2 (1.78) .07 64.2 by dual-energy (1.42) absorptiometry, car- 69.2 (1.78) –6.5 (1.42) Diastolic BP, mm Hg 67.8 (2.03) 66.2 (1.80) indirect (1.61) by body composition (1.58) –6.5 x-ray .07 91.7 (2.03) arterial–3.0 (1.27) this concept, deviations89.5 (1.78) –3.0 (1.27) (1.12) (2.18)and self-reported hunger. (1.12) Mean cording mm Hg 96.6 (2.18) pressure, to 94.1 (2.48) 91.7in(2.03) –6.5 risk96.6 diovascular disease factors, .04 89.5 (1.78) –6.5 .04 body weight from baseline elicitLDL-C, low-density lipoprotein. model assessment; LDL-C, low-density lipoprotein. physi-oprotein cholesterol; HOMA, homeostasis model high-density lipoprotein cholesterol; HOMA, Resting energy expenditure decreased less with the low–glycemic load diet Abbreviations: BP, blood pressure; HDL-C, assessment; SI conversions: ological adaptations that antagonize fur- Results homeostasismultiply by 0.0259; triglycerides to mmol/L,and LDL-C bymmol/L, multiply by 0.0259; triglycerides to mmol/L, multiply by 0.0113. To convert HDL-C multiply to 0.0113. *Effect of dietary treatment on % change. than with the low-fat diet, expressed in absolute terms (mean [SE], 96 [24] vs 176 ther weight change. During energy re- †For low-fat diet group, n=11; for low–glycemic load diet group, n=14. [27] kcal/d; P=.04) or as a proportion (5.9% [1.5%] vs 10.6% [1.7%]; P=.05). Par- oup, n=14. striction, humans and experimental ticipants receiving the low–glycemic load diet reported less hunger than those receiv- animals have increased hunger, de- ©2004 American Medical Association. All rights reserved. ing the low-fat diet (P=.04). Insulin resistance 24, 2004—Vol 292, triglycerides (P=.01), (Reprinted) JAMA, November (P=.01), serum No. 20 2489 creased thyroid hormone levels, and C-reactive protein (P=.03), and blood pressure (P=.07 for both systolic and diastolic) s reserved. (Reprinted) JAMA, November 24, 2004—Vol 292, No. 20 2489 down-regulation of reproductive and improved more with the low–glycemic load diet. Changes in body composition (fat growth functions,3-5 changes that in- and lean mass) in both groups were very similar (P=.85 and P=.45, respectively). crease energy intake and lower energy ex- Conclusions Changes in dietary composition within prevailing norms can affect physi- penditure. Downloaded this phenom- ological adaptations UNIVERSITAET weight. Reduction in glycemic load may aid in To examine from jama.ama-assn.org at LUNDS that defend body on May 4, 2011
    • CRP LDL 2,5 2 1,5 1 0,5 0 1 2 3 4 5QUINTIS DE RISCO RELATIVO PARA TODOS OS ACIDENTES CARDIOVASCULARES 109 Ridker PM et al. N Engl J Med 2002;347:1557-65.
    • See corresponding editorial on page 1541.Intake of carbohydrates compared with intake of saturated fatty acidsand risk of myocardial infarction: importance of the glycemic index1–3Marianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjønneland, Erik B Schmidt,and Kim OvervadABSTRACT concentration is tightly regulated by homeostatic regulatoryBackground: Studies have suggested that replacing saturated fatty systems, but the rapid absorption of carbohydrates after con-acids (SFAs) with carbohydrates is modestly associated with a high- sumption of a high-GI meal challenges these homeostaticer risk of ischemic heart disease, whereas replacing SFAs with mechanisms (4). A high-GI meal results in a high blood glucose Downloaded from www.ajcn.org at Lund University Libraries on November 5, 2010polyunsaturated fatty acids is associated with a lower risk of ische- concentration and a high insulin-to-glucagon ratio, followed bymic heart disease. The effect of carbohydrates, however, may de- hypoglycemia, counterregulatory hormone secretion, and ele-pend on the type consumed. vated plasma free fatty acid concentration (4). These events mayObjectives: By using substitution models, we aimed to investigate affect the risk of IHD through promoting dyslipidemia, in-the risk of myocardial infarction (MI) associated with a higher en- flammation, and endothelial dysfunction (4).ergy intake from carbohydrates and a concomitant lower energy The aim of this study was to investigate the risk of myocardialintake from SFAs. Carbohydrates with different glycemic index infarction (MI) with a higher energy intake from carbohydrates(GI) values were also investigated. and a concomitant lower energy intake from SFAs. CarbohydratesDesign: Our prospective cohort study included 53,644 women and with different GI values were investigated. Furthermore, potentialmen free of MI at baseline. effect modification by sex was investigated because of differencesResults: During a median of 12 y of follow-up, 1943 incident MI in the underlying biology such as hormonal differences.cases occurred. There was a nonsignificant inverse association be-tween substitution of carbohydrates with low-GI values for SFAsand risk of MI [hazard ratio (HR) for MI per 5% increment of SUBJECTS AND METHODSenergy intake from carbohydrates: 0.88; 95% CI: 0.72, 1.07). Incontrast, there was a statistically significant positive association Study populationbetween substitution of carbohydrates with high-GI values for SFAs Between December 1993 and May 1997, 160,725 women andand risk of MI (HR: 1.33; 95% CI: 1.08, 1.64). There was no men were invited by mail to participate in the Danish prospectiveassociation for carbohydrates with medium-GI values (HR: 0.98; cohort study Diet, Cancer, and Health. The criteria for invitation95% CI: 0.80, 1.21). No effect modification by sex was observed. were as follows: age between 50 and 64 y, born in Denmark, andConclusion: This study suggests that replacing SFAs with carbohy- no previous cancer diagnosis registered in the Danish Cancerdrates with low-GI values is associated with a lower risk of MI, Registry. All persons fulfilling these criteria and living in thewhereas replacing SFAs with carbohydrates with high-GI values is greater Copenhagen or Aarhus areas were invited. With the in-associated with a higher risk of MI. Am J Clin Nutr 2010;91:1764–8. 1 From the Department of Clinical Epidemiology Aarhus University Hos- pital, Aalborg, Denmark (MUJ); the Department of Cardiology, Center for Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital,INTRODUCTION Aalborg, Denmark (MUJ, CD, AMJ, JS, EBS, and KO); the Danish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark (AT); and Epidemiologic prospective cohort studies have suggested that the Department of Epidemiology, School of Public Health, Aarhus Univer-replacing saturated fatty acids (SFAs) with carbohydrates is sity, Aarhus, Denmark (KO).modestly associated with a higher risk of ischemic heart disease 2
    • org at Lund University Libraries on November 5, 2010values (HR in the second tertile of dietary GI: 0.98; 95% CI: carbohydrates and a concomitant lower energy intake from SFAs.0.80, 1.21) (Table 3). As assessed from the 95% CIs, the Relevant control for established risk factors for IHD did not changemeasures of associations for extreme tertiles of GI were statis- corresponding editorial on pageand thus residual confounding seems See the measures of associations, 1541.tically significantly different. The P value for effect modification unlikely. However, confounding from other IHD risk factors notIntake of dietary GI The P value for effect0.29 in men, and taken into accountsaturated fatty acidsthe observedby tertiles of carbohydrates compared with intake of remains a possible explanation for0.16 in all participants. was 0.06 in women, modification by associations. 1–3and risk of myocardial infarction: importance 2of the glycemichave investigated the sub-sex was 0.86. Only epidemiologic studies index stitution of carbohydrates for SFAs (1, 18). In the prospectiveMarianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjønneland, al (18), Schmidt, cohort study by Hu et Erik B substitution of carbohydrates forDISCUSSIONand Kim Overvad SFAs was nonsignificantly associated with a lower risk of IHD, The findings from this study suggest that the effect of sub- whereas in the prospective cohort study by Jakobsen et al (1), inABSTRACT concentration data from 11 American and European cohort studies werestitution of carbohydrates for SFAs varies depending on the type of which is tightly regulated by homeostatic regulatoryBackground: Studies have suggested that replacinginverse associationcarbohydrates. There was a nonsignificant saturated fatty systems, but the rapid absorption of carbohydrates after con- modestly pooled, substitution of carbohydrates for SFAs wasacids (SFAs) with carbohydrates is modestly associated with a high- sumption of a high-GI meal challenges these homeostaticer risk of ischemic heart disease, whereas replacing SFAs withTABLE 3 mechanisms (4). A high-GI meal results in a high blood glucose Downloaded from www.ajcn.org at Lund University Libraries on November 5, 2010polyunsaturated fatty acids is associated with per 5% increment of energy intake from carbohydrates with low–glycemic ratio, followed byHazard ratios (HRs) for myocardial infarction a lower risk of ische- concentration and a high insulin-to-glucagon index (low-GI), medium-GI, ormic heart disease. The effect of carbohydrates,intake frommay de- fatty acids1high-GI values and a concomitant lower energy however, saturated hypoglycemia, counterregulatory hormone secretion, and ele-pend on the type consumed. vated plasma free fatty acid concentration (4). These events may All participantsObjectives: By using substitution models, we aimed to investigate Women affect the risk of IHD through promoting dyslipidemia, in- Menthe risk of myocardial infarction (MI) associated with a higher en- flammation, and endothelial dysfunction (4).Tertiles of Median dietary GIergy intake from carbohydrates and a concomitant lower energy The aimdietary GI Median of this study was to investigateMedian dietary GI the risk of myocardialintake GI2dietary from SFAs. Carbohydrates with different glycemic (95% CI) (80% central range) HR index (80% central range) HR (95% CI) (80% central range) HR (95% CI) infarction (MI) with a higher energy intake from carbohydrates(GI) values were also investigated.Carbohydrates with low-GI 82 (77, 85) 0.88 (0.72, 1.07)and a concomitant lower energy intake from SFAs. Carbohydrates (0.65, 1.04) 80 (75, 82) 1.17 (0.80, 1.71) 84 (79, 86) 0.83Design: Our prospective cohort study included 53,644 women and with different GI values were investigated. Furthermore, potential values (first tertile)men free of MI at baseline.Carbohydrates with medium-GI 88 (86, 90) 0.98 (0.80, 1.21)effect modification by sex was investigated because of91) 85 (84, 87) 0.80 (0.54, 1.18) 89 (87, differences (0.84, 1.38) 1.08Results: During a median of 12 y of follow-up, 1943 incident MI in the underlying biology such as hormonal differences. values (second tertile)cases occurred. There was a nonsignificant inverse association be-Carbohydrates with high-GI 93 (91, 98) 1.33 (1.08, 1.64) 91 (88, 96) 1.10 (0.75, 1.63) 94 (92, 98) 1.34 (1.04, 1.71)tween substitution of carbohydrates with low-GI values for SFAs values (third tertile)and risk of MI [hazard ratio (HR) for MI per 5% increment of SUBJECTS AND METHODS 1energyAll models included intake of glycemic carbohydrates, proteins, monounsaturated fatty acids, and polyunsaturated fatty acids expressed as percentages intake from carbohydrates: 0.88; 95% CI: 0.72, 1.07). Incontrast, there intake, total energy intake (kcal/d), an indicator variable for alcohol consumption (0 and .0 g/d), alcohol consumption (g/d), BMI (in kg/m2;of total energy was a statistically significant positive association Study population,25, 25–29, and 30), carbohydrates 8–10, and .10 y), for SFAsbetween substitution of education (,8,with high-GI valuessmoking status (never, former, and currently and May1–14, 15–24, or 25 g tobacco/d), physical Between December 1993 smoking 1997, 160,725 women andand risk(,3.5 and 3.51.33; 95% CI: 1.08, hypertension (yes, no, andmennot know). HRs with 95%participate in the Danishmyocardial infarction wereactivity of MI (HR: h/wk), and history of 1.64). There was no do were invited by mail to CIs for the incidence of prospectiveassociationby using Cox proportionalmedium-GI values with age as the cohort study In analyses among all participants, sex was entered into the model.calculated for carbohydrates with hazards regression (HR: 0.98; time metric. Diet, Cancer, and Health. The criteria for invitation 295% CI: 0.80, of dietary GI were based on theby sex was observed. GI amongas follows:22,144, 17,000, and 14,400 for allin Denmark,in the first, second, Tertiles 1.21). No effect modification distribution of dietary were cases. n = age between 50 and 64 y, born participants andConclusion: This study suggests that replacing 9594, with carbohy-and third tertiles of dietary GI, respectively; n = SFAs 10,202, and 8699 for women in the first, diagnosis registered in of dietary GI,Cancer no previous cancer second, and third tertiles the Danish respectively; and n =drates 8127, low-GI values is associated with a lowerthird tertiles of dietary GI, respectively. fulfilling these criteria and living in the8941, with and 8081 for men in the first, second, and risk of MI, Registry. All personswhereas replacing SFAs with carbohydrates with high-GI values is greater Copenhagen or Aarhus areas were invited. With the in-associated with a higher risk of MI. Am J Clin Nutr 2010;91:1764–8. 1 From the Department of Clinical Epidemiology Aarhus University Hos- pital, Aalborg, Denmark (MUJ); the Department of Cardiology, Center for Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital,INTRODUCTION Aalborg, Denmark (MUJ, CD, AMJ, JS, EBS, and KO); the Danish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark (AT); and Epidemiologic prospective cohort studies have suggested that the Department of Epidemiology, School of Public Health, Aarhus Univer-replacing saturated fatty acids (SFAs) with carbohydrates is sity, Aarhus, Denmark (KO).modestly associated with a higher risk of ischemic heart disease 2
    • with dietary intake cannot be completely adjusted for in ob- 95% CI: 1.25, 1.60), breast cancer (GI RR 2 major GL RR ҃ 1.41, certain chronic diseases with high-GI diets. Specifically, ҃ 1.08, Mo by Custodio Cesar on November 18, 2008 servational studies. Therefore, a meta-analysis of intervention1.16), and all diseases combined (GI RR ҃ 1.14, 95% 95% CI: 1.02, pathways have been proposed to explain the association with por studies looking at “hard” clinical endpoints, not chronic- type 2 diabetes risk (57). First, the same amount of carbohydrate disease risk factors, may be warranted, when CI:sufficient data GL RR ҃ 1.09, 95% CI: higher blood glucose concentra- 1.09, 1.19; from high-GI foods produces 1.04, 1.15). tionGlycemic index, glycemic load, and chronic disease risk—a meta- have accumulated. Conclusions: Low-GI and/or low-GLfor insulin. The chronically increased tions and a greater demand diets are independently asso- deranalysis of observational studies glycemia, in ciated to chronic insulin demand maymeta- result in pancreatic ␤ cell failure, Our findings support the hypothesis that postprandial hyper- 1,2 Glycemicindividuals glycemic load, and with a reduced risk of certainimpaired glucose tolerance. Second, there index, without diabetes, contributeschronic diseasea consequence, chronic diseases. In diabetes and and, as risk—a eventually stud disease. Higher observational studies1,2 disease,athe protection ishigh-GI diets may directly increase insulin re- analysis of glucose concentrations areheart to play thought is evidence that comparable with that seen for whole a thAlan W Barclay, role in Petocz, Joanna McMillan-Price, Victoria M Flood, Taniaeffect on glycemia,the hypothesis that direct pathogenic Peter the disease process. The DECODE fiber intakes. The findings support free fatty acids, and grain and high sistance through their Prvan, Alan W Barclay, Peter Petocz, 13 studies involving 25 000 M Flood, Tania Prvan, study, a meta-analysis of Joanna McMillan-Price, Victoria individu-PaulMitchell, and Jennie Jennie C Brand-Miller Mitchell, and C Brand-Miller counter-regulatory hormone secretion. High glucose and insulin O als, found an almost 2-fold increased risk ofhigher postprandial glycemiaare associated with mechanism profiles for concentrations is a universal increased risk for disease Paul all-cause mortality stud in individuals ABSTRACT progression. cereal products cereal products 2008;87:627–37. Am J Clin Nutrhave replaced more traditionally processedABSTRACT with an elevated 2-h postchallenge blood glucose have replaced more traditionally including decreased concentrations of cardiovascular disease, processed drat Background: Inconsistent findings from observational studies have grains. Because carbohydrate is the main dietary componentBackground: Inconsistent findings from observational studies havesecretion and postprandial glycemia (3), it is is the main dietary component grains. Because carbohydrate prolonged the controversy over the effects of dietary glycemic index TABLE 4 affecting insulinprolonged the controversy over the effects of dietary glycemic index etiology of many chronic diseases. Both the postprandial glycemia (3), it is (GI) and glycemic load (GL) on the risk of certain chronic diseases. implicated in the affecting insulin secretion and hyd(GI) and glycemic load to evaluate the associationthe KEYwith the and type of carbohydrate consumedindex, glycemicincreasingdietaryindex WORDS highest amount lowest quantile for developing chronic an effect because of load, glycemic carbo- Objective: The objectiveCIs) for the on the risk of certain chronic diseases. Rate ratios (and 95% was (GL) comparison of between Glycemic have disease on sho Downloaded from www.ajcn.org by Custodio Cesar on November 18, 2008 GI,glycemic load disease risk with the use of meta-analysis tech- a priori insulin secretion and postprandialin the food-frequencymany chronic diseases. Both the implicated etiology of or GL, and chronic in 27 prospective cohort studies meeting both exclusion criteria (correlation between with differ- questionnaire and weighed foodObjective: The objective was to evaluate the association epidemiology and glycemia, carbohydrate consumed have an effect on hydrates, not explained by amount length (4). In 1981, the between glucose chain type of Downloaded from www.ajcn.org by Custodio Cesar on November 18, 2008 niques. records/24-h dietary recall ͧ 0.5 in representative subgroups)encesGI, GL, and chronic disease riskreports identified a total concept of the glycemic index (GI) was introduced by Jenkins et Design: A systematic review of published with the use of meta-analysis tech- Ano both insulin secretion and postprandial glycemia, with differ-niques. were cohort studies of GI and GLto thechronic disease al (5) to quantify theindex rate not explained by glucose chain length (4). In 1981, the of 37 prospective risk. Studies stratified further according and validity of the Glycemic glycemic response to carbohydrates inGlycemic load rate ences but Chronic A systematic review of published reports different a total ratio1 P ratio1Design:disease dietary intake. Rate ratios (RRs) were estimated identified foods. Glycemic load (GL), the mathematical product (GI) was introduced by Jenkins et P tools used to assess concept of the glycemic index of the GI of a food and its carbohydrate content, has been pro-of 37 2 diabetes (6–11) random-effects model. INTRODUCTION1.59)theto quantify the glycemic (1.12, 1.45) to carbohydrates in in a Cox proportional hazards model and of GI and GL and chronic disease Type prospective cohort studies combined by using a posed as a global (1.23,al of 1.40 indicator (5) glucose response and insulin 1.27 response 0.0001 0.0001 1risk. Studies (14, 16) follow-up across studies, a total of 40to the validity of1.25by a serving of food (6). 0.050 Heart disease were stratified further according 129 the demand induced (1.00, 1.56) 1.57 (0.87, 2.84) 0.140 Worldwide,studies that investigated havefood inconsistent. 1.28 (0.83,the content, has0.270 pro- The results of (0.86,different foods.0.805 between Glycemic load (GL), 1.98) mathematical product Results: From 4 to 20 y of Stroke casesto assess dietary intake. Rate ratios (RRs) were estimatedchronic diseases such as diabetes, cardiovasculartools used incident (15) were identified. For the comparison between the high- 1.02 1.21) the association lia (A Breast cancer (17–19, GI hazards model and combined by dietary GI, GL, and disease risk a 0.015and its carbohydrate overall of the GI of beenin a Cox proportionaland GL, significant positive associa- With stroke, (1.02, a cancer contribute to Ȃ60% 1.06)all deaths, and est and lowest quantiles of21, 30) using a and1.16) association was documented 0.99 (0.92, of 1.09 been 0.797 disease, tions were found in fully adjusted models of validated studies for respect to diabetes,posed as a global indicator of the glucose response and insulin positive rie Urandom-effectsRR ҃ 1.40, 34, 35) 1.23, 1.59; GL RR ҃ 1.27, in 6 large cohort studies (6 –11), but no association was seen in 2 1.11 (0.88, 1.40) Colorectal cancer (23, 29, type 2 diabetes (GI model. 95% CI: 1.11 (0.99, 1.24) 0.059 0.385 95% CI: 1.12, 1.45), coronaryy of disease (GI RR ҃ 1.25, 95% CI: proportion is predicted to 2 studies the others (12, 129 cardiovascular Pancreatic cancer (11, 24) 0.98 (0.78,demanddisease, increase toa75% by the year 2020 (1, 1.25) induced by areported 0.96food (6). 0.896 serving of (0.75, 1.23) 0.733 moloResults: From 4 to 20 32) follow-up across studies, a total of 4013). In(0.80, 1.60) heart Endometrial cancer (26, (GI RR ҃ 1.26, 95% CI: 1.13, 1.40; 1.13 (14, 15), whereas 1 foundstudies that investigated the association between 0.489 1.72 (0.75, 3.95) 0.204incident 1.41, 95% CI: 1.25, 1.60), breast cancercomparison betweenof the studies thatis The results of0.320 have re- 0.76 (0.46, 1.25) Wes positive association 1.00, 1.56), gallbladder disease Gastric cancer GL RR ҃ were 1.08, Most the high- diet 1.29) majornomodifiable risk factor, and the cases(28) identified. For the (GI RR ҃2). Habitual0.77 (0.46, have investigated cancer risk the relation (16). 0.282est and1.02, 1.16),quantiles of combined GL, significant positive no associations (11, 17–29),dietary are notable excep- 1.41 (1.25, 1.60) been inconsistent. 95% CI: lowest and(38, 39) GI and (GI RR ҃ 1.14, 95% overall ported associa- (1.13, 1.40) GI, GL, and disease risk have PM) Gallbladder disease all diseases identificationfor studies that respect to 0.323 a positive association was documented 1.26 simple, but there of 1.31) cost-effective strategies for prevention 0.0001 CI: 1.09, 1.19; found ҃ fully adjusted models of validated studies1.10 (0.91,With investigated the risk of gallblad- 0.96 (0.82, 1.12)tionsdisease (40–42)in1.09, 95% CI: 1.04, 1.15). Eye were GL RR tions (30 –37). Two diabetes, 0.0001 0.590 Unit Conclusions: Low-GI and/or low-GL diets are independently asso- and management is association with eye disease, whereastypediseases (6–11, 14–19,҃ 1.40, 95% CI: 1.23, 1.59; GL RR(40,1.27, All 21, 23, 24, 26, 28–30, 32, 34, 35, ciated2 diabetes (GI of certain chronic diseases. In diabetes and with a reduced risk RR studies ҃ 41) reported an in a matter of urgency. der disease showed positive large cohort studies (6 –11), but no association was seen in 2 6 associations (38, 39). Finally, 2 2 38–42)1.12,protection is comparable with diseasefor whole ҃ a third found1.14 (1.09,others (12, 13). In cardiovascular disease, 2 studies reported a 1.19)95%disease, the 1.45), coronary heart that seen (GI RR 1.25, 95% changes(42). the quantity and quality of fat have re- 1.09 (1.04, 1.15) heart CI: Although no association in CI: 0.0001 0.0001 grain and high fiber intakes. The findings support the hypothesis that1.00,11.56),fully adjusted models only. RR ҃ 1.26, 95% CI: 1.13, 1.40; Final gallbladder disease (GI Of concern, 5 (13%) (22, 25, 27, 31, 33) of the 37 prospective whereas 1 found no relation (16). positive association (14, 15), Nutr higher postprandial glycemia is a universal mechanism for diseaseGL RR ҃ 1.41, 95% Nutr 1.25, 1.60), breast cancer (GI progression. Am J Clin CI: 2008;87:627–37. ceived RR that1.08, Most of the studies that have investigated cancer risk have re- considerable attention, dietary carbohy- of carbohydrates is less studies ҃ investigated the relation between the role j.bra drates, GI, GL, and chronic disease risk did not validate carbo-95% CI: 1.02, 1.16), and all diseases combined (GI RR ҃ 1.14, 95% an additional no associations (11, 17–29), but there areaccompa- clear (2). Increases in refined sugar36, 37) have been notable excep- hydrate intake, and ported 5 (13%) (12, 13, 20, intake R KEY WORDS Glycemic index, glycemic load, dietary carbo-CI: 1.09, 1.19; GL RR ҃ 1.09, 95% CI: 1.04,nied by more subtle changes instudies that investigated the risk of gallblad- showed correlation coefficients (30total carbohydrate of 0.5. tions for –37). Two Another 2 (5%) studies (29, 32) appear to have been starchy foods, eg, processed hydrates, epidemiology 1.15). A validated,Conclusions: Low-GI and/or low-GL diets are independently asso-study has notdisease showedothers (5%) associations (38, 39). Finally, 2 but the validation der been published, and 2 positiveciated with a reduced risk of certain chronic diseases. In diabetes and studies (40, 41) reported an association with eye disease, whereas INTRODUCTIONheart disease, the protection is comparable with that Clinfor whole Nutrition Unit, University of Sydney, Sydney, Austra-(42).© 2008 American Society Am J seen Nutr 2008;87:627–37. no association 1 From the Human a third found Printed in USA. for Nut Worldwide, chronic diseases such as diabetes, cardiovascular lia (AWB, JM-P, VMF, and JCB-M); the Department of Statistics, Macqua-grain and high fiber intakes. TheȂ60% of all support the hypothesis Sydney, AustraliaOf and TP); the Department of Ophthal- 27, 31, 33) of the 37 prospective disease, stroke, and cancer contribute to findings deaths, and rie University, that (PP concern, 5 (13%) (22, 25,higher postprandial the proportion is predictedglycemiato 75%universal2020 (1, to increase is a by the year mechanism for Centre for Vision Research, Westmead Millennium Institute, mology, disease 2). Habitual diet is the major modifiable risk factor, and the Westmead Hospital, University of Sydney, Sydney, Australia (VMF and relation between dietary carbohy- studies that investigated the
    • MITO 2 massa, batata ou pão. As pessoas com Diabetes devem evitar comer arroz,MITO 2 • Estes alimentos são grandes fornecedores de hidratos de carbono massa, batata ou pão. (HC), os nutrientes que mais influenciam os níveis de glicemia após as refeições. No entanto, ao contrário dos alimentos ricos em açúcar, estes alimentos contêm HC de absorção lenta, permitindo um melhor• Estes alimentos são grandes fornecedores de hidratos de carbono controlo da glicemia ao longoe-Book do dia. (HC), os nutrientes que mais influenciam os níveis de glicemia após as refeições. No entanto, ao contrário dos alimentos ricos em açúcar, • A sua ingestão é indispensável, pois devem fornecer um melhor estes alimentos contêm HC de absorção lenta, permitindoa maior parte da controlo da glicemia nosso organismo necessita, cerca de 45 a 60% das energia que o ao longo do dia. calorias totais por dia.• A sua ingestão é indispensável, pois devem fornecer a maior parte da • Desta forma, estes alimentos devem fazer parte 45 a 60% das energia que o nosso organismo necessita, cerca dede todas as refeições calorias totais por longo do dia. realizadas ao dia.• Desta forma, estes alimentos devem fazer parte de todas as refeições realizadas ao longo do dia.
    • CEREAIS INTEGRAIS
    • dex diet than in the high–cereal fiber did not alter Mitchell, BASc, RD the as- Sandy the significance of been associa ResultsEither a High–Cereal Fiber Diet dietsa Low–Glycemic MSc glycemic in- diet at week 24. Viscous fibers or or Azadeh Emam, sociation of the change in of diabetes units (95% Effect of a Low–Glycemic Index A. Augustin, MSc Livia S. compared low–glyce Tina L. 2 Diabetes Completing Either a High–Cereal Fib Figure 3.High–Cereal Fiber Diet on Type 2 Diabetes Parker, BASc, RD or a Mean Study Measurements in Participants With Type A. Leiter, MD Index Diet Lawrence protein ch dL) comp A Randomized Trial T (95% CI,diet (n = 80) dietary gly HE High–cereal fiber diet (n = 75) NEED FOR IMPLEMENTA - Low–glycemic index diet (n = 80) David J. A. Jenkins, MD Context Clinical trials using antihyperglycemic medications to improve glycemicstrate- tion of effective dietary con- PϽ.001) Cyril W. C. Kendall, PhD trol have not demonstrated the anticipated cardiovascular benefits. Low–glycemic in- P=.009). Gail McKeown-Eyssen, PhD weight dex diets may improve both glycemic control andin HbA1c Body gies cardiovascular risk factors for pa- diabetes prevention and 90 Robert G. Josse, MB, BS Fasting glucose tients with type 2 diabetes but debate over their effectiveness continues due to trial 7.30 management has been empha- Conclus 146 limitations. 146 Jay Silverberg, MD 88 Objective To test the effectssized by the success glycemic control and 7.10 of low–glycemic index diets on of diet and life- glycemic 138 cardiovascular risk factors in patients with type 2 diabetes. cereal fib 6.90 style changes in preventing diabetes in Gillian L. Booth, MD 86 mg/dL Edward Vidgen, BSc Design, Setting, and Participants A randomized, parallel study design at a Ca- 130 Trial Reg kg 1 nadian university hospital research center of 210 patients. There is also con- high-risk participants with type 2 diabetes treated % 84 138 Andrea R. Josse, MSc 6.70 with antihyperglycemic medications who were recruited by antihyperglycemic cern that use of newspaper advertisement JAMA. 2008 122 mg/dL Tri H. Nguyen, MSc 82 6.50 and randomly assigned to receive 1 of 2 diet treatments each for 6 months between P = .052 September 16, 2004, and Maymedications to improve glycemic con- 22, P <.001 2007. P = .0 80 130 Sorcha Corrigan, BSc 6.30 114 Monica S. Banach, BSc 8 0 4 12 20 24 trol in 4type 8 diabetesadvice.20 always 16 Intervention High–cereal fiber0 low–glycemic index12 or 2 may not 24 dietary16 control 0 Sophie Ares, MA, RD, CDETime, wk significantly improve cardiovascular Main Outcome Measures Absolute change in glycated hemoglobin A1c (HbA1c), with Time, wk fasting blood glucose and cardiovascular disease2-7 factors as secondary measures. risk density 122 Sandy Mitchell, BASc, RD outcomes. (HDL-C Results In the intention-to-treat analysis, HbA1c decreased by −0.18% absolute HbA1c Azadeh Emam, MSc P = .04 One dietary strategy aimed at im- units (95% confidence interval [CI], −0.29% to −0.07%) in the high–cereal fiber diet compared with −0.50% absolute HbA1c units (95% CI, −0.61% to −0.39%) in the ide, plasm Livia S. A. Augustin, MSc HDL-C Triglycerides 46.0 114 proving both diabetes control and car- low–glycemic index diet (P Ͻ .001). There was also an increase of high-density lipo- 140 and high 4.5 Tina L. Parker, BASc, RD 24 0 4 8 12 diovascular risk 24 16 20 factors is the use of protein cholesterol in the low–glycemic index diet by 1.7 mg/dL (95% CI, 0.8-2.6 mg/ dL) compared with a decrease of high-density lipoprotein cholesterol by −0.2 mg/dL tein (CR Lawrence A. Leiter, MD 8-10 44.0 Time, wk low–glycemic index diets. These diets 130 duce dia 4.3 T (95% CI, −0.9 to 0.5 mg/dL) in the high–cereal fiber diet (P = .005). The reduction in HE NEED FOR IMPLEMENTA - dietary glycemic index related positively to the reduction in HbA1c concentration (r=0.35, have been reported to benefit the cardiova mg/dL mg/dL Ratio 42.0 tion of effective dietary strate- PϽ.001) and negatively to120increase in high-density lipoprotein cholesterol (r=−0.19, the 4.1 gies in diabetes prevention and P = .009). 40.0 management has been empha- Conclusion In patients110 2742 2 diabetes, 6-month treatment with a300, No. with type JAMA, December 17, 2008—Vol low– 23 (Reprinted) 3.9 sized by the success of dietPand life- = .01 glycemic index diet resulted in moderately lower HbA1c levels compared with a high– P = .90 style changes in preventing diabetes in 38.0 cereal fiber diet. 100 3.7
    • dex diet than in the high–cereal fiber did not alter Mitchell, BASc, RD the as- been associa Sandy the significance of Resultsn Participants With Type 2 Diabetessociation of the change in glycemic in- of diabetes diet at week 24. Viscous fibers or diets Completing Either a High–Cereal Fibe Azadeh Emam, MSc units (95% Effect of a Low–Glycemic Index A. Augustin, MSc Livia S. compared low–glyce Tina L. 2 Diabetes Completing Either a High–Cereal Fib Figure 3.High–Cereal Fiber Diet on Type 2 Diabetes Parker, BASc, RD or a Mean Study Measurements in Participants With Type A. Leiter, MD Index Diet Lawrence protein ch dL) comp A Randomizeddiet (n = 75) High–cereal fiber Trial T Low–glycemic index diet (n = 80) (95% CI, HE High–cereal fiber diet (n = 75) NEED FOR IMPLEMENTA - Low–glycemic index diet (n = 80) dietary gly David J. A. Jenkins, MD Context Clinical trials using antihyperglycemic medications to improve glycemicstrate- tion of effective dietary con- PϽ.001) Cyril W. C. Kendall, PhD trol have not demonstrated the anticipated cardiovascular benefits. Low–glycemic in- P=.009). Gail McKeown-Eyssen, PhD weight dex diets may improve both glycemic control andin HbA1c Body HbA gies cardiovascular risk factors for pa- diabetes prevention and 90 Robert G. Josse, MB, BS 1c tients with type 2 diabetes but debate over their effectiveness continues due to trial 7.30 management has been empha- Conclus 146 limitations. 7.30 Jay Silverberg, MD 88 Objective To test the effectssized by the success glycemic control and 7.10 of low–glycemic index diets on of diet and life- 146 glycemic 138 cardiovascular risk factors in patients with type 2 diabetes. cereal fib 6.90 style changes in preventing diabetes in Gillian L. Booth, MD 86 7.10 mg/dL Design, Setting, and Participants A randomized, parallel study design at a Ca- nadian university hospital research center of 210 patients. There is also 138 Edward Vidgen, BSc 130 Trial Reg kg 1 high-risk participants with type 2 diabetes treatedcon- % 84 Andrea R. Josse, MSc 6.70 with antihyperglycemic medications who were recruited by antihyperglycemic cern that use of newspaper advertisement JAMA. 2008 6.90 122 mg/dL Tri H. Nguyen, MSc 82 6.50 and randomly assigned to receive 1 of 2 diet treatments each for 6 months between September 16, 2004, and Maymedications to improve glycemic con- 22, P <.001 P = .0 P = .052 2007. 130 % Sorcha Corrigan, BSc 80 6.30 114 0 6.70 Monica S. Banach, BSc 8 4 12 16 20 24 trol in 4type 8 diabetesadvice.20 always Intervention High–cereal fiber0 low–glycemic index12 or 2 may not 24 dietary16 control 0 Sophie Ares, MA, RD, CDETime, wk significantly improve cardiovascular Main Outcome Measures Absolute change in glycated hemoglobin A1c (HbA1c), with Time, wk fasting blood glucose and cardiovascular disease2-7 factors as secondary measures. risk density outcomes. 122 (HDL-C 6.50 Sandy Mitchell, BASc, RD Results In the intention-to-treat analysis, HbA1c decreased by −0.18% absolute HbA1c Azadeh Emam, MSc P <.001 One dietary strategy aimed at im- units (95% confidence interval [CI], −0.29% to −0.07%) in the high–cereal fiber diet compared with −0.50% absolute HbA1c units (95% CI, −0.61% to −0.39%) in the ide, plasm P = .0 Livia S. A. Augustin, MSc HDL-C proving both diabetes control and114Triglycerides car- and high 46.0 6.30 Tina L. Parker, BASc, RD low–glycemic index diet (P Ͻ .001). There was also an increase of high-density lipo- 140 4.5 24 Lawrence A. Leiter, MD 0 4 8 12 16 20 24 diovascular risk factors is the use of protein cholesterol in the low–glycemic index diet by 1.7 mg/dL (95% CI, 0.8-2.6 mg/ dL) compared with a decrease of high-density lipoprotein cholesterol by −0.2 mg/dL 0 (CR tein 8-10 Time, wk low–glycemic index diets. These diets duce dia 44.0 130 4.3 T (95% CI, −0.9 to 0.5 mg/dL) in the high–cereal fiber diet (P = .005). The reduction in HE NEED FOR IMPLEMENTA - dietary glycemic index related positively to the reduction in HbA1c concentration (r=0.35, have been reported to benefit the cardiova mg/dL mg/dL Ratio 42.0 tion of effective dietary strate- PϽ.001) and negatively to120increase in high-density lipoprotein cholesterol (r=−0.19, the 4.1 gies in diabetes prevention and P = .009). 40.0 management has been empha- Conclusion In patients110 2742 2 diabetes, 6-month treatment with a300, No. with type JAMA, December 17, 2008—Vol low– 23 (Reprinted) 3.9 sized by the success of dietPand life- = .01 glycemic index diet resulted in moderately lower HbA1c levels compared with a high– P = .90 style changes in preventing diabetes in 38.0 cereal fiber diet. 100 3.7
    • dex diet than in the high–cereal fiber did notSandy the significance of the as- alter Mitchell, BASc, RD been associa Results diet at week 24. Viscous fibers or diets Triglycerides Azadeh Emam, MSc sociation of the change in glycemic in- Total cholesterol : HDL-C of diabetes units (95% Effect of a Low–Glycemic Index 140 4.5 compared Livia S. A. Augustin, MSc 130 4.3 low–glyce Tina L.2Parker, BASc, RD Either a High–Cereal Fib or a High–Cereal Fiber Diet on Type 2 Diabetes Figure 3. Mean Study Measurements in Participants With Type Diabetes Completing protein ch mg/dL Ratio Index Diet 120 Lawrence A. Leiter, MD 4.1 dL) comp A Randomized Trial T (95% CI, 110 3.9 dietary gly High–cereal fiber diet (n = HE NEED FOR IMPLEMENTA - 75) Low–glycemic index diet (n = 80) P = .90 David J. A. Jenkins, MD P = .12 100 Context Clinical trials using antihyperglycemic medications to improve glycemicstrate- 3.7 tion of effective dietary con- PϽ.001) Cyril W. C. Kendall, PhD trol have not demonstrated the anticipated cardiovascular benefits. Low–glycemic in-0 24 0 4 8 12 16 20 24 0 4 8 12 16 20 24 P=.009). Gail McKeown-Eyssen,Body weight wk dex diets may improve both glycemic control andinHbA1c PhD Time, gies cardiovascular risk factors for pa- diabetes prevention and Time, wk tients with type 2 diabetes but debate over their effectiveness continues due to trial 90 Robert G. Josse, MB, BS limitations. 7.30 management has been empha- 146 Conclus Jay Silverberg, MD 88 Objective To test the 7.10 sized by the success glycemic control and effects of low–glycemic index diets on of diet and life- glycemic 138 Gillian L. Booth, MD 86 130 Systolic BP style changes in preventing diabetes in cereal fib cardiovascular risk factors in patients with type 2 diabetes. 6.90 Diastolic BP mg/dL Edward Vidgen, BSc 76 Design, Setting, and Participants A randomized, parallel study design at a Ca- high-risk patients.1 There is also con- 130 Reg Trial kg % 84 128 nadian university hospital6.70 research center of 210 participants with type 2 diabetes treated Andrea R. Josse, MSc with antihyperglycemic medications who were recruited by antihyperglycemic cern that use of newspaper advertisement 74 JAMA. 2008 122 Tri H.126 82 Nguyen, MSc and randomly assigned to receive 1 of 2 diet treatments each for 6 months between 6.50 September 16, 2004, and Maymedications to improve glycemic con- mm Hg mm Hg 22, 2007. P <.001 P =. 124P = .052 Sorcha Corrigan, BSc 72 80 Intervention High–cereal trol in type 2 diabetes may 6.30fiber or low–glycemic index dietary advice. not always 114 control Monica S. Banach, BSc 0 122 4 8 12 16 20 24 0 4 8 12 16 20 24 0 Sophie Ares, MA, RD, CDE Time, wk significantly Time, wksecondary measures. 70 improve cardiovascular density Main Outcome Measures Absolute change in glycated hemoglobin A1c (HbA1c), with 120 fasting blood glucose and cardiovascular disease2-7 factors as risk Sandy Mitchell, = .39 P BASc, RD P = .43 outcomes.1c decreased by −0.18% absolute HbA1c (HDL-C 118 Results In the intention-to-treat 68 analysis, HbA0 24 Azadeh Emam, MSc4 0 8 12 16 20 24 One dietary strategy aimed 20 im- ide, plasm units (95% confidence interval [CI], −0.29% to4 0 −0.07%) in the12 8 16 at high–cereal fiber diet 24 Livia S. A. Augustin, MSc HDL-C compared with −0.50% absolute HbA1c units (95% CI, −0.61% to −0.39%) in the Time, wk Triglycerides wk Time, low–glycemic index diet (P Ͻ .001). There was also diabetesof high-density lipo- proving both an increase control and car- and high 46.0 L. Parker, BASc, RD Tina protein cholesterol in the 140 diovascularby 1.7 mg/dL (95% CI, 0.8-2.6use of low–glycemic index diet risk factors is the mg/ 4.5 (CR teinDL-C, high-density lipoprotein cholesterol; LDL-C, low-density Lawrence A. Leiter, MD dL) compared with lipoprotein high-density lipoprotein cholesterol by −0.2 mg/dL indi- a decrease of cholesterol; BP, blood pressure. Error bars 8-10 (95% CI, −0.9 to 0.5 mg/dL) in the high–cereal fiber diet as change reduction diets 130 low–glycemic index diets. These in duce dia Tach panel indicates the comparison between high–cereal fiber diet vs a low–glycemic index diet (P = .005). Thefrom week 0 to 4.3 44.0 HE NEED FOR IMPLEMENTA - dietary glycemic index related positively to the reduction in HbA1c concentration (r=0.35,n-to-treat analysis using an analysis of covariance model. negatively to the increase in been reportedcholesterol (r=−0.19, have high-density lipoprotein to benefit the cardiova mg/dL mg/dL PϽ.001) and Ratio 42.0 tion of effective dietary strate- 120 4.1 gies in diabetes prevention and P = .009). 2742 JAMA, December 17, 2008—Vol low– management has been empha- Conclusion In patients with type 2 diabetes, 6-month treatment with a300, No. 23 (Reprinted) 40.0n. All rights reserved. 110in moderately lower HbA1c levels comparedNo. 23 2751 3.9 sized by the success of diet and life- glycemic(Reprinted) JAMA, December 17, 2008—Vol 300, with a high– index diet resulted P = .01 style changes in preventing diabetes in cereal fiber diet. P = .90
    • 3 Clinical Nutrition and Metabolism, Department of Public Health and Caring Sciences, Uppsala University, 751 85 Uppsala, Sw and 4Department of Food Science,Foods Do Not Affect Insulin (SLU), 750 07 Uppsala, Sweden Whole-Grain the Swedish University of Agriculture Sciences Sensitivity or Markers of Lipid Peroxidation and Inflammation in Healthy, Moderately 1,2 Abstract Overweight SubjectsTABLE 5 BMI, blood pressure, and bloodKarlstrom,3 Afaf of all participants beforeSamar Basu,3 6 wk consuming Agneta Andersson,3* Siv Tengblad,3 Brita chemistry Kamal-Eldin,4 Rikard Landberg,4 and after ¨ whole-grain or refined-grain diets1 High intakesPer A of whole grain foods ˚ man,4 and Bengt Vessby3 are inversely related to the incidence of coronary heart diseases and type 2 diabete the mechanisms remain unclear. Our studyHealth and Caringevaluate the effectsUppsala, diet rich in whole grains compared with Clinical Nutrition and Metabolism, Department of Public aimed to Sciences, Uppsala University, 751 85 of a Sweden 3 Whole-grain period Refined-grain period and 4Department of Food Science, the Swedish University of Agriculture Sciences (SLU), 750 07 Uppsala, Sweden containing the same amount of refined grains on insulin sensitivity and markers of lipid peroxidation and inflammatio 2 Before After Before After P-value treatment effect randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain pro Abstractn 30 30 30 30 Sem diferenças entre os grupos (3 bread slices, intakes of whole grain foods are inversely related to the incidence of coronaryportion pasta) 2to include in their habitual daily diet for two High 2 crisp bread slices, 1 portion muesli, and 1 heart diseases and type diabetes, but Downloaded from jn.nutrition.org by guest on February 9, 2011BMI, kg/m2 28.5 6 2.4 28.8 6 2.5a the mechanisms remain unclear. Our study aimed to evaluate the effects of a6 2.1 in whole grains compared with a diet 28.4 diet rich 28.6 6 2.1 0.046Fasting blood glucose, mmol/Linsulin sensitivity was determined5.2 6 of lipid peroxidationhyperinsulinemic 0.28 periods. Peripheralthe same amount of6 0.8 grains on 5.3 6sensitivity and markers 0.9 containing 5.2 refined insulin 0.8 by euglycemic 6 0.8 5.2 and inflammation. In a clamp tests. 8-Iso-prostagland randomized crossover study, 22 women and 8 men (BMI 28 6 2) were given either whole-grain or refined-grain productsFasting insulin, pmol/L breadF2-isoprostane,22.9 measured in the urine astheirmarker25.7lipid peroxidation, and highly sensitive C-re (8-iso PGF2a), an slices, 2 crisp bread slices, was muesli, and 24.3 pasta) to include in a habitual6 of for two 6-wk (3 56.2 6 1 portion 57.6 6 1 portion 60.4 6 30.6 57.6 daily diet 0.47 3Insulin sensitivity, Mperiods. Peripheral insulin sensitivity was determined 6 euglycemic hyperinsulinemic clamp tests. 6 2.0 5.9 6 2.1 5.5 by 1.7 5.7 6 1.9 6.0 8-Iso-prostaglandin F2a 0.24 protein and IL-6PGF ), an Fanalyzedwas measured in the urine as a marker ofof inflammation. sensitive C-reactiveinsulin sensitivity [mg glucose Á kg were -isoprostane, in plasma as markers lipid peroxidation, and highly Peripheral M/I (8-iso 2a 2 6.8 6 3.0 6.5 6 2.7 6.4 6 2.9 6.9 6 3.2 0.79 21 21protein and IL-6 were analyzed in plasma as markers of inflammation. Peripheral insulin sensitivity [mg glucose Á kg bodyTotal cholesterol, mmol/L unit plasma insulin (mU/L) 3 100] did not improve when0.7 wt Á min per 21 5.5 6 0.7 5.5 6 0.7 5.5 6 0.8 5.5 6 subjects consumed whole-grain products (6.8 0.76 wt21 Á min per unit plasma insulin (mU/L) 3 100] did not improve when subjects consumed whole-grain products (6.8 6 3.0HDL cholesterol, mmol/L6.5 6 2.7 2.7 after 66 wk) or refined 0.32.9 and 6.91.23.2, respectively) and 6 were no3.2, respectively) and there were no differ at baseline and at baseline and 6.5 6 after 6 0.3 1.3 wk) or refined products6 products (6.4 6 2.9 and there 0.3 differences 1.2 (6.4 6 6 6 0.2 1.2 6.9 6 0.15LDL cholesterol, mmol/L 3.7 6 0.8 3.7 6 0.7 3.7 6 0.8 3.6 6 0.7 between the 2 periods. Whole-grain consumption also did not affect 8-iso-PGF2a in urine, IL-6 and C-reactive protein in 0.40 between the 2 periods. Whole-grain consumption also didofnot affect 8-iso-PGF2a in urine, IL-6 and C-reactive prot c plasma, blood pressure, or serum lipid concentrations. In conclusion, substitution whole grains (mainly based on milledTG cholesterol, mmol/L 1.4 6 0.8 1.5 6 0.8 1.3 6 0.6 1.6 6 1.0 0.19 wheat) for refined-grain products in the habitual daily diet of healthy moderately overweight adults for 6-wk did not affectFree fatty acid,blood pressure,markers of6 0.19 plasma, mmol/L sensitivity or or0.56 lipid peroxidation and 6 0.18 insulin serum lipid concentrations. In137: 1401–1407, 2007.substitution of whole grains (mainly based on 0.61 inflammation. J. Nutr. conclusion, 0.18 0.63 6 0.17 0.62 6 0.99Systolic bloodfor refined-grain products in the 129 6 15 daily diet 16 healthy 6 15 wheat) pressure, mm Hg 130 6 17 habitual 130 6 of 130 moderately overweight adults for 6-wk did not 0.35*Diastolic blood pressure, mm Hg 81 6 9 81 6 8 80 6 10 81 6 9 0.60 insulin sensitivity or markers of lipid peroxidation and inflammation. J. Nutr. 137: 1401–1407, 2007.8-iso-PGF2a, nmol/mmol creatinine Introduction 0.43 6 0.14 0.43 6 0.14 0.42grain products in many 0.21 6 0.15 0.44 6 countries including the 0.48 the U.K., U.S.,a-tocopherol, mmol/mmol lipid products are reported to have several positive effects and Sweden. The claims must, however, be set within the context Whole-grain 4.68 6 0.72 4.78 6 0.61 4.38 6 1.07 4.64 6 0.61 0.08 on human health (1). An inverse, relatively strong correlation of other lifestyle factors such as exercise and healthy eating habitsg-tocopherol, mmol/mmol lipid intake of0.26 6grain foods 0.24 6 0.07 from in general (1). 0.26 6 0.10 between the whole 0.12 (2–6) and fiber 0.26 6 0.10 0.10CRP, mg/L grains (7–10), based mainly6 1.62 and the incidence of coro- 2.03 on FFQ 2.38 6 2.29 2.86 6 2.96 2.34 6 1.57 0.55 Despite indications that whole grain foods may beneficially nary heart disease, is consistently shown in epidemiological studies influence glucose and lipid metabolism, knowledge of how IntroductionIL-6, ng/L of both men and women. In6 32.2 recent studies33.2 linked 14.8 addition, 15.2 6 have 15.9biological mechanisms contribute to the health effects of whole 6 32.4 15.8 6 30.9 0.79PAI-1 activity, kU/L cereal fiber and whole-grain foods to a reduced risk of type 2 grain remain weak. Several bioactive components, such asin many countries in 24.7 6 15.8 26.9 6 20.3 24.8 6 19.9 22.1 6 19.5 grain products die- 0.26 diabetes (11–16) and of the metabolic syndrome (6,17). These tary fiber, vitamins, minerals, antioxidants, and other phyto-1 Whole-grain products be most striking among overweightseveral positive effects mayand Sweden. lower the relations seem to are reported to have subjects protectants in whole grain act synergistically to The claims must, howev Data are means 6 SD. P-values (treatment effect) for differences between the 137: 1401–1407, stress are both adjusted for changes in BMI. Differences within such as exerci J. Nutr. whole-grain and refined-grain diet 2007. (11,18,19). The scientific evidence is considered sufficient to permit risk of chronic diseases (20,21). Insulin resistance and oxidative2 on human health (1). An inverse, relatively strong correlation health claims regarding the cardio-protective effect of whole- of other lifestyle factors important factors in the pathogenesis of type 2 a b c diabetes design, only in general (1).groups when compared to baseline: P , 0.001; grain foods0.05. *Parallel groupand cardiovascular diseases (22–25) and may poten- between the intake of whole P , 0.01; P , (2–6) and fiber from from 1st diet period (because carryovereffect was found). tially be affected by whole-grain intake. Induction of lipid per-
    • chroni chroni wheat large c Effect of Wheat Bran on Glycemic Control wheatc large o ment wheat sociati and Risk Factors for CardiovascularOBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and ment o ment ocoronary heart — Cohort studies indicate Diabetesthe effect of the risk of diabetes andOBJECTIVE disease (CHD).Type 2 we assessedfiber reduces wheat bran on glycemic Disease in Therefore, that cereal either sociatioOBJECTIVE — risk factors in Therefore, we assessedfiber effect of wheat bran diabetes and control and CHDJ. A. J ,(CHD). typeH2 diabetes. cereal the reducesinterest in the possible on glycemic Cohort studies indicate that the risk of sociati to con either coronary heart disease T either 1,2,3,4 7,8 D AVID ENKINS MD L , ERB AU MD here is muchcoronary heart diseasefactors in Therefore, we , assessed the effect of wheat bran on glycemic control and CHDS.risk (CHD). typeP 2 diabetes. C L W. C. K YRIL A. A , ENDALL PHD , 1,3 1,3 J W. C T HILIP , ONNELLY PHD 7,8 2,9,10 health benefits of fiber-containing crease to con cereals (1–3). The exact component to con IVIA UGUSTIN MSC EROME EITEL MD RESEARCHMDESIGN risk , AND METHODScontrol and CHD A C. M,factors in typeW diabetes. —, A total or facet of fiber that is responsible has nottype 2 diabetes 2 C. V , of 23 subjects with source 5 M creases 2 ARGARET ARTINI PHD 6 S ILLIAM INGER MD 7,10 ETTE XELSEN PHD A RTHUR ANDENBROUCKE PHD been clearly defined, and there are indi- V , DWARD IDGEN BSC , OROTHEA AULKNER RD 1,3 1 (16 men and E7 postmenopausal METHODS — A total cationsbenefits (4) andphasesrisk of a randomized RESEARCHT DESIGN AND women) completed twoabolic23 the whole grain confers met- D F L R G. J A. L AWRENCE OBERT , , EITER MD OSSE MD 1,2,3,4 1,2,3,4 3-month reduces the of of that subjects with type 2 diabetes creases cemic sourceRESEARCH 7 In the testAND METHODS — A cereals werestudies have Thewithproducts high in crossover and DESIGN phase, bread andcompletedtotal chronic disease (1,5,6). suggested oftype 2 diabetes 1 P , (16 men study. postmenopausal women) breakfast twolarge cohort subjects resultsthat a randomized of 23 provided as of source INA ARKER RD 3-month phases studie cemic c(16 men and 7g/day additional cereal fiber).breakfast cereals3-month against the develop- a randomized postmenopausal bread andcompleted twowheatoffiber protects phases of cereal fiber (19 In the test phase, crossover study. women) In the control phase, supplements products high in were provided as were low in fiber cemic ment diabetes (1–3). Many diabetes as- proved studiescrossoveradditionalthe testfiber). bread fiber reduces the risk of diabetes and phase,advise glycemic controlintake, low in fiber (4 g/day study. In heart additional cereal fiber). breakfast glycemic sociationsimprove increased fiberas were cereal fiber (19 g/day — Cohort studies indicate we assessed and Inwheat bran on cereals were provided (7)products high in OBJECTIVE phase, cereal(CHD). Therefore, that cereal the effect of the control either to supplements or studie coronary diseasecereal fiber (19control and cereal fiber).diabetes. fiber). In the control phase,fiber from a variety of (8). In- low in fiber (10) an proved (4 g/day additional CHD risk factors in type 2cereal g/day additional supplements were to confer general health benefits proved RESULTS — Between fiber). completed controlphases oftyperandomized cemic control in type 2 diabetes (9). gly- creases in(4 g/day additionaland 7DESIGNthe METHODS — A total of 23 subjectstreatments, sources have been shown to improveEarly seen in body RESEARCH cereal AND test and two 3-month with a 2 diabetes no differences were dietary subjec (10) an (16 men postmenopausal women) (10)eff cial an subject RESULTS — blood glucose, test In the,control phase, lipids, apolipoproteins, blood pressure, serum uric weight, fastingcereal fiber (19 g/day additional cereal fiber).andserumsupplements were low in fiber proved both glycemic control inwere seen in body Between the HbA1c control treatments, no differences diabetes crossover study. In the test phase, bread and breakfast cereals were provided as products high in studies suggested that cereal fiber im-RESULTS — blood glucose,test andserum lipids, apolipoproteins, tolerance fornondiabetic seen in body acid, clotting factors, homocysteine,, C-reactivetreatments, (10) anddifferences the benefi- subjecC clear. cial effe weight, fastingRESULTS — Betweenthe and control treatments, no differences protein, magnesium,reason in pressure, serum uric Between HbA1c control were seen in body subjects (11). Theblood were no glucose calcium, iron, or ferritin. (4 g/day additional cereal fiber). the testweight, fastingfactors,testglucose, HbAHbAlipids,C-reactivethatapolipoproteins, blood pressure, serum uric blood glucose, serum , serum lipids,iron, or ferritin. clear. control phase the iron, 5.4%, P Ͻ LDL oxidationweight,thefactors, homocysteine,,was1cprotein, magnesium,bloodprotein,uric theCereal nonviscous cereal fiber israte Ϯor ferritin. acid, clotting acid, clotting blood phase C-reactivehigher than pressure, serum in cial effects of fibers docalcium, not in fasting homocysteine, apolipoproteins, calcium, seen magnesium, not reduce (12.1 1c cialgas of eff clear. Cacid, oxidation0.034).the test phasehigher thanhigheroutcontrolstudyprotein,food the controlthe postprandial gly- Ϯ orand food 0.034). Of theLDL oxidation inhomocysteine, dropped thethanphasefordropped of gastric emptying study intestinal LDL clotting factors,subjects originally recruited,recruited, the that seenPin absorption orthe calcium, iron, 5.4%, P Ͻ in Of the the test phase was wasmore C-reactive (12.1 Ϯ 5.4%, Ͻ out of flatten and small for health ferritin. subjects originally that seen in of more health and magnesium, phase (12.1 clear. C of gast absorpLDL oxidation preference reasons fromthe controlsubjects) thanthan thatsubjects). in thethe thecontrast, viscous fibers subjects). food preference the in the testoriginally recruited,(16phase (11 seen thanmeal (12). Into astudy for health5.4%, P Ͻ 0.034). Of reasons from phase was higher the more dropped outcontrol phase (11 Ϯ and subjects the control phase (16 phase test subjects) cemic response phase (12.1 test of test high-carbohydrate of gast absorp cemic0.034). Of the CONCLUSIONSfactors for CHD cereal foods did not improve(16 subjects) are out guar test gastric emptying (13)subjects). food preference reasons from the control phase conventional longer studies than the and pectin have been(11health and mic control or risk originally recruited, more dropped to reduce thethe study for subjects — High-fiber in type 2 diabetes over 3 months. Possibly markers of glyce- such as of rate of phase shown absorp cemic test m CONCLUSIONS another High-fiber cereal foodssubjects) than theconventional(14),preference reasonstofrom component of of cereal fiber.that imparts(16 advantagesnot improveproviding a phase (11 subjects). a marker for — the control phase health did or a healthy required demonstrate the benefits whole grains Alternatively, cereal fiber in the diet may be thereby test mechanism for po- and small intestinal absorption markers of glyce- cemic test me such a CONCLUSIONS — High-fiber in type 2 diabetes over shown to conventional longer studies are lifestyle. mic control or risk factors for CHD cereal foods 25:1522–1528, 2002 3tential benefits. These fibers have been Diabetes Care months. Possibly markers of glyce- did not improve reduce postprandial glycemia suchm test as to reduCONCLUSIONS — High-fiber cereal foods did not improve conventionalwhenthe diet mayare required to demonstrate the benefits of cereal fiber. Alternatively, urinary meals. They alsomarkers of glyce- mic control or risk factors for CHD in type 2 diabetes over 3when added cereal fiber in months. Possibly longer studies be to test de- such a to redu crease 24-h glucose losses and smic control oranother component of of cereal fiber.that imparts (15).diets of subjects with type 2the or a may are a markerto demonstrate the benefits whole grains Alternatively, cerealadvantages diet healthy required for risk factors for CHD in type 2 diabetes over 3added to the Possiblyin ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● health months. fiber longer studies be to redu diabetes From the 1Clinical Nutrition and Risk Factor Modification Center, St. Michael’s Hospital, Toronto, Ontario, and sm therebrequired to demonstrate the benefits of cereal fiber.that imparts health wheat fiber, rathertheor a healthy lifestyle. for another component of whole grains Alternatively, cerealadvantages diet may be a marker Furthermore, it is Canada; the 2Department of Medicine, Division of Endocrinology and Metabolism, St. Michael’s Hospital, fiber in lifestyle.a marker for another component of whole grains that impartsstudies to be associated with a re- or a healthy than viscous fiber, that for more than two Toronto, Ontario, Canada; the 3Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; the 4Department of Medicine, Faculty of Medicine, University of health advantages decades has been shown consistently in and s thereb tential Toronto, Toronto, Ontario, Canada; 5Kraft Foods, Glenview, Illinois; the 6Lundberg Laboratory for Diabeticlifestyle. ¨ cohort Research, Department of Internal Medicine, Sahlgrenska University Hospital, Goteborg, Sweden; the 7De- Diabetes heart disease25:1522–1528, 2002 duced risk of Care (5,6,16,17). partment of Laboratory Medicine, Division of Clinical Biochemistry, St. Michael’s Hospital, Toronto, On- thereb tential shown 9 These effects are seen despite the fact that tario, Canada; the 8Department of Hematology, St. Michael’s Hospital, Toronto, Ontario, Canada; the viscous fibers Care 25:1522–1528, 2002 Diabetesfromgum have been shown Department of Biochemistry, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; and Jenkins D, et al. Diabetes Care 25:1522–1528, 2002 and guar the 10Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, oats, barley, psyllium, tential shown when pectins, Toronto, Ontario, Canada. the blood lipid Care 25:1522–1528, 2002 Diabetes profile, whereas the insol- to lower serum cholesterol and improve Address correspondence and reprint requests to David J. A. Jenkins, Clinical Nutrition and Risk Factor when a shown crease Modification Center, St. Michael’s Hospital, 61 Queen St. East, Toronto, Ontario, Canada, M5C 2T2. E-mail: cyril.kendall@utoronto.ca. uble fibers were largely without effect
    • AUMENTO DA INGESTÃO DE FIBRA A PARTIR DE CEREAIS INTEGRAIS DE 9 PARA 17 GRAMAS AUMENTO NÃO SIGNIFICATIVO DO RISCO RELATIVO EM 18% Diet And Reinfarction Trial Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.
    • Diabetologia DOI 10.1007/s00125-007-0716-y ARTICLE A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease S. Lindeberg & T. Jönsson & Y. Granfeldt & E. Borgstrand & J. Soffman & K. Sjöström & B. Ahrén 1,400 Received: 1 May 2007 / Accepted: 4 May 2007 Início Incremental AUC Glucose0–30 a # Springer-Verlag 2007 Insulin0–30, did not change signif Início 6 sem 12 sem Abstract1,200 p=0.03). In the study population as a whole, there was no a trend towards lowe although Aims/hypothesis Most studies of diet in glucose intolerance relationship between change in AUC Glucose and and type 2 diabetes have focused on intakes of fat, carbo- 0–120 Insulin0–30 was seen in both group changes in weight (r=−0.06, p=0.9) or waist circumference hydrate, fibre, fruits and vegetables. sem we aimed to 6 Instead, Reported food composition dif (r=0.01, p=1.0). There was a tendency for a larger decrease compare 1,000 were available during human evolution diets that of AUC Insulin 0–120 in the Palaeolithic group, but because of with more recently introduced ones. the strong association between change in groups such that subjects in the P AUC Insulin Glucose AUC0−120 (mmol/l x min) 12 sem Methods Twenty-nine patients with ischaemic heart disease 0–120 and change in waist circumference (r=0.64, p=0.0003), this plus either glucose intolerance or type 2 diabetes were ran- did not remain after multivariate analysis. much lower intake of dairy pro domised to receive (1) a Palaeolithic (‘Old Stone Age’) diet 800 (n=14), based on lean meat, fish, fruits, vegetables, root margarine, and a higher intake of f Conclusions/interpretation A Palaeolithic diet may im- prove glucose tolerance independently of decreased waist vegetables, eggs and nuts; or (2) a Consensus (Mediterra- circumference. The intake of vegetables, meat, m nean-like) diet (n=15), based on whole grains, low-fat dairy products, vegetables, fruits, fish, oils and margarines. Pri- Keywords Diet . Evolution . Glucose intolerancediffer significantly between the not . 600 mary outcome variables were changes in weight, waist cir- Ischaemic heart disease . Palaeolithic diet . Type 2 diabetes cumference and plasma glucose AUC (AUC Glucose 0–120 ) was low with no difference betwee and plasma insulin AUC (AUC Insulin 0–120 ) in OGTTs. Results Over 12 weeks, there was a 26% decrease of AUC Abbreviations BIA Absolute protein intake was ident bioelectrical impedance analysis Glucose 400 (p=0.0001) in the Palaeolithic group and a 7% 0–120 E% while relative protein intake (as a pe percentage of total energy intake decrease (p=0.08) in the Consensus group. The larger (p= HOMA-IR homeostasis model assessment 0.001) improvement in the Palaeolithic group was indepen- of insulin resistance intake [E%]) was higher in the Pala dent (p=0.0008) of change in waist circumference (−5.6 cm IFG impaired fasting glucose 200 in the Palaeolithic group, −2.9 cm in the Consensus group; IGT impaired glucose tolerance carbohydrate intake was 43% low IHD ischaemic heart disease group, and 23% lower in terms of E Electronic supplementary material The online version of this article NGT normal glucose tolerance (doi:10.1007/s00125-007-0716-y) contains supplementary material, 47% lower in the Palaeolithic group which is available 0 authorised users. to S. Lindeberg (*) : T. Jönsson : E. Borgstrand : J. Soffman : with cereal intake (r=0.75, p<0.00 Palaeolithic Introduction Consensus : B. Ahrén K. Sjöström Energy intake was 25% lower iFig. 2 Mean SwedenHs 32,AUCs (0–120 min) during OGTTs at tolerance start and type 2 diabetes are Department of Medicine, SE-221 85 Lund, glucose University of Lund, Impaired glucose study (IGT)(baseline, light grey columns) and after 6 weeks (dark factors for ischaemic heart disease (IHD) [1, 2], Table 6) despite similar e-mail: staffan.lindeberg@med.lu.se common risk grey columns) (p=0.004;
    • DiabetologiaDOI 10.1007/s00125-007-0716-y ARTICLEA Palaeolithic diet improves glucose tolerancemore than a Mediterranean-like diet in individualswith ischaemic heart diseaseS. Lindeberg & T. Jönsson & Y. Granfeldt &E. Borgstrand & J. Soffman & K. Sjöström & B. AhrénReceived: 1 May 2007 / Accepted: 4 May 2007# Springer-Verlag 2007Abstract p=0.03). In the study population as a whole, there was noAims/hypothesis Most studies of diet in glucose intolerance relationship between change in AUC Glucose0–120 andand type 2 diabetes have focused on intakes of fat, carbo- changes in weight (r=−0.06, p=0.9) or waist circumferencehydrate, fibre, fruits and vegetables. Instead, we aimed to (r=0.01, p=1.0). There was a tendency for a larger decreasecompare diets that were available during human evolution of AUC Insulin0–120 in the Palaeolithic group, but because ofwith more recently introduced ones. the strong association between change in AUC Insulin0–120Methods Twenty-nine patients with ischaemic heart disease and change in waist circumference (r=0.64, p=0.0003), thisplus either glucose intolerance or type 2 diabetes were ran- did not remain after multivariate analysis.domised to receive (1) a Palaeolithic (‘Old Stone Age’) diet Conclusions/interpretation A Palaeolithic diet may im-(n=14), based on lean meat, fish, fruits, vegetables, root prove glucose tolerance independently of decreased waistvegetables, eggs and nuts; or (2) a Consensus (Mediterra- circumference.nean-like) diet (n=15), based on whole grains, low-fat dairyproducts, vegetables, fruits, fish, oils and margarines. Pri- Keywords Diet . Evolution . Glucose intolerance .mary outcome variables were changes in weight, waist cir- Ischaemic heart disease . Palaeolithic diet . Type 2 diabetescumference and plasma glucose AUC (AUC Glucose0–120)and plasma insulin AUC (AUC Insulin0–120) in OGTTs. AbbreviationsResults Over 12 weeks, there was a 26% decrease of AUC BIA bioelectrical impedance analysisGlucose0–120 (p=0.0001) in the Palaeolithic group and a 7% E% percentage of total energy intakedecrease (p=0.08) in the Consensus group. The larger (p= HOMA-IR homeostasis model assessment0.001) improvement in the Palaeolithic group was indepen- of insulin resistancedent (p=0.0008) of change in waist circumference (−5.6 cm IFG impaired fasting glucosein the Palaeolithic group, −2.9 cm in the Consensus group; IGT impaired glucose tolerance IHD ischaemic heart diseaseElectronic supplementary material The online version of this article NGT normal glucose tolerance(doi:10.1007/s00125-007-0716-y) contains supplementary material,which is available to authorised users.S. Lindeberg (*) : T. Jönsson : E. Borgstrand : J. Soffman : IntroductionK. Sjöström : B. AhrénDepartment of Medicine, Hs 32, University of Lund,SE-221 85 Lund, Sweden Impaired glucose tolerance (IGT) and type 2 diabetes aree-mail: staffan.lindeberg@med.lu.se common risk factors for ischaemic heart disease (IHD) [1, 2],
    • Diabetologia DOI 10.1007/s00125-007-0716-y ARTICLE A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease S. Lindeberg & T. Jönsson & Y. Granfeldt & E. Borgstrand & J. Soffman & K. Sjöström & B. Ahrén Received: 1 May 2007 / Accepted: 4 May 2007 # Springer-Verlag 2007 Dieta Paleolitica Dieta Med Abstract P p=0.03). In the study population as a whole, there was no (n=14) Aims/hypothesis Most studies of diet in glucose intolerance relationship (n=15) in AUC Glucose between change and 0–120 and type 2 diabetes have focused on intakes of fat, carbo- changes in weight (r=−0.06, p=0.9) or waist circumference hydrate, fibre, fruits and vegetables. Instead, we aimed to (r=0.01, p=1.0). There was a tendency for a larger decreaseInício do Estudo 10 compare diets that were available during human evolution with more recently introduced ones. 9 0.4 of AUC Insulin0–120 in the Palaeolithic group, but because of the strong association between change in AUC Insulin0–120 Methods Twenty-nine patients with ischaemic heart disease and change in waist circumference (r=0.64, p=0.0003), this 6 Semanas 1 plus either glucose intolerance or type 2 diabetes were ran- domised to receive (1) a Palaeolithic (‘Old Stone Age’) diet 3 did not remain after multivariate analysis. 0.2 Conclusions/interpretation A Palaeolithic diet may im- (n=14), based on lean meat, fish, fruits, vegetables, root prove glucose tolerance independently of decreased waist12 Semanas 0 vegetables, eggs and nuts; or (2) a Consensus (Mediterra- nean-like) diet (n=15), based on whole grains, low-fat dairy circumference. 5 0.01 products, vegetables, fruits, fish, oils and margarines. Pri- Keywords Diet . Evolution . Glucose intolerance . mary outcome variables were changes in weight, waist cir- Ischaemic heart disease . Palaeolithic diet . Type 2 diabetes Nº INDIVÍDUOS COM DIABETES (GLICEMIA PÓS OGT) cumference and plasma glucose AUC (AUC Glucose0–120) and plasma insulin AUC (AUC Insulin0–120) in OGTTs. Abbreviations Results Over 12 weeks, there was a 26% decrease of AUC BIA bioelectrical impedance analysis Glucose0–120 (p=0.0001) in the Palaeolithic group and a 7% E% percentage of total energy intake decrease (p=0.08) in the Consensus group. The larger (p= HOMA-IR homeostasis model assessment 0.001) improvement in the Palaeolithic group was indepen- of insulin resistance dent (p=0.0008) of change in waist circumference (−5.6 cm IFG impaired fasting glucose in the Palaeolithic group, −2.9 cm in the Consensus group; IGT impaired glucose tolerance IHD ischaemic heart disease Electronic supplementary material The online version of this article NGT normal glucose tolerance (doi:10.1007/s00125-007-0716-y) contains supplementary material, which is available to authorised users. S. Lindeberg (*) : T. Jönsson : E. Borgstrand : J. Soffman : Introduction K. Sjöström : B. Ahrén Department of Medicine, Hs 32, University of Lund, SE-221 85 Lund, Sweden Impaired glucose tolerance (IGT) and type 2 diabetes are e-mail: staffan.lindeberg@med.lu.se common risk factors for ischaemic heart disease (IHD) [1, 2],
    • NUTRITION MYTHS
    • MITO 2 massa, batata ou pão. As pessoas com Diabetes devem evitar comer arroz,MITO 2 • Estes alimentos são grandes fornecedores de hidratos de carbono massa, batata ou pão. (HC), os nutrientes que mais influenciam os níveis de glicemia após as refeições. No entanto, ao contrário dos alimentos ricos em açúcar, estes alimentos contêm HC de absorção lenta, permitindo um melhor• Estes alimentos são grandes fornecedores de hidratos de carbono controlo da glicemia ao longoe-Book do dia. (HC), os nutrientes que mais influenciam os níveis de glicemia após as refeições. No entanto, ao contrário dos alimentos ricos em açúcar, • A sua ingestão é indispensável, pois devem fornecer um melhor estes alimentos contêm HC de absorção lenta, permitindoa maior parte da controlo da glicemia nosso organismo necessita, cerca de 45 a 60% das energia que o ao longo do dia. calorias totais por dia.• A sua ingestão é indispensável, pois devem fornecer a maior parte da • Desta forma, estes alimentos devem fazer parte 45 a 60% das energia que o nosso organismo necessita, cerca dede todas as refeições calorias totais por longo do dia. realizadas ao dia.• Desta forma, estes alimentos devem fazer parte de todas as refeições realizadas ao longo do dia.
    • James M Shikany, KarenBackground: Glycemic effects of the Women’s Health Initiative L Margolis, Mary Pettinger, Rebecca D Jackson, Marian C Limacher, Simin Liu, during a mLawrence S Phillips, and(WHI) low-fat dietary intervention are unknown. Lesley F Tinker carbohydraABSTRACT Objective: low-fatobjective was to on glucose,the incidence in postmenopausal women increa Effects of a Our dietary intervention analyze insulin, and colorectal cancer effects of the WHI ated and insulin resistance in the Women’s Health Initiative (WHI)Background: Glycemic effects of the dietary Health Initiative on serum glucose of 8.1 y. Despite the increased intake of low-fat Modification trial1–3 Women’s intervention during a mean follow-up and insulin and in- observed. S Dietary(WHI) low-fat dietary intervention are unknown. sulinMresistance upofto Pettinger,after Drandom inC the intervention group, and question of associ-Objective: Our objective was toJames analyze Karen effects Mary Shikany, the L Margolis, the carbohydrate 6WHIRebecca Jackson, Marianassignment. y Limacher, Simin Liu, percentage ated increased risk of diabetes, no increase in diabetes risk waslow-fat dietary interventionDesign:glucose and insulin and in- on serum Postmenopausal WHI Dietary Modification trial that greater decreases in observed. Subgroup analysis suggested interven- Lawrence S Phillips, and Lesley F Tinker trend = 0.sulin resistance up to 6 y after random assignment. comparison (DM-C) participantstotal fat blood meas- risk (P for ABSTRACT tion (DM-I) and and colorectal cancer incidence in postmenopausal women of energy from with intake of percentage follow-up of 8.1 y. Despite the increasedreduced diabetes Background: Glycemic effects of the Women’s Health InitiativeDesign: Postmenopausal WHI Dietary Modification trial interven- during a mean trend = 0.04); however, that finding was (WHI) low-fat dietary intervention are unknown. nificant aft carbohydrate in the intervention group, and question of associ- not statistically sig-tion (DM-I) and comparisonures at least at baseline and ated increased risk(ndiabetes, 2263)greater decreasesincluded. effect of year 1 of = no increase in diabetes risk was Objective: Our objective was to analyze the effects of the WHI (DM-C) participants with blood meas- nificant after adjustment for weight loss—a common low-fat dietary intervention on serum glucose and insulin and in- observed. Subgroup analysis suggested that were in eating a loures at least at baseline and year 1 (n = 2263) were included. dietary aassessments, serum risk (P for Anthropometric measures, sulin resistance up to 6 y after random assignment. glucose and eating = 0.04);energy from total fat reducednot statistically sig- percentagelow-fat diet (2). of diabetes Design: Postmenopausal WHI Dietary Modification trial interven-Anthropometric measures, dietary assessments, serum glucose and trend however, that finding was nificant afterof the effects of the WHI diet intervention on glucose, Details adjustment for weight loss—a common effect of tion (DM-I) and comparison (DM-C) participants with blood meas- Details o insulin concentrations, homeostasis modelresistance have not been insulin The aim of ures at least at baseline and year 1 (n = 2263) were included.insulin concentrations, homeostasis model assessment of insulin assessment of insulin, low-fatinsulinthe WHI diet intervention on glucose, reported. eating a and diet (2). Anthropometric measures, dietary assessments, serum glucose and insulin, and Details of the effects ofresistance (HOMA-IR) measures, and quantitative insulin sensitiv- resistance (HOMA-IR) measures,report insulin resistancethe effectbeen theoverall diet in-sensitiv- diet in- report insulin, and quantitative insulin of insulin concentrations, homeostasis model assessment of insulin this report was to analyze reported. The aim of the overall and have not effect resistance (HOMA-IR) measures, and quantitative insulin sensitiv-ity check index (QUICKI) values were obtained at baseline, year 1, this was to analyze of the tervention, andspecific effects of fibereffects of fiber and whole grain this tervention, and the the specific ity check index (QUICKI) values were obtained at baseline, year 1,year 3, and year 6. Changes in measures index (QUICKI) values weredietary glycemic index (GI) and glycemic load tervention, ity check were compared between intakes,and dietaryobtained at glycemic load (GL) year 1, baseline, and whole grain year 3, and year 6. Changes in measures were compared between intakes, and glycemic index (GI) and groups at years 1, 3, and 6 overall and within stratified analyses. on glucose, insulin, and insulin resistance in the WHI DM trial. (GL)groups at years 1, 3, and 6 year 3, and year 6.analyses. overall and within stratified Changes on glucose, insulin, and insulin resistancebetween DM trial. in measures were compared in the WHI intakes, an Results: Mean (6SD) differences in changes at year 1 between the DM-I and DM-C groups were as follows: glucose, 21.7 6 17.9 mg/Results: Mean (6SD) differences in changes at year 1 between theDM-I and DM-C groups were as follows: glucose, 21.7 3, 17.9 mg/ overall and within stratified analyses. groups at years 1, 6 and 6 dL; insulin, 20.7 6 5.1 lIU/mL; HOMA-IR, 20.2 6 1.9; and SUBJECTS AND METHODS QUICKI, 0.004 6 0.019 (all P , 0.05). Similar findings resulted from repeated-measures analyses comparing the intervention and WHI DM trial on glucose Results: Mean (6SD) differences in changes at year 1 between thedL; insulin, 20.7 6 5.1 lIU/mL; HOMA-IR, 20.2 6 1.9; and comparison groups over the 6 y. Whereas normoglycemic womenSUBJECTS AND METHODS RecruitmentQUICKI, 0.004 6 0.019 (all P , 0.05). Similar findings resulted at baseline had a decrease in glucose at year 1 that was 1.9 6 as Details of thewomendesign andwritten 21.7 6and DM-I and DM-C groups were WHI DMAlltrial glucose, informedpublished pre- 17.2 mg/dL greater in the DM-I than in the DM-C group, diabeticfrom repeated-measures analyses comparing the intervention and follows: provided methods were consent, 17.9 mg/ viously (3). women had an increase in glucose that was 7.9 6 20.3 mg/dL greater study in the DM-I than in the DM-C group (P for interaction ,0.001). dL; insulin, 20.7 6 5.1 Recruitment Birmingham, Birmingham, 20.2 6 1.9; andcomparison groups over the 6 y. Whereas normoglycemic women lIU/mL; Division of Preventive Medicine, School of Medicine, Univer- Conclusions: A low-fat diet was not significantly associated with From the HOMA-IR, 1 sity of Alabama at AL (JMS); HealthPartners SUBJECTat baseline had a decrease in glucose at year 1 that was 1.9 6 adverse glycemic effects up to 6 y after random assignment in post-17.2 mg/dL greater in the DM-I than in the DM-C 6 0.019 (all P ,LFT); of Department of Internal Medicine, and methods were published pre- QUICKI, 0.004 group, diabetic Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA resulted 0.05). study design findings the Similar Research Foundation, Minneapolis, MN (KLM); the Division of Public menopausal women. However, diabetic women experienced adverse Details glycemic effects of the low-fat diet. This trial is registered at clin- (MP and the Division of Endocri- viously comparing Ohio State University,written informed consent, and (3). All women the intervention and from repeated-measures analyses the Division of Cardiovascular Medicine, University of Florida Col- icaltrials.gov as NCT00000611. Am J Clin Nutr doi: 10. provided Columbus, OHwomen had an increase in glucose that was 7.9 6 20.3 mg/dL greater 3945/ajcn.110.010843. nology, Diabetes and Metabolism, The (RDJ); WHI DMin the DM-I than in the DM-C group (P for interaction ,0.001). lege of Medicine, Gainesville, FL (MCL); the Department of Epidemiology,Conclusions: A low-fat diet was not significantly associated with 6 lanta VA MedicalDivisionDivision of Endocrinology, DepartmentSchool of Medicine, Univer- comparison groups over the 1University ofthe CenterLos Angeles, Los Angeles, CA (SL); and the At- women INTRODUCTION y. Whereas of Preventive Medicine, of From California, and normoglycemic Recruitmenadverse glycemic effects up at 6The optimal macronutrientin nutritional science.post- healthsity glucose National Heart, Lung, and Blood Institute, was 1.9 6 toremainsafter random assignment in human diets Medicine, Emory University Birmingham, Atlanta, GA (LSP). AL (JMS); HealthPartners baseline had aof the diet for Low-fat in of Alabama at School of Medicine, Birmingham, the Division of Public y a major controversy content decrease Supported by the at year 1 that National 2 Researchof Health, US Department of Health and HumanMN (KLM); Institutes Foundation, Minneapolis, Services (contractmenopausal women. However,indiabetic women experienced adverse general, and the Women’s Health Initiative (WHI) low-fat Detailsglycemic effects of the low-fat diet.toThis trial greater inatthe 17.2 mg/dL is registered for fat, potentially numbers32118-32119, 32122, 42107-26, 42129-32, and 44221). dietary intervention in particular, have been criticized forDM-I than in Fred Hutchinson Cancer32111-13, diabetic Seattle, WA the DM-C group, their Health Sciences, 24152, 32100-2, 32105-6, 32108-9, Research Center, N01WH22110, potential substitute unhealthy carbohydrates clin- 32115, (MP and LFT); the Department of Internal Medicine, Division of Endocri- contributing resistance had Clin Nutr doi: 10. cine, 3 Address correspondence to JM Shikany, Division of Preventive Medi-icaltrials.gov as NCT00000611. (1).to hyperglycemia, hyperinsulinemia, andglucose School of Medicine, University of6 20.3Ohio 1530 3rd University, Columbus, OH women Am J an increase in insulinnology,that610, Birmingham, AL 35294. E-mail:Birmingham, State greater was 7.9 Alabama The mg/dL Diabetes and Metabolism, at jshikany@dopm.uab. viously (3) Avenue S, MT3945/ajcn.110.010843. fat, DM-C group (P for interaction ,0.001). The WHI Dietary Modification (DM) trial was designed to test (RDJ); the Division of Cardiovascular Medicine, University of Florida Col- inthethe DM-I pattern low in totalthealong with in-lege of Medicine, Gainesville, FL (MCL); the Department of Epidemiology, effects of a dietary than in edu. Received December 21, 2010. Accepted for publication April 15, 2011. creased vegetables, fruit, and grains, on primarily breast cancer 1 Conclusions: A low-fat diet University of California, Los Angeles, Los 1Angeles, CA (SL); and the At-From the doi: 10.3945/ajcn.110.010843.INTRODUCTION was not significantly associated with Am J Clin Nutr doi: 10.3945/ajcn.110.010843. Printed in USA. Ó 2011 American Society for Nutrition of 11 Shikany JM, et al. Am J Clin Nutr. 2011 Jul;94(1):75-85. lanta VA Medical Center and Division of Endocrinology, Department of of Alab sity The optimal macronutrient content of the diet for human health to 6 y after randomSchool of Medicine, in post- (LSP). adverse glycemic effects up Medicine, Emory University assignment Atlanta, GAremains a major controversy in nutritional science. Low-fat diets the American Societyby the National Heart, Lung, and adverse Research Fo menopausal women. (C) 2011 by Copyright However, diabetic for Nutrition experienced Blood Institute, National Supported women 2
    • dL; insulin, 20.7 6 5.1 lIU/mL; HOMA-IR, 20.2 6 1.9; and SUQUICKI, 0.004 6 0.019 (all P , 0.05). Similar findings resulted Effects of a low-fat dietary intervention on glucose, insulin,from repeated-measures analyses comparing the intervention and and insulin resistance in the Women’s Health Initiative (WHI) 1–3 WH Dietary Modification trialcomparison groups over the 6 y. Whereas normoglycemic women James M Shikany, Karen L Margolis, Mary Pettinger, Rebecca D Jackson, Marian C Limacher, Simin Liu, Lawrence S Phillips, and Lesley F Tinker Recat baseline had a decrease in glucose at year 1 that was 1.9 6 ABSTRACT and colorectal cancer incidence in postmenopausal women Background: Glycemic effects of the Women’s Health Initiative17.2 mg/dL greater in the DM-I than in the DM-C group, diabetic (WHI) low-fat dietary intervention are unknown. Objective: Our objective was to analyze the effects of the WHI during a mean follow-up of 8.1 y. Despite the increased intake of carbohydrate in the intervention group, and question of associ- ated increased risk of diabetes, no increase in diabetes risk was D vio low-fat dietary intervention on serum glucose and insulin and in- observed. Subgroup analysis suggested that greater decreases inwomen had an increase in glucose that was 7.9 6 20.3 mg/dL greater sulin resistance up to 6 y after random assignment. Design: Postmenopausal WHI Dietary Modification trial interven- tion (DM-I) and comparison (DM-C) participants with blood meas- percentage of energy from total fat reduced diabetes risk (P for trend = 0.04); however, that finding was not statistically sig- nificant after adjustment for weight loss—a common effect ofin the DM-I than in the DM-C group (P for interaction ,0.001). ures at least at baseline and year 1 (n = 2263) were included. Anthropometric measures, dietary assessments, serum glucose and insulin concentrations, homeostasis model assessment of insulin eating a low-fat diet (2). Details of the effects of the WHI diet intervention on glucose, insulin, and insulin resistance have not been reported. The aim of resistance (HOMA-IR) measures, and quantitative insulin sensitiv- 1Conclusions: A low-fat diet was not significantly associated with this report was to analyze the effect of the overall diet in- ity check index (QUICKI) values were obtained at baseline, year 1, tervention, and the specific effects of fiber and whole grain year 3, and year 6. Changes in measures were compared between intakes, and dietary glycemic index (GI) and glycemic load (GL) groups at years 1, 3, and 6 overall and within stratified analyses.adverse glycemic effects up to 6 y after random assignment in post- Results: Mean (6SD) differences in changes at year 1 between the DM-I and DM-C groups were as follows: glucose, 21.7 6 17.9 mg/ on glucose, insulin, and insulin resistance in the WHI DM trial. sity dL; insulin, 20.7 6 5.1 lIU/mL; HOMA-IR, 20.2 6 1.9; and SUBJECTS AND METHODS Resmenopausal women. However, diabetic women experienced adverse QUICKI, 0.004 6 0.019 (all P , 0.05). Similar findings resulted from repeated-measures analyses comparing the intervention and WHI DM trial comparison groups over the 6 y. Whereas normoglycemic women at baseline had a decrease in glucose at year 1 that was 1.9 6 Recruitment Heaglycemic effects of the low-fat diet. This trial is registered at clin- 17.2 mg/dL greater in the DM-I than in the DM-C group, diabetic Details of the study design and methods were published pre- women had an increase in glucose that was 7.9 6 20.3 mg/dL greater in the DM-I than in the DM-C group (P for interaction ,0.001). viously (3). All women provided written informed consent, and (MPicaltrials.gov as NCT00000611. Am J Clin Nutr doi: 10. 1 Conclusions: A low-fat diet was not significantly associated with From the Division of Preventive Medicine, School of Medicine, Univer- sity of Alabama at Birmingham, Birmingham, AL (JMS); HealthPartners adverse glycemic effects up to 6 y after random assignment in post- menopausal women. However, diabetic women experienced adverse Research Foundation, Minneapolis, MN (KLM); the Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA nolo3945/ajcn.110.010843. glycemic effects of the low-fat diet. This trial is registered at clin- icaltrials.gov as NCT00000611. 3945/ajcn.110.010843. Am J Clin Nutr doi: 10. (MP and LFT); the Department of Internal Medicine, Division of Endocri- nology, Diabetes and Metabolism, The Ohio State University, Columbus, OH (RDJ); the Division of Cardiovascular Medicine, University of Florida Col- (RD lege of Medicine, Gainesville, FL (MCL); the Department of Epidemiology, INTRODUCTION The optimal macronutrient content of the diet for human health University of California, Los Angeles, Los Angeles, CA (SL); and the At- lanta VA Medical Center and Division of Endocrinology, Department of Medicine, Emory University School of Medicine, Atlanta, GA (LSP). lege 2 remains a major controversy in nutritional science. Low-fat diets Supported by the National Heart, Lung, and Blood Institute, National in general, and the Women’s Health Initiative (WHI) low-fat Institutes of Health, US Department of Health and Human Services (contract UniINTRODUCTION dietary intervention in particular, have been criticized for their potential to substitute unhealthy carbohydrates for fat, potentially numbers N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122, 42107-26, 42129-32, and 44221). contributing to hyperglycemia, hyperinsulinemia, and insulin resistance (1). 3 Address correspondence to JM Shikany, Division of Preventive Medi- cine, School of Medicine, University of Alabama at Birmingham, 1530 3rd lant The optimal macronutrient content of the diet for human health Avenue S, MT 610, Birmingham, AL 35294. E-mail: jshikany@dopm.uab. The WHI Dietary Modification (DM) trial was designed to test the effects of a dietary pattern low in total fat, along with in- creased vegetables, fruit, and grains, on primarily breast cancer edu. Received December 21, 2010. Accepted for publication April 15, 2011. doi: 10.3945/ajcn.110.010843. Med 2remains a major controversy in nutritional science. Low-fat diets Am J Clin Nutr doi: 10.3945/ajcn.110.010843. Printed in USA. Ó 2011 American Society for Nutrition Shikany JM, et al. Am J Clin Nutr. 2011 Jul;94(1):75-85. 1 of 11in general, and the Women’s Health Initiative (WHI) low-fat Copyright (C) 2011 by the American Society for Nutrition Inst
    • INCIDÊNCIA DE DIABETES MED C/ AZEITE VIRGEM: 10.1 (5.1–15.1) MED C/ FRUTOS SECOS: 11.0 (5.9–16.1) DIETA LOW FAT: 17.9 (11.4–24.4) Diabetes Care January 2011 vol. 34 no. 1 14-19
    • Nutrition Research xx (2011) xxx–xxx RESTRINGIR HIDRATOS DE CARBONO É PERIGOSO ge Table 5 t5:1 ts, Definitions for low-carbohydrate diets [59] t5:2 to Absolute carbohydrate Relative carbohydrate t5:3ost content (g/d) content (percentage of energy/d)er- he Low-carbohydrate- b50 b10 t5:4 ketogenic diet al- Low-carbohydrate 50-b130 10-b25 t5:5 le, dietain Moderate ≥130 26-45 t5:6 on carbohydratef a dietrnser- Ströhle A, Hahn A. Diets of modern hunter-gatherers vary substantially in their carbohydrate content dependingrce Ludwig and Jenkins [67] may have been correct when they on ecoenvironments: results from an ethnographic analysis. Nutrition Research 2011, em publicação 262 261 260 259 258 257 256 255 254 253 252 251 250 249 he stated that “humans can probably do well over the long term 263
    • REDUÇÃO FARMACOLÓGICA DA GLICEMIA PÓS-!! PRANDIAL DIMINUIU RISCO DE:!!!ü DT2!ü Aumento de peso!ü DCV! Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M. Lancet 2002;359:2072– 2077
    • Brewer N, et al. Diabetes Care. 2008 Jun;31(6):1144-9
    • or the association between A1C levels and mortality in a New Zealand population-based Zealandby cause of death sample by ca 1.79 (0.35–9.18 2.12 (1.58–2.85 1.50 (0.90–2.48 2.46 (1.44–4.19 1.75 (0.88–3.49 19 2 27. 1.33 (1.05–1.70) 87 129 2. 1.10 (0.72–1.68) 23 44 1. 1.43 (0.89–2.30) 32 54 2. 1.27 (0.71–2.30) 23 26 2. 1.41 (0.96–2.06) 13 29 1. A1C level 6 HR (95% CI)* diabetes), but this risk reealand population-based sample by cause of death CONCLUSIONS (2.46 [1.86 –3.26]) wh n A1C. If the adjustment w n Before discussing the ing A1C as a categorical study, several limitatio Ͻ7.0% 6.0n to HRHR (95% CI)* 449 2.12 (1.58–2.85) 154 1.50 (0.90–2.48) 2 6 1.79 (0.35–9.18) 151 2.46 (1.44–4.19) 26 91 1.75 (0.88–3.49) 138 2.52 (1.47–4.31) tinuous variablemain knowledged. The (to Table 3—HRs for the association between A1C levels and mortality in a New sample population-based (95% CI)* to to Ͻ6.0% nonlinear association bd lack of anthropometric 6.05.0 Ͻ7.0% mortality), thecardiovas tion on other HR in th 1.0† sex, ethnicity, and smoking status.ethnicity, and smoking status. †Reference category. ‡Not calculated due to zero deaths. diabetes diagnosis reduc The short follow-up ti CI 1.82–3.26).could no meant that we A1C levels levels yses to the cases diagn n 129 44 54 29 CONCLUSIONS test A1C years after the A1C Before discussing the jects with undetected d n HR (95% CI)*CI)* study, severaltest. Ther of the blood limitation 821.33 (1.05–1.70) 261.10 (0.72–1.68) 201.43 (0.89–2.30) 131.27 (0.71–2.30) 361.41 (0.96–2.06) 4.0 to Ͻ5.0% 1.0† 1.0† 1.0† 1.0† 1.0† HR (95% knowledged. The main exclude the possibility th ‡ 5.0 to Ͻ6.0% Brewer N, et al. Diabetes Care. 2008 Jun;31(6):1144-9 129 44 2 54 26 lack of anthropometricm time of the A1C test d n tion on other cardiovasc elevated glucose levels 01.0† *Adjusted for age, sex, †Reference category. ‡Not calculated due to zero deaths. The short follow-up pa separate analyses for ti meant that we could not previous diagnosis of di 2.90 (0.91–9.19)449 154 6 151 6.26 (0.81–48.13)91 138 yses to the cases diagn n sis of hospitalizations o 3.95 (0.53–29.51) 4.53 (1.09–18.85) 5.0 (95% CI)* n n n HR (95%(95% CI)* years after thefor insulin prescriptions A1C test 1.33 (1.05–1.70) 1.10 (0.72–1.68) 1.43 (0.89–2.30) 1.27 (0.71–2.30) jects with aundetected d HR CI)* cemic, or home glucos HR (95% CI)* Ͻ4.0% of the blood may have but there still test. Ther 4.0 to Ͻ5.0% 1.0† ‡ 1.0† 1.0† 1.0† 1.0† exclude the possibility th ‡ ‡ ipants with diagnosed d time of the A1C test m being treated with lifes HR to Ͻ6.0% elevated glucose levels rather than medication 82 3 26 0 0 0 20 1 13 1 36 2 separate analyses forpar also have been some pa previous diagnosis of (p diagnosed diabetes di 2.90 (0.91–9.19) 815 262 47 3.95 (0.53–29.51)280 6.26 (0.81–48.13)166 Other and unknown causes 4.53 (1.09–18.85)226 sis ofA1C levels Ն7.0%) with hospitalizations o 1.0† prescriptions for insulin ies of this type, there ma ry system (390–459) of circulatory system (390–459) cemic, or a homespecific classification of glucos Ͻ4.0% ease (410–414) Ischemic heart disease (410–414) Endocrine, nutritional & metabolic, but thereof the well-reco because still may have b ipants with diagnosed d for diabetes to be und ‡ ‡ being of deathwith lifest cause treated (19,20). and immunity disorders rather than medication 3 All cancers (140–239)0 0 1 1 2 n The current study w also have in an intensive ticipants been some par 449 154 6 151 91 All deaths 815 262 47 280 166 226 diagnosed screening (p hepatitis B diabetes pr n Site (ICD-9) n (240–279) with A1C levels Ն7.0%) “volunteers ” may not be ies of this type, there ma Diseases the general populatio classification of specific have made internal com al & metabolic, because of the well-reco for diabetes to be und CI)* DIABETES CARE, VOLUME 31, NUMBER 6, JUNE 2008 causes orders cause of death (19,20). 9)
    • res ate mia ow- not ••]. rol, on ces da 8••] ave not and ete- ght rate the diet hatmost ion Stratton IM, et al. BMJ 2000, 321(7258):405-412. Fig. 3 Hazard ratios with 95% confidence intervals as estimate ofs at
    • requirement of the diet above. Although most in total fat, substitutiont, for carbohydrate is ateficial for markers of andorates all of the featureseas higher carbohydratetprandial hyperglycemia32].hydrate restriction do notilar narrative review ona global perspective and aAs such, one would havehy its promise should notve been almost complete- ea that low-carbohydrate popular media and thed. The net effect is thatduced. Fig. 3 Hazard ratios with 95% confidence intervals as estimate of association between hemoglobin A1c (HbA1c) concentration and BMJ 2000, 321(7258):405-412. Stratton IM, et al. to CVD: Saturated Fat myocardial infarction or microvascular end points. (Modified from Stratton et al. [36])
    • Nutrition & Metabolism BioMed Central Brief communication Open Access Low-carbohydrate diet in type 2 diabetes: stable improvement of bodyweight and glycemic control during 44 months follow-up Jörgen V Nielsen* andNutrition & Metabolism 2008, 5:14 Eva A Joensson http://www.nutritionandmetabolism.com/content/5/1/14 Address: Department of Medicine, Blekingesjukhuset, Karlshamn, 37480 Karlshamn, SwedenTable 1: Effect Nielsen*on weight, BMI, HbA1c and fasting A Joensson - eva-a.jonsson@ltblekinge.setype 2 diabetes started at month 0 on a Email: Jörgen V of diet - jorgen.vesti-nielsen@ltblekinge.se; Eva lipids. Sixteen obese patients with * Corresponding authordiet with the proportions: 20% carbohydrates, 30% protein and 50% fat. The figures shown are means before, 3, 6, 22 and 44 monthsafter the dietary change. Month 0 3 P* 6 P* 22 44 P* Published: 22 May 2008 Received: 24 January 2008 Accepted: 22 May 2008 Weight (kg) 100.6 14.7 91.9 ± 14.7 Nutrition & Metabolism 2008, 5:14 ± doi:10.1186/1743-7075-5-14 <0.001 89.2 ± 14.3 <0.001 92.0 ± 14.0 93.1 ± 14.5 <0.001 This (kg/m2 36.1 ± 4.2 33.0 ± 4.5 <0.001 32.0 BMIarticle is)available from: http://www.nutritionandmetabolism.com/content/5/1/14 ± 4.3 <0.001 32.9 ± 3.5 33.4 ± 3.9 <0.001 HbA1c (%) 8.0 ± 1.5 5.9 ± 0.7 <0.001 6.6 ± 1.0 <0.001 6.9 ± 1.1 6.8 ± 1.3 <0.001 © 2008 Nielsen and Joensson; licensee BioMed Central Ltd. Lipids(mmol/l) This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), Tot-Chol. unrestricted use, distribution, and5.8 ± 1.1 which permits 5.6 ± 1.2 0.4 6.1 ± 1.1 0.06 5.7 ± 1.2 reproduction in any medium, provided the original work is properly cited. 5.4 ± 1.0 0.8 HDL-Chol. 1.1 ± 0.2 1.2 ± 0.2 <0.002 1.3 ± 0.2 <0.001 1.3 ± 0.3 1.3 ± 0.2 <0.001 §Triglycerides 1.4 (1;1.8) 1.2(0.8;1,4) 0.01 1.4(0.9;1.7) 0.4 1.4(1.2;1.9) 1.4(1.2–2) 0.9 Chol/HDL 5.4 ± 1.5 5.0 ± 1.5 0.02 5.0 ± 1.7 0.07 4.6 ± 1.6 4.1 ± 0.9 <0.001 §TG/HDL Abstract 1.4(0.9;1.7) 1.0(0.6;1.2) 0.003 1.0(0.7;1.5) 0.03 1.3(0.8;1.5) 1.1(0.9;1.7) 0.7 Background: Low-carbohydrate diets, due to their potent antihyperglycemic effect, are an §given as medians with 25 and 75 percentiles. * p to the are for differences obese patients with type 2 diabetes. We intuitively attractive approach values management of from baseline. previously reported that a 20% carbohydrate diet was significantly superior to a 55–60% carbohydrate diet with regard to bodyweight and glycemic control in 2 groups of obese diabetesResults patients observed closely over 6 months (intervention At the n = 16; controls, n = 15) and we used metformin and group, start of the study 15 of the 16Table 1 shows the measured parametersgains after 22&to 44 The present study documents the degree to patients were treated reported maintenance of these from start months. 5 2008, 5:14 Nutrition Metabolism sulfonylurea (SU). Eleven of the http://www.nutritionandmetabol which these changes were preserved in the low-carbohydrate insulin at a mean daily dosage of 60 ± 33 IU.months. Triglycerides (TG) and HbA1c, both parameters with group after 44 months observation time, without close follow-up. In addition, we assessed the performance of the two thirds ofof adherence to the diet, were at their lowest after 3 control patients from the high-carbohydrate diet group that had changed to a low-carbohydrate
    • Nutrition & Metabolism Vital signsing for weight change or BMI change, the between group BioMed Centralcomparison in change in hemoglobin A1c approached sta- There was significantly greater weight loss for the LCKDtistical significance (p = 0.06). Additionally, there was no than the LGID group over the 24 weeks: body weightcorrelation between change in hemoglobin A1c and Research decreased from 108.4 ± 20.5 kg to 97.3 ± 17.6 kg for the Open Accesschange in weight (Figure 2). LCKD group, and from 105.2 ± 19.8 to 98.3 ± 20.3 kg for The effect of a low-carbohydrate, ketogenic diet versus a groups had reductions in the LGID group (Table 2). Both low-glycemic index diet on glycemic control in type 2and diastolic blood pressureMedication changes systolic blood pressure diabetesAt baseline, 22 (75.9%) of the LGID group were taking (Table 4). mellitushypoglycemic medications (insulin only n = 3, oral agentsonly n = 19), and 20 (95.2%) of the LCKD S Yancy Jr1,2, John C Mavropoulos1, Eric C Westman*1, William group were tak- Other metabolic effectsingMegan Marquart1 and Jennifer R McDuffieFor fasting lipid profiles, the LCKD group had an increase hypoglycemic medications (insulin + oral agents n = 1,24, insulin only n = 4, oral agents only n = 12). Twenty of in HDL cholesterol (+12.7%), while the LGID group had21 (95.2%) LCKD group participants had an elimination no change over the 24 weeks. All 7 parameters associated Address: Department of Medicine, Duke University Medical Center, Durham, NC, USA and Center for Health Services Research in Primary Care, 1 2 Department of Veterans Affairs Medical Center, Durham, NC, USATable 1: Baseline participant characteristics* Email: Eric C Westman* - ewestman@duke.edu; William S Yancy - yancy006@mc.duke.edu; John C Mavropoulos - jcm10@duke.edu; Megan Marquart - mlmarquart@cox.net; Jennifer R McDuffie - mcduf011@mc.duke.edu Characteristic Low -glycemic, reduced-calorie diet Low-carbohydrate, ketogenic diet * Corresponding author Enrollees Completers Non-completers Enrollees Completers Non-completers (n = 46) (n = 29) (n = 17) (n = 38) (n = 21) (n = 17) Age, years 19 December 2008 Published: 51.8 ± 7.8 50.0 ± 8.4 54.9 ± 5.7 Received: 15 July 2008 51.8 ± 7.3 51.2 ± 6.1 52.4 ± 8.7 Female gender, % 80.4 79.3 Accepted: 19 December 200876.3 82.3 66.7 88.2 Nutrition & Metabolism 2008, 5:36 doi:10.1186/1743-7075-5-36 White race, % 45.7 44.8 47.1 57.9 66.7 47.1 This article is available from: http://www.nutritionandmetabolism.com/content/5/1/36 African-American race, % 50 51.7 47.1 36.8 23.8 52.9 © 2008 Westman et al; licensee BioMed Central Ltd. College degree, % 58.7 68.9 41.2 57.9 61.9 52.9 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), Body weight, kg 106.3 ± 20.1 105.2 ± 19.8 108.1 ± 20.9 105.5 ± 19.5 108.4 ± 20.5 101.9 ± 18.1 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Body mass index, kg/m2 38.5 ± 5.6 37.9 ± 6.0 39.4 ± 5.0 37.7 ± 6.1 37.8 ± 6.7 37.6 ± 5.3 * Values with plus/minus signs are means ± SD. Abstract Objective: Dietary carbohydrate is the major determinant of postprandial glucose levels, and several clinical studies have shown that low-carbohydrate diets improve glycemic control. In this Page 4 of 9 (page number not for citation purposes) study, we tested the hypothesis that a diet lower in carbohydrate would lead to greater improvement in glycemic control over a 24-week period in patients with obesity and type 2 diabetes mellitus. Nutrition & Metabolism 2008, 5:36 http://www.nutritionandme Research design and methods: Eighty-four community volunteers with obesity and type 2 diabetes were randomized to either a low-carbohydrate, ketogenic diet (<20 g of carbohydrate daily; LCKD) or a low-glycemic, reduced-calorie diet (500 kcal/day deficit from weight maintenance
    • Nutrition & Metabolism BioMed Central Research Open Access The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitusNutrition & Metabolism 2008, 5:36 http://www.nutritionandmetabolism.com/content/5/1/36 Eric C Westman* , William S Yancy Jr1,2, John C Mavropoulos1, 1 Megan Marquart1 and Jennifer R McDuffie1,2Table 4: Effect of diet programs on metabolic syndrome parameters and fasting lipid profiles Address: 1Department of Medicine, Duke University Medical Center, Durham, NC, USA and 2Center for Health Services Research in Primary Care, Low glycemic, reduced-calorie diet group (n = 29) Low carbohydrate, ketogenic diet group (n = 21) Department of Veterans Affairs Medical Center, Durham, NC, USA Email: Eric C Westman* - ewestman@duke.edu; William S Yancy - yancy006@mc.duke.edu; John C Mavropoulos - jcm10@duke.edu; Test Marquart - mlmarquart@cox.net; Jennifer R McDuffie - mcduf011@mc.duke.edu0 to 24 Megan Week 0 Week 24 Week Week 0 Week 24 Week 0 to 24 * Corresponding author mean ± sd mean ± sd mean change mean ± sd mean ± sd mean change Fasting glucose, mg/dL 166.8 ± 63.7 150.8 ± 47.4 -16.0 * 178.1 ± 72.9 158.2 ± 50.0 -19.9* Published: 19 December 2008 Received: 15 July 2008 Waist circumference, inches 47.0 ± 5.1 42.4 ± 5.5 -4.6 * 47.1 ± 5.5 41.8 ± 5.3 -5.3 * Accepted: 19 December 2008 Triglycerides, mg/dL 2008, 5:36 doi:10.1186/1743-7075-5-36 147.8 ± 128.5 Nutrition & Metabolism 167.1 ± 125.7 -19.3 210.4 ± 10.3 142.9 ± 76.9 -67.5 * HDL article is available from: http://www.nutritionandmetabolism.com/content/5/1/36 This cholesterol, mg/dL 48.7 ± 11.8 48.7 ± 10.1 -0 † 44.0 ± 8.7 49.6 ± 11.7 +5.6 * † Systolic blood pressure, mmHg 140.8 ± 15.7 130.1 ± 17.1 -10.7 * 144.4 ± 15.0 127.8 ± 13.4 -16.6 * © 2008 Westman et al; licensee BioMed Central Ltd. Diastolic blood Access article distributed under the terms of the Creative ± 8.7 This is an Open pressure, mmHg 84.1 ± 11.0 78.5 Commons Attribution License (http://creativecommons.org/licenses/by/2.0), * -5.6 * 83.9 ± 10.3 75.8 ± 10.9 -8.1 Body mass index, kg/m2 use, distribution, and reproduction in any 35.2 ± 6.1 which permits unrestricted 37.9 ± 6.0 -2.7 * † work is 37.8 ± 6.7 medium, provided the original properly cited. 33.9 ± 5.8 -3.9 * † Total cholesterol, mg/dL 190.6 ± 43.8 184.8 ± 45.6 -5.8 191.4 ± 32.0 187.0 ± 35.8 -4.4 LDL cholesterol, mg/dL 113.8 ± 40.9 111.0 ± 42.2 -2.8 105.8 ± 25.7 107.1 ± 26.3 +1.3 VLDL cholesterol, mg/dL 27.7 ± 13.2 24.4 ± 12.3 -3.3* 37.3 ± 14.9 27.3 ± 15.2 -10.0* Total cholesterol/HDL cholesterol ratio 4.1 ± 1.3 3.9 ± 1.2 -0.2 4.5 ± 1.1 4.1 ± 4.1 -0.4 Abstract Triglyceride/HDL cholesterol ratio 3.9 ± 3.7 3.3 ± 3.1 -0.6 5.2 ± 3.4 3.4 ± 3.0 -1.8* Objective: Dietary carbohydrate is the major determinant of postprandial glucose levels, and These changes were observed with a reduction shown that low-carbohydrate diets improve glycemic control. In this several clinical studies have or elimination of diabetic medication as shown in Table 3. HDL = high-density lipoprotein; LDL = low-density lipoprotein; VLDL lower in carbohydrate would lead to greater study, we tested the hypothesis that a diet = very-low-density lipoprotein * p < 0.05 for within-group change from Baseline to Week 24.a 24-week period in patients with obesity and type 2 improvement in glycemic control over † p < 0.05, for between-groups comparison of changes from Baseline to Week 24. diabetes mellitus. Nutrition & Metabolism 2008, 5:36 http://www.nutritionandme P values with adjustment for baseline values: fasting glucose: 0.76, waist circumference: 0.43, triglycerides: 0.17, HDL: 0.09, systolic blood pressure: Research design and methods: Eighty-four community volunteers with obesity and type 2 0.89, diastolic blood pressure: 0.48, body mass index: 0.10, total cholesterol: 0.85, LDL: 0.79, VLDL: 0.24, total cholesterol/HDL ratio: 0.92, triglyceride/HDLdiabetes were randomized to either a low-carbohydrate, ketogenic diet (<20 g of carbohydrate ratio: 0.54. daily; LCKD) or a low-glycemic, reduced-calorie diet (500 kcal/day deficit from weight maintenance
    • t the of a Thedrate diet tric- them of the easeotherhavebolicetes, Fig. 2 Comparison ofincereal-based diets and low-GIApr;11(2):128-35 Feinman RD. Fad diets the treatment of diabetes. Curr Diab Rep. 2011 diets of Jenkins et ould al. [16] and comparison of low-GI diets with low-carbohydrate diets of Westman et al. [17]. Changes are shown as percentage for the indicated
    • Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55
    • to show improvements in atherogenic dyslipidemia most clinically usefPerspective [5,8,9] and there is an evolving picture that the effects of Access Open (CVD) and there seLow carbohydrate diets improve atherogenic dyslipidemia even in LDL, especially if ef CR, notably in lowering insulin and thereby changing metabolic regulation of lipid, may be more importantthe absence of weight loss accompanied by subRichard D than the total amount of lipid substrate. Feinman*1 and Jeff S Volek2 ovascular events. T marker, however, mAddress: Department of Biochemistry, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA and Human Performance Laboratory, 1 2Department of Kinesiology, University of Connecticut, Storrs, CT 06269-1110, USA LDL is not homogenEmail: Richard D Feinman* - rfeinman@downstate.edu; Jeff S Volek - jeff.volek@uconn.edu* Corresponding author a function of partic more atherogenic [Published: 21 June 2006Nutrition & Metabolism 2006, 3:24 doi:10.1186/1743-7075-3-24 Received: 09 June 2006 Accepted: 21 June 2006 Nutrition & high triglyceride (TA are frequently increaThis article is available from: http://www.nutritionandmetabolism.com/content/3/1/24 [8]. The atherogenic© 2006 Feinman and Volek; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), particles is reflectedwhich permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Perspective (apoB) since each a Low carbohydrate d tains one molecule Abstract Because of its effect on insulin, carbohydrate restriction is one of the obvious dietary choices for the absencetowards low results of weigh weight reduction and diabetes. Such interventions generally lead to higher levels of dietary fat Richard evidence that apoB a than D Feinman*1 i official recommendations and have long been criticized because of potential effects on cardiovascular risk although many literature reports have shown that they are actually protective LDL and further tha even in the absence of weight loss. A recent report of Krauss et al. (AJCN, 2006) separates the conventional choles effects of weight loss and carbohydrate restriction. They clearly confirm that carbohydrate Address: 1Department of Biochemistry, SUN restriction leads to an improvement in atherogenic lipid states in the absence of weight loss or in Department of of considerable imp Kinesiology, University of C the presence of higher saturated fat. In distinction, low fat diets seem to require weight loss for effective improvement in atherogenic dyslipidemia. Email: Richard mechanistically link D Feinman* - rfeinman@do * Corresponding author particles, and is highBackgroundThe recent report of Krauss et al. [1] highlights the rather the practical implications of macronutrient composition. Criticism of the use of CR for weight loss has traditionally Study synopsisdramatic differences in the effects of carbohydrate focused on the potential effect on risk of CVD because June 2006 Published: 21 of Details of the dietarrestricted (CR) and low fat (LF) diets on the lipid changes the substitution of fat for carbohydrate. It is now clear thatthat may predispose to atherosclerosis. By first imple- such a change is beneficial and the demonstration that shown in Table 1. D Nutrition & Metabolism 2006, 3:24 doi:10.118 Figure dietary interventions on reduction in TAG Effect of1menting weight maintenance diets of different composi- actual weight loss is not required for the benefits of CR periods in which en This article is available from: http://www.nutrittions followed by calorie reduction, the authors show that suggests the need for reevaluation of current guidelines.
    • Perspective Open AccessLow carbohydrate diets improve atherogenic dyslipidemia even in http://www.nutritionandmetabolism.com/content/3/1/24the absence of weight lossRichard D Feinman*1 and Jeff S Volek2Address: 1Department of Biochemistry, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA and 2Human Performance Laboratory,Department of Kinesiology, University of Connecticut, Storrs, CT 06269-1110, USAEmail: Richard D Feinman* - rfeinman@downstate.edu; Jeff S Volek - jeff.volek@uconn.edu* Corresponding authorPublished: 21 June 2006Nutrition & Metabolism 2006, 3:24 doi:10.1186/1743-7075-3-24 Received: 09 June 2006 Accepted: 21 June 2006 Nutrition &This article is available from: http://www.nutritionandmetabolism.com/content/3/1/24© 2006 Feinman and Volek; licensee BioMed Central Ltd. PerspectiveThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Low carbohydrate d Abstract the absence of weigh Because of its effect on insulin, carbohydrate restriction is one of the obvious dietary choices for weight reduction and diabetes. Such interventions generally lead to higher levels of dietary fat than official recommendations and have long been criticized because of potential effects on Richard D Feinman* a 1 cardiovascular risk although many literature reports have shown that they are actually protective even in the absence of weight loss. A recent report of Krauss et al. (AJCN, 2006) separates the effects of weight loss and carbohydrate restriction. They clearly confirm that carbohydrate Address: 1Department of Biochemistry, SUN Department of Kinesiology, University of C restriction leads to an improvement in atherogenic lipid states in the absence of weight loss or in the presence of higher saturated fat. In distinction, low fat diets seem to require weight loss for effective improvement in atherogenic dyslipidemia. Email: Richard D Feinman* - rfeinman@do * Corresponding authorBackground the practical implications of macronutrient composition.The recent report of Krauss et al. [1] highlights the rather Criticism of the use of CR for weight loss has traditionallydramatic differences in the effects of carbohydrate focused on the potential effect on risk of CVD because June 2006 Published: 21 ofrestricted (CR) and low fat (LF) diets on the lipid changes the substitution of fat for carbohydrate. It is now clear thatthat may predispose to atherosclerosis. By first imple- Nutrition & Metabolism 2006, 3:24 doi:10.118 such a change is beneficial and the demonstration that Figure in Change 3 the ratio of total cholesterol to HDL with dietmenting weight maintenance diets of different composi- actual weight loss is not required for the benefits of CR This article is available from: http://www.nutrittions followed by calorie reduction, the authors show that suggests the need for reevaluation of current guidelines.
    • Perspective Open Access http://www.nutritionandmetabolism.com/content/3/1/24Low carbohydrate diets improve atherogenic dyslipidemia even inthe absence of weight lossRichard D Feinman*1 and Jeff S Volek2Address: 1Department of Biochemistry, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA and 2Human Performance Laboratory,Department of Kinesiology, University of Connecticut, Storrs, CT 06269-1110, USAEmail: Richard D Feinman* - rfeinman@downstate.edu; Jeff S Volek - jeff.volek@uconn.edu* Corresponding authorPublished: 21 June 2006Nutrition & Metabolism 2006, 3:24 doi:10.1186/1743-7075-3-24 Received: 09 June 2006 Accepted: 21 June 2006 Nutrition &This article is available from: http://www.nutritionandmetabolism.com/content/3/1/24© 2006 Feinman and Volek; licensee BioMed Central Ltd. PerspectiveThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Low carbohydrate d Abstract the absence of weigh Because of its effect on insulin, carbohydrate restriction is one of the obvious dietary choices for weight reduction and diabetes. Such interventions generally lead to higher levels of dietary fat than official recommendations and have long been criticized because of potential effects on Richard D Feinman* a 1 cardiovascular risk although many literature reports have shown that they are actually protective even in the absence of weight loss. A recent report of Krauss et al. (AJCN, 2006) separates the effects of weight loss and carbohydrate restriction. They clearly confirm that carbohydrate Address: 1Department of Biochemistry, SUN Department of Kinesiology, University of C restriction leads to an improvement in atherogenic lipid states in the absence of weight loss or in the presence of higher saturated fat. In distinction, low fat diets seem to require weight loss for effective improvement in atherogenic dyslipidemia. Email: Richard D Feinman* - rfeinman@do * Corresponding authorBackground the practical implications of macronutrient composition.The recent report of Krauss et al. [1] highlights the rather Criticism of the use of CR for weight loss has traditionallydramatic differences in the effects of carbohydrate focused on the potential effect on risk of CVD because June 2006 Published: 21 ofrestricted (CR) and low fat (LF) diets on the lipid changes the substitution of fat for carbohydrate. It is now clear thatthat may predispose to atherosclerosis. By first imple- Nutrition & Metabolism 2006, 3:24 doi:10.118 such a change is beneficial and the demonstration thatmenting weight maintenance diets of different composi- actual weight loss is not required for the benefits of CR This article is available from: http://www.nutrit Figure in Change 5 peak diameter of LDL particlestions followed by calorie reduction, the authors show that suggests the need for reevaluation of current guidelines.
    • ARQGA/1482 ARTIGO ORIGINAL / ORIGINAL ARTICL INSULIN RESISTANCE INDEX (HOMA-IR) IN THE DIFFERENTIATION OF PATIENTS WITH Insulin resistance index (HOMA-IR) in the differentiation of patients with non-alcoholic fatty NON-ALCOHOLIC FATTY LIVER DISEASE AND HEALTHY INDIVIDUALS Ana Lúcia Farias de Azevedo SALGADO1, Luciana de CARVALHO1, Ana Claudia OLIVEIRA1, Virgínia Nascimento dos SANTOS1, Jose Gilberto VIEIRA2 and Edison Roberto PARISE1,s with TABLE 1. Characteristics of the studied groups virus Characteristics - Due to its good correlation group clamp, HOMA-IR has been widely utilized as insulin resistance index in ABSTRACT – Context Control to glycemic NAFLD group P clinical and epidemiological studies involving non-alcoholic fatty liver disease carriers. However, values used for this parameter havehod), n shown large variability. Objective – To identify the HOMA-IR cut value that best distinguishes non-diabetic non-alcoholic fatty liver 88 116 disease patients from a control group. Methods - One hundred sixteen non-alcoholic fatty liver disease patients were studied, diagnosed byeases, Age clinical, biochemical, and liver image or biopsy± 11.7 88 healthy individuals, without any liver disease and testing for oral glucose (years) 42.3 criteria, and 41.2 ± 11.0 0.488group Maletolerancewere (%) for glucosegroups did(61%) in age andimmunofluorometric method. HOMA-IR was calculated and blood gender collected These and 54 not differ samples within normality. insulin measurements by gender. All were submitted to oral glucose tolerance test 86 (74%) 0.075 according BMIto(kg/height ) <0.001 2 insulin ( U/L) x fasting glucose (nmol/L)/22.5. Results - NAFLD patients showed higher insulin, glycemia, and 20.41 ± 0.31 30.05 ± 0.51sease, the formula: fasting HOMA-IR values than control group, even when excluding glucose intolerant and diabetes mellitus patients by their glycemic curves. Glucose (mg/dL) 84.7 ± 6.8 94.5 ± 9.9 <0.001le age HOMA-IR 75th percentile for control group was 1.78 and the best area under the curve index was obtained for HOMA-IR values of 2.0 [AUC= 0.840 (0.781–0.899 CI 95%), sensitivity (Se): 85%, specificity (Sp): 83%] while value 2.5 showed best specificity without Insulin (µUi/mL) 6.04 ± 2.8 15.7 ± 7.6 <0.001 important loss in sensitivity [AUC=0,831 (0.773-0.888) Se = 72%, Sp = 94%]. Conclusion: HOMA-IR values above or equal to 2.0 or 2.5 show enhanced diagnostic value in distinguishing non-alcoholic fatty liver disease carriers from control group individuals. HOMA-IR 1.2 ± 0.6 3.9 ± 2.8 <0.001neous HEADINGS - Insulin resistance. Fatty liver.rding Salgado AL, Carvalho L, Oliveira AC, Santos VN, Vieira JG, Parise ER. Arq Gastroenterol. 2010 Jun;47(2):165-9Brunt Control group presented HOMA-IR mean the most frequently INTRODUCTIONassay (HOMA-IR) has been value of 1.27 employed technique both in clinical practice and in Non-alcoholic fatty liver disease (NAFLD) has epidemiological studies. HOMA-IR, as proposed by
    • See corresponding CME exam on page 268.Dietary glycemic index and liver steatosis1–3Silvia Valtuena, Nicoletta Pellegrini, Diego Ardigo, Daniele Del Rio, Filippo Numeroso, Francesca Scazzina, ˜ `Lucilla Monti, Ivana Zavaroni, and Furio BrighentiABSTRACT syndromes, the development of dietary strategies to prevent thBackground: Insulin resistance (IR) GLYCEMIC INDEX AND LIVER STEATOSIS of NAFLD and its progression141NASH is of majo and liver steatosis (LS) are occurrence tointerlinked metabolic derangements whose prevalence is rapidly interest. Weight loss and supplementation with dietary antiox TABLE 4increasing, but the effect of dietary carbohydrate quality on LS is dants have been proposed for potential use in the prevention o Percentage prevalence, unadjusted and adjusted odds ratios (ORs), and 95% CIs for high-grade liver steatosis in relation to sex, waist circumference,unknown. model assessment index for insulin resistance (HOMA-IR), and dietary glycemic index1 and NASH, but little or no attention has been paid to th homeostasis NAFLDObjective: The objective was to describe the relation of IR and LS effect of carbohydrate quality on fat accretion in the liver (2-4 Risk factors Prevalence Unadjusted ORs (95% CIs) P Adjusted ORs (95% CIs)2 Pto total carbohydrate, total dietary fiber, and the glycemic index (GI) It is well documented that both excess body fat and resistanc % (n/total)and glycemic load of the diet. to the action of insulin impair the suppression of circulatin SexDesign: The study was a cross-sectional evaluation of 247 appar- Females 15.9 (17/107) 1 nonesterified fatty acids (NEFAs) in the postprandial stat 1ently healthy subjects who had no evidence of viral, toxic, or auto- Males 23.9 (32/134) 1.66 (0.87, 3.19) which favors a 5.76 (2.21, 15.01) influx into the hepatocyte an 0.1283 greater NEFA  0.001 Waist circumference and who were unselected for alcohol intake. Theimmune hepatitis subsequent synthesis of triacylglycerols. In addition, the meta Low 9.9 (14/141) 1 1homeostasis model assessment index was used as a(2.46, 9.72) mea- High 35.0 (35/100) 4.89 surrogate  0.001 pathway controlling mitochondrial 0.001 bolic 9.29 (3.54, 24.43)  fat oxidation is downsure of IR, and a liver echography was used as a proxy for LS grading. HOMA-IR regulated in the presence of IR, which further contributes tDietary data were collected by using 3-d food records. Total carbo- Low 10.5 (19/181) 1 1 intracellular fat accretion (5). Because weight loss and insulin High 50.0 (30/60) 7.83 (3.93, 15.6)  0.001 6.17 (2.83, 13.44)  0.001hydrate intake, total dietary fiber, GI, and glycemic load were cal- Glycemic index sensitizing medications have shown some efficacy in the treaculated by using a semiquantitative food-frequency questionnaire Low 16.5 (30/182) 1 ment of NAFLD, we 1 hypothesize that diets that can modulaconcerning the dietary sources of carbohydrates. (1.23, 4.71) High 32.2 (19/59) 2.41 either body weight or the metabolic consequences of IR coul 0.010 3.15 (1.34, 7.39) 0.009Results: The prevalencemodels, values for waist circumference were ͨ88 and ͨ102 cm for females and males, respectively (low), and Œ88 and Œ102 1 In the logistic regression of high-grade LS (HG-LS) increased sig- also have an effect on liver steatosis (LS).nificantly across quartiles of cm for females and males, respectively dietary GI for HOMA-IR and  0.034): are first 3 quartiles (low) and 4th quartile (high). a low dietary glycemic inde (high); values (P for trend glycemic index Epidemiologic data indicate that Downloaded from www.ajcn 2 Adjusted for sex, waist circumference, HOMA-IR, and glycemic index. Additional terms for plasma concentrations of triacylglycerols and HDLHG-LS inalcohol intake, intakes of carbohydrates andtwiceand dietarythe firstload (first(GI) is associated with4th quartile) did intake and body weight (6, 7 cholesterol, the 4th quartile (high GI) was fiber, that in glycemic 3 3 quartiles compared with the lower food not modify anyquartiles (low to medium GIs), whereas noin which glucose ҃ 100. risk estimate. Glycemic index was calculated on a scale relation was observed In addition, low dietary GI and glycemic load (GL) seem to bwith total carbohydrates, total S, Pellegrini N, Ardigo D, etload. In Am J Clin to favorable lipid profiles and lower concentrations o 3 Valtuena dietary fiber, or glycemic The sex ҂ waist circumference interaction was significant, P ҃ 0.008.al (2006). linked Nutr 84:136–142insulin-sensitive subjects (first 3 quartiles of homeostasis model C-reactive protein only in overweight and obese persons, whicassessment index of IR), the prevalence of HG-LS did not differ suggests that the metabolic effects of dietary carbohydrates ma effect of high-GI foods may exacerbate liver fat depositionsignificantly between GI groups, but, in insulin-resistant subjects only of the total amount of glucose consumed but also of role not be particularly important in insulin-resistant persons (8 –10). In through multiple mechanisms related to the reciprocal control of the glucose delivery rate (33). However, the availability of fatty
    • ü  MELHORA RIü  REDUÇÃO DA INGESTÃO CALÓRICA (> SACIEDADE)ü  6 A 12 MESES: ü  > PERDA DE PESO ü  > DIMINUIÇÃO TRIGLICÉRIDOS ü  > AUMENTO HDLü  MELHORA VÁRIOS MARCADORES DE DCV, MESMO NA AUSÊNCIA DE PERDA DE PESO
    • NUTRITION MYTHS
    • HIDRATOS DE CARBONO SÃO TODOS MAUS
    • Clinical Care/Education/Nutrition B R I E F R E P O R T A Low–Glycemic Load Diet Facilitates Greater Weight Loss in Overweight Adults With High Insulin Secretion but Not in Overweight Adults With Low InsulinGlycemic load and weight loss Secretion in the CALERIE Trial ANASTASSIOS G. PITTAS, MD1 SAI KRUPA DAS, PHD2 EDWARD SALTZMAN, MD2 PAUL C. STARK, SCD3 estimated daily glycemic index of 53, and weight gain upon ex CHERYL L. HAJDUK, MS, MPH, RD2 ANDREW S. GREENBERG, MD1,2 NÃO FOI of 45 g/1,000 kcals)baseline glycemic load SIGNIFICATIVO calorie restriction compared with at 30% glycemic load diet (35 JULIE GOLDEN, MD2 SUSAN B. ROBERTS, PHD2 individual energy needs. The glycemic in- dex and glycemic load of the diets were can be hypothesized determined using the International Ta- glycemic load diets, L ifestyle changes, in particular reduc- domized to a low– glycemic load diet bles of Glycemic Index and Glycemic ing energy intake, are the corner- compared with a high– glycemic load Load (23) and the Nutrition Data System ported by our presen stone of current approaches to diet. for Research (version 4.05_33) developed weight loss and prevention of type 2 dia- by the Nutrition Coordinating Center, Our results requ betes. However, there is currently no con- RESEARCH DESIGN AND sensus that one dietary regimen is more METHODS — This study was per- ent Database 33, released in 2002 (24). University of Minnesota, Food and Nutri- further studies with effective than another for weight loss (1) formed as part of the Comprehensive During the 6-month intervention period, subjects, but neverth or whether particular diets work better for Assessment of Long-term Effects of Re- all food was provided by the research cen- identifiable groups of individuals. There ducing Intake of Energy (CALERIE) trial ter, and participants were requested to evidence that simple is evidence, however, to suggest that both at the Human Nutrition Research Center consume only this food and report addi- insulin resistance and insulin secretion on Aging at Tufts University with ap- tional foods if they were eaten. To maxi- secretion may help e play a role in body weight regulation (2– proval from the Tufts-New England mize adherence to the study diet, regular 12). Therefore, dietary factors such as the Medical Center Human Investigation Re- behavioral group meetings and individual success in overwe dietary glycemic load (glycemic load ϭ view Committee. Written informed con- sessions with a dietitian were held. From through the use of targ glycemic index [GI] ϫ available carbohy- sent was obtained from all participants. participants’ reports of leftover food and drate amount) that influence these pa- Healthy women and men aged 24 – 42 extra items, actual daily nutrient intake mendations specific f rameters may theoretically interact with years with a BMI of 25–29.9 kg/m2 and during the intervention period was calcu- subject-specific characteristics of glucose- fasting plasma glucose Ͻ100 mg/dl were lated (24). status. insulin dynamics to influence the effect of recruited. After a 6-week baseline period Height (Ϯ0.1 cm) was measured at different hypocaloric diets on weight loss when usual energy requirements for baseline, and body weight (Ϯ100 g) was or maintenance (13,14). Weight loss weight stability were assessed using the measured weekly. Insulin secretion was studies using the concept of the dietary doubly labeled water method (22), partic- also estimated at baseline, as was the in- Acknowledgments — T glycemic index or glycemic load have ipants were randomized for 24 weeks to sulin value at 30 min (INS-30) after a 75-g shown conflicting results for heteroge- either a high– glycemic load diet (60% oral glucose tolerance test (25). Insulin ported by National Insti neous groups of individuals (15–21). carbohydrate, 20% protein, 20% fat, 15 g sensitivity in the fasting state was esti- K23-DK61506 (to A.G.P In a 6-month controlled feeding trial fiber/1,000 kcal, mean estimated daily mated at baseline by the homeostasis in healthy overweight adults with normal glycemic index of 86, and glycemic load model assessment of insulin resistance FOI SIGNIFICATIVO S.B.R.), and U.S. Depa glucose tolerance, we tested the hypothe- of 116 g/1,000 kcal) or a low– glycemic (HOMA-IR) (26). Glucose was measured cooperative agreement n sis that individuals with higher insulin load diet (40% carbohydrate, 30% pro- by the hexokinase method, and insulin secretion lose more weight when ran- tein, 30% fat, 15 g giber/1,000 kcal, mean was measured by radioimmunoassay. To S.B.R. and A.S.G.). ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● examine change in weight at 6 months, We thank the study p From the 1Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, we used general linear models adjustingFigure 1—Mean (ϮSEM) weightal. DiabetesUSDA Human Nutrition Researchfeeding study ofHOMA-IR and(HG) vs. Boston, Massachusetts; the 2Energy Metabolism Laboratory, Jean Mayer Care. 2005 Dec;28(12):2939-41. weight, a high– INS- Pittas AG, et change during a 6-month for baseline the MRU at the USDA Center on Aging, Tufts University, Boston, Massachusetts; and the 3Institute for Clinical Research and Health 30, and the interaction between diet ϫlow– (LG) glycemic England Medical Center, Boston, Massachusetts. Policy Studies, Tufts-New load diet in overweight adults stratified by baseline insulin secretion based on HOMA-IR and diet ϫ INS-30 (PROC search Center on Aging.serumDiabetes, and Metabolism,min after aMedical Center, 750glucose St., #268, Boston, MA GLM procedure in SAS software,pmol/l [66 insulin at 30 Tufts-New England to75-g oral Washington tolerance test (low INS-30 Ͻ 473 version Address correspondence and reprint requests Anastassios G. Pittas, M.D., Division of Endocrinology, 8.2; SAS Institute, Cary, NC).mU/l] Ͻ high INS-30). P values are adjusted for baseline weight. *P Ͻ 0.005 for within-group 02111. E-mail: apittas@tufts-nemc.org.
    • ROCIO ROCIO PEREIRA, GUREVICH, RICKARD RICKARD those on the LC/H PEREIRA, INGA INGA GUREVICH, women,WESTERGREN, SVEN ENERBACK, PETER J. ECKEL, J. ECKEL, their initial BW t WESTERGREN, SVEN ENERBACK, PETER 0.001) of 0.001) of a MARC Insulin Sensitivity Determines the Effectiveness 0.001)MARC L. GOALSTONE, JAMES O. JAMES O. HILL, ROBERT H. lost by those on th L. GOALSTONE, HILL, ROBERT H. Ͻ Ͻ 0.001) lo AND of Dietary BORIS AND Macronutrient Composition onECKEL,ECKEL,BORIS DRAZNIN.DRAZNIN. Insulin sensitivity Insulin sensitivity two groups). These groups two differedetermines the Weight Loss inof dietary of dietary macronutrientin resting metabol effectiveness Obese Women determines the effectivenessPereira,* Inga Gurevich,¶ Rickard Westergren,**macronutrient changes changes incomposition on Marc-Andre Cornier,*††J.W.Eckel,‡Donahoo,*†† Rocio in obeseRobert H.Res. and Obes changes in Si were asso Sven Enerback,**loss in Marc L. Goalstone,*¶ James O. Hill,†§ weighton weight losswomen. Obes Eckel,*‡ composition Peter Troy obese women. all, Res. Ϫ0.57, p change all, loss (r ϭ loss Ͻ 0.05 Boris Draznin*¶2005;13:703–709. (r ϭ Ϫ 2005;13:703–709. Discussion: The state of SiObjective: To determine whether macronutrient composi- the insulin-resistant Abstract on the LC/HF diet lost 6.8 Ϯ 1.2% (p Ͻ 0.001; p Ͻ 0.002 Discussion Objective: PEREIRA,determine RICKARD betweenofthe groups). InLC/HFcompared with 8.5 1.3% macronutrient composition ROCIO To CORNIER, MARC-ANDRE, W. TROY DONAHOO, INGA GUREVICH, whether those on theBW as diet lost 13.4 Ϯ Ϯcomposi- women, macronutrient contrast, among (p Ͻtion of a hypocaloric GOALSTONE, JAMES O. HILL, ROBERT H. effectiveness HC/LF diet (p Ͻ 0.04 between diet can enhance its 0.001) lost byinitial on the and WESTERGREN, SVEN ENERBACK, PETER J. ECKEL, their 1.4% (p macronutri tion of sensitivity (Si) affects the two groups). Thesemetaboliceffectiveness and For maximal bene a hypocaloric diet sensitivity enhance its rate,could not be intake. Over- ECKEL, AND BORIS DRAZNIN. Insulin can MARC L. Ͻ 0.001) response thosewhether insulin determines the effectiveness of dietary macronutrient changes in resting to hy- or differences women. explained by whether2005;13:703–709. sensitivity (Si) loss (r ϭ Ϫ0.57, p Ͻthe response to hy-a hypocaloric die insulin composition on weight loss in obese women. Obes Res. affects 0.05). activity, tion of all, changes in Si were associated with the degree of weight women. Fopocaloric diets. Objective: To determine whether macronutrient composi- Discussion: The state of Si determines the effectiveness of tion of a correspond to the state of SResearch Methodsofdiets. diet can enhance its effectiveness and macronutrientmaximal benefit, the macronutrient composi- pocaloric andsensitivity (Si) affects the response to hy- women. For composition of hypocaloric diets in obese tion a hypocaloric Procedures: Obese nondiabetic in- whether insulin correspond Research Methods and10 ␮U/mL; n toϭstate of Si. and Procedures: the 12) nondiabetic in- Obese tion of a hypocaloric diet may need to be adjusted tosulin-sensitive (fasting (fasting insulin Ͻ 10 Obese nondiabeticand insulin Ͻ n ϭ 12) in- pocaloric diets. correspond Research Methods and Procedures: sulin-sensitive ␮U/mL; Key words: CHO, fat, insobese nondiabetic insulin-resistantwere(fasting insulin Ͼ 15 n ϭ 12) and sulin-sensitive (fastingold)insulin Ͻ words: CHO, fat, insulin resistance 10 ␮U/mL; Key obese nondiabetic insulin-resistant (fasting insulin Ͼ 15 ␮U/mL; n ϭ 9) women (23 to 53 years (60% CHO, 20% (23 to (LC)/high fat 53 years random-␮U/mL; obese nondiabeticCHOinsulin-resistant dietary interventions are based on a significant Ͼ 15 n ϭ 9) women fat) or lowdiet. Primary outcome(HF) (40%old)Successful (fasting insulin ized to either a high carbohydrate (CHO) (HC)/low fat (LF) were random- Introduction Key word CHO, 40% fat) hypocaloric measures reduction in caloric intake, relative to energy expenditureized to either a high (BW), Si,9) women fasting lipids. (HC)/lowof fat (LF)the effectiveness of carbohydrate and (23 to 53 years old) onwere random- (CHO) (1).hypocaloric dietswhether impact ␮U/mL; n ϭ resting metabolicon the HC/LF diet lost of The question has an the macronutrient composition after a 16-week dietary intervention were: changes in body weight rate, Intro(60% CHO, 20%either(p Ͻ low their initial BW,(LC)/high fat (HF) (40% (LC), hypoca- Successful dietary interve ized to 13.5 Ϯ 1.2%ora0.001) of CHO whereas those popularizationregimens (2–11). (CHO) fat) Results: Insulin-sensitive women these diets, however, has gained substantial interest with the high carbohydrate dietary of low-carbohydrate loric (CHO) (HC)/low fat (LF) 1CHO, 40% fat) CHO, 20% diet. or low CHO body insulin sensitivity (Si) isfat (HF) (40% in caloric intake (60% hypocaloric fat) Primary outcome Insulin-resistantglucoseindividuals require Total measures overall measure of insulin (LC)/high uptake and metab- an reduction the ability of to regulate Successf Received for review June 7, 2004. Accepted in final form January 20, 2005.after a 16-week dietary intervention were: changes levels ofbody to maintain normal The question of whethe higher than normal in insulinemia olism (12,13). (IR) The costs of publication of this article were defrayed, in part, by the payment of page (1). CHO, 40% fat) hypocaloric diet.glycemia. Thus, either fasting or postprandial hyperinsulin- Primary outcome measures charges. This article must, therefore, be hereby marked “advertisement” in accordance withweight (BW), Si, resting metabolic rate, and prevents the development of impaired glucose toler- hypocaloric reductionan i 18 U.S.C. Section 1734 solely to indicate this fact. fasting lipids. Departments of *Medicine and †Pediatrics, ‡Adult General Clinical Research Center, and emia the §Center for Human Nutrition, University of Colorado Health Sciences Center, ¶Research of diets has after a 16-week dietary intervention were: changes in body Service of the Denver Veterans Administration Medical Center, Denver, Colorado; and these diets, however, has qu (1). The ga **Medical Genetics, Department of Medical Biochemistry, Gothenburg University, Gote-Results: Insulin-sensitive women on the HC/LF diet lost borg, Sweden. ††These authors contributed equally to the design and implementation of this study. 1 Nonstandard abbreviations: CHO, carbohydrate; LC, low CHO; Si, insulin sensitivity; IR,13.5 Ϯ 1.2% (p Ͻ 0.001) of resting metabolic rate, and fasting lipids. weight (BW), Si, their initial BW, whereas those Address correspondence to Boris Draznin, Veterans Administration Medical Center, (151) insulin resistant; IS, insulin sensitive; HC, high CHO; LF, low fat; HF, high fat; BW, body 1055 Clermont Street Denver, CO 80220. E-mail: Boris.Draznin@med.va.gov Copyright © 2005 NAASO of hypocal weight; GCRC, General Clinical Research Center; RMR, resting metabolic rate; RQ, popularization of low-carb respiratory quotient; FFA, free fatty acid; HDL, high-density lipoprotein; LDL, low-density lipoprotein. Results: Insulin-sensitive Obes Res. 2005 Apr;13(4):703-9. HC/LF diet lost Cornier MA, et al. women on the these diets, loric dietary regimens (2–1 OBESITY RESEARCH Vol. 13 No. 4 April 2005 703 13.5 Ϯ 1.2% (p Ͻ 0.001) of their initial BW, whereas Total body insulin sensiti those popularizat
    • concentrations (from 1 0.05). As predicted, lepInsulin Sensitivity Determines the Effectiveness groups with weight loof Dietary Macronutrient Composition on composition of the hypWeight Loss in Obese WomenMarc-Andre Cornier,*†† W. Troy Donahoo,*†† Rocio Pereira,* Inga Gurevich,¶ Rickard Westergren,**Sven Enerback,** Peter J. Eckel,‡ Marc L. Goalstone,*¶ James O. Hill,†§ Robert H. Eckel,*‡ and Measures of Energy BBoris Draznin*¶ IS subjects in the LCAbstract on the LC/HF diet lost 6.8 Ϯ 1.2% (p Ͻ 0.001; p Ͻ 0.002 HC/LF group lost theCORNIER, MARC-ANDRE, W. TROY DONAHOO,ROCIO PEREIRA, INGA GUREVICH, RICKARD between the groups). In contrast, among the insulin-resistant women, those on the LC/HF diet lost 13.4 Ϯ 1.3% (p Ͻ caloric deficit imposedWESTERGREN, SVEN ENERBACK, PETER J. ECKEL,MARC L. GOALSTONE, JAMES O. HILL, ROBERT H. 0.001) of their initial BW as compared with 8.5 Ϯ 1.4% (p Ͻ 0.001) lost by those on the HC/LF diet (p Ͻ 0.04 between HC/LF and IR patientsECKEL, AND BORIS DRAZNIN. Insulin sensitivitydetermines the effectiveness of dietary macronutrient two groups). These differences could not be explained by changes in resting metabolic rate, activity, or intake. Over- almost twice the expect all, changes in Si were associated with the degree of weightcomposition on weight loss in obese women. Obes Res.2005;13:703–709. loss (r ϭ Ϫ0.57, p Ͻ 0.05). subjects received all of Discussion: The state of Si determines the effectiveness ofObjective: To determine whether macronutrient composi-tion of a hypocaloric diet can enhance its effectiveness and macronutrient composition of hypocaloric diets in obese and frequent dietary re women. For maximal benefit, the macronutrient composi-whether insulin sensitivity (Si) affects the response to hy-pocaloric diets. tion of a hypocaloric diet may need to be adjusted to correspond to the state of Si. ences between the grouResearch Methods and Procedures: Obese nondiabetic in-sulin-sensitive (fasting insulin Ͻ 10 ␮U/mL; n ϭ 12) and Key words: CHO, fat, insulin resistance weight and those that loobese nondiabetic insulin-resistant (fasting insulin Ͼ 15␮U/mL; n ϭ 9) women (23 to 53 years old) were random- cannot definitively ruleized to either a high carbohydrate (CHO) (HC)/low fat (LF) Introduction(60% CHO, 20% fat) or low CHO (LC)/high fat (HF) (40% Successful dietary interventions are based on a significant the etiology for the diffeCHO, 40% fat) hypocaloric diet. Primary outcome measures reduction in caloric intake, relative to energy expenditureafter a 16-week dietary intervention were: changes in body (1). The question of whether the macronutrient composition energy expenditure seemweight (BW), Si, resting metabolic rate, and fasting lipids. of hypocaloric diets has an impact on the effectiveness ofResults: Insulin-sensitive women on the HC/LF diet lost these diets, however, has gained substantial interest with the We addressed the energ13.5 Ϯ 1.2% (p Ͻ 0.001) of their initial BW, whereas those popularization of low-carbohydrate (CHO)1 (LC), hypoca- loric dietary regimens (2–11). only through self-repor Total body insulin sensitivity (Si) is an overall measure ofReceived for review June 7, 2004.Accepted in final form January 20, 2005. the ability of insulin to regulate glucose uptake and metab- olism (12,13). Insulin-resistant (IR) individuals require jects were pooled, RMRThe costs of publication of this article were defrayed, in part, by the payment of pagecharges. This article must, therefore, be hereby marked “advertisement” in accordance with18 U.S.C. Section 1734 solely to indicate this fact. higher than normal levels of insulinemia to maintain normal glycemia. Thus, either fasting or postprandial hyperinsulin- 36 to 1221 Ϯ 43 kcal/dDepartments of *Medicine and †Pediatrics, ‡Adult General Clinical Research Center, andthe §Center for Human Nutrition, University of Colorado Health Sciences Center, ¶ResearchService of the Denver Veterans Administration Medical Center, Denver, Colorado; and emia prevents the development of impaired glucose toler- significant changes in R**Medical Genetics, Department of Medical Biochemistry, Gothenburg University, Gote-borg, Sweden.††These authors contributed equally to the design and implementation of this study. 1 Nonstandard abbreviations: CHO, carbohydrate; LC, low CHO; Si, insulin sensitivity; IR, analyzed separately, anFigure 1: Absolute (A) and percentage (B) change in BW in IS andAddress correspondence to Boris Draznin, Veterans Administration Medical Center, (151)1055 Clermont Street Denver, CO 80220. insulin resistant; IS, insulin sensitive; HC, high CHO; LF, low fat; HF, high fat; BW, body weight; GCRC, General Clinical Research Center; RMR, resting metabolic rate; RQ, found. Therefore, changE-mail: Boris.Draznin@med.va.gov respiratory quotient; FFA, free fatty acid; HDL, high-density lipoprotein; LDL, low-densityIR women randomized to 16 weeks of hypocaloric HC/LF orCopyright © 2005 NAASO lipoprotein. Cornier MA, et al. Obes Res. 2005 Apr;13(4):703-9. weight loss differencesLC/HF diet. (*) p Ͻ 0.01 for diet effect within ISVol. 13 No. 4 April 2005 Ͻ OBESITY RESEARCH group. (†) p 7030.05 for Si effect within HC/LF diet. (‡) p Ͻ 0.05 for diet effect
    • Trial in Obese Young AdultsDiet Effects of a Low–Glycemic LoadTrial Context The results of clinical trials involving diet in the treatment of obesity have been vs Low-Fat Diet in Obese Young Adults A Randomized Trial inconsistent, possibly due to inherent physiological differences among study participants. Cara B. Ebbeling, PhD Context ObjectiveThe results of clinical trials involvingresultsdueclinical trials involving dietdifferences among studywith 2 popu- Michael M. Leidig, whether insulin secretion affects weight obesity have been To determineRD Context The diet in thephysiological in the treatment of obesity have been inconsistent, possibly of to inherent treatment of loss participants. inconsistent, possibly due to inherent physiological differences among study participants. lar diets. Henry A. Feldman, PhD Objective To determine whether insulin secretion affects weight loss with 2 popu- lar diets. Margaret M. Lovesky, RD Objective To determine whether insulin secretion affects weight loss with 2 (aged Design, Setting, and Participants Randomized trial of obeseDecember 2006adultspopu- David S. Ludwig, MD, PhD Design, Setting, and Participants Randomized trial of obese young adults (aged 18-35 years; n = 73) conducted from September 2004 to young in Boston, W lar diets. ITH PREVALENCE proaching one Mass, and consisting of a 6-month intensive intervention period and a 12-month fol- 18-35 years; n = 73) conducted thirdAPof low-up period. Serum insulin concentrationDecember a2006 of oral from September 2004 to at 30 minutes after 75-g dose in Boston, - glucose was determined at baseline as a measure of insulin secretion. Outcomes were Mass, and consisting of theamong the most im-intensive12, and 18 months. Missingperiod and a 12-month fol- Design, Setting, and is a population, obesity assessed at 6, intervention data were imputed conservatively. 6-month ParticipantsInterventions A low–glycemic load (40% obese young adults (aged Randomized trial of carbohydrate and 35% fat) vs low-fatCE AP - low-upyears; n =States and identification of effective di- September 2004 to December 2006 in Boston, 18-35 period. Serum insulin from portant medical problems in concentration at and 20% fat) diet. 73) conducted the United (55% carbohydrate 30 minutes after a 75-g dose of oral hird of 1 glucose was determinedahas become a major as a measure of and cardiovascular diseaseand determined by dual- were Mass, and consisting ofpriority.baselineintensiveabsorptiometry, insulin secretion. a 12-month fol- etary treatment at Outcomes Main Outcome Measures Body weight, body fat percentage 6-month energy x-ray intervention period risk factors.obesityCE AP - public health 2 Three popular assessedperiod. Serumfat, low months. Missingoverall.in body weight and body fatafter a 75-g betweenglu-of oral low-up at 6, 12, glycemic18 carbohydrate, and Results Change However,minutes percentage did not differ dose and diets—low insulin concentration at 30 data were concentration at 30 conservatively. imputed minutes after a dose of oral the load—have recently re- diet groups insulinost im- hird of low Interventions ceived much attention. However, clini-as a(40% and P=.01 forinsulin secretion. Outcomes were glucose was determined at baseline cosebody weight carbohydrate and those with30 fat) vs low-fat A low–glycemic load atmeasure ofmedian (57.5 µIU/mL; n=28), the low–glycemic load diet was an effect modifier (groupϫtimeϫinsulin concentration at minutes: P=.02 for body fat percentage). For 35%insulin concentra- obesity United cal trials have produced inconsistent (55% carbohydratesuperior for months. diet.(–2.6% vs –0.9%; P=.03) thanimputedat 18 months. There werepercent- assessed at 6, 12, and 18 suggesting that one tion 30 a greaterabove thein weight (–5.8 vs –1.2 kg;conservatively. findings,and 20% fat) Missing data were with some produced minutes decrease P=.004) and body fat ost im- tive di- 3-8 diet is weight loss and age the low-fat diet no sig- Interventions tween low–glycemic load (40%minutes below the percentage35% fat) minutes Main OutcomeA diets. This inconsistency may weight, body fat median level (n=28). Insulindetermined by dual- Measures Body centration at 30 carbohydrate and concentration at 30 vs low-fat others indicating no difference be- nificant differences in these end points between diet groups for those with insulin con- United 9-11 major energycarbohydrate and between trials, such cardiovascularimproved more onrisk factors.cholesterol andlow- (55% x-ray absorptiometry, and as after risk factors. In glucosedisease high-densitymodifier for cardiovascular dis- arise from methodological fat) diet. a dose of oral 20% problems ease was not a significant effect the full cohort, plasma lipoprotein tri-ctive di- opular both within and different treatment intensity between glyceride concentrations the low–glycemic load diet, whereas Main Outcome Measures Body weight, fat percentageimprovednotondiffer between the Results Change in inadequate attention to treat- Conclusions body fat percentage determined by dual- groups, body weight and body density lipoprotein cholesterol concentration did more the low-fat diet. major te, and ment fidelity, variable nutrition edu- Variability in dietary weight loss trials may be partially attributable topopularntly re- diet groups overall. and confounding by dietary andconcentration response. individuals withfactors. dose of oral energy x-ray absorptiometry, and cardiovascularloss among Reducing glycemicafter secretion. Regardless glu- However, insulin tant to achieve weight disease risk high insulin be cation and dietary counseling strate- differences in hormonal at 30 minutes load maya especially impor- gies, te, and cose was an effect in body An(groupϫtimeϫinsulin concentrationbut notdiffer high-density P=.02 Results Change modifierweight andlipoprotein cholesterol and triglyceride concentrationsnot 30 minutes: the nondietary factors. alternative ex- body fat percentage did at on low-density lipopro- of insulin secretion, a low–glycemic load diet has beneficial effects on betweenr, clini- planation for this inconsistency re- tein cholesterol concentration. for body weight lates to inherent physiological differ-concentration at 30 minutes after a dose of oral glu-ntly re- diet groups overall. However, insulin fat Registration clinicaltrials.gov Identifier: NCT00130299insulin concentra- and P=.01 for body Trial percentage). For those with sistent ences among study participants. tion at 30an effect above the median (57.5 µIU/mL; n=28), the low–glycemic load diet cose was minutes modifier mechanism that One physiological (groupϫtimeϫinsulin concentration at 30 minutes: P=.02 JAMA. 2007;297:2092-2102 www.jama.com r, clini-hat one producedweight position is individualEbbeling CB,in- al. (–5.8 vsMay 16;297(19):2092-102 with insulinfat percent- for body a greater decreasefor weightofJAMA. 2007 index and kg; P=.004) and body concentra- in body the glycemic –1.2 the carbo- might relate weight loss to dietary com- and P=.01differences in et fat percentage). For those Author Affiliations: Department of Medicine, Chil- dren’s Hospital Boston, Boston, Mass.nsistents3-8 and age (–2.6% vs –0.9%; P=.03)a than the low-fatresult in higher calo- months. There were no diet Corresponding Author: David S. Ludwig, MD, PhD, Chil- tion at 30 minutes abovemathematicalhigh gly- (57.5 insulin )concentration, post- the low–glycemic load sig- diet at 18 cemic load (the the median prandial µIU/mL; n=28), 12 sulin secretion. Diets with hydrate amount dren’s Hospital Boston, 300 Longwood Ave, Boston, MA product 02115 (david.ludwig@childrens.harvard.edu). hat one ce be- nificant differences in these end points(–5.8 vs –1.2 kg; P=.004)those withfat percent- produced a greater decrease in weight between diet groups for and body insulin con- 2092 JAMA, May 16, 2007—Vol 297, No. 19 (Reprinted) ©2007 American Medical Association. All rights reserved.
    • Low–Glycemic ronutrient content, some clinical trials Load Diet Low-Fat Diet P (n = 32) (n = 34) Value† show benefits of a low–glycemic in- How satisfied are you with this diet? 7.0 (0.4) 6.9 (0.3) .80 dex diet on LDL cholesterol concen- How easy has this diet been? Effects of a Low–Glycemic Load 5.3 (0.3) 5.1 (0.4) .68 tration.11,14 Therefore, we speculate that a low–glycemic load diet in which satu- vs Low-Fat Diet in Obese Young Adults How tasty have the foods been? How satisfied are you with your weight loss to date? 6.9 (0.3) 4.1 (0.4) 6.8 (0.3) 4.7 (0.5) .92 .37 rated fat is kept low (eg, by substitut- ing monounsaturated or polyunsatu- †Testing for group difference using the t test. A Randomized Trial *On 10-cm visual analog scale with 0 indicating not at all and 10, extremely. rated fat from vegetable sources for Cara B. Ebbeling, PhD Context The results of clinical trials involving diet in the treatment of obesity have been Michael M. Leidig, RD inconsistent, possibly due to inherent physiological differences among study participants. Figure 3. Change in Body Weight Feldman, PhD Henry A. Objective To determine whether insulin secretion affects weight loss with 2 popu- NÃO FOI SIGNIFICATIVORD Margaret M. Lovesky, NÃOlar diets. SIGNIFICATIVO FOI FOI SIGNIFICATIVO David S. Ludwig, MD, PhD Design, Setting, and Participants Insulin Concentration ≤57.5 µIU/mL at Randomized trial ofInsulin young adults (aged obese Concentration >57.5 µIU/mL at All 30 min After 75-g = 73) conducted from September 2004 to 30 min After 75-g Dose of Oral Glucose 18-35 years; n Dose of Oral Glucose December 2006 in Boston, W Mass, and consisting of a 6-month intensive intervention period and a 12-month fol- 5 ITH PREVALENCE AP - low-up period. Serum insulin concentration at 30 minutes after a 75-g dose of oral Low–Glycemic Load Diet Low-Fat DietChange From Baseline, kg proaching one third of glucose was determined at baseline as a measure of insulin secretion. Outcomes were the population, obesity assessed at 6, 12, and 18 months. Missing data were imputed conservatively. 0 is among the most im- Interventions A low–glycemic load (40% carbohydrate and 35% fat) vs low-fat portant medical problems in the United (55% carbohydrate and 20% fat) diet. States1 and identification of effective di- etary treatment has become a major Main Outcome Measures Body weight, body fat percentage determined by dual- –5 energy x-ray absorptiometry, and cardiovascular disease risk factors. public health priority.2 Three popular diets—low fat, low carbohydrate, and Results Change in body weight and body fat percentage did not differ between the P = .99 low glycemic load—have recently = .90 diet groups overall. However, insulin concentration at 30P = .02 after a dose of oral glu- P re- minutes cose was an effect modifier (groupϫtimeϫinsulin concentration at 30 minutes: P=.02 –10 ceived much attention. However, clini- for body weight and P=.01 for body fat percentage). For those with insulin concentra- 0 6 cal trials have produced inconsistent tion at 30 minutes above the median (57.5 µIU/mL; n=28), the low–glycemic load diet 12 12 18 0 6 12 18 0 6 18 Time, mo Time, mo findings, with some suggesting that one produced a greater decrease in weight (–5.8 vs –1.2 kg; P=.004) and body fat percent- Time, mo diet is superior for weight loss3-8 and age (–2.6% vs –0.9%; P=.03) than the low-fat diet at 18 months. There were no sig- others indicating no difference be- nificant differences in these end points between diet groups for those with insulin con- In the full cohort (left panel), weight loss did9-11 differ significantly between participants assigned to the low–glycemic load diet vs the low-fat diet. Among participants not tween diets. This inconsistency may centration at 30 minutes below the median level (n=28). Insulin concentration at 30 minutes for whom data were available at baseline (right 2 panels), insulin concentration dose of oral glucose was not adose of oral glucose wasforsignificant effect modifier (P = .02). at 30 minutes after a 75-g significant effect modifier a cardiovascular dis- arise from methodological problems after a Error bars indicate 95% confidence intervals. Data based on repeated-measures analysis, accounting for plasma high-density lipoprotein cholesterol and tri- variability. The ease risk factors. In the full cohort, within-subject correlation and between-subject both within and between trials, such as P value at the lower left of each panel tests the groupϫ time interaction. Missing data were imputed conservatively. different treatment intensity between glyceride concentrations improved more on the low–glycemic load diet, whereas low- density lipoprotein cholesterol concentration improved more on the low-fat diet. groups, inadequate attention to treat- ment fidelity, variable nutrition edu- Conclusions Variability in dietary weight loss trials may be partially attributable to cation and dietary counseling strate- differences in hormonal response. Reducing glycemic load may be especially impor- Table 3. Changes in Adiposity and Cardiovascular Disease Risk Factors* weightlow–glycemic load diet withbeneficial effects on high-density tant to achieve gies, and confounding by dietary and of insulin secretion, a loss among individuals has high insulin secretion. Regardless nondietary factors. An alternative ex- lipoprotein cholesterol and triglyceride concentrations but not on low-density lipopro- 6-mo Follow-up, Mean (SE) 18-mo Follow-up, Mean (SE) planation for this inconsistency re- tein cholesterol concentration. lates to inherent physiological differ- Low–Glycemic P Low–Glycemic Trial Registration clinicaltrials.gov Identifier: NCT00130299 P ences among study participants. Load Diet Low-Fat Diet JAMA. 2007;297:2092-2102 Value Load Diet Low-Fat Diet www.jama.com Value One physiological mechanism that Body fat percentage† might relate weight loss to dietary com- Author Affiliations: Department of Medicine, Chil- All position is individual differences in in- al. JAMA. 2007 May 16;297(19):2092-102−1.5 (0.4) Boston, Mass. −1.1 (0.3) Ebbeling CB, et of the−1.4 (0.3)index and .94 carbo- dren’s Hospital Boston, −1.3 (0.4) glycemic the .50 sulin secretion. Diets with a (0.5) gly- hydrate amount12) result in higher post- CorrespondingBoston, 300 Longwood Ave, Boston,Chil- Insulin concentration Յ57.5 µIU/mL −0.9 high −2.2 (0.6) .11 −0.9 (0.5) dren’s Hospital Author: David S. Ludwig, MD, PhD, −1.4 (0.6) MA .56 at 30 min‡ cemic load (the mathematical product prandial insulin concentration, calo- 02115 (david.ludwig@childrens.harvard.edu). Insulin concentration Ͼ57.5 µIU/mL May 16, 2007—Vol 297, No. 19 (Reprinted) −0.4 (0.5) 2092 JAMA, −2.0 (0.6) .04 ©2007 American −2.6 (0.6) −0.9 (0.5) Medical Association. All rights reserved. .03
    • 0163-769X/09/$20.00/0 Endocrine Reviews 30(1):96 –116Printed in U.S.A. Copyright © 2009 by The Endocrine Society doi: 10.1210/er.2008-0033Hypothesis: Could Excessive Fructose Intake and UricAcid Cause Type 2 Diabetes?Richard J. Johnson, Santos E. Perez-Pozo, Yuri Y. Sautin, Jacek Manitius, Laura Gabriela Sanchez-Lozada,Daniel I. Feig, Mohamed Shafiu, Mark Segal, Richard J. Glassock, Michiko Shimada, Carlos Roncal,and Takahiko NakagawaDivision of Nephrology (R.J.J., Y.Y.S., L.G.S.-L., M.Sha., M.Se., R.J.G., M.Shi., C.R., T.N.), University of Florida,Gainesville, Florida 32620-0224; Division of Nephrology (S.E.P.-P.), Mateo Orfila Hospital, 07703 Minorca (BalearicIslands), Spain; Division of Nephrology (J.M.), The Ludwig Rydygier Medical University, 85-067 Bydgoszcz, Poland;Department of Nephrology (L.G.S.-L.), Instituto Nacional de Cardiología Ignacio Chavez, 14080 Mexico City, Mexico; ´Division of Pediatric Nephrology (D.I.F.), Baylor College of Medicine, Houston, Texas 77030; and Retired Professor(R.J.G.), Torrance, CaliforniaWe propose that excessive fructose intake (>50 g/d) may be uric acid in the pathogenesis of metabolic syndrome.one of the underlying etiologies of metabolic syndrome and Fourth, environmental and genetic considerations providetype 2 diabetes. The primary sources of fructose are sugar a potential explanation of why certain groups might be(sucrose) and high fructose corn syrup. First, fructose intake more susceptible to developing diabetes. Finally, we discusscorrelates closely with the rate of diabetes worldwide. Sec- the counterarguments associated with the hypothesis and aond, unlike other sugars, the ingestion of excessive fructose potential explanation for these findings. If diabetes mightinduces features of metabolic syndrome in both laboratory result from excessive intake of fructose, then simple publicanimals and humans. Third, fructose appears to mediate the health measures could have a major impact on improvingmetabolic syndrome in part by raising uric acid, and there are the overall health of our populace. (Endocrine Reviews 30:now extensive experimental and clinical data supporting 96 –116, 2009) I. Introduction overweight or obese subject (likely type 2 diabetes) (1, 2).
    • Johnson et al. • Fructose as a Cause of Type 2 Diabetes Endocrine Reviews, February 2009, 30(1):96 –116 101FIG. 3. Potential mechanisms by which fructose and uric acid may induce insulin resistance. Fructose enters cell via a transporter (primarilyGlut 5) where it is acted on by fructokinase (KHK). As part of this metabolism, ATP depletion may occur, generating uric acid with systemic
    • 100 Endocrine Reviews, February 2009, 30(1):96 –116 Johnson et al. • Fructose as a Cause of Type 2 DiabetesFIG. 2. Effect of fructose on various organ systems. Table sugar, HFCS, and natural sources provide fructose, which in excess has numerous effectson the brain, liver, vasculature, kidney, and adipocyte. The net effects induce all features of the metabolic syndrome and ultimately type 2 diabetes.adipocyte. There is evidence that insulin resistance is medi- ability of fructose to induce features of the metabolic syn-ated in part by inflammation and oxidative stress within the drome. As mentioned, lowering uric acid was found to ame-adipocyte (109). Sautin et al. (104) have recently shown that liorate a number of features of metabolic syndrome in fructose-uric acid induces this phenotype in cultured adipocytes. In fed rats, including hypertension, hypertriglyceridemia,
    • ALIMENTO! DOSE  (GRS)! CARGA  GLICÉMICA! FRUTOSE! Maçã! 120" 5,5! 11,2! Alperces! 120" 5,2! 4,0!Banana  crua! 120" 12,4! 7,2! Cerejas! 120" 2,7! 4,3! Tâmaras! 60! 41,6! 13,4! Figos! 60" 15,7! 1,8! Toranja! 120" 2,7! 3,5! Uvas! 120" 8,2! 9,1! Kiwi! 120" 6,2! 5,9! Manga! 120" 8,5! 9,5! Laranja! 120" 4,6! 5,5! Papaia! 120" 10,2! 4,3! Pêssegos! 120" 4,6! 4,9! Pêras! 120" 4,2! 8,8! Ananás! 120" 7,4! 4,4! Ameixa! 120" 4,8! 4,0! Passas! 60! 28,5! 20,3! Meloa! 120" 3,7! 5,4! Morangos! 120" 1,3! 3,6! Melancia! 120" 4,3! 6,1!
    • M ET ABOL I SM CL IN I CA L A N D E XP E RI ME N TAL XX ( 2 0 11 ) XXX– X XX available at www.sciencedirect.com www.metabolismjournal.comThe effect of two energy-restricted diets, a low-fructose dietversus a moderate natural fructose diet, on weight loss andmetabolic syndrome parameters: a randomized controlled trialMagdalena Madero a,⁎, Julio C. Arriaga a , Diana Jalal b , Christopher Rivard b , Kim McFann b ,Oscar Pérez-Méndez a , Armando Vázquez a , Arturo Ruiz a , Miguel A. Lanaspa b ,Carlos Roncal Jimenez b , Richard J. Johnson b , Laura-Gabriela Sánchez Lozada a,ba Division of Nephrology, Department of Medicine, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano no 1 Col Seccion XVITlalpan, México City, 14080, Méxicob Division of Renal Diseases and Hypertension, University of Colorado, Denver, CO, USAA R T I C LE I N FO AB S T R A C TArticle history: One of the proposed causes of obesity and metabolic syndrome is the excessive intake of
    • natural fructose diet, on weight loss and metabol..., Metabolism (2011), doi:10.1016/j.metabol.2011.04.001Please cite this article as: Madero M, et al, The effect of two energy-restricted diets, a low-fructose diet versus a moderate M ET ABOL I SM CL IN I CA L A N D E XP E RI ME N TAL XX ( 2 0 11 ) XXX–X XX Table 2 – Differences in diet compositions at baseline and among intervention groups Baseline % Low- % Moderate- % Low- % Moderate- % Low- % Moderate- % energy intake fructose fructose fructose fructose fructose fructose (kcal) total diet diet diet diet diet diet cohort 1500 kcal 1500 kcal 1800 kcal 1800 kcal 2000 kcal 2000 kcal Pyramid food groups Protein 416.4 14 264 18 227 15 308 17 272 15 344 17 296 15 Fat 764.3 26 427.5 29 441 29 508.5 28 504 28 571.5 29 625.5 32 Carbohydrate 1818.9 61 796 54 832 56 971 54 1014 57 1062 54 1104 56 Major food groups Dairy products 363.9 13 220 15 220 15 220 12 110 6 220 11 220 11 Fruits 528.1 17 60 4 480 32 60 3 540 30 60 3 540 27 Animal products 228.3 7 225 15 225 15 225 13 300 17 300 15 300 15 Vegetables 178.5 6 100 7 100 7 100 6 50 3 87.5 4 75 4 Leguminous products 99.9 3 60 4 60 4 120 7 240 13 120 6 180 9.1 Cereals 899.2 30 665 45 280 19 770 43 280 16 875 44 350 18 Fat 154.6 6 157.5 11 135 9 292.5 16 270 15 315 16 315 16 Candies 71.7 2 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 Juices and soft drinks 263.8 9 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 Snacks 154.8 4 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 Added sugars 56.8 3 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 0 0.0 Average caloric intake 2999.7 100 1487.5 100 1500.0 100 1787.5 100 1790.0 100 1977.5 100 1980.0 100 “%” refers to the percentage of calories from each food group. 5
    • 3 2 1WEIGHT LOSS (kilograms) 0 -1 -2 -3 -4 -5 -6 -7 BASELINE FINAL LOW FRUCTOSE GROUP MODERATE NATURAL FRUCTOSE GROUP
    • 6 ME TA BOL I SM CL IN I CA L A N D E XP E RI ME N TAL XX ( 2 0 11 ) XXX– X XX Table 3 – Within- and between-group changes in the low-fructose group and the moderate-fructose group with natural fruit supplements Δ = final − baseline Low fructose Moderate natural fructose Comparison between intervention groups Δ Mean ± SD P value Δ Mean ± SD P value P value Weight (kg) −2.94 ± 2.18 <.0001 −4.07 ± 2.39 <.0001 .002 Systolic BP (mm/Hg) −9.46 ± 7.77 <.0001 −7.85 ± 8.73 <.0001 .09 Diastolic BP (mm/Hg) −5.17 ± 4.69 <.0001 −6.04 ± 5.40 <.0001 .57 Fat (%) −2.09 ± 6.32 .02 −2.89 ± 6.33 .002 .10 Waist to hip ratio −0.03 ± 0.02 <.0001 −0.18 ± 1.04 .21 .41 BMI (kg/m2) −1.18 ± 0.82 <.0001 −1.57 ± 1.08 <.0001 .02 Uric acid (mg/dL) −0.24 ± 0.60 .004 −0.22 ± 0.56 .01 .90 sICAM (ng/dL) −0.28 ± 0.78 .01 −0.42 ± 0.67 <.0001 .19 Urine microalbumin (µg/mg) 0.19 ± 7.70 .85 −0.42 ± 1.84 .11 .32 Total cholesterol (mg/dL) −9.75 ± 24.4 .004 −12.76 ± 33.31 .01 .95 Triglycerides (mg/dL) −23.50 ± 69.2 .01 −31.76 ± 55.36 <.0001 .48 HDL (mg/dL) −0.75 ± 19.67 .79 0.107 ± 12.36 .95 .93 Insulin resistance (HOMA) −0.29 ± 0.93 .02 −0.37 ± 0.57 <.0001 .12 Blood glucose (mg/dL) −6.14 ± 30.83 .14 −6.96 ± 9.37 <.0001 .07compared with baseline. Because subjects were assigned to deviation). The number of patients required to have a powerdifferent caloric intakes, ANCOVA was then performed, of 80% was 64 patients in each arm.adjusting for baseline and caloric intake. Data from ANCOVAare reported as adjusted least square means ± SE. Paired ttests were used to compare within-group changes from 3. Resultsbaseline to 6 weeks. The data were analyzed first for
    • DiabetologiaDOI 10.1007/s00125-007-0716-y ARTICLEA Palaeolithic diet improves glucose tolerancemore than a Mediterranean-like diet in individualswith ischaemic heart diseaseS. Lindeberg & T. Jönsson & Y. Granfeldt &E. Borgstrand & J. Soffman & K. Sjöström & B. AhrénReceived: 1 May 2007 / Accepted: 4 May 2007# Springer-Verlag 2007Abstract p=0.03). In the study population as a whole, there was noAims/hypothesis Most studies of diet in glucose intolerance relationship between change in AUC Glucose0–120 andand type 2 diabetes have focused on intakes of fat, carbo- changes in weight (r=−0.06, p=0.9) or waist circumferencehydrate, fibre, fruits and vegetables. Instead, we aimed to (r=0.01, p=1.0). There was a tendency for a larger decreasecompare diets that were available during human evolution of AUC Insulin0–120 in the Palaeolithic group, but because ofwith more recently introduced ones. the strong association between change in AUC Insulin0–120Methods Twenty-nine patients with ischaemic heart disease and change in waist circumference (r=0.64, p=0.0003), thisplus either glucose intolerance or type 2 diabetes were ran- did not remain after multivariate analysis.domised to receive (1) a Palaeolithic (‘Old Stone Age’) diet Conclusions/interpretation A Palaeolithic diet may im-(n=14), based on lean meat, fish, fruits, vegetables, root prove glucose tolerance independently of decreased waistvegetables, eggs and nuts; or (2) a Consensus (Mediterra- circumference.nean-like) diet (n=15), based on whole grains, low-fat dairy FRUTA:products, vegetables, fruits, fish, oils and margarines. Pri-mary outcome variables were changes in weight, waist cir- Keywords Diet . Evolution . Glucose intolerance . Ischaemic heart disease . Palaeolithic diet . Type 2 diabetes 160-1435 g/dcumference and plasma glucose AUC (AUC Glucose0–120)and plasma insulin AUC (AUC Insulin0–120) in OGTTs. AbbreviationsResults Over 12 weeks, there was a 26% decrease of AUC BIA bioelectrical impedance analysisGlucose0–120 (p=0.0001) in the Palaeolithic group and a 7% E% percentage of total energy intakedecrease (p=0.08) in the Consensus group. The larger (p= HOMA-IR homeostasis model assessment0.001) improvement in the Palaeolithic group was indepen- of insulin resistancedent (p=0.0008) of change in waist circumference (−5.6 cm IFG impaired fasting glucosein the Palaeolithic group, −2.9 cm in the Consensus group; IGT impaired glucose tolerance IHD ischaemic heart diseaseElectronic supplementary material The online version of this article NGT normal glucose tolerance(doi:10.1007/s00125-007-0716-y) contains supplementary material,which is available to authorised users.S. Lindeberg (*) : T. Jönsson : E. Borgstrand : J. Soffman : IntroductionK. Sjöström : B. AhrénDepartment of Medicine, Hs 32, University of Lund,SE-221 85 Lund, Sweden Impaired glucose tolerance (IGT) and type 2 diabetes aree-mail: staffan.lindeberg@med.lu.se common risk factors for ischaemic heart disease (IHD) [1, 2],
    • European Journal of Clinical Nutrition (2009), 1–9 & 2009 Macmillan Publishers Limited All rights reserved 0954-3007/09 $32.00 www.nature.com/ejcnORIGINAL ARTICLEMetabolic and physiologic improvements fromconsuming a paleolithic, hunter-gatherer type dietLA Frassetto, M Schloetter, M Mietus-Synder, RC Morris Jr and A SebastianDepartment of Medicine, University of California San Francisco School of Medicine, San Francisco, CA, USABackground: The contemporary American diet figures centrally in the pathogenesis of numerous chronic diseases—‘diseases ofcivilization’. We investigated in humans whether a diet similar to that consumed by our preagricultural hunter-gathererancestors (that is, a paleolithic type diet) confers health benefits.Methods: We performed an outpatient, metabolically controlled study, in nine nonobese sedentary healthy volunteers,ensuring no weight loss by daily weight. We compared the findings when the participants consumed their usual diet with thosewhen they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets ofincreasing potassium and fiber for 7 days, then a paleolithic type diet comprising lean meat, fruits, vegetables and nuts, andexcluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, for 10 days. Outcomes included arterial bloodpressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and insulin areas under the curve (AUC) during a 2 horal glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery reactivity in response toischemia.Results: Compared with the baseline (usual) diet, we observed (a) significant reductions in BP associated with improved arterialdistensibility (À3.1±2.9, P ¼ 0.01 and þ 0.19±0.23, P ¼ 0.05);(b) significant reduction in plasma insulin vs time AUC, duringthe OGTT (P ¼ 0.006); and (c) large significant reductions in total cholesterol, low-density lipoproteins (LDL) and triglycerides(À0.8±0.6 (P ¼ 0.007), À0.7±0.5 (P ¼ 0.003) and À0.3±0.3 (P ¼ 0.01) mmol/l respectively). In all these measured variables,either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, nearconsistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.Conclusions: Even short-term consumption of a paleolithic type diet improves BP and glucose tolerance, decreases insulinsecretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.European Journal of Clinical Nutrition advance online publication, 11 February 2009; doi:10.1038/ejcn.2009.4Keywords: paleolithic diet; blood pressure; glucose tolerance; insulin sensitivity; lipidsIntroduction plants (predominantly cereal grains) and domesticate animals (Brandt, 2007). During that interval (more thanIn 1985, anthropologists Eaton and Konner (1985) intro- 2-million year), culminating in the emergence of today’s soleduced the general medical community in ‘paleolithic Homo species, Homo sapiens, about 200 kya (McDougall et al.,nutrition. A consideration of its nature and current implica- 2005), our ancestors, including Homo sapiens, lived astions’. ‘Paleolithic’ refers to the period of history of the genus hunter-gatherers, eating wild animal-source foods (lean
    • Health benefits of a Paleo diet LA Frassetto et al 5Table 2 Menu: 1 week of increasing fiber and potassium diets (‘ramp’ diets) and Paleo diet (per 3000 kcal)Diet Ramp 1 Ramp 2 Ramp 3 Paleo dietPotassium content 125 mmol 180 mmol 259 mmol 339 mmolBreakfast Honey Honey Honey Honey Fresh pineapple Orange juice Orange juice Carrot Juice Scrambled eggs Fresh pineapple Fresh pineapple Fresh pineapple Pork tenderloin Pork tenderloin Pork tenderloinAM snack Lettuce, cucumber, celery Celery, cucumber, red Low salt tomato soup Almonds and tomatoes with oil and peppers and tomatoes with vinegar dressing oil and vinegar dressing Carrot juice Carrot juiceLunch Stir-fried fresh zucchini Carrot juice Carrot juice Carrot juice Tuna salad (tuna, radish, Tuna salad/mayo on lettuce Tuna salad/mayo on lettuce Tuna Salad (mayo, radishes, shallots, mayo) on lettuce shallots) on lettuce Applesauce Honey Low-salt tomato soup with chopped tomatoes HoneyDay Snack Lettuce, carrot and peppers Turkey/mayo in lettuce wrap Turkey/mayo with lettuce Turkey, guacamole and tomato with oil and vinegar dressing wrap lettuce roll-ups Canned pears Carrots and tomatoes with oil Carrots and tomatoes with oil and vinegar dressing nd vinegar dressing Honey Tomato juiceDinner Chicken breast stir-fry with Chicken breast stir-fry with Chicken breast stir-fry with Chicken breast stir-fry with fresh broccoli and garlic fresh spinach, garlic and fresh spinach, broccoli and spinach, garlic and broccoli broccoli garlic Mandarin oranges Mandarin oranges Mandarin oranges Roasted parsnips and mushrooms with thyme Honey Tomato juice Low salt tomato soupPM Snack Turkey and tomatoes with Cantaloupe Cantaloupe Cantaloupe mayo in lettuce wrap Carrot juice Carrot juice Carrot juice Honey
    • and vinegar dressing nd vinegar dressing Honey Tomato juiceDinner European Journal of Clinical Nutrition (2009), 1–9 & 2009 Macmillan Publishers Limited All rights reserved 0954-3007/09 $32.00 Chicken breast stir-fry with Chicken breast stir-fry with www.nature.com/ejcn Chicken breast stir-fry with Chicken breast stir-fry with fresh broccoli and garlic fresh spinach, garlic and fresh spinach, broccoli and spinach, garlic and broccoli broccoli garlic ORIGINAL ARTICLE Mandarin oranges Mandarin oranges Mandarin oranges Roasted parsnips and mushrooms with thyme Honey Tomato juice Low salt tomato soupPM Snack Metabolic and physiologic improvements from consumingwrap with Cantaloupe hunter-gatherer type diet Turkey and tomatoes paleolithic, mayo in lettuce a Cantaloupe Cantaloupe Carrot juice Carrot juice Carrot juice LA Frassetto, M Schloetter, M Mietus-Synder, RC Morris Jr andHoney A Sebastian Department of Medicine, University of California San Francisco School of Medicine, San Francisco, CA, USA Background: The contemporary American diet figures centrally in the pathogenesis of numerous chronic diseases—‘diseases of civilization’. We investigated in humans whether a diet similar to that consumed by our preagricultural hunter-gathererTable 3 Effect of the paleolithic diet on metabolic variables ancestors (that is, a paleolithic type diet) confers health benefits. Methods: We performed an outpatient, metabolically controlled study, in nine nonobese sedentary healthy volunteers,Category ensuring no weight loss by daily weight. We compared the findings when the participants Paleolithic their usual diet with% Change Variable Usual diet consumed diet those P-value when they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets ofLipids increasing potassium and fiber for 7 days, then a paleolithic type diet0.9 Total cholesterol (mmol/l) 4.7± comprising lean meat, fruits, vegetables and nuts, and 4.0±0.7 À16 0.007 excluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, for 10 days. Outcomes included arterial blood HDL (mmol/l) 1.3±0.2 1.3±0.3 þ4 NS pressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and insulin areas under the curve (AUC) during a 2 h LDL (mmol/l) 3.0 ±0.7 2.3±0.6reactivity in responseÀ22 oral glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery to 0.003 ischemia. VLDL (mmol/l) 0.4±0.2 0.3±0.1 À35 0.01 Triglycerides (mmol/l) 0.9±0.4 0.6±0.1 À35 Results: Compared with the baseline (usual) diet, we observed (a) significant reductions in BP associated with improved arterial 0.01 distensibility (À3.1±2.9, P ¼ 0.01 and þ 0.19±0.23, P ¼ 0.05);(b) significant reduction in plasma insulin vs time AUC, duringFasting the OGTT (P ¼ 0.006); and insulin (pmol/l) reductions in total cholesterol, low-density lipoproteins (LDL) and triglycerides Fasting (c) large significant 69±63 21±7 À68 0.07 (À0.8±0.6 (P ¼ 0.007), À0.7±0.5 (P ¼ 0.003) and À0.3±0.3 (P ¼ 0.01) mmol/l respectively). In all these measured variables, either nine participants (mmol/l) 18±3 17±2Insulin and Glucose eight or all Fasting glucose had identical directional responses when switched to paleolithic type diet, that is, near À5 NS consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.OGTT Insulin AUC (pmol  h/l) 533±222 361±194 Conclusions: Even short-term consumption of a paleolithic type diet improves BP and glucose tolerance, decreases insulin À39 0.006 secretion, increases insulinasensitivity and improves lipid profiles3.2±3.2 HOMA 1.0±0.4 without weight loss in healthy sedentary humans. À72 0.07 European Journal of Clinical Nutrition advance online publication, 11 February 2009; doi:10.1038/ejcn.2009.4Abbreviation: HOMA ¼ homeostatic assessment.a Keywords: paleolithic diet; blood pressure; glucose tolerance; insulin sensitivity; lipids Equation for HOMA ¼ (fasting insulin  fasting glucose)/22.4. European Journal of Clinical Nutrition Introduction plants (predominantly cereal grains) and domesticate animals (Brandt, 2007). During that interval (more than In 1985, anthropologists Eaton and Konner (1985) intro- 2-million year), culminating in the emergence of today’s sole duced the general medical community in ‘paleolithic Homo species, Homo sapiens, about 200 kya (McDougall et al., nutrition. A consideration of its nature and current implica- 2005), our ancestors, including Homo sapiens, lived as tions’. ‘Paleolithic’ refers to the period of history of the genus hunter-gatherers, eating wild animal-source foods (lean
    • 0.04 ∆ Arterial cross-sectional area, ∆ Insulin AUC, pmol*hr/L 0 0.02 European Journal of Clinical Nutrition (2009), 1–9 & 2009 Macmillan Publishers Limited All rights reserved 0954-3007/09 $32.00 www.nature.com/ejcn -140 0.00 -280 ORIGINAL ARTICLE -0.02 -420 Metabolic and physiologic improvements from consuming 20 40 60 80 100 120 140 160 180 -560 0 20 40 60 80 100 120 140 160 180 -0.04 0 a paleolithic, hunter-gatherer type diet ∆ Daily Urine K excretion, mmol/day ∆ Daily Urine K excretion, mmol/day LA Frassetto, M Schloetter, M Mietus-Synder, RC Morris Jr and A SebastianFigure 1 (a and b) Physiological changes correlating with increases in average daily urine potassium excretion (an index of dietary potassiumintake. (a) Increasing arterial Medicine, University of California San Francisco School ofduring 2-h oral glucose tolerance test. Department of dilation and (b) decreasing insulin secretion Medicine, San Francisco, CA, USA Background: The contemporary American diet figures centrally in the pathogenesis of numerous chronic diseases—‘diseases ofTable 4 Resting civilization’. We investigated in humans whetherartery reactivity data consumed by our preagricultural hunter-gatherer blood pressure measurements and brachial a diet similar to that ancestors (that is, a paleolithic type diet) confers health benefits. Methods: We performed an outpatient, metabolically controlled study, in nine nonobese sedentary healthy volunteers,Factor Days –2 to 0 (usual diet) Days 15 to 17 (Paleo diet) ensuring no weight loss by daily weight. We compared the findings when the participants consumed their usual diet with those P-value when they consumed a paleolithic type diet. The participants consumed their usual diet for 3 days, three ramp-up diets ofResting BP increasing potassium and fiber for 7 days, then a paleolithic type diet comprising lean meat, fruits, vegetables and nuts, and 116± for À2.6± blood excluding nonpaleolithic type foods, such as cereal grains, dairy or legumes, 10 10 days. Outcomes included arterial5.1 Systolic BP (mm Hg) NS pressure (BP); 24-h urine sodium and potassium excretion; plasma glucose and 6 Diastolic BP (mm Hg) 71± insulin areas under the curve (AUC) during a 2 h À3.4±2.7 0.006 oral glucose tolerance test (OGTT); insulin sensitivity; plasma lipid concentrations; and brachial artery reactivity in response to MAP (mm Hg) ischemia. 86±7 À3.1±2.9 0.01 Results: Compared with the baseline (usual) diet, we observed (a) significant reductions in BP associated with improved arterial 3.97±0.88 3.98± duringBrachial artery diameter at baseline (BAD;¼ 0.01 and þ 0.19±0.23, P ¼ 0.05);(b) significant reduction in plasma insulin vs time AUC, 0.85 distensibility (À3.1±2.9, P mm) 0.14Peak brachial artery diameter ¼ 0.006);hyperemia (pkFMD; mm) 4.25± low-density lipoproteins (LDL) and triglycerides the OGTT (P during and (c) large significant reductions in total cholesterol, 0.83 4.35±0.73 0.05Absolute difference (pkFMD-BAD; mm)À0.7±0.5 (P ¼ 0.003) and À0.3±0.3 (P ¼ 0.01) mmol/l respectively). In all these measured ±0.158 (À0.8±0.6 (P ¼ 0.007), 0.288±0.089 0.371 variables, 0.06 either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, near consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.Abbreviations: BAD, brachial artery diameter; BP, blood pressure. paleolithic type diet improves BP and glucose tolerance, decreases insulin Conclusions: Even short-term consumption of a secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans. European Journal of Clinical Nutrition advance online publication, 11 February 2009; doi:10.1038/ejcn.2009.4and in the brachial artery cross-sectional area, all are insulin AUC occurring in participants with the highest Keywords: paleolithic diet; blood pressure; glucose tolerance; insulin sensitivity; lipidscorrelated (r ¼ 0.71, P ¼ 0.047; r ¼ 0.72, P ¼ 0.04; r ¼ 0.74, increase in urinary potassium (index of dietary potassium);P ¼ 0.04, respectively). (g) a significantly lower integrated value of plasma insulin In all the consistency data reported, the Wilcoxon concentration over the period of the OGTT (that is, thesigned-rank test gave significant P-values, ranging from plasma insulin AUC) relative to the corresponding integratedo0.004 to o0.04.Introduction value of plasma glucose concentration (that is, the plasma plants (predominantly cereal grains) and domesticate animals (Brandt, 2007). During that interval (more than In 1985, anthropologists Eaton and Konner (1985) intro- glucose AUC)—an index of improved insulin sensitivity; 2-million year), culminating in the emergence of today’s sole duced the general medical community in ‘paleolithic (h) improved insulin sensitivity by homeostatic model Homo species, Homo sapiens, about 200 kya (McDougall et al.,Discussion nutrition. A consideration of its nature and current implica- 2005), our ancestors, including Homo sapiens,sensitivity proportional to assessment; (i) improved insulin lived as tions’. ‘Paleolithic’ refers to the period of history of the genus hunter-gatherers, eating wild animal-source foods (lean
    • Lindeberg S, Lundh B. J Intern Med. 1993; 233: 269-275!
    • 1990: Não existia Electricidade, Telefones, Veículos a Motor Alguns produtos ocidentais eram recebidos da Nova Guiné, mas a influência do estilo de vida ocidental era minímo
    • DIETA TÍPICA EM KITAVA! Nov-Dec 1990" ""Alimentos !Total !Prot ! Gor !HC !Ener!(médias) "(g) "(g) "(g) "(g) "(kJ) "" ""Tubérculos "1200 "25 "2 "300 "5600"Fruta "400 "3 "<1 "50 "920"Coco "110 "4 "43 "7 "1865"Peixe "85"Porco "<1 "- "- "- "-"Outras Carnes "<5 "- "- "- "-"Outros "200 "5 "<1 "14 "360"Processados "<1 "0 "<1 "<1 "20""Total "2 000 "54 "50 "370 "9200" " Lindeberg S et al. AJCN 1997;66:845
    • Insulina jejum!(Ul/ml)! ! 8 7 Homens Mulheres 6Insulina jejum 5 4 3 Kitava 2 Suécia 1 0 25-39 40-59 60-74 25-39 40-59 Idade 60-74 Lindeberg S, Eliasson M, Lindahl B, Ahren B. Metabolism 1999; 48:1216-9 !
    • ÍNDICE HOMA!4 Males 4 Females3 32 21 10 0-1 -1-2 -2-3 -3 Kitava Sweden Kitava Sweden Carrera-Bastos P, Fontes-Villalba M, OKeefe JH, Lindeberg S, Cordain L. Res Rep Clin Cardiol 2011;2:15-35. Fig. log HOMA in the age group 50-86 years in Kitava and Sweden. HOMA = fP-
    • 54 Índice Cintura (cm)/altura (m)5250 Kitava48 Suécia464442 Homens Mulheres Lindeberg, S, Soderberg, S, Ahren, B, Olsson, T. J Intern Med, 2001;  249: 553-8!
    • 848 LINDEBERG ET AL G) 0 0 C’) N 0.5 :, Cl) Cl) 0 0. 0 0 0 -0.5 .0 0 0 -1 Cl) C’) -1.5 -2 Downloaded from www.ajcn.org at Lund University Libraries on Dece 1.5 a) 0 0 Cl) N 0.5 a) 0 U) U) a) 0. -0.5 0 0 0 .0 -1 0 0 -1.5 U) CO 0 -2 20 30 40 50 60 70 80 Age (y) FIGURE 1. Systolic and diastolic blood pressure in Kitavan and Swedish al. males and females in relation to means and SDs in Swedish males aged 20-29 Lindeberg S et AJCN 1997;66:845y old (systolic blood pressure: 129 ± 10 mm, diastolic blood pressure: 84 ± 7 mm). Values are expressed as ratios of Swedish SDs (z scores). For example,systolic blood pressure in Kitavan males aged 20-69 y is l.5 SD below the mean of Swedish 20-29-y-old males, whereas systolic blood pressure of
    • ü  ENFARTE E AVC RAROS! ü  INEXISTÊNCIA DE SOBREPESO, HIPERTENSÃO E SUBNUTRIÇÃO! ü  BAIXOS VALORES DE INSULINA E LEPTINA! ü  MUITAS PESSOAS ALCANÇAM + 75 ANOS!Lindeberg S et al. J Intern Med 1993;233:269-75;Lindeberg S et al. J Intern Med 1994;236:331-40; Lindeberg S et al. Metabolism 1999;48:1216-19
    • Cereal Grains: Humanity’s Double-Edged Sword Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 Loren Cordain ............................ Department of Exercise and Sport Science, Colorado State University, Fort Collins, Cereal Grains: Colo., USA Humanity’s Double-Edged Sword ‘Here is bread, which strengthens man’s heart, and therefore called the staV of life’ Loren Cordain (Mathew Henry: 1662–1714, Commentary on Psalm 104) yet, Department of Exercise and Sport Science, Colorado State University, Fort Collins, Colo., USA ‘Man cannot live on bread alone’ (Bible, Matthew 4:4) ‘Here is bread, which strengthens man’s heart, and therefore called the staV of life’ Contents (Mathew Henry: 1662–1714, Commentary on Psalm 104) yet,20 Introduction ‘Man cannot live on bread alone’ (Bible, Matthew 4:4)22 Archaeological Perspective24 Dietary Imbalances of Cereal Grains Contents26 Vitamins A, C and Beta-Carotene27 20B Vitamins Introduction29 22Minerals Archaeological Perspective34 24Essential Imbalances of Cereal Grains Dietary Fatty Acids 26 Vitamins A, C and Beta-Carotene36 Amino Acids 27 B Vitamins41 Antinutrients in Cereal Grains 29 Minerals43 34Alkylresorcinols Acids Essential Fatty43 36Alpha-Amylase Inhibitors Amino Acids44 41Protease Inhibitors Antinutrients in Cereal Grains 43 Alkylresorcinols45 Lectins 43 Alpha-Amylase Inhibitors47 Autoimmune Diseases and Cereal Grain Consumption 44 Protease Inhibitors48 45Autoimmunity Lectins49 47Molecular Mimicry and Cereal Grain Consumption Autoimmune Diseases49 48Genetic and Anthropological Factors Autoimmunity 49 Molecular Mimicry51 49 Autoimmune Diseases Associated with Cereal Grain Consumption Genetic and Anthropological Factors56 Psychological and Neurological Illnesses Cereal Grain with Cereal Grain Consumption 51 Autoimmune Diseases Associated with Associated Consumption58 Conclusions 56 Psychological and Neurological Illnesses Associated with Cereal Grain Consumption60 58 Conclusions Acknowledgments 60 Acknowledgments60 References 60 References
    • Adaptado de Cordain L, 2009 LECTINAS (com permissão)Leguminosas ü  Glicoproteínas com capacidade para se ligarem de forma reversiva a mono e oligossacarídeos específicos! ü  São resistentes à cozedura e às Cereais enzimas proteoliticas e são reconhecidas como o maior antinutriente dos alimentos.! Cordain L, et al. Br J Nutr. 2000 Mar;83(3):207-17 Cordain L. World Rev Nutr Diet 1999; 84:19-73
    • WGAü  Gérmen de Trigo: 300 – 350 mg/kg WGA (1)ü  Farinha de trigo integral: 30-50 mg/kg WGA (2)ü  Farinha de trigo refinado: 4.4 mg/kg WGA (2) 1. Vincenzi S, et al. J Agric Food Chem. 2002 Oct 23;50(22):6266-70. 2.  Matucci A et al. Food Control 2004;15: 391-95
    • Adaptado de Cordain L, 2009 (com permissão) Villi LUMEN WGA/PHA Enterócitos Junções Estreitas Integridade Hiperpermeabilidade1.  Sjolander A et al. The effect of concanavalin A and wheat germ agglutinin on the ultrastructure and permeability of rat intestine. Int Arch Allergy Appl Immunol 1984; 75, 230–236.2.  Greer F & Pusztai A. Toxicity of kidney bean (Phaseolus vulgaris) in rats: changes intestinal permeability. Digestion 1985; 32, 42–46.3.  Pellegrina CD et al. Plant lectins as carriers for oral drugs: Is wheat germ agglutinin a suitable candidate? Toxicol Appl Pharmacol 2005;207:170-78
    • Proc. Nat. Acad. Sci. USA Vol. 70, No. 2, pp. 485-489, February 1973 Insulin-Like Activity of Concanavalin A and Wheat Germ Agglutinin-Direct Interactions with Insulin Receptors (glucose transport/lipolysis/adenylate cyclase/affinity chromatography/lymphocyte transformation/growth factors) PEDRO CUATRECASAS AND GUY P. E. TELLDepartment of Medicine, and Department of Pharmacology and Experimental Therapeutics, The Johns Hopkins UniversitySchool of Medicine, Baltimore, Maryland 21205Communicated by Saul Roseman, December 7, 1972 ABSTRACT Concanavalin A and wheat germ agglu- mined by a modification (10) of the technique of Pohl et al. tinin are as effective as insulin in enhancing the rate of (11). Fat cell membranes (10) were freshly prepared for eachglucose transport and in inhibiting epinephrine-stimu-lated lipolysis in isolated adipocytes. These lectins, also like experiment by homogenization (Polytron), centrifugation, andinsulin, inhibit basal as well as epinephrine-stimulated suspension of the pellet in 50 mMI Tris HCl (pH 7.6); aden- -adenylate cyclase activity of membranes obtained from ylate cyclase assays were begun within 10 min. Concanavalinhomogenates of fat cells. Low concentrations of wheat A (three-times crystallized) was from Miles. Wheat germgerm agglutinin enhance the specific binding of insulin to agglutinin, a gift from Dr. V. Marchesi, was purified byreceptors of fat cells and liver membranes. Higher con-centrations of this plant lectin, as well as of concanavalin affinity chromatography and was homogeneous on NaA, competitively displace the binding of insulin to recep- dodecylsulfate disc gel electrophoresis (12).tors in these tissues. These effects are equally apparent Agarose derivatives of the lectins were prepared by thein insulin-binding proteins solubilized from membranes, CNBr procedure (13), or by reaction with activated N-indicating that the plant lectins interact directly with hydroxysuccinimide esters of diaminodipropylaminosuccinyl-insulin receptors. All of the effects observed with the plantlectins are reversed by simple sugars that bind specifically agarose (14). 40 ml of Sepharose 4B was activated with 6 g of
    • BMC Endocrine Disorders BioMed CentralResearch article Open AccessAgrarian diet and diseases of affluence – Do evolutionary noveldietary lectins cause leptin resistance?Tommy Jönsson*1, Stefan Olsson2, Bo Ahrén1, Thorkild C Bøg-Hansen3,Anita Dole3 and Staffan Lindeberg1Address: 1Department of Clinical Sciences, Lund University, Lund, Sweden, 2Department of Ecology, The Royal Veterinary and AgriculturalUniversity, Copenhagen, Denmark and 3Institute of Molecular Pathology, University of Copenhagen, Copenhagen, DenmarkEmail: Tommy Jönsson* - Tommy.Jonsson@med.lu.se; Stefan Olsson - stefan.olsson@ecol.kvl.dk; Bo Ahrén - Bo.Ahren@med.lu.se;Thorkild C Bøg-Hansen - tcbh@plab.ku.dk; Anita Dole - Anita@plab.ku.dk; Staffan Lindeberg - staffan.lindeberg@med.lu.se* Corresponding authorPublished: 10 December 2005 Received: 24 June 2005 Accepted: 10 December 2005BMC Endocrine Disorders 2005, 5:10 doi:10.1186/1472-6823-5-10This article is available from: http://www.biomedcentral.com/1472-6823/5/10© 2005 Jönsson et al; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
    • GLIADINA LIGA-SE A RECEPTOR CXR3 Fasano A. Scientific American. August 2009
    • RESPOSTA INFLAMATÓRIAPodolsky. N Engl J Med. 2002 Aug 8;347(6):417-29
    • TLR4 EM MONÓCITOS DE DIABÉTICOS TIPO II!Dasu MR. Increased Toll-Like Receptor (TLR) Activation and TLR Ligands in Recently Diagnosed Type 2 Diabetic Subjects. Diabetes Care 33:861–868, 2010
    • NUTRITION MYTHS
    • Greater WeightWeight Loss and Hormonal Changes Greater Loss and Hormonal ChangesAfter 6 MonthsMonths Diet WithCarbohydrates Eaten Mostly at With After 6 Diet Dinner CarbohydratesEaten Mostly at Dinner Sigal Sofer1,2, Abraham Eliraz1, Sara Kaplan2, Hillary Voet1, Gershon Fink3, Tzadok Kima4 and Zecharia Madar1Sigal Sofer1,2, Abraham Eliraz1,designed toKaplanthe effect of a low-calorie diet with carbohydrates eaten 3, at dinner on This study was Sara investigate 2, Hillary Voet1, Gershon Fink mostly anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated.Tzadok Kima4 and Zecharia Madar1 (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at Seventy-eight police officers dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimentalThis study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, averageanthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumorSeventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at necrosis factor- (TNF- ), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimentaldinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when comparedcollected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify theGreater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes,diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average and achieves improved metabolic response, compared to a more conventional dietary approach.daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, Obesity (2011) doi:10.1038/oby.2011.48low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor INTRODUCTION crucial hormone responsible for satiety is at its highest levelsnecrosis factor- (TNF- ), and interleukin-6 pathways in order towere observed in comparison to controls. The experimental Manipulation of physiological (IL-6) levels reduce when individuals are sleeping.diet modified daily leptin andofadiponectin concentrations major insulin resistance, and the metabolic syndrome”between obesity, and to a control obesity and symptoms of the metabolic syndrome is a focus research worldwide. Recent data show that adipose Adiponectin is considered to be “the link compared to those observed at baseline (6). Adiponectindiet. A simple dietary manipulation of carbohydrate distribution appears to regulation additionaland carbohy- when compared tissue, the energy storage site of the body, is also an endocrine plays a role in energy have as well as in lipid benefits organ that synthesizes and secretes a variety of adipocytokines. drate metabolism, reducing serum glucose and lipids, improvingto a conventional weight loss diet in individuals suffering as well obesity. It might also be beneficial for individuals This includes hormones that regulate hunger and satiety from insulin sensitivity and having an anti-inflammatory effect (7). as those associated with the development of insulin resistance, Adiponectin’s diurnal secretion pattern has been described insuffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the the metabolic syndrome and inflammation (1). obese individuals (particularly with abdominal obesity), as low Leptin “the satiety hormone” has been described as the throughout the day. In normal weight subjects or overweightmechanisms by which this relatively simple diet approach enhances satiety, leads to increase in adiponectin “information provider” of adipose tissue status to receptors in subjects following weight loss, a general better anthropometric outcomes,and achieves improved metabolic response, compared and foodmore conventionalwell at 1100 andthe diurnal pattern the brain. In short term, it regulates hunger, satiety, to a concentrations is detected as dietary approach. intake (1–3). Previous studies have described a typical diurnal during the daytime, with zeniths as a rise in 0100 hours and a pattern of leptin secretion that falls during the day from 0800 decline at night, reaching a nadir at 0400 hours (5,8).Obesity (2011) doi:10.1038/oby.2011.48 hours, reaching a nadir at 1300 hours and increases to 1600 Innovative dietary regimens that will be able to modify from 1600 with a zenith at 0100 hours (4,5). Ironically, this these hormonal secretion patterns may be beneficial to people 1 The Robert H. Smith Faculty of Agriculture, Food and Environment, Institute of Biochemistry and Food Science, The Hebrew University of Jerusalem, Rehovot, Israel; 2Meuhedet Medical Services, Diet and Nutrition Department, Israel; 3Kaplan Medical Center, Rehovot, Israel; 4Israeli Police Force, Tel Aviv District, Israel.INTRODUCTION Correspondence: Zecharia Madar (Madar@agri.huji.ac.il) crucial hormone responsible for satiety is at its highest levels Obesity 19, 2006-2014 (October 2011) Received 28 June 2010; accepted 29 January 2011; advance online publication 7 April 2011. doi:10.1038/oby.2011.48Manipulation of physiological pathways in order to reduce when individuals are sleeping.obesity and symptoms of the metabolic syndrome is a major OBESITY Adiponectin is considered to be “the link between obesity, 1
    • Greater Weight Loss and Hormonal Changes After 6 Months Diet With Carbohydrates Eaten Mostly at Dinner Sigal Sofer1,2, Abraham Eliraz1, Sara Kaplan2, Hillary Voet1, Gershon Fink3, Tzadok Kima4 and Zecharia Madar1 ARTICLES This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on INTERVENTION AND PREVENTION anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores wereTable 3 Changes in anthropometric parameters2000 hours. Anthropometricdiet collected every 4 h from 0800 to after 6 months on measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental Units Experimental group (n = 30) Control group (n = 33) diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average Comparison of groupsWeight loss daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor- (TNF- ), and interleukin-6 (IL-6) levels were 0.84* in comparison to controls. ± 0.84* (kg) 11.6 ± observed 9.06 The experimental P = 0.024 diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control (%) 11.7 ± 0.66* 9.96 ± 0.79* diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared P = 0.053 to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individualsBMI reduction suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, Original (g/m2) 3.99 ± 0.24* and achieves improved metabolic response, compared to a more conventional dietary approach. 3.16 ± 0.27* Adjusted for baseline differences(2011) doi:10.1038/oby.2011.48 2) Obesity (g/m 3.85 ± 0.25* 3.28 ± 0.24* P = 0.115 (%) 11.7 ± 0.66* 9.68 ± 0.79* P = 0.053 INTRODUCTIONAbdominal circumference decrease crucial hormone responsible for satiety is at its highest levels Manipulation of physiological pathways in order to reduce when individuals are sleeping. Original obesity and symptoms of the metabolic syndrome is a 11.7 ± 0.89* (cm) major Adiponectin is considered to be “the± 0.98* 9.39 link between obesity, focus of research worldwide. Recent data show that adipose insulin resistance, and the metabolic syndrome” (6). Adiponectin Adjusted for baseline differences the energy storage site of the body, is also an endocrine ± plays a role in energy regulation as well as in lipid and carbohy- tissue, (cm) 11.1 0.92* 10.0 ± 0.88* P = 0.408 organ that synthesizes and secretes a variety of adipocytokines. drate metabolism, reducing serum glucose and lipids, improving This includes hormones that regulate hunger and satiety as well ± insulin sensitivity and having an8.80 ± 0.90* effect (7). (%) 10.5 0.70* anti-inflammatory P = 0.159 as those associated with the development of insulin resistance, Adiponectin’s diurnal secretion pattern has been described inBody fat percent reduction the metabolic syndrome and inflammation (1). obese individuals (particularly with abdominal obesity), as low Leptin “the satiety hormone” has been described as the throughout the day. In normal weight subjects or overweight Absolute “information provider” of adipose tissue status to receptors in ± subjects following weight loss, a general increase in adiponectin (%) 6.98 0.95* 5.13 ± 0.59* P = 0.710 the brain. In short term, it regulates hunger, satiety, and food concentrations is detected as well as a rise in the diurnal pattern Relative intake (1–3). Previous studies have described a typical diurnal ± during the daytime, with zeniths 14.1 ± 1.71* hours and a (%) 18.1 2.45* at 1100 and 0100 P = 0.122 pattern of leptin secretion that falls during the day from 0800 decline at night, reaching a nadir at 0400 hours (5,8).Mean ± s.e. Analysis by two-factor ANOVA. reaching a nadir at 1300 hours and increases to 1600 hours, Innovative dietary regimens that will be able to modify*Significant difference from day 0 (P < 0.0001). a zenith at 0100 hours (4,5). Ironically, this these hormonal secretion patterns may be beneficial to people from 1600 with 1 The Robert H. Smith Faculty of Agriculture, Food and Environment, Institute of Biochemistry and Food Science, The Hebrew University of Jerusalem, Rehovot, Israel; 2Meuhedet Medical Services, Diet and Nutrition Department, Israel; 3Kaplan Medical Center, Rehovot, Israel; 4Israeli Police Force, Tel Aviv District, Israel. Correspondence: Zecharia Madar (Madar@agri.huji.ac.il) Obesity 19, 2006-2014 (October 2011) Received 28 June 2010; accepted 29 January 2011; advance online publication 7 April 2011. doi:10.1038/oby.2011.48 a OBESITY 1 150% Experimental diet
    • 10 ated with a decl Greater Weight Loss and Hormonal Changes our control gro 5 After 6 Months Diet With Carbohydrates satiety reductio Eaten Mostly at Dinner of the study, the 0 Sigal Sofer1,2, Abraham Eliraz1, Sara Kaplan2, Hillary Voet1, Gershon Fink3, Tzadok Kima4 and Zecharia Madar1 Day 0 Day 90 Day 180 comparison to b This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. It is proposed b Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at 80 Experimental diet dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were * leptin concentr be an importan collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average 70 Control diet daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor during the day. necrosis factor- (TNF- ), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimental 60 diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control 143.5% that during wei diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals ety levels were r Adiponectin (ng/ml) suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the 50 mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, 115.3% and achieves improved metabolic response, compared to a more conventional dietary approach. 113.9% of body weight Obesity (2011) doi:10.1038/oby.2011.48 40 101.9% tions that will m INTRODUCTION crucial hormone responsible for satiety is at its highest levels during daylight Manipulation of physiological pathways in order to reduce when individuals are sleeping. 30 obesity and symptoms of the metabolic syndrome is a major focus of research worldwide. Recent data show that adipose Adiponectin is considered to be “the link between obesity, insulin resistance, and the metabolic syndrome” (6). Adiponectin Our experimen tissue, the energy storage site of the body, is also an endocrine organ that synthesizes and secretes a variety of adipocytokines. plays a role in energy regulation as well as in lipid and carbohy- drate metabolism, reducing serum glucose and lipids, improving tion, leading to 20 This includes hormones that regulate hunger and satiety as well insulin sensitivity and having an anti-inflammatory effect (7). as those associated with the development of insulin resistance, the metabolic syndrome and inflammation (1). Adiponectin’s diurnal secretion pattern has been described in obese individuals (particularly with abdominal obesity), as low day. We propos Leptin “the satiety hormone” has been described as the throughout the day. In normal weight subjects or overweight 10 “information provider” of adipose tissue status to receptors in the brain. In short term, it regulates hunger, satiety, and food subjects following weight loss, a general increase in adiponectin concentrations is detected as well as a rise in the diurnal pattern helped particip intake (1–3). Previous studies have described a typical diurnal pattern of leptin secretion that falls during the day from 0800 during the daytime, with zeniths at 1100 and 0100 hours and a decline at night, reaching a nadir at 0400 hours (5,8). hours, enhance to 01600 hours, reaching a nadir at 1300 hours and increases Innovative dietary regimens that will be able to modify from 1600 with a zenith at 0100 hours (4,5). Ironically, this these hormonal secretion patterns may be beneficial to people anthropometric Day 0 Day 90 Day 180 1 The Robert H. Smith Faculty of Agriculture, Food and Environment, Institute of Biochemistry and Food Science, The Hebrew University of Jerusalem, Rehovot, Israel; 2Meuhedet Medical Services, Diet and Nutrition Department, Israel; 3Kaplan Medical Center, Rehovot, Israel; 4Israeli Police Force, Tel Aviv District, Israel. Correspondence: Zecharia Madar (Madar@agri.huji.ac.il) Although, no Obesity 19, 2006-2014 (October 2011) Received 28 June 2010; accepted 29 January 2011; advance online publication 7 April 2011. doi:10.1038/oby.2011.48Figure 3 Mean ± s.e. for absolute values, least squares mean for balance, lipids p ticipants, impro OBESITY 1percentage of baseline (shown in boxes on bars) in the experimental
    • study was conducted according to the guidelines laid testing, and were instructed to avoid over- or under-down in the Declaration ofJournal of Nutrition and page 1 procedures British Helsinki, (2011), all of 7 eating. Smokers doi:10.1017/S0007114510005192 abstain on the morning were instructed toinvolving human subjectsThe Authors 2011 q were approved by the Human before testing. On the night before testing, participantsResearch Ethics Committee of the University of Sydney. were instructed to consume a high-CHO, low-fat eveningWritten informed consent was obtained fromand -glycaemic load meals increase the availability order to avoid extreme High-glycaemic index all subjects meal devoid of legumes inbefore participation. of tryptophan in healthy volunteers hunger and variation in basal blood glucose concentration. Self-reported compliance with these instructions was eval- Christopher P. Herrera *†, Keir Smith , Fiona Atkinson , Patricia by a, researcher (C. P. H. and K. S.) each morning 1 2 2 uated Ruell1 Chin Moi Chow1,Meals Helen O’Connor1 and Jennie Brand-Miller2,3 1 before testing. Discipline of Exercise and Sport Science, Faculty of Health Sciences, University of Sydney, Sydney, NSW, AustraliaThe energy and macronutrient composition of the of Science,are School of Molecular Bioscience, Faculty meals University of Sydney, Sydney, NSW, Australia 2 3 Participants initially completed three independent Boden Institute of Obesity, Nutrition, and Exercise, University of Sydney, Sydney, NSW, Australiasummarised in Table 1. The CHGI meal, 3212 kJ, was repli- reference glucose tests separated by at least 48 h (Received 12 July 2010 – Revised 29 October 2010 – Accepted 12 November 2010) (11)cated from a previous study and consisted of a large apart. Each reference test used a standard glucose drink Table 1. Energy and macronutrient composition of the carbohydrate (CHO) high-glycaemic index (CHGI), mixed-macro- Abstract British Journal of Nutrition nutrient high-glycaemic of the present study andtomixed-macronutrient low-glycaemic index (MLGI) meals the ratio The purpose index (MHGI) was determine the influence of the glycaemic index (GI) and glycaemic load (GL) on of tryptophan (TRP) relative to other large neutral amino acids (LNAA). Ten healthy men (age 22·9 (SD 3·4) years; BMI 23·5 (SD 1·6) kg/m2) underwent standard GI testing, and later consumed each of a mixed-macronutrient (1915 kJ; 66·5 % carbohydrate Fat Protein CHO (CHO), 17 % protein and 16·5 % fat) high-GI (MHGI), an isoenergetic, mixed-macronutrient low-GI (MLGI) and a CHO-only (3212 kJ; 90 % CHO, 8 % protein, 2 % fat) high-GI (CHGI) meal on separate days. The GI, GL and insulin index values (e.g. area under the curve) were largest after the CHGI meal (117, 200, 158), followed by the MHGI (79, 59, 82) and MLGI (51, 38, 56) meals, respectively Meal Energy (kJ) significantly different, P,0·05). After the MHGI and MLGI meals but(%)after the CHGI meal, TRP was elevated at 120 (all values were g Energy (%) g Energy not g Energy (%) GI* GL† and 180 min (P, 0·05). After the CHGI, LNAA was lower compared with the MLGI (P,0·05); also the rate of decline in LNAA was CHGI‡ higher after CHGI compared with MHGI1·6 MLGI (both 16·8 3212 0·4 and comparisons P,0·05). The percentage171·4 from baseline in TRP:LNAA 8 increase 90·4 117 200 after CHGI (23 %) was only marginally higher than after the MHGI meal (17 %; P¼0·38), but it was threefold and nearly significantly greater MHGI 1916 7·9 16·2 18·2 17·2 75 66·6 than MLGI (8 %; P¼ 0·05). The present study demonstrates that the postprandial rise in TRP:LNAA was increased by additional CHO 79 59 MLGI ingestion and higher GI. Therefore, the 16·1 appears to18·6 important factor influencing the postprandial TRP:LNAA concentration. 1913 7·9 meal GL be an 17·5 75 66·4 51 38 Key words: Glycaemic index: Glycaemic load: Tryptophan: Amino acids: Carbohydrate GI, glycaemic index; GL, glycaemic load. * GI was determined using the average glucose response (n 9) and the incremental area under the curve method(12)). † GL was calculated availability of dietary tryptophan by the to the brain The by multiplying each meal GI (TRP) available CHO meal would elicit a greater insulin release, and therefore (g). ‡ GI for the CHGI meal was approximate due to a largerlarge neutral a larger postprandial rise in plasma TRP:LNAA levels(3,6,7). depends on its concentration relative to other CHO content of this test meal compared with the reference glucose drink providing 75 g CHO(12). amino acids (LNAA), which compete for a common trans- The proportion of CHO relative to either protein or fat may (1) port mechanism across the blood– brain barrier . similarly influence the TRP:LNAA response after mixed- Increased consumption of carbohydrate (CHO) elicits a macronutrient meals. Berry et al.(8) suggested that a meal con- marked demand in insulin secretion, which enhances per- taining a CHO:protein ratio of approximately 5:1 would ipheral, skeletal muscle uptake of LNAA. However, TRP is neither raise nor lower postprandial LNAA, given that the largely albumin bound and therefore protected from this LNAA-lowering effect of the insulin demand would be offset absorption(2). Previous studies have shown that the post- by the contribution of LNAA provided by the protein prandial concentration of TRP:LNAA increases between source. Since TRP is the least abundant amino acid found 20 and 50 % compared with baseline after predominately in protein, a protein-rich, low-CHO meal lowers TRP:LNAA CHO-rich meals(3 – 5). In one study, consumption of a due to a greater contribution of LNAA relative to TRP in (3)
    • British Journal of Nutrition (2011), page 1 of 7 doi:10.1017/S0007114510005192 q The Authors 2011 High-glycaemic index and -glycaemic load meals increase the availability of tryptophan in healthy volunteers Christopher P. Herrera1*†, Keir Smith2, Fiona Atkinson2, Patricia Ruell1, Chin Moi Chow1, Helen O’Connor1 and Jennie Brand-Miller2,3 1 Discipline of Exercise and Sport Science, Faculty of Health Sciences, University of Sydney, Sydney, NSW, Australia 2 School of Molecular Bioscience, Faculty of Science, University of Sydney, Sydney, NSW, Australia Meal composition and tryptophan 3 Boden Institute of Obesity, Nutrition, and Exercise, University of Sydney, Sydney, NSW, Australia (Received 12 July 2010 – Revised 29 October 2010 – Accepted 12 November 2010) 25 Tryp/LNAA composition Change from baseline (%) Abstract and each coBritish Journal of Nutrition The purpose of the present study was to determine the influence of the glycaemic index (GI) and glycaemic load (GL) on the ratio 20 of tryptophan (TRP) relative to other large neutral amino acids (LNAA). Ten healthy men (age 22·9 (SD 3·4) years; BMI 23·5 (SD 1·6) kg/m2) underwent standard GI testing, and later consumed each of a mixed-macronutrient (1915 kJ; 66·5 % carbohydrate breast sache (CHO), 17 % protein and 16·5 % fat) high-GI (MHGI), an isoenergetic, mixed-macronutrient low-GI (MLGI) and a CHO-only (3212 kJ; 90 % CHO, 8 % protein, 2 % fat) high-GI (CHGI) meal on separate days. The GI, GL and insulin index values (e.g. area under the an identical 15 curve) were largest after the CHGI meal (117, 200, 158), followed by the MHGI (79, 59, 82) and MLGI (51, 38, 56) meals, respectively (all values were significantly different, P,0·05). After the MHGI and MLGI meals but not after the CHGI meal, TRP was elevated at 120 and 180 min (P, 0·05). After the CHGI, LNAA was lower compared with the MLGI (P,0·05); also the rate of decline in LNAA was was greater higher after CHGI compared with MHGI and MLGI (both comparisons P,0·05). The percentage increase from baseline in TRP:LNAA after CHGI (23 %) was only marginally higher than after the MHGI meal (17 %; P¼0·38), but it was threefold and nearly significantly greater mainly rice a 10 than MLGI (8 %; P¼ 0·05). The present study demonstrates that the postprandial rise in TRP:LNAA was increased by additional CHO ingestion and higher GI. Therefore, the meal GL appears to be an important factor influencing the postprandial TRP:LNAA concentration. cant increase Key words: Glycaemic index: Glycaemic load: Tryptophan: Amino acids: Carbohydrate 5 the MHGI a The availability of dietary tryptophan (TRP) to the brain depends on its concentration relative to other large neutral meal would elicit a greater insulin release, and therefore a larger postprandial rise in plasma TRP:LNAA levels(3,6,7). (Table 2). C 0 amino acids (LNAA), which compete for a common trans- port mechanism across the blood– brain barrier(1). The proportion of CHO relative to either protein or fat may baseline in L 0 120 180 240 similarly influence the TRP:LNAA response after mixed- macronutrient meals. Berry et al.(8) suggested that a meal con- Increased consumption of carbohydrate (CHO) elicits a marked demand in insulin secretion, which enhances per- taining a CHO:protein ratio of approximately 5:1 would meals (240 m ipheral, skeletal muscle uptake of LNAA. However, TRP is Time (min) neither raise nor lower postprandial LNAA, given that the LNAA after t largely albumin bound and therefore protected from this LNAA-lowering effect of the insulin demand would be offset absorption(2). Previous studies have shown that the post- Fig. 2. Effects of the carbohydrate-only high-glycaemic index (CHGI), mixed- by the contribution of LNAA provided by the protein prandial concentration of TRP:LNAA increases between source. Since TRP is the least abundant amino acid found MLGI meals. macronutrient high-glycaemic index (MHGI) and mixed macronutrient low 20 and 50 % compared with baseline after predominately in protein, a protein-rich, low-CHO meal lowers TRP:LNAA CHO-rich meals(3 – 5). In one study, consumption of a glycaemic index (MLGI) meals on postprandial tryptophan (TRP)/large neu- (3) due to a greater contribution of LNAA relative to TRP in prandial dec
    • after the meal. Respective ratings immediately after the meal and bedtiat bedtime were 3.21 and 2.17 for theshorten sleep onset ingested 4 h High-glycemic-index carbohydrate meals low-GI meal 1–3before bedtime; 3.17 and 2.13 for high-GI meal ingested 4 h Ahmad Afaghi, Helen O’Connor, and Chin Moi Chow 6-SMbefore bedtime; and 3.17 and 2.25 for the high-GI meal ingested ABSTRACT Background: Dietary carbohydrate intake has been shown to in- considered the best practice. Other popular remedies used to treat sleep difficulties include prescribed sedatives and tranquilizers, Th crease the plasma concentration of tryptophan, a precursor of sero- herbal extracts and complimentary medicines, massage and re- tonin and sleep-inducing agent. Objective: To investigate the role of carbohydrate in sleep induc- laxation techniques, regular physical activity, and avoidance of stimulants such as caffeine before sleeping. mela tion, we explored the effect of glycemic index (GI) and meal time on Both the timing (4, 5) and macronutrient content (6 –9) of sleep in healthy volunteers. Design: We compared the effect of high- and low-GI carbohydrate– meals are known to influence sleep. A meal consumed close to bedtime is associated with sleep disturbance (4). A number of high- CV ҃ based meals ingested 4 h before bedtime on sleep quality. We also macronutrients influence sleep through tryptophan (Trp), which Downloaded from www.ajcn.org by guest on March 26, 2011 evaluated the effect of the timing of high-GI meals (4 h compared serves as a precursor for brain serotonin, a sleep-inducing agent with 1 h) on sleep quality. Twelve healthy men (aged 18-35 y) were (10, 11). A factor that promotes the entry of Trp into the brain is administered standard, isocaloric (3212 kJ; 8% of energy as protein, 1.6% of energy as fat, and 90.4% of energy as carbohydrate) meals of either Mahatma (low GI ҃ 50) or Jasmine (high GI ҃ 109) rice 4 h its plasma concentration relative to that of the other large neutral amino acids (LNAAs: tyrosine, phenylalanine, leucine, isoleu- (556 cine, valine, and methionine) (12). It is now known that high- before their usual bedtime. On another occasion, the high-GI meal was given 1 h before bedtime. The participants underwent a famil- glycemic-index (GI) carbohydrates have the ability to increase the ratio of circulating Trp to LNAAs (Trp:LNAA) via a direct inges iarization night followed by 3 test nights in random order 1 wk apart. Results: A significant (P ҃ 0.009) reduction in the mean (ȀSD) sleep onset latency (SOL) was observed with a high-GI (9.0 Ȁ 6.2 action of insulin, which promotes a selective muscle uptake of LNAAs (13). Thus, a high-GI meal would be expected to pro- mote sleep via an increase in brain Trp and serotonin as the P҃0 min) compared with a low-GI (17.5 Ȁ 6.2 min) meal consumed 4 h before bedtime. The high-GI meal given 4 h before bedtime showed a significantly shortened SOL compared with the same meal given plasma Trp:LNAA increases (12). It would also be expected that a meal containing a high protein content, which contributes less for th Trp to the circulating blood compared with the other LNAAs (12) 1 h before bedtime (9.0 Ȁ 6.2 min compared with 14.6 Ȁ 9.9 min; P ҃ 0.01). No effects on other sleep variables were observed. Conclusions: We showed that a carbohydrate-based high-GI meal and thus a lower plasma Trp:LNAA, would reduce serotonin. Serotonin function may be measured indirectly through changes 1718 ng/h, in melatonin concentrations, because serotonin is an intermedi- resulted in a significant shortening of SOL in healthy sleepers com- ary product in the production of melatonin, a pineal hormone pared with a low-GI meal and was most effective when consumed 4 h (14). Urinary 6-hydroxymelatonin sulfate, a stable end product before bedtime. The relevance of these findings to persons with sleep of melatonin, is often used as a surrogate measure of melatonin, disturbance should be determined in future trials. Am J Clin given their linear relation (14). Nutr 2007;85:426 –30. Therefore, the aim of the present study was to investigate the KEY WORDS sleep timing Carbohydrates, glycemic index, sleep quality, role of carbohydrate in inducing sleep, and specifically the effect of GI on sleep patterns in healthy sleepers. We hypothesized that carbohydrate-based high- compared with low-GI meals ingested Bloo 4 h before bedtime would improve sleep quality because of a INTRODUCTION greater insulin response and that the timing of the high-GI meal (4 h compared with 1 h) before bedtime would also influence Th FIGURE According tonot sleep wellAm. J.nights/mo, 10 – 40%onset latency (SOL) between the high- tenance. 1. Comparison of sleepin Common sleep difficulties include sleep initiation and main- sleep quality. the United States do The Gallup Organization, 49% of adults for ͧ5 Clin. Nutr. 2007 Feb.;85(2):426–430. 1 From the School of Exercise and Sport Science, Faculty of Health Sci- mealglycemic-index (GI) Australia,10ingested 1 h or 4 h before bedtime and the low-GI meala –15% have long-term and 4 have intermittent insomnia, and ences, The University of Sydney, Sydney, Australia. 2 sleep difficulties (1). In survey reported an in- Supported by Sydney University’s PhD student research budget. The ricemeal ingested 4 h (2). before bedtime. PC, subject who showed an inappropriate somnia prevalence of 17% in men and 25% in women in an was provided by Riviana Food Pty Ltd, Victoria, Australia. The 3 Reprints not available. Address correspondence to CM Chow, Delta urban community Sleep Research Unit, School of Exercise and Sport Science, Faculty of Healthtrend in theandcurrent treatment options for insomnia are pharmacother-mean (ȀSD) SOLs for the low-GI meal apy SOL for the 3 meals. The The cognitive behavioral therapy. Treatments are considered Sciences, The University of Sydney, PO Box 170, Lidcombe NSW 1825
    • NUTRITION MYTHS
    • " " " ! ! “A ASSOCIAÇÃO ?? ENTRE DIETA E ACNE É UM MITO!” ! " Dose Extra " Batata Doce " Controlo " "" "1.  " Smolinski KN, Yan AC. Curr Opin Pediatr 2004; 16: 385-3912.  Thiboutot DM, Strauss JS: Diseases of the sebaceous glands, in Freedberg IM, Eisen AZ, Wolff K, et al, (eds.): Fitzpatrick’s Dermatology in General Medicine, vol 1. (ed 6). New York: McGraw-Hill, 2003 p 6833.  Cunliffe WJ, Simpson NB: Disorders of sebaceous glands. In: Champion RH, Wilkinson DS, Ebling FJG, et al, (eds): Rook/ Wilkinson/Ebling Textbook of Dermatology (ed 6). Oxford: Blackwell Science, Ltd, 1998 p 1951
    • ALUNOS DE MEDICINA RESPONDEMIMEDIATAMENTE QUE ACNE E DIETA É UM MITO
 !
    • EUA!ü 28-61 % Crianças (10-12 a)!ü 79-95 % Adolescentes (16-18 a) ! White GM. J Am Acad Dermatol 1998;39:S34-S37 Goulden V, Stables, GI Cunliffe WJ. J Am Acad Dermatol 1999;41:577-80
    • OKINAWA !1946: !! !! Médicos americanos ! administraram extensos questionários a médicos locais que mostraram:! !AUSÊNCIA DE ACNE VULGARIS NESTA POPULAÇÃO RURAL Steiner PE. Arch Pathol 1946;42:359-380.
    • ALASCASchaefer O. When the Eskimo comes to town. Nutr Today 1971;6:8-16
    • ACNE NOS ESQUIMÓS “Another condition has become prevalent, one obvious even to the layman: acne vulgaris. The condition used to be unknown among Eskimos, but one can see it readily amongst teenagers on the streets of Inuvik, Frobisher Bay, and Cambridge Bay. It is far less Prevalent in the smaller centers” “Old Northmen, such as missionaries, traders, trappers, men of the Royal Canadian Mounted Police and others who have known and watched the Eskimos closely for many years, frequently remark to their physician friends on the change in the complexions of the young people. Many Eskimos themselves blame their pimples on the pop, chocolate, and candies the youngsters consume as if addictedEsquimó, 1913 Otto Schaefer, M.D. – 1971 Schaefer O. When the Eskimo comes to town. Nutr Today 1971;6:8-16
    • DIETA ORIGINAL: ! ü Carne de Animais selvagens (caça e peixe)! ü Vegetação e bagas (Verão)!ü  Modificações na dieta à Controlo medida que foram ocidentalizados:! Açúcar, Doces, Cereais, Lacticínios" Schaefer O. When the Eskimo comes to town. Nutr Today 1971;6:8-16
    • HABITANTES DE KITAVA!ü  Área de 25 Km2!ü  Nº Habitantes: 2250!ü  Estilo de Vida: Horticultura e Pesca!
    • AVALIAÇÃO MÉDICA!ü  Durante 7 semanas, em 1990, o Dr. Lindeberg visitou 494 casas!ü  AVALIOU 1200 pessoas com 10 anos ou mais!ü  Incluindo 300 pessoas entre 15-25 anos ! Cordain L, et al. Arch Dermatol 2002;138:1584-90
    • Consumo muito reduzido de:! ü  Álcool, café e chá! ü  Lacticínios! ü  Cereais! ü  Açúcar! ü  Sal refinado! ü  Óleos vegetais e Margarina! ü  Alimentos processados!Cordain L, et al. Arch Dermatol 2002;138:1584-90
    • !NÃO ENCONTROU UM ÚNICO CASO DE ACNE NESTA POPULAÇÃO.! Cordain L, et al. Arch Dermatol 2002;138:1584-90
    • ACNE É RARA OU INEXISTENTE EM POPULAÇÕES ! PRIMITIVAS " Dose Extra Batata Doce ControloCordain L, Lindeberg S, Hurtado M, et al: Acne vulgaris: a disease of Western civilization. Arch Dermatol 2002;138:1584-90
    • ESTUDO DE INTERVENÇÃO DIETÉTICA RANDOMIZADO E CONTROLADO Dieta LGL: •  25% P •  45% HC de Bx IG •  30% L Smith RN et al. Am J Clin Nutr. 2007 Jul;86(1):107-15
    • Smith RN et al. Am J Clin Nutr. 2007 Jul;86(1):107-15
    • Smith RN et al. Am J Clin Nutr. 2007 Jul;86(1):107-15
    • Smith RN et al. Am J Clin Nutr. 2007 Jul;86(1):107-15
    • Costa, A et al. An. Bras. Dermatol. 2010; 85(3): 346-353
    • ASSOCIAÇÃO POSITIVA COMCARGA GLICÉMICA ELEVADA E COM LACTICÍNIOS
    • LEITE E ACNE
 
ESTUDOS EPIDEMIOLÓGICOS ! Adebamowo CA, Spiegelman D, Danby FW, et al High school dietary dairy intake and teenage acne. J Am Acad Dermatol; 52(2):207-14, 2005. Adebamowo CA, Spiegelman D, Berkey CS, et al. Milk consumption and acne in adolescent girls. Dermatol Online J; 12(4):1, 2006. Dose Extra Adebamowo CA, Spiegelman D, Berkey CS, et al. Batata Doce Milk consumption and acne in teenaged boys. J Am Acad Dermatol. Controlo 2008 May;58(5):787-93
    • NUTRITION MYTHS
    • DDR: 0,8 G/KG/DIANational Academy of Sciences. Dietary Reference Intakes – The essential guide to nutritional requirements. The National Academy Press, 2006.
    • ATLETAS: 1,2 – 2 G/KG/DIAGreenwood M, Kalman D, Antonio J. Nutritional Supplements in Sports and Exercise. Humana Press, Totowa, NJ, 2009
    • PROTEÍNA tem > Efeito na Saciedade que GORDURA e HC Porrini M et al. Physiol Behav 1997;62:563-70 Batterham RL, et al. Cell Metabolism 2006 Sept; 4:223-233.
    • N Engl J Med 2010;363:2102-13
    • N Engl J Med 2010;363:2102-13
    • PROTEÍNA E DCV NURSES HEALTH STUDY:ü  80,082 Mulheres seguidas desde 1976ü  Proteína (animal e vegetal) associada com menor risco de DAC Hu FB et al. Am J Clin Nutr 1999;70:221-7
    • DIETA HIPERPROTEICA MELHORA DISLIPIDEMIASubstituição de CHO(11% ingestão calórica total diária) porProteína:1. Diminuiu LDL (9%),2. Reduziu Col total /HDL (15%)3. Diminuiu Triglicéridos (23%)4. Aumentou HDL (12%) Wolfe BM et al. Can J Cardiol 1995 11:127G-31G
    • DIETA HIPERPROTEICA MELHORA DISLIPIDEMIA,GLICEMIA E SENSIBILIDADE À INSULINA EM DT2, OBESIDADE E/OU SÍNDROME METABÓLICA1.  O’Dea K. Diabetes 1984; 33, 596-603.2.  O’Dea K, et al. J. Am. Diet. Assoc. 1989; 89, 1076-1086.3.  Wolfe BM & Piche LA. Clin. Invest. Med. 1999; 22, 140-148.4.  Layman DK, et al. J Nutr. 2003 Feb;133(2):411-7.5.  Farnsworth E, et al. Am J Clin Nutr. 2003 Jul;78(1):31-9.6.  Aude YW, et al. Arch Intern Med. 2004 Oct 25;164(19):2141-6.7.  McAuley KA, et al. Diabetologia. 2005 Jan;48(1):8-16.8.  Luscombe-Marsh ND, et al. Am J Clin Nutr. 2005 Apr;81(4):762-729.  Noakes M, Keogh JB, Foster PR, Clifton PM. Am J Clin Nutr. 2005 Jun;81(6):1298-306.10.  Appel LJ, et al. JAMA. 2005 Nov 16;294(19):2455-64
    • Substituição moderada de CHO por Proteína poderá reduzir PA em HipertensosHodgson JM, et al. Am J Clin Nutr. 2006 Apr;83(4):780-7
    • NUTRITION MYTHS
    • PROTEÍNA ANIMAL AUMENTA RISCO DE OSTEOPOROSE
 
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    • PRAL DE ALGUNS ALIMENTOS ACIDIFICANTES ALCALINIZANTES PRAL(mEq/100 kcal) PRAL (mEq/100 kcal) Peixe 14,6 Oleaginosas -1,1 Carne 12,4 Fruta -5,2 Aves 7,8 Tubérculos -5,4 Ovo 7,3 Cogumelos -11,2Marisco 7,3 RaízesQueijo 3,3 (Cenoura, nabo) -17,1 Leite 1,3 Tomate -17,5Cereais 1,1 Hortaliças -23,4NEUTROS PAEL (mEq/100 kcal)Leguminosas -0,4 Frassetto L.A. et al. J Nephrol. 2006 Mar-Apr;19 Suppl 9:S33-40.
    • Dietary protein and calcium interact to influence calcium retention: acontrolled feeding study1–4Janet R Hunt, LuAnn K Johnson, and ZK Fariba RougheadABSTRACT and possible negative consequences for bone health (11, 12),Background: The effect of meat protein on calcium retention at especially if calcium intakes are low.different calcium intakes is unresolved. In this controlled feeding study, the objectives were to de-Objective: The objective was to test the effect of dietary protein on termine the nature of interaction between dietary protein andcalcium retention at low and high intakes of calcium. calcium on 1) calcium retention (by using 47Ca radiotracer and Downloaded from www.ajcn.org at Lund University Libraries on February 16, 2010Design: In a randomized controlled feeding study with a 2 3 2factorial crossover design, healthy postmenopausal women (n ¼27) consumed either ’675 or ’1510 mg Ca/d, with both low and ü  Proteína aumenta whole-body scintillation counting) and 2) blood and urinary biomarkers of calcium and bone metabolism. Multiple urinary measurements during a 7-wk dietary treatment period also en-high protein (providing 10% and 20% energy) for 7 wk each, sep-arated by a 3-wk washout period. After 3 wk, the entire diet was Excreção de Ca! abled examination of possible adaptations in urinary acidifica- tion and calciurea.extrinsically labeled with 47Ca, and isotope retention was monitoredby whole-body scintillation counting. Clinical markers of calciumand bone metabolism were measured. SUBJECTS AND METHODS ü  Proteína aumentaResults: High compared with low dietary protein significantly in-creased calcium retention from the low-calcium (29.5% compared General protocol and treatment assignmentwith 26.0% absorbed) but not the high-calcium diet (18% absorbed). This controlled feeding trial was conducted as a randomizedFor the low-calcium diet, this effect nearly balanced a protein-related crossover design (2 3 2 factorial); de Ca! Absorção each subject consumed one0.5-mmol/d greater urinary calcium excretion. Protein-related calciu- amount of dietary calcium but alternately consumed 2 amountsretic effects were independent of dietary calcium. Testing at 1, 2, 3, 5,and 7 wk showed no long-term adaptation in urinary acidity or urinarycalcium excretion. High compared with low dietary protein decreased ! of dietary assigned After statistically blocking to),orattain an were protein. distribution of body mass index (BMI; in kg/m subjects randomly to either high-calcium (HC) 2 even low-calciumurinary deoxypyridinoline and increased serum insulin-like growthfactor I without affecting parathyroid hormone, osteocalcin, bone-specific alkaline phosphatase, or tartrate-resistant acid phosphatase. ! (LC) treatment groups. Subjects were further randomly assigned to a sequence for consuming both low-protein (LP) and high- protein (HP) diets. Thus, every subject consumed 2 experimentalConclusions: In healthy postmenopausal women, a moderate in-crease in dietary protein, from 10% to 20% of energy, slightlyimproved calcium absorption from a low-calcium diet, nearly com- ! diets for 7 wk each. The 2 diet periods were separated by a 3-wk washout period when diets were not controlled.pensating for a slight increase in urinary calcium excretion. Underpractical dietary conditions, increased dietary protein from animalsources was not detrimental to calcium balance or short-term indi- ! Subjects Healthy postmenopausal women were recruited through publiccators of bone health. Am J Clin Nutr 2009;89:1357–65. ! advertising and direct mailings. The women were selected after an interview and blood analysis if they met the following criteria:INTRODUCTION ! 1 From the US Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND (JRH and
    • Nutrient Physiology, Metabolism, and Nutrient-Nutrient InteractionsA Diet High in Meat Protein and Potential RenalAcid Load Increases Fractional CalciumAbsorption and Urinary Calcium Excretionwithout Affecting Markers of Bone Resorptionor Formation in Postmenopausal Women1–4Jay J. Cao,* LuAnn K. Johnson, and Janet R. HuntUSDA, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202Abstract Downloaded from jn.nutrition.org by Janet Hunt on February 3, 2011Our objective in this study was to determine the effects of a high-protein and high-potential renal acid load (PRAL) diet oncalcium (Ca) absorption and retention and markers of bone metabolism. In a randomized crossover design, 16postmenopausal women consumed 2 diets: 1 with low protein and low PRAL (LPLP; total protein: 61 g/d; PRAL: 248mEq/d) and 1 with high protein and high PRAL (HPHP; total protein: 118 g/d; PRAL: 33 mEq/d) for 7 wk each separated by a1-wk break. Ca absorption was measured by whole body scintillation counting of radio-labeled 47Ca. Compared with theLPLP diet, the HPHP diet increased participants’ serum IGF-I concentrations (P , 0.0001), decreased serum intact PTHconcentrations (P , 0.001), and increased fractional 47Ca absorption (mean 6 pooled SD: 22.3 vs. 26.5 6 5.4%; P , 0.05)and urinary Ca excretion (156 vs. 203 6 63 mg/d; P = 0.005). The net difference between the amount of Ca absorbed andexcreted in urine did not differ between 2 diet periods (55 vs. 28 6 51 mg/d). The dietary treatments did not affect othermarkers of bone metabolism. In summary, a diet high in protein and PRAL increases the fractional absorption of dietary Ca,which partially compensates for increased urinary Ca, in postmenopausal women. The increased IGF-I and decreased PTHconcentrations in serum, with no change in biomarkers of bone resorption or formation, indicate a high-protein diet has noadverse effects on bone health. J. Nutr. doi: 10.3945/jn.110.129361.Introduction impairs bone, many epidemiological observations link a high-Although being essential to bone health, protein intake, espe- protein intake with bone anabolism, including an associationcially from animal sources, in high amounts has also been with increased bone mineral density or decreased fracture riskconsidered a risk factor for osteoporosis or bone fractures (1–4) (9–14), with few reports showing negative associations (15,16).due to the increase in urinary calcium (Ca) excretion resulting The results of well-controlled human trials with Ca isotopesfrom the metabolic acidity of protein metabolism (5–8). How- show that a high-protein intake increases intestinal Ca absorp-
    • NaCl determina ~ 50% da PRALFrassetto LA, Morris RC Jr, Sebastian A. Am J Physiol Renal Physiol. 2007 Aug;293(2):F521-5
    • ü  40 H e M > 50 anosü  Duração: 60 diasü  2 Grupos: GRUPO 1: Elevada ingestão de Fruta e Vegetais GRUPO 2: Fruta e Legumes substituidas por Cereais Jajoo R, et al. J Am Coll Nutr. 2006 Jun;25(3):224-30.
    • GRUPO 2: ü  PTH ü  Excreção UCa ü  Excreção urinária de N-Telopéptido Jajoo R, et al. J Am Coll Nutr. 2006 Jun;25(3):224-30.
    • NUTRITION MYTHS
    • INSUFICIÊNCIA RENAL E PROTEÍNAAumento daingestão deproteína empacientes cominsuficiênciarenal acelera aprogressão Brenner BM, Meyer TW, Hostetter TH. N Engl J Med. 1982 Sep 9;307(11):652-9
    • ü  Dieta em que Proteína foi 25 % energia não levou a alterações renais adversas ao fim de 6 meses ü  Sem alterações na albumina urinária (pré/pós dieta) ü  Taxa de Filtração Glomerular por volume de rim não mudou ü  Conclusão: Rim adapta-se a dieta hiperproteica em pessoas sem patologia renalSkov AR et al. Int J Obes Metab Disord 1999;23:1170-77.
    • CONCLUSÃO: ! "“Apesar da restrição de Proteína poder ser apropriada no tratamento de patologias renais, não encontrámos evidencia que una ingestão elevada de proteína afecte de forma negativa a função renal de indivíduos saudáveis.”! "" " "
    • NUTRITION MYTHS
    • LEITE, CA E FRACTURAS
    • LEITE E FRACTURAS" Sem associação em adultos RR/+1glass"Pooled analysis for categories of milk intake and hip fracture risk in womenfrom prospective cohort studies (6 studies, 195 102 women, 3574 fractures). ! Bischoff-Ferrari HA et al. J Bone Mineral Res 2011; online Oct 2010, DOI 10.1002/jbmr.279!
    • " . ü  7 estudos prospectivos, 170 " " " . " " 991 mulheres, 2954 " " " " " fracturas da anca. ü  5 estudos prospectivos, 68 606 Homens, 214 fracturas da anca. ü  5 intervenções (5666 Mulheres + 1074 Homens), 814 fracturas não-vertebrais. ü  4 intervenções c/ resultados separados para fracturas da anca (6504 pessoas, 139 fracturas da anca). 248Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Am J Clin Nutr. 2007 Dec;86(6):1780-90
    • Total n: 252,841 ü Estudos Prospectivos NÃO MOSTRAM ASSOCIAÇÃO ENTRE INGESTÃO DE CA E FRACTURAS DA ANCA em Homens e Mulheres ü RCTs observam um LIGEIRO AUMENTO DO RISCO DE FRACTURAS DA ANCA com a SUPLEMENTAÇÃO DE CA249 . . Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Am J Clin Nutr. 2007 Dec;86(6):1780-900
    • Bolland MJ, et al. BMJ. 2008 Feb 2;336(7638):262-6
    • NUTRITION MYTHS
    • Obrigado 
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