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/
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
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 26 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
EFEITOS A LONGO PRAZO 3 grupos de Consumo de ovos por semana (Framingham Heart Study)27 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
EFEITOS A LONGO PRAZO Colesterol Total nos 3 grupos28 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
of each that th Dietary cholesterol The changes 1.4 1 trolling models 1.2 statistica erate 1.0 0) a manipul I 0.8 more a 0) function -C E 0.6 reduction in dieta 0.4 shown 0.2 tions 35.43 . Confined Inst meals Free : :ii- mg/dL; Location of subjects mmol/L 0.6% FIGURE 2. Regression WH, et al. Am J Clin Nutr. 1997 Jun;65(6):1747-64. Howell coefficients of saturated fatty acids, poly- Onunsaturated fatty acids, and &holesterol for studies of subjects free-living analysis
US NATIONAL HEALTH AND NUTRITIONAL SURVEY (1984–1994)30 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-
826 HERRON ET AL Table 1. Distribution of Cholesterol in LDL Subclasses and LDL Peak Diameter of Hypo- and Hyper-responders During the EGG or SUB Periods LDL Peak LDL-1 (mg/dL) LDL-2 (mg/dL) LDL-3 (mg/dL) Diameter (nm) Women Hyper-responders (n ϭ 14) EGG 31.7 Ϯ 12.2a 22.1 Ϯ 10.7b 5.1 Ϯ 5.5a 26.90 Ϯ 0.25a SUB 28.1 Ϯ 10.4b 16.6 Ϯ 7.8a 4.1 Ϯ 5.5a 26.99 Ϯ 0.33a Hypo-responders (n ϭ 13) EGG 21.8 Ϯ 7.8c 19.4 Ϯ 10.5ab 4.5 Ϯ 5.5a 26.58 Ϯ 0.57b SUB 21.9 Ϯ 8.0c 19.1 Ϯ 11.5ab 4.6 Ϯ 6.8a 26.67 Ϯ 0.62b Men Hyper-responders (n ϭ 12) EGG 23.3 Ϯ 8.4c 19.6 Ϯ 8.2ab 16.6 Ϯ 16.2c 26.24 Ϯ 0.58b SUB 20.0 Ϯ 7.9c 25.6 Ϯ 5.6b 9.9 Ϯ 10.4bc 26.40 Ϯ 0.53b Hypo-responders (n ϭ 13) EGG 18.2 Ϯ 8.8d 20.5 Ϯ 5.6ab 6.8 Ϯ 6.1ab 26.75 Ϯ 0.35a SUB 20.5 Ϯ 9.0c 20.5 Ϯ 9.0ab 7.8 Ϯ 7.5b 26.67 Ϯ 0.52b Sex effect P Ͻ .05 NS P Ͻ .01 P Ͻ .01 Response effect P Ͻ .05 NS NS NS Diet effect NS NS P Ͻ .05 NS Interaction sex ϫ response NS NS NS P Ͻ .001 Interaction sex ϫ diet NS NS NS NS Interaction response ϫ diet P Ͻ .001 P Ͻ .05 P Ͻ .001 NS Interaction sex ϫ diet ϫ response NS P Ͻ .01 P Ͻ .05 NS NOTE. Values are presented as mean Ϯ SD for the number of subjects indicated in parentheses. Values in the same column with differentsuperscripts are signiﬁcantly different as determined by 3-way ANOVA and LSD as post hoc test. Abbreviations: EGG, egg; SUB,KL, Lofgren NS,Sharman M, Volek JS, Fernandez ML. Metabolism. 2004 Jun;53(6):823-30. Herron substitute; IE, not signiﬁcant.consumption, while hyporesponders experienced no change for contrast, plasma LCAT and CETP activities were signiﬁcantly
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 . significant increases in LDL-C of 7.8% and 3.3%, respec- Clinical trials conducted in children , 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)  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)  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)  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) . These recommendations are mostly based onMen/women (n=34)  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 .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 , and India , 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” . In contrast to US policies, Europeans have no Keywords Dietary cholesterol . LDL cholesterol . dietary guidelines for DC . 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 SOFREROXIDAÇÃO37
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.
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. !
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
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 firstname.lastname@example.org. 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 74–80 Effects of an Indo-Mediterranean Diet on the Omega–6/Omega–3 Ratio in Patients at High Risk of Coronary Artery Disease: The Indian Paradox Daniel Pellaa, Gal Dubnovb, Ram B. Singhc, Rakesh Sharmad, Elliot M. Berryb, Orly Manor ba 2nd Interna Klinika,Safaric University, Kosice, Slovakia;b Department of Human Nutrition and Metabolism, Hebrew University, Hadassah Medical School, Jerusalem, Israel;c Subharti Medical College, Medical Hospital and Research Centre, Moradabad, India;d Department of Medicine, Columbia University, New York, N.Y., USA
> PREVALÊNCIA DE DAC NOS INDIVÍDUOS DA REGIÃO URBANA Pella D et al. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 74-80.
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 , increasing their consumption has been promoted in the management of coronary artery disease (CAD) .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  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 . A recent meta-analysis showed that both dietary and non-dietary sources are equally beneficial , and the health benefits of plant- derived or fish- derived omega–3 fatty acids now seem to have a sound basis . 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)