Download as PDF, PPTX
![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) 12:377–383
which 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 had
regarding 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 in
that 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. These
individuals considered hyper-responders to & a cholesterol
Maria Luz Fernandez Mariana Calle studies suggest that dietary management of OIR individuals
challenge 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 2010
Population Duration Additional dietary cholesterol LDL-C HDL-C LDL-C/HDL-C ratio LDL size HDL size
Children (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) has
Women (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
no
Men (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 scientific
Men/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 on
Men/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 many
Men/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 the
Men/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](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-12-320.jpg)
![dification Trial (CVD) prevention, butand some trials have linked diet needed.
Context Multiple epidemiologic studies
cation Trial disease
diovascular long-term intervention data are
with car-
Linda Objective To test the hypothesis that a dietary intervention, intended to be low in
Context Multiple epidemiologic some trials some trials have linked diet with risk.
Context Multiple epidemiologic studies andstudies andhave linked diet with reduce CVD car-
Hsia, MD; fat and high in vegetables, fruits, and grains to reduce cancer, wouldcar-
.
D;
diovascular disease (CVD) prevention, but long-term intervention data are needed. are needed.
diovascular disease (CVD) prevention, but long-term intervention data
L. ; L. Design, Setting, and Participants Randomized controlled trial of 48 835 post-
arcia
D Objective To test the that a dietary intervention, intended to be low in
Objective To test the hypothesishypothesis that a dietary intervention, intended to be low in
menopausal women aged 50 tograins to reduce cancer, would reduce CVD risk.
79 years, of diverse backgrounds and ethnicities, who
fat and highand high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk.
s; H. fat in vegetables, fruits, and
Lewis H. participated in the Women’s Health Initiative Dietary Modification Trial. Women were
Croix, PhDDesign,Design, Setting, and Participants 541 [40%]) or of 48 835trial of 48 835 post-
PhD; ; Setting, and Participants Randomized controlled trial
an intervention (19 Randomized controlled
post-
randomly assigned to 50 to 79 years, of diverse backgrounds and ethnicities, whogroup (29 294
comparison
L. menopausal women aged
orman L. [60%]) menopausal women agedStudy79 years, of diverse backgrounds and ethnicities, who
in in the Women’s Health 50 to Dietary Modification Trial. Women 1993 and 1998 in
; , MD; participateda free-living setting.InitiativeenrollmentDietary Modification were Women were
participated in the Women’s Health Initiative
occurred between
Trial.
s 40 US clinical centers;intervention (19 541 in this 541 [40%]) orgroup (29 294 group (29 294
randomly assigned to an mean follow-up [40%]) analysis was 8.1 years.
or comparison
L.
Karen L. [60%]) in a free-living setting.to an intervention (19 between 1993 and 1998 in
randomly assigned
Study enrollment occurred
comparison
MD;
D; , MD; InterventioninIntensive behavior Study enrollment group and individual sessions de-
ysiw
. 40 US clinical centers; mean follow-up in this analysis wasin occurred between 1993 and 1998 in
[60%]) a free-living setting. modification 8.1 years.
inda M. signed to reduce total fat intake tofollow-up calories and increase intakes of vegetables/
PhD;
40 US clinical centers; mean 20% of in this analysis was 8.1 years.
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 diet-related educationgrains to at intake servings/d. The comparison group received of vegetables/
fruits to 5 servings/d and materials.
signed to reduce total fat least 6 to 20% of calories and increase intakes
bins, G. ; Main Outcome Measures grains to at least 6 servings/d. The comparison group received
fruits to 5 servings/d and
nda MD diet-related education materials.
E. Fatal and nonfatal coronary heart disease (CHD), fatal
diet-related education materials.
RISCO
0%
5%
10%
15%
20%
25%
DAC
Total
DCV
RELATIVO
GloriaG. and nonfatal stroke, and CVD and nonfatal coronary heart disease (CHD), fatal
Linda E. Main Outcome Measures Fatal (composite of CHD and stroke).
PhD;
ns, MD; ;Linda G.nonfatal stroke, and CVD (compositeFatal and nonfatal coronary heart disease (CHD), fatal
z, PhD and Main Outcome Measures of CHD and stroke).
Results By year 6, mean fat intakeintake decreased byenergy intake in the inter- in the inter-
Resultsand nonfatal stroke, and CVD (composite of CHD and stroke). intake
Stevens, PhD; By year 6, mean fat decreased by 8.2% of 8.2% of energy
PH; ; ventionvs the comparison group, with small decreases in saturated (2.9%), monoun-
DrPH
aurizio vention Results By year 6, mean fatwith small decreases in saturated (2.9%), monoun-
vs the comparison group,
intake decreased by 8.2% of energy intake in the inter-
se R. ,
ouise R. DrPH;
tolins saturated (3.3%),the comparison group, withincreases occurred :in-intakes of veg-intakes of veg-
saturated (3.3%), and polyunsaturated (1.5%) (1.5%) fat; increases occurred in
and polyunsaturated fat; small decreases in saturated (2.9%), monoun-
TRANS 22%
D; vention vs
; 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 cholesterol
saturated servings/d) polyunsaturated (1.5%) fat; increases occurred in intakes of veg-
and and
y R. MD; levels,diastolic blood pressure, and factor VIIc levels were+11% Low-density lipoprotein cholesterol
enry R.
ord,; levels, diastolic blood pressure, and factor VIIc levels were significantly reduced16%
HORTALIÇAS/FRUTA: +30% CEREAIS: significantly reduced by FIBRA: +
etables/fruits and 4.29%, respectively; levels of high-density lipoprotein cho-
(1.1 servings/d) and grains (0.5 serving/d).
3.55 by 3.55
PhD mg/dL, 0.31 mm Hg,
D; ; Henry mg/dL, levels, mm Hg,blood 4.29%, respectively; levels of high-density lipoprotein 3.55
hD R. 0.31 diastolic and pressure, and factor VIIc levels were significantly reduced by cho-
lesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention
unner, PhDlesterol,mg/dL, 0.31 mm numbers who developed CHD,significantly differ in the intervention
ski, MD; ;vs comparison groups. The Hg, and 4.29%, respectively;stroke, of high-density lipoprotein cho-
triglycerides, glucose, and insulin did not levels and CVD (annual-
,ette; ; vs comparison groups. 1000glucose, and JAMA.developed CHD, stroke, and CVD (annual-
MD MD ized incidence rates) were The (0.63%), et al. insulin didand 1357 (0.86%)differ in the intervention
lesterol, triglycerides, numbers who 2006 Feb 8;295(6):655-66
Howard BV, 434 (0.28%), not significantly in the in-
hlebowski, ized incidence rates) were 1000 (0.63%), 434 (0.28%),CHD, 1357 (0.86%) in the in-
D; MD;
tervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. CVD (annual-
vs comparison groups. The numbers who developed and stroke, and
ranek, MD; The diet ized no significant effects on incidence of CHD434 (0.28%), and 0.97; 95%
had incidence rates) were 1000 (0.63%), (hazard ratio [HR], 1357 (0.86%) in the in-](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-19-320.jpg)
![Based on Evolutionary, Historical,
Dietary Fat Quality and Coronary Heart
Global, and Modern ed Theory
Disease Prevention: A Unifi Perspectives
Christopher E.on Evolutionary, Historical,
Based Ramsden, MD
Global, and Modern Perspectives
Keturah R. Faurot, PA, MPH
Pedro ChristopherFaurot, PA, MPH
Carrera-Bastos, MD
Keturah R.
E. Ramsden, BA
Loren Pedro Carrera-Bastos, BA
Cordain, PhD
Loren Cordain, PhD
Michel De De Lorgeril, MD, PhD PhD
Michel
Lorgeril, MD,
Laurence S. Sperling, MD
Laurence S. Sperling, MD
Corresponding author
Corresponding author
Christopher E. Ramsden, MD
Department of Physical Medicine and Rehabilitation, Program on
Christopher E. Ramsden,University of North Carolina–Chapel Hill School
Integrative Medicine, MD
Department Medicine, CB# 7200, Chapel Hill, and Rehabilitation, Program on
of of Physical Medicine NC 27599, USA.
E-mail: cramsden@med.unc.edu
Integrative Current Treatment Options in Cardiovascular Medicine 2009, 11:289–301Hill School
Medicine, University of North Carolina–Chapel
of Medicine, CB# 7200, Chapel Hill, NC 27599, USA.
Current Medicine Group LLC ISSN 1092-8464
Copyright © 2009 by Current Medicine Group LLC
E-mail: cramsden@med.unc.edu
Current Treatmentstatement in Cardiovascular Medicine 2009, 11:289–301
Opinion Options
Current Medicine and growing body of evidence indicates that dietary fatty acids regulate
A large Group LLC ISSN 1092-8464
Copyright © 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 shortcomings
Opinion 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](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-26-320.jpg)
![Orange Juice on Inflammation, Endoto
C l li in i icca l l C a rree//EEd uucca t t i o n / N u t r i t oo Expression e of cToll-Like Recept
C n a Ca d a andu the nn / P s y c h o s o c aa l R R s s e a r h h
ion/N tritii /Psychosoci i l e ear c
O R I I G I I N A LL
O R G N A
and Suppressor of Cytokine Signaling-
A R TT I I CC L L EE
A R
RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD vital to the protection fro
Differential Effects of Cream, Glucose, and
Differential Effects of Cream, Glucose, andHUSAM GHANIM, PHD
JAY FRIEDMAN, PHD
PRABHAKAR VISWANATHAN, PHD
AJAY CHAUDHURI, MD
ins and immunological
commensal and patho
Orange Juice on Inflammation, Endotoxin,
Orange Juice on Inflammation, Endotoxin,
SANAA ABUAYSHEH, BSC PARESH DANDONA, MD, PHD bacteria.
CHANG LING SIA, BSC In this context, we w
which macronutrient wa
and the Expression of Toll-Like Receptor-4
and the Expression of Toll-Like Receptor-4 the induction of oxidati
OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on the one h
and Suppressor of Cytokine Signaling-3
and Suppressor of Cytokine Signaling-3
induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the crease in LPS concent
expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in
mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated
expression of TLR-4 and
fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and tokine signaling (SOCS)
RUPALI DEOPURKAR, ,PHD
RUPALI DEOPURKAR PHD PPRIYA induce an , MD in LPS, TLR-4, and SOCS3. toto the protection from To elucidate this, we inv
inflammation, alsoMOHANTYMD
RIYA MOHANTY, increase vital the protection from bacterial tox-
vital bacterial tox-
HUSAM GHANIM, ,PHD
HUSAM GHANIM PHD PPRABHAKAR VISWANATHANPHD
RABHAKAR VISWANATHAN, , PHD ins and immunological responses glucose,
fect ofto the the most
ins and immunological responses to the
JJAYFRIEDMAN, ,PHD
AY FRIEDMAN PHD RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- hydrate, cream, a sat
AAJAY CHAUDHURIMD
JAY CHAUDHURI, , MD commensal and pathogenic intestinal
commensal and pathogenic intestinal
SANAA ABUAYSHEH, ,BSC
SANAA ABUAYSHEH BSC calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood orange juice, a carbohy
PPARESH DANDONAMD, PHD
ARESH DANDONA, , MD, PHD bacteria.
CHANG LING SSIA,BSC bacteria. food product, which do
CHANG LING IA, BSC samples were obtained at 0, 1, 3, and 5 h for analysis.
InIn this context, we wanted to analyzestress or in
this context, we wanted to analyze
ther oxidative
which macronutrient was responsible for is a protein
RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, andwas responsible for
which macronutrient the SOCS3
the induction ofof in MNCs, stress and in-
expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 oxidative
the induction oxidative stress and in-
shown to interfere with i
OBJECTIVE — We have recently shown thatsignificantly high-carbohydrate (HFHC) meal TLR-4 expressionon the one LPS signal transduction (2–
OBJECTIVE — We have recently shown thata ahigh-fat after glucose and cream intake, but flammation, and plasma hand, and the in-
increased high-fat high-carbohydrate (HFHC) meal flammation, on the one hand, and the in-
induces an increase in plasma concentrations of endotoxin (lipopolysaccharide intake. The intake of orangein LPS water did not work has shown that SO
concentrations increased only after cream [LPS]) and the
induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the crease juice LPS concentrations and the
expression of Toll-like receptor-4 (TLR-4) andany change inof cytokineindexes measured. crease in or concentrations and the
induce suppresser of of the signaling-3 (SOCS3) in
expression of Toll-like receptor-4 (TLR-4) and suppresser anycytokine signaling-3 (SOCS3) in expression of TLR-4 and suppresser of cy-
mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated expression of TLR-4 and suppressercirculating mo
mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated tokine signaling (SOCS)-3 on the other. obese hu
in the of cy-
(MNCs) of the
fat and carbohydrates, components of the HFHC meal, known toto induce oxidative stress and tokine signalingand an in- on the other.
fat and carbohydrates, components of CONCLUSIONSknown induce oxidative stress and induce NF-B binding (SOCS)-3 increased when compar
the HFHC meal, — Although both glucose and cream
To elucidate this, we investigated the ef-
inflammation, also induce an increase in LPS, the expression of SOCS3, TNF-␣, and IL-1 in MNCs, onlyelucidate this, increase normalthe ef-
inflammation, also induce an increase in LPS, inTLR-4, and SOCS3.
crease TLR-4, and SOCS3. To cream caused an we investigated subjects
fectorange juice or watermost important carbo- (6). I
in LPS concentration and TLR-4 expression. Equicaloric amounts of ofof glucose, the did not work carbo-
fect glucose, the most important demonstrated that
hydrate, cream, a a saturated fat, and
hydrate, cream, saturated fat, and
RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300-are relevant to the pathogenesis of sion in MNCs is inverse
induce a change in any of these indexes. These changes
RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- orange juice, a carbohydrate-containing
calorie drinks of either glucose, saturatedatherosclerosisorange juice,resistance. water to ingest. Blood orange juice, a carbohydrate-containing
fat as cream, and insulin or only water to ingest. Blood
calorie drinks of either glucose, saturated fat as cream, orange juice, or only tyrosine phosphorylatio
samples were obtained at 0, 1, 3, and 55 h for analysis.
samples were obtained at 0, 1, 3, and h for analysis. food product, which does not induce and directly rel
product, which does receptor ei-
foodCare 33:991–997, 2010 not induce ei-
Diabetes
ther oxidative stress oror inflammation.
ther oxidative stress inflammation.insulin resistance (home
O
SOCS3 is is a protein that has been
RESULTS — Indexes of inflammation including nuclear factor-Bshown thatbinding, and the because the content of LPS sessment of a protein that has been insulin res
ur recent work has (NF-B) binding, and the shown to interfere with insulin and leptin
RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) a great interest SOCS3
expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 ininthese meals is not to interfere with insulin and leptin
MNCs, IR]), consistent with
expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs, shown significantly differ-
high-fat high-cholesterol (HFHC)
increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS signal transduction (2–5). Our recent of insulin r
increased significantly after glucose and cream intake, butoxidative and inflam- plasma LPS signal transduction (2–5). Our recent
pathogenesis
meal induces TLR-4 expression and ent, and, thus, it would appear that the
concentrations increased only after cream intake. The intake ofof orange juice or water did not work has shown that SOCS3 resistance in human obe
concentrations increased only after cream intake. The intake orange juice oran inflammatory work has shownmay lead
water did not expression
matory stress in addition to inducing nature of the meal that SOCS3 expression
induce any change in any of the indexes measured. inability of leptin to ca](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-31-320.jpg)
![(R01-D
Differential Effects of Cream, Gluco the Am
Orange Juice on Inflammation,The da End
and we
and the Expression of Toll-Likepretatio Rec
and Suppressor of Cytokine Signal investig
vestiga
RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD vitalfor the
to the pro
HUSAM GHANIM, PHD PRABHAKAR VISWANATHAN, PHD ins and immu
JAY FRIEDMAN, PHD AJAY CHAUDHURI, MD commensal p
No a
SANAA ABUAYSHEH, BSC PARESH DANDONA, MD, PHD bacteria. art
this
CHANG LING SIA, BSC In this con
Nata which macron
the induction
OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on
induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the Referen
crease in LPS
expressionGh
1. of T
expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in
mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated
fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and tokine signalin
nie
inflammation, also induce an increase in LPS, TLR-4, and SOCS3. To elucidate th
JM
fect of glucose,
RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- tox
hydrate, crea
calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood orange juice,
samples were obtained at 0, 1, 3, and 5 h for analysis. Sumo de of
food product,
Laranja cyt
ther oxidative
RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, and the SOCS3 is
expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs,
fol
shown to inter
increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS me
signal transdu
concentrations increased only after cream intake. The intake of orange juice or water did not work has show
induce any change in any of the indexes measured. Dia
in the circul
(MNCs) ofRu
2. the
CONCLUSIONS — Although both glucose and cream induce NF-B binding and an in- increased whe
crease in the expression of SOCS3, TNF-␣, and IL-1 in MNCs, only cream caused an increase normal subje
Wh
in LPS concentration and TLR-4 expression. Equicaloric amounts of orange juice or water did not work demonstsul
induce a change in any of these indexes. These changes are relevant to the pathogenesis of sion in MNCs
atherosclerosis and insulin resistance. deg
Figure 3—Change in NFB binding activity in MNC (A) and plasma endotoxin concentrations tyrosine phosp
Diabetes Care juice (OJ, ‚),
Ch
receptor and d
(B) in normal subjects after a 300-calorie drink of cream (E), glucose (Œ), orange 33:991–997, 2010
3. Sen
insulin resistan
and ؉, P Ͻ 0.05 with a great interest because the content of LPS
or water (F). Data are means Ϯ SEM. *ur recent work has shown thatRMANOVA comparing changes in sessment of in
TA
IR]), consiste
relation to baseline after cream and glucose challenges; # andin $, P meals 0.05 significantly differ-
high-fat high-cholesterol (HFHC) these Ͻ is not with two-way](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-32-320.jpg)
![Macronutrients, oxidative stress, and inflammation
Differential
Effects of Cream, Gluco
Orange Juice on Inflammation, Endcytok
and the Expression of Toll-Like Rec
know
and Suppressor of Cytokine Signal
anim
RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD
but
vital to the pro
HUSAM GHANIM, PHD
JAY FRIEDMAN, PHD
PRABHAKAR VISWANATHAN, PHD
AJAY CHAUDHURI, MD
creas
ins and immu
commensal a
SANAA ABUAYSHEH, BSC
CHANG LING SIA, BSC
PARESH DANDONA, MD, PHD and
bacteria.
In this con
creas
which macron
Nata SOC
the induction
OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on
induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the
expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in
of in
crease in LPS
Glucose expression of T
mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated
fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and
juice
tokine signalin
inflammation, also induce an increase in LPS, TLR-4, and SOCS3. stres
To elucidate th
fect of glucose,
RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- Sumo de an in
hydrate, crea
orange juice,
calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood
samples were obtained at 0, 1, 3, and 5 h for analysis.
Laranja food product,
ther oxidative
RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, and the SOCS3 is
expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs, Ackn
shown to inter
increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS signal transdu
concentrations increased only after cream intake. The intake of orange juice or water did not porte
work has show
induce any change in any of the indexes measured. Flori
in the circul
(MNCs) of the
CONCLUSIONS — Although both glucose and cream induce NF-B binding and an in- supp
increased whe
crease in the expression of SOCS3, TNF-␣, and IL-1 in MNCs, only cream caused an increase
in LPS concentration and TLR-4 expression. Equicaloric amounts of orange juice or water did not (R01
normal subje
work demonst
induce a change in any of these indexes. These changes are relevant to the pathogenesis of
atherosclerosis and insulin resistance.
the A
sion in MNCs
tyrosine phosp
The
receptor and d
Diabetes Care 33:991–997, 2010
and w
insulin resistan
sessment of in
ur recent work has shown that a great interest because the content of LPS preta
IR]), consiste
high-fat high-cholesterol (HFHC) in these meals is not significantly differ-](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-35-320.jpg)
![dex diet than in the high–cereal fiber did not alter Mitchell, BASc, RD the as- been associa
Sandy the significance of
Results
n 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](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-46-320.jpg)
![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, HbA
0 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
tein
DL-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
T
ach 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)
40.0
n. 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](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-47-320.jpg)
![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 Subjects
TABLE 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
Abstract
n 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, 2011
BMI, 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 0.046
Fasting 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 products
Fasting 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
3
Insulin 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 body
Total 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 3.0
HDL 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 0.15
LDL 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 milled
TG 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 affect
Free 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 0.99
Systolic 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 habits
g-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 0.10
CRP, 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
Introduction
IL-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 0.79
PAI-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 betweenutr.
whole-grainwhole- stress are both adjusted for changes in BMI. Differences within such as exerci
(11,18,19). The scientific evidence is considered 37:
1401–1407,
2007.
chronic diseases (20,21). Insulin resistance and oxidative
J.
N the 1 sufficient to permit risk of
2 on human health (1). An inverse, relatively strong correlation of other lifestyle factors
health claims regarding the cardio-protective effect of and refined-grain diet 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 carryover
effect was found). tially be affected by whole-grain intake. Induction of lipid per-](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-48-320.jpg)
![EPA
DHA
Calder PC. Biochimie. 2009 Feb 3. [Epub ahead of print]](https://image.slidesharecdn.com/dietaeprevencaocvdversaoslideshare-130327150722-phpapp02/85/Dieta-e-prevencao-cvd-versao-slideshare-68-320.jpg)
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- 3. COLESTEROL DIETÉTICO <300 MG/DIA Dietary Guidelines for Americans, USDA, 2005
- 4. 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 408 Tabela de Composição dos Alimentos. Centro de Segurança Alimentar e Nutrição. Instituto nacional de Saúde Dr. Ricardo Jorge, 2006
- 5. Limite o consumode gemas de ovo
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- 7. BMJ 2013;346:e8539 doi:10.1136/bmj.e8539 (Published 7 January 2013) BMJ 2013;346:e8539 doi: 10.1136/bmj.e8539 (Published 7 January 2013) Page 1 of 13 Research RESEARCH Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies OPEN ACCESS 12 12 12 Ying Rong doctoral student , Li Chen research fellow , Tingting Zhu research fellow , Yadong 12 12 12 Song research fellow , Miao Yu research fellow , Zhilei Shan research fellow , Amanda Sands 3 3 12 doctoral student , Frank B Hu professor , Liegang Liu professor 1 Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, People’s Republic of China; 2Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, People’s Republic of China; 3Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA Abstract Conclusions Higher consumption of eggs (up to one egg per day) is Objective To investigate and quantify the potential dose-response not associated with increased risk of coronary heart disease or stroke. The increased risk of coronary heart disease among diabetic patients Fig 3 Forest plot of egg consumption and risk of coronary heart disease association between egg consumption and risk of coronary heart disease and stroke. and reduced risk of hemorrhagic stroke associated with higher egg consumption in subgroup analyses warrant further studies. Design Dose-response meta-analysis of prospective cohort studies. RISCO DE DOENÇA CARDÍACA CORONÁRIA Introduction Data sources PubMed and Embase prior to June 2012 and references of relevant original papers and review articles. Cardiovascular disease is now a public health crisis, affecting Eligibility criteria for selecting studies Prospective cohort studies millions of people in both developed and developing countries. with relative risks and 95% confidence intervals of coronary heart disease Although the rate of death attributable to the disease has declined or stroke for three or more categories of egg consumption. in developed countries in the past several decades, it is still the Results Eight articles with 17 reports (nine for coronary heart disease, leading cause of death and extorts a heavy social and economic eight for stroke) were eligible for inclusion in the meta-analysis (3 081 toll globally.1-3 In low and middle income countries, the
- 8. Fig 4 Dose-responseanalyses of egg consumption and risk of stroke BMJ 2013;346:e8539 doi: 10.1136/bmj.e8539 (Published 7 January 2013) Page 1 of 13 Research RESEARCH Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies OPEN ACCESS 12 12 12 Ying Rong doctoral student , Li Chen research fellow , Tingting Zhu research fellow , Yadong 12 12 12 Song research fellow , Miao Yu research fellow , Zhilei Shan research fellow , Amanda Sands 3 3 12 doctoral student , Frank B Hu professor , Liegang Liu professor 1 Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, Tongji Medical College, Huazhong University of Science and Technology, 430030 Wuhan, People’s Republic of China; 2Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, People’s Republic of China; 3Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA Abstract Conclusions Higher consumption of eggs (up to one egg per day) is Fig 5 Forest plot of egg consumption and risk of stroke Objective To investigate and quantify the potential dose-response association between egg consumption and risk of coronary heart disease not associated with increased risk of coronary heart disease or stroke. The increased risk of coronary heart disease among diabetic patients and stroke. and reduced risk of hemorrhagic stroke associated with higher egg consumption in subgroup analyses warrant further studies. Design Dose-response meta-analysis of prospective cohort studies. RISCO DE AVC Introduction Data sources PubMed and Embase prior to June 2012 and references of relevant original papers and review articles. Cardiovascular disease is now a public health crisis, affecting Eligibility criteria for selecting studies Prospective cohort studies millions of people in both developed and developing countries. with relative risks and 95% confidence intervals of coronary heart disease Although the rate of death attributable to the disease has declined or stroke for three or more categories of egg consumption. in developed countries in the past several decades, it is still the Results Eight articles with 17 reports (nine for coronary heart disease, leading cause of death and extorts a heavy social and economic eight for stroke) were eligible for inclusion in the meta-analysis (3 081 toll globally.1-3 In low and middle income countries, the
- 9. EFEITOS NO CURTOPRAZO INCREMENTO DE 100 MG/D DE COLESTEROL DIETÉTICO AUMENTOU: ü CT: 2.2 mg/dl ü C- HDL: 0.3 mg/dl 9 Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.
- 10. 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, 2003 Figure 26–6. Transport of cholesterol between the tissues in humans. (C, unesterified cholesterol; CE, cho-
- 11. LDL PEQUENAS EDENSAS ü > Entrada no espaço subendotelial ü Menos Vit E ü + Susceptível à oxidação ü Elevado TG/HDL-C é um bom preditor de sdLDL Griffin BA. Proc Nutr Soc 1999;58:163-69
- 12. 24, 25]. Othercholesterol-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) 12:377–383 which 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 had regarding 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 in that 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. These individuals considered hyper-responders to & a cholesterol Maria Luz Fernandez Mariana Calle studies suggest that dietary management of OIR individuals challenge 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 2010 Population Duration Additional dietary cholesterol LDL-C HDL-C LDL-C/HDL-C ratio LDL size HDL size Children (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) has Women (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 no Men (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 scientific Men/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 on Men/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 many Men/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 the Men/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
- 13. REDUZIR INGESTÃO DEGORDURA TOTAL DIMINUI RISCO DE DCV
- 15. 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 averaged within -10 to +20 per- to find the actual composition of the diets. No alcohol was in- tropolitan Life Insur- values from the 1983 TABLE 1 r chronic disease was Composition of HNS*27 Diets, Proximal Analysis a on was not an exclu- Low-fat diets High-fat diets cruited tended to have (% of total calories) e for men in this age Target Target nsumption, and evi- Measured value Measured value sionary. Macronutrient energy eers 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 10 heir 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
- 16. dicated an increasein 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 w DL 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 co nsated 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
- 17. misnomer. The countriesaround 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 oxidant is 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 (Table environmental 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 basin major 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 Sta placedecrease 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 Study ical 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 St terized 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 is 16.74:1, whereas during evolution aasdecrease inCrete, according to data compiled by the (n-6) to (n-3) fatty and1). trans fatty acids and low a death rate as (n-3) fatty status of intake; 3)ofathe dietary MediterraneanhealthDIETÉTICA:and © beforeusually IIforand G the patterns and basin United Nationsperin0022-3166/01 $3.00 2001yearbook for 1948. Nutritional Sciences. and th on. Although Greece acid the countries surroundingORDURA it was 2–1:1 (Table 1, Fig. their demographic It Recent investigations decrease in complex was 11.3–13.7 1000 inhabitants American Society considered to be area carbohydrates World War 37% E T fiber 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 DA NERGIA OTALas CONSUMIDA and 1946 –1948 many fruit and vegetable intake; and 5) a decrease in protein,Greece before 1960.Crete have been below this l United States anti- (14.0 –18.0 in Crete (19). The diet of Crete represents the traditional diet of The Seven Coun- 3065S 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. Guest it 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,
- 18. DIMINUIÇÃO DA GORDURA TOTALDE 35% PARA 32.3% Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.
- 19. dification Trial (CVD)prevention, butand some trials have linked diet needed. Context Multiple epidemiologic studies cation Trial disease diovascular long-term intervention data are with car- Linda Objective To test the hypothesis that a dietary intervention, intended to be low in Context Multiple epidemiologic some trials some trials have linked diet with risk. Context Multiple epidemiologic studies andstudies andhave linked diet with reduce CVD car- Hsia, MD; fat and high in vegetables, fruits, and grains to reduce cancer, wouldcar- . D; diovascular disease (CVD) prevention, but long-term intervention data are needed. are needed. diovascular disease (CVD) prevention, but long-term intervention data L. ; L. Design, Setting, and Participants Randomized controlled trial of 48 835 post- arcia D Objective To test the that a dietary intervention, intended to be low in Objective To test the hypothesishypothesis that a dietary intervention, intended to be low in menopausal women aged 50 tograins to reduce cancer, would reduce CVD risk. 79 years, of diverse backgrounds and ethnicities, who fat and highand high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk. s; H. fat in vegetables, fruits, and Lewis H. participated in the Women’s Health Initiative Dietary Modification Trial. Women were Croix, PhDDesign,Design, Setting, and Participants 541 [40%]) or of 48 835trial of 48 835 post- PhD; ; Setting, and Participants Randomized controlled trial an intervention (19 Randomized controlled post- randomly assigned to 50 to 79 years, of diverse backgrounds and ethnicities, whogroup (29 294 comparison L. menopausal women aged orman L. [60%]) menopausal women agedStudy79 years, of diverse backgrounds and ethnicities, who in in the Women’s Health 50 to Dietary Modification Trial. Women 1993 and 1998 in ; , MD; participateda free-living setting.InitiativeenrollmentDietary Modification were Women were participated in the Women’s Health Initiative occurred between Trial. s 40 US clinical centers;intervention (19 541 in this 541 [40%]) orgroup (29 294 group (29 294 randomly assigned to an mean follow-up [40%]) analysis was 8.1 years. or comparison L. Karen L. [60%]) in a free-living setting.to an intervention (19 between 1993 and 1998 in randomly assigned Study enrollment occurred comparison MD; D; , MD; InterventioninIntensive behavior Study enrollment group and individual sessions de- ysiw . 40 US clinical centers; mean follow-up in this analysis wasin occurred between 1993 and 1998 in [60%]) a free-living setting. modification 8.1 years. inda M. signed to reduce total fat intake tofollow-up calories and increase intakes of vegetables/ PhD; 40 US clinical centers; mean 20% of in this analysis was 8.1 years. 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 diet-related educationgrains to at intake servings/d. The comparison group received of vegetables/ fruits to 5 servings/d and materials. signed to reduce total fat least 6 to 20% of calories and increase intakes bins, G. ; Main Outcome Measures grains to at least 6 servings/d. The comparison group received fruits to 5 servings/d and nda MD diet-related education materials. E. Fatal and nonfatal coronary heart disease (CHD), fatal diet-related education materials. RISCO 0% 5% 10% 15% 20% 25% DAC Total DCV RELATIVO GloriaG. and nonfatal stroke, and CVD and nonfatal coronary heart disease (CHD), fatal Linda E. Main Outcome Measures Fatal (composite of CHD and stroke). PhD; ns, MD; ;Linda G.nonfatal stroke, and CVD (compositeFatal and nonfatal coronary heart disease (CHD), fatal z, PhD and Main Outcome Measures of CHD and stroke). Results By year 6, mean fat intakeintake decreased byenergy intake in the inter- in the inter- Resultsand nonfatal stroke, and CVD (composite of CHD and stroke). intake Stevens, PhD; By year 6, mean fat decreased by 8.2% of 8.2% of energy PH; ; ventionvs the comparison group, with small decreases in saturated (2.9%), monoun- DrPH aurizio vention Results By year 6, mean fatwith small decreases in saturated (2.9%), monoun- vs the comparison group, intake decreased by 8.2% of energy intake in the inter- se R. , ouise R. DrPH; tolins saturated (3.3%),the comparison group, withincreases occurred :in-intakes of veg-intakes of veg- saturated (3.3%), and polyunsaturated (1.5%) (1.5%) fat; increases occurred in and polyunsaturated fat; small decreases in saturated (2.9%), monoun- TRANS 22% D; vention vs ; 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 cholesterol saturated servings/d) polyunsaturated (1.5%) fat; increases occurred in intakes of veg- and and y R. MD; levels,diastolic blood pressure, and factor VIIc levels were+11% Low-density lipoprotein cholesterol enry R. ord,; levels, diastolic blood pressure, and factor VIIc levels were significantly reduced16% HORTALIÇAS/FRUTA: +30% CEREAIS: significantly reduced by FIBRA: + etables/fruits and 4.29%, respectively; levels of high-density lipoprotein cho- (1.1 servings/d) and grains (0.5 serving/d). 3.55 by 3.55 PhD mg/dL, 0.31 mm Hg, D; ; Henry mg/dL, levels, mm Hg,blood 4.29%, respectively; levels of high-density lipoprotein 3.55 hD R. 0.31 diastolic and pressure, and factor VIIc levels were significantly reduced by cho- lesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention unner, PhDlesterol,mg/dL, 0.31 mm numbers who developed CHD,significantly differ in the intervention ski, MD; ;vs comparison groups. The Hg, and 4.29%, respectively;stroke, of high-density lipoprotein cho- triglycerides, glucose, and insulin did not levels and CVD (annual- ,ette; ; vs comparison groups. 1000glucose, and JAMA.developed CHD, stroke, and CVD (annual- MD MD ized incidence rates) were The (0.63%), et al. insulin didand 1357 (0.86%)differ in the intervention lesterol, triglycerides, numbers who 2006 Feb 8;295(6):655-66 Howard BV, 434 (0.28%), not significantly in the in- hlebowski, ized incidence rates) were 1000 (0.63%), 434 (0.28%),CHD, 1357 (0.86%) in the in- D; MD; tervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. CVD (annual- vs comparison groups. The numbers who developed and stroke, and ranek, MD; The diet ized no significant effects on incidence of CHD434 (0.28%), and 0.97; 95% had incidence rates) were 1000 (0.63%), (hazard ratio [HR], 1357 (0.86%) in the in-
- 20. 50% 45% RISCO RELATIVO 40% EM MULHERES 35% QUE TINHAM DCV 30% 25% RISCO 0% 5% 10% 15% 20% 25% DAC Total DCV RELATIVO 20% 15% 10% 5% 0% DAC Total DCV Howard BV, etet al. JAMA. 2006 Feb 8;295(6):655-66 Howard BV, al. JAMA. 2006 Feb 8;295(6):655-66
- 21. 80 % Pessoas c/ Sd LDL 60 r = -0.95 P< 0.001 40 20 0 % Gordura 0 10 20 30 40 50 % CHO 75 65 55 45 35 Krauss RM. J Nutr 2001;131:340s-43s
- 22. ÁCIDOS GORDOS SATURADOS USDA,AHA: < 10% DO TOTAL CALÓRICO Dietary Guidelines for Americans, USDA, 2010
- 24. Δ de TC/HDL-C Δ de LDL-C Δ de HDL-C Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55
- 25. larger effect ofchanges in the amount and quality of dieta and carbohydrates on CAD risk (89), and the possible reaso this were discussed elsewhere (90, 91). Effects of fatty acids and carbohydrates on serum lipid lipoproteins Our results suggest that isoenergetic replacement of SFA carbohydrates does not improve the serum total:HDL chole All natural fats contain both SFAs, which do not change this and unsaturated fatty acids, which lower it. As a result, ev replacement of dairy fat and tropical fats with carbohydrate Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55 FIGURE 3. Predicted changes (⌬) in the ratio of serum total t
- 26. Based on Evolutionary,Historical, Dietary Fat Quality and Coronary Heart Global, and Modern ed Theory Disease Prevention: A Unifi Perspectives Christopher E.on Evolutionary, Historical, Based Ramsden, MD Global, and Modern Perspectives Keturah R. Faurot, PA, MPH Pedro ChristopherFaurot, PA, MPH Carrera-Bastos, MD Keturah R. E. Ramsden, BA Loren Pedro Carrera-Bastos, BA Cordain, PhD Loren Cordain, PhD Michel De De Lorgeril, MD, PhD PhD Michel Lorgeril, MD, Laurence S. Sperling, MD Laurence S. Sperling, MD Corresponding author Corresponding author Christopher E. Ramsden, MD Department of Physical Medicine and Rehabilitation, Program on Christopher E. Ramsden,University of North Carolina–Chapel Hill School Integrative Medicine, MD Department Medicine, CB# 7200, Chapel Hill, and Rehabilitation, Program on of of Physical Medicine NC 27599, USA. E-mail: cramsden@med.unc.edu Integrative Current Treatment Options in Cardiovascular Medicine 2009, 11:289–301Hill School Medicine, University of North Carolina–Chapel of Medicine, CB# 7200, Chapel Hill, NC 27599, USA. Current Medicine Group LLC ISSN 1092-8464 Copyright © 2009 by Current Medicine Group LLC E-mail: cramsden@med.unc.edu Current Treatmentstatement in Cardiovascular Medicine 2009, 11:289–301 Opinion Options Current Medicine and growing body of evidence indicates that dietary fatty acids regulate A large Group LLC ISSN 1092-8464 Copyright © 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 shortcomings Opinion 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
- 27. CHINA RURAL: <5% EUA: 11-12% CRS: 4-18% KITAVA: 17% MAASAI: 30-35% TOKELAU: 40%
- 29. Ameta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD
- 30. AUMENTO DO RÁCIOPUFA/SAFA EM 100% DIMINUIÇÃO DA GORDURA TOTAL DE 35% PARA 32.3% Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.
- 31. Orange Juice onInflammation, Endoto C l li in i icca l l C a rree//EEd uucca t t i o n / N u t r i t oo Expression e of cToll-Like Recept C n a Ca d a andu the nn / P s y c h o s o c aa l R R s s e a r h h ion/N tritii /Psychosoci i l e ear c O R I I G I I N A LL O R G N A and Suppressor of Cytokine Signaling- A R TT I I CC L L EE A R RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD vital to the protection fro Differential Effects of Cream, Glucose, and Differential Effects of Cream, Glucose, andHUSAM GHANIM, PHD JAY FRIEDMAN, PHD PRABHAKAR VISWANATHAN, PHD AJAY CHAUDHURI, MD ins and immunological commensal and patho Orange Juice on Inflammation, Endotoxin, Orange Juice on Inflammation, Endotoxin, SANAA ABUAYSHEH, BSC PARESH DANDONA, MD, PHD bacteria. CHANG LING SIA, BSC In this context, we w which macronutrient wa and the Expression of Toll-Like Receptor-4 and the Expression of Toll-Like Receptor-4 the induction of oxidati OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on the one h and Suppressor of Cytokine Signaling-3 and Suppressor of Cytokine Signaling-3 induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the crease in LPS concent expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated expression of TLR-4 and fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and tokine signaling (SOCS) RUPALI DEOPURKAR, ,PHD RUPALI DEOPURKAR PHD PPRIYA induce an , MD in LPS, TLR-4, and SOCS3. toto the protection from To elucidate this, we inv inflammation, alsoMOHANTYMD RIYA MOHANTY, increase vital the protection from bacterial tox- vital bacterial tox- HUSAM GHANIM, ,PHD HUSAM GHANIM PHD PPRABHAKAR VISWANATHANPHD RABHAKAR VISWANATHAN, , PHD ins and immunological responses glucose, fect ofto the the most ins and immunological responses to the JJAYFRIEDMAN, ,PHD AY FRIEDMAN PHD RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- hydrate, cream, a sat AAJAY CHAUDHURIMD JAY CHAUDHURI, , MD commensal and pathogenic intestinal commensal and pathogenic intestinal SANAA ABUAYSHEH, ,BSC SANAA ABUAYSHEH BSC calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood orange juice, a carbohy PPARESH DANDONAMD, PHD ARESH DANDONA, , MD, PHD bacteria. CHANG LING SSIA,BSC bacteria. food product, which do CHANG LING IA, BSC samples were obtained at 0, 1, 3, and 5 h for analysis. InIn this context, we wanted to analyzestress or in this context, we wanted to analyze ther oxidative which macronutrient was responsible for is a protein RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, andwas responsible for which macronutrient the SOCS3 the induction ofof in MNCs, stress and in- expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 oxidative the induction oxidative stress and in- shown to interfere with i OBJECTIVE — We have recently shown thatsignificantly high-carbohydrate (HFHC) meal TLR-4 expressionon the one LPS signal transduction (2– OBJECTIVE — We have recently shown thata ahigh-fat after glucose and cream intake, but flammation, and plasma hand, and the in- increased high-fat high-carbohydrate (HFHC) meal flammation, on the one hand, and the in- induces an increase in plasma concentrations of endotoxin (lipopolysaccharide intake. The intake of orangein LPS water did not work has shown that SO concentrations increased only after cream [LPS]) and the induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the crease juice LPS concentrations and the expression of Toll-like receptor-4 (TLR-4) andany change inof cytokineindexes measured. crease in or concentrations and the induce suppresser of of the signaling-3 (SOCS3) in expression of Toll-like receptor-4 (TLR-4) and suppresser anycytokine signaling-3 (SOCS3) in expression of TLR-4 and suppresser of cy- mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated expression of TLR-4 and suppressercirculating mo mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated tokine signaling (SOCS)-3 on the other. obese hu in the of cy- (MNCs) of the fat and carbohydrates, components of the HFHC meal, known toto induce oxidative stress and tokine signalingand an in- on the other. fat and carbohydrates, components of CONCLUSIONSknown induce oxidative stress and induce NF-B binding (SOCS)-3 increased when compar the HFHC meal, — Although both glucose and cream To elucidate this, we investigated the ef- inflammation, also induce an increase in LPS, the expression of SOCS3, TNF-␣, and IL-1 in MNCs, onlyelucidate this, increase normalthe ef- inflammation, also induce an increase in LPS, inTLR-4, and SOCS3. crease TLR-4, and SOCS3. To cream caused an we investigated subjects fectorange juice or watermost important carbo- (6). I in LPS concentration and TLR-4 expression. Equicaloric amounts of ofof glucose, the did not work carbo- fect glucose, the most important demonstrated that hydrate, cream, a a saturated fat, and hydrate, cream, saturated fat, and RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300-are relevant to the pathogenesis of sion in MNCs is inverse induce a change in any of these indexes. These changes RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- orange juice, a carbohydrate-containing calorie drinks of either glucose, saturatedatherosclerosisorange juice,resistance. water to ingest. Blood orange juice, a carbohydrate-containing fat as cream, and insulin or only water to ingest. Blood calorie drinks of either glucose, saturated fat as cream, orange juice, or only tyrosine phosphorylatio samples were obtained at 0, 1, 3, and 55 h for analysis. samples were obtained at 0, 1, 3, and h for analysis. food product, which does not induce and directly rel product, which does receptor ei- foodCare 33:991–997, 2010 not induce ei- Diabetes ther oxidative stress oror inflammation. ther oxidative stress inflammation.insulin resistance (home O SOCS3 is is a protein that has been RESULTS — Indexes of inflammation including nuclear factor-Bshown thatbinding, and the because the content of LPS sessment of a protein that has been insulin res ur recent work has (NF-B) binding, and the shown to interfere with insulin and leptin RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) a great interest SOCS3 expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 ininthese meals is not to interfere with insulin and leptin MNCs, IR]), consistent with expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs, shown significantly differ- high-fat high-cholesterol (HFHC) increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS signal transduction (2–5). Our recent of insulin r increased significantly after glucose and cream intake, butoxidative and inflam- plasma LPS signal transduction (2–5). Our recent pathogenesis meal induces TLR-4 expression and ent, and, thus, it would appear that the concentrations increased only after cream intake. The intake ofof orange juice or water did not work has shown that SOCS3 resistance in human obe concentrations increased only after cream intake. The intake orange juice oran inflammatory work has shownmay lead water did not expression matory stress in addition to inducing nature of the meal that SOCS3 expression induce any change in any of the indexes measured. inability of leptin to ca
- 32. (R01-D Differential Effects of Cream, Gluco the Am Orange Juice on Inflammation,The da End and we and the Expression of Toll-Likepretatio Rec and Suppressor of Cytokine Signal investig vestiga RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD vitalfor the to the pro HUSAM GHANIM, PHD PRABHAKAR VISWANATHAN, PHD ins and immu JAY FRIEDMAN, PHD AJAY CHAUDHURI, MD commensal p No a SANAA ABUAYSHEH, BSC PARESH DANDONA, MD, PHD bacteria. art this CHANG LING SIA, BSC In this con Nata which macron the induction OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the Referen crease in LPS expressionGh 1. of T expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and tokine signalin nie inflammation, also induce an increase in LPS, TLR-4, and SOCS3. To elucidate th JM fect of glucose, RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- tox hydrate, crea calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood orange juice, samples were obtained at 0, 1, 3, and 5 h for analysis. Sumo de of food product, Laranja cyt ther oxidative RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, and the SOCS3 is expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs, fol shown to inter increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS me signal transdu concentrations increased only after cream intake. The intake of orange juice or water did not work has show induce any change in any of the indexes measured. Dia in the circul (MNCs) ofRu 2. the CONCLUSIONS — Although both glucose and cream induce NF-B binding and an in- increased whe crease in the expression of SOCS3, TNF-␣, and IL-1 in MNCs, only cream caused an increase normal subje Wh in LPS concentration and TLR-4 expression. Equicaloric amounts of orange juice or water did not work demonstsul induce a change in any of these indexes. These changes are relevant to the pathogenesis of sion in MNCs atherosclerosis and insulin resistance. deg Figure 3—Change in NFB binding activity in MNC (A) and plasma endotoxin concentrations tyrosine phosp Diabetes Care juice (OJ, ‚), Ch receptor and d (B) in normal subjects after a 300-calorie drink of cream (E), glucose (Œ), orange 33:991–997, 2010 3. Sen insulin resistan and ؉, P Ͻ 0.05 with a great interest because the content of LPS or water (F). Data are means Ϯ SEM. *ur recent work has shown thatRMANOVA comparing changes in sessment of in TA IR]), consiste relation to baseline after cream and glucose challenges; # andin $, P meals 0.05 significantly differ- high-fat high-cholesterol (HFHC) these Ͻ is not with two-way
- 33.
- 34. LPS • Citoquinas • Enzimas • Moléculas de adesão TLR IkB Cinase P
- 35. Macronutrients, oxidative stress,and inflammation Differential Effects of Cream, Gluco Orange Juice on Inflammation, Endcytok and the Expression of Toll-Like Rec know and Suppressor of Cytokine Signal anim RUPALI DEOPURKAR, PHD PRIYA MOHANTY, MD but vital to the pro HUSAM GHANIM, PHD JAY FRIEDMAN, PHD PRABHAKAR VISWANATHAN, PHD AJAY CHAUDHURI, MD creas ins and immu commensal a SANAA ABUAYSHEH, BSC CHANG LING SIA, BSC PARESH DANDONA, MD, PHD and bacteria. In this con creas which macron Nata SOC the induction OBJECTIVE — We have recently shown that a high-fat high-carbohydrate (HFHC) meal flammation, on induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in of in crease in LPS Glucose expression of T mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and juice tokine signalin inflammation, also induce an increase in LPS, TLR-4, and SOCS3. stres To elucidate th fect of glucose, RESEARCH DESIGN AND METHODS — Fasting normal subjects were given 300- Sumo de an in hydrate, crea orange juice, calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood samples were obtained at 0, 1, 3, and 5 h for analysis. Laranja food product, ther oxidative RESULTS — Indexes of inflammation including nuclear factor-B (NF-B) binding, and the SOCS3 is expression of SOCS3, tumor necrosis factor-␣ (TNF-␣), and interleukin (IL)-1 in MNCs, Ackn shown to inter increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS signal transdu concentrations increased only after cream intake. The intake of orange juice or water did not porte work has show induce any change in any of the indexes measured. Flori in the circul (MNCs) of the CONCLUSIONS — Although both glucose and cream induce NF-B binding and an in- supp increased whe crease in the expression of SOCS3, TNF-␣, and IL-1 in MNCs, only cream caused an increase in LPS concentration and TLR-4 expression. Equicaloric amounts of orange juice or water did not (R01 normal subje work demonst induce a change in any of these indexes. These changes are relevant to the pathogenesis of atherosclerosis and insulin resistance. the A sion in MNCs tyrosine phosp The receptor and d Diabetes Care 33:991–997, 2010 and w insulin resistan sessment of in ur recent work has shown that a great interest because the content of LPS preta IR]), consiste high-fat high-cholesterol (HFHC) in these meals is not significantly differ-
- 36. Lipids (2008) 43:65–77 DOI 10.1007/s11745-007-3132-7 ARTICLE Comparison of Low Fat and Low Carbohydrate Diets on Circulating Fatty Acid Composition and Markers of Inflammation Cassandra E. Forsythe Æ Stephen D. Phinney Æ Maria Luz Fernandez Æ 40 H e M c/ IMC> 25 Erin E. Quann Æ Richard J. Wood Æ Doug M. Bibus Æ William J. Kraemer Æ Richard D. Feinman Æ Jeff S. Volek RCT de 12 semanas: Received: 5 July 2007 / Revised: 24 October 2007 / Accepted: 25 October 2007 / Published online: 29 November 2007 Ó AOCS 2007 Dieta Very Low Carb - Dieta Prudente - Abstract Abnormal distribution of plasma fatty acids and and 16:1n-7 were consistently decreased following the increased inflammation are prominent features of meta- VLCKD. Both diets significantly decreased the concen- bolic syndrome. We tested whether these components of tration of several serum inflammatory markers, but there 1504 kcal: metabolic syndrome, like dyslipidemia and glycemia, are responsive to carbohydrate restriction. Overweight men and women with atherogenic dyslipidemia consumed 1478 kcal: was an overall greater anti-inflammatory effect associated with the VLCKD, as evidenced by greater decreases in TNF-a, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1. ad libitum diets very low in carbohydrate (VLCKD) Increased 20:4n-6 and the ratios of 20:4n-6/20:5n-3 and ¤ %CHO = 12 (1504 kcal:%CHO:fat:protein = 12:59:28) or low in fat (LFD) (1478 kcal:%CHO:fat:protein = 56:24:20) for ¤ %CHO = 56 n-6/n-3 are commonly viewed as pro-inflammatory, but unexpectedly were consistently inversely associated with ¤ % Lípidos = 59 12 weeks. In comparison to the LFD, the VLCKD resulted in an increased proportion of serum total n-6 PUFA, mainly ¤ % Lípidos = 24 responses in inflammatory proteins. In summary, a very low carbohydrate diet resulted in profound alterations in attributed to a marked increase in arachidonate (20:4n-6), fatty acid composition and reduced inflammation compared while its biosynthetic metabolic intermediates were to a low fat diet. decreased. The n-6/n-3 and arachidonic/eicosapentaenoic acid ratio also increased sharply. Total saturated fatty acids Keywords Arachidonic acid Á Palmitoleic acid Á 36,4 g de SAFA 11,7 g de SAFA Ketogenic diet Á Saturated fat Á Metabolic syndrome Abbreviations VLCKD Very low carbohydrate ketogenic diet C. E. Forsythe Á E. E. Quann Á W. J. Kraemer Á J. S. Volek (&) LFD Low fat diet Department of Kinesiology, University of Connecticut, 2095 Hillside Road, Unit 1110, Storrs, CT 06269-1110, USA PL Phospholipid e-mail: jeff.volek@uconn.edu CE Cholesteryl ester CVD Cardiovascular disease S. D. Phinney
- 37. ÁCIDOS GORDOS NOSÉSTERES DE COLESTEROL 14 12 10 8 Low Carb 6 Prudente 4 2 0 14:O 16:O Total SAFA mg/dl
- 38. Mensink RP, ZockPL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55
- 39. See corresponding editorialon page 1541. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index1–3 Marianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjønneland, Erik B Schmidt, and Kim Overvad ABSTRACT concentration is tightly regulated by homeostatic regulatory Background: 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 homeostatic er 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, 2010 polyunsaturated fatty acids is associated with a lower risk of ische- concentration and a high insulin-to-glucagon ratio, followed by mic 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 may Objectives: 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 myocardial intake 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. Carbohydrates Design: Our prospective cohort study included 53,644 women and with different GI values were investigated. Furthermore, potential men free of MI at baseline. effect modification by sex was investigated because of differences Results: 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 SFAs and risk of MI [hazard ratio (HR) for MI per 5% increment of SUBJECTS AND METHODS energy intake from carbohydrates: 0.88; 95% CI: 0.72, 1.07). In contrast, there was a statistically significant positive association Study population between substitution of carbohydrates with high-GI values for SFAs Between December 1993 and May 1997, 160,725 women and and 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 prospective association for carbohydrates with medium-GI values (HR: 0.98; cohort study Diet, Cancer, and Health. The criteria for invitation 95% CI: 0.80, 1.21). No effect modification by sex was observed. were as follows: age between 50 and 64 y, born in Denmark, and Conclusion: This study suggests that replacing SFAs with carbohy- no previous cancer diagnosis registered in the Danish Cancer drates with low-GI values is associated with a lower risk of MI, Registry. All persons fulfilling these criteria and living in the whereas 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
- 40. 0.80, 1.21) (Table3). As assessed from the 95% CIs, the Lund University Libraries on November 5, 2010 measures of associations for extreme tertiles of GI were statis- the measures of associations, and thus residual confounding seems tically significantly different. The P value for effect modification unlikely. However, confounding from other IHD risk factors not See corresponding editorial on page 1541. by tertiles of dietary GI was 0.06 in women, 0.29 in men, and taken into account remains a possible explanation for the observed 0.16 in all participants. The P value for effect modification by associations. Intake of carbohydrates compared with intake of saturated fatty acids sex was 0.86. Only 2 epidemiologic studies have investigated the sub- 1–3 stitution of carbohydrates for SFAs (1, 18). In the prospective and risk of myocardial infarction: importance of the glycemic index cohort study by Hu et al (18), substitution of carbohydrates for DISCUSSION SFAs was nonsignificantly associated with a lower risk of IHD, Marianne U Jakobsen, Claus Dethlefsen, Albert M Joensen, Jakob Stegger, Anne Tjønneland, Erik B Schmidt, The findings from this study suggest that the effect of sub- whereas in the prospective cohort study by Jakobsen et al (1), in and Kim Overvad stitution of carbohydrates for SFAs varies depending on the type of which data from 11 American and European cohort studies were carbohydrates. There was a nonsignificant inverse association pooled, substitution of carbohydrates for SFAs was modestly ABSTRACT concentration is tightly regulated by homeostatic regulatory Background: Studies have suggested that replacing saturated fatty TABLE 3 systems, but the rapid absorption of carbohydrates after con- acids (SFAs) (HRs)carbohydrates is modestly associated with a high- intake from carbohydrates withmeal challenges these homeostatic or Hazard ratios with for myocardial infarction per 5% increment of energy sumption of a high-GI low–glycemic index (low-GI), medium-GI, high-GI values and a concomitant lower energy intake from SFAs with acids1 er risk of ischemic heart disease, whereas replacing saturated fatty mechanisms (4). A high-GI meal results in a high blood glucose Downloaded from www.ajcn.org at Lund University Libraries on November 5, 20 polyunsaturated fatty acids is associated with a lower risk of ische- concentration and a high insulin-to-glucagon ratio, followed by All participants mic heart disease. The effect of carbohydrates, however, may de- Women Men hypoglycemia, counterregulatory hormone secretion, and ele- pend on the type consumed. vated plasma free fatty acid concentration (4). These events may Tertiles of Median dietary GI Median dietary GI Median dietary GI Objectives: By using substitution models, we aimed to investigate 2 affect the range)of HR (95% CI) promoting dyslipidemia, (95% CI) risk IHD through (80% central range) HR in- dietary GI (80% central range) HR (95% CI) (80% central the risk of myocardial infarction (MI) associated with a higher en- flammation, and endothelial dysfunction (4). Carbohydratesfrom low-GI ergy intake with carbohydrates and a concomitant lower energy 82 (77, 85) 0.88 (0.72, 1.07) 80 (75, 82) this study was to investigate (79, risk of myocardial 1.04) The aim of 1.17 (0.80, 1.71) 84 the 86) 0.83 (0.65, intake from SFAs. Carbohydrates with different glycemic index values (first tertile) infarction (MI) with a higher energy intake from carbohydrates Carbohydrates withalso investigated. 88 (86, 90) (GI) values were medium-GI 0.98 (0.80, 1.21) and a (84, 87) 85 concomitant lower energy intake from SFAs. Carbohydrates 1.38) 0.80 (0.54, 1.18) 89 (87, 91) 1.08 (0.84, Design: (second tertile) cohort study included 53,644 women and values Our prospective with different GI values were investigated. Furthermore, potential CarbohydratesMI at high-GI men free of with baseline. 93 (91, 98) 1.33 (1.08, 1.64) effect(88, 96) 91 modification1.10sex was investigated because of differences 1.71) by (0.75, 1.63) 94 (92, 98) 1.34 (1.04, Results:(third tertile) values During a median of 12 y of follow-up, 1943 incident MI in the underlying biology such as hormonal differences. cases All models There was a nonsignificant inverse association be- 1 occurred. included intake of glycemic carbohydrates, proteins, monounsaturated fatty acids, and polyunsaturated fatty acids expressed as percentages of total substitution total energy intake (kcal/d), an values variable for tween energy intake,of carbohydrates with low-GIindicator for SFAs alcohol consumption (0 and .0 g/d), alcohol consumption (g/d), BMI (in kg/m2; ,25, risk of and 30), education (HR) 8–10,MI per 5% increment of (never, former, and currently smoking 1–14, 15–24, or 25 g tobacco/d), physical and 25–29, MI [hazard ratio (,8, for and .10 y), smoking status SUBJECTS AND METHODS activity (,3.5 and 3.5 h/wk), and history of95% CI: 0.72, 1.07). and do not know). HRs with 95% CIs for the incidence of myocardial infarction were energy intake from carbohydrates: 0.88; hypertension (yes, no, In contrast, there was a statistically significant positive association Study population calculated by using Cox proportional hazards regression with age as the time metric. In analyses among all participants, sex was entered into the model. 2 between substitution ofGI were based on the high-GI values for SFAsamong cases. n = December 1993 and Mayfor all participantswomen andsecond, Tertiles of dietary carbohydrates with distribution of dietary GI Between 22,144, 17,000, and 14,400 1997, 160,725 in the first, and third tertiles of(HR: 1.33; respectively; n = 9594, 10,202, and 8699 for women in the first, second, and third tertiles in dietary GI, respectively; and n = and risk of MI dietary GI, 95% CI: 1.08, 1.64). There was no men were invited by mail to participate of the Danish prospective 8941, 8127, and 8081 for men in withfirst, second, and third (HR: 0.98; association for carbohydrates the medium-GI values tertiles of dietary GI, respectively. Cancer, and Health. The criteria for invitation cohort study Diet, 95% CI: 0.80, 1.21). No effect modification by sex was observed. were as follows: age between 50 and 64 y, born in Denmark, and Conclusion: This study suggests that replacing SFAs with carbohy- no previous cancer diagnosis registered in the Danish Cancer drates with low-GI values is associated with a lower risk of MI, Registry. All persons fulfilling these criteria and living in the whereas 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-
- 41. with dietary intakecannot 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). tion Glycemic 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- der analysis 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 th Alan 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 processed ABSTRACT 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 component Background: 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 insulin prolonged 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 food Objective: 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)ences GI, 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 ratio1 Design: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 1 risk. 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, cardiovascular tools 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 been in 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 U random-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 molo Results: 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) 0.204 incident 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). 0.282 est 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, whereas typediseases (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 that 1.00,11.56),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 disease GL 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 positive ciated with a reduced risk of certain chronic diseases. In diabetes and studies (40, 41) reported an association with eye disease, whereas INTRODUCTION heart 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
- 42. • 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
- 43. ÍNDICE GLICÉMICO ECARGA GLICÉMICA Alimento IG Dose Hidratos CG Carbono Pão branco 70 60 grs 30 grs 21 Baguete francesa 62 70 grs 42 grs 26 Pão centeio 50 60 grs 24 grs 12 Cheerios 74 30 grs 20 grs 15 Chocapic 84 30 grs 25 grs 21 CornFlakes 92 30 grs 26 grs 24 Golden Grahams 71 30 grs 25 grs 18 Special K 84 30 grs 24 grs 20 Bran Flakes 74 30 grs 16 grs 13 Cream Crackers 65 25 grs 17 grs 11 Alpen 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.
- 44. ÍNDICE GLICÉMICO ECARGA GLICÉMICA Alimento IG Dose HC CG Arroz branco Uncle Ben’s 10 min 68 150 grs 37 grs 25 Arroz branco 56 150 grs 41 grs 23 Arroz branco Basmati 58 150 grs 38 grs 22 Arroz integral 55 150 grs 33 grs 18 Esparguete de milho 78 180 grs 42 grs 32 Fettucine com ovo 40 180 grs 46 grs 18 Gnocchi 68 180 grs 48 grs 33 Linguini 46 180 grs 48 grs 22 Macarroni 47 180 grs 48 grs 23 Ravioli 40 180 grs 42 grs 32 Spaghetti, cozido 5 min 38 180 grs 48 grs 18 Spaghetti, cozido 20 min 61 180 grs 44 grs 27 Esparguete 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.
- 45.
- 46. dex diet thanin the high–cereal fiber did not alter Mitchell, BASc, RD the as- been associa Sandy the significance of Results n 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
- 47. dex diet thanin 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, HbA 0 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 tein DL-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 T ach 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) 40.0 n. 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
- 48. 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 Subjects TABLE 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 Abstract n 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, 2011 BMI, 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 0.046 Fasting 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 products Fasting 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 3 Insulin 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 body Total 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 3.0 HDL 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 0.15 LDL 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 milled TG 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 affect Free 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 0.99 Systolic 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 habits g-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 0.10 CRP, 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 Introduction IL-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 0.79 PAI-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 betweenutr. whole-grainwhole- stress are both adjusted for changes in BMI. Differences within such as exerci (11,18,19). The scientific evidence is considered 37: 1401–1407, 2007. chronic diseases (20,21). Insulin resistance and oxidative J. N the 1 sufficient to permit risk of 2 on human health (1). An inverse, relatively strong correlation of other lifestyle factors health claims regarding the cardio-protective effect of and refined-grain diet 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 carryover effect was found). tially be affected by whole-grain intake. Induction of lipid per-
- 49. chroni chroni wheat large c Effect of Wheat Bran on Glycemic Control wheatc large o ment wheat sociati and Risk Factors for Cardiovascular OBJECTIVE — Cohort studies indicate that cereal fiber reduces the risk of diabetes and ment o ment o coronary heart — Cohort studies indicate Diabetesthe effect of the risk of diabetes and OBJECTIVE disease (CHD).Type 2 we assessedfiber reduces wheat bran on glycemic Disease in Therefore, that cereal either sociatio OBJECTIVE — 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 much coronary 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 HILIP T 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 METHODS control 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 , , OROTHEA AULKNER RD DWARD IDGEN BSC 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 AWRENCE G. J OBERT A. L , , 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 source RESEARCH 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 studies crossoveradditionalthe 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 disease cereal 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 test weight, 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. C acid, 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 absorp LDL 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 cemic 0.034). 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 redu CONCLUSIONS — 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 s mic 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 thereb required 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 Canada; the 2Department of Medicine, Division of Endocrinology and Metabolism, St. Michael’s Hospital, Furthermore, it is fiber in lifestyle. a marker for another component of whole grains that impartsstudies to be associated with a re- or a healthy Toronto, Toronto, Ontario, Canada; the 4Department of Medicine, Faculty of Medicine, University of than viscous fiber, that for more than two Toronto, Ontario, Canada; the 3Department of Nutritional Sciences, 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 Diabetic lifestyle. ¨ 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 tario, Canada; the 8Department of Hematology, St. Michael’s Hospital, Toronto, Ontario, Canada; the 9 These effects are seen despite the fact that 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
- 50. AUMENTO DA INGESTÃODE FIBRA A PARTIR DE CEREAIS INTEGRAIS DE 9 PARA 17 GRAMAS AUMENTO NÃO SIGNIFICATIVO DO RISCO RELATIVO EM 18% Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.
- 51.
- 52. Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-‐55
- 53. The n e w e ng l a n d j o u r na l of m e dic i n e original article N Engl J Med 2013. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet Ramón Estruch, M.D., Ph.D., Emilio Ros, M.D., Ph.D., Jordi Salas-Salvadó, M.D., Ph.D., Maria-Isabel Covas, D.Pharm., Ph.D., Dolores Corella, D.Pharm., Ph.D., Fernando Arós, M.D., Ph.D., Enrique Gómez-Gracia, M.D., Ph.D., Valentina Ruiz-Gutiérrez, Ph.D., Miquel Fiol, M.D., Ph.D., José Lapetra, M.D., Ph.D., Rosa Maria Lamuela-Raventos, D.Pharm., Ph.D., Lluís Serra-Majem, M.D., Ph.D., Xavier Pintó, M.D., Ph.D., Josep Basora, M.D., Ph.D., Miguel Angel Muñoz, M.D., Ph.D., José V. Sorlí, M.D., Ph.D., José Alfredo Martínez, D.Pharm, M.D., Ph.D., and Miguel Angel Martínez-González, M.D., Ph.D., for the PREDIMED Study Investigators* A bs t r ac t
- 54. The n e w e ng l a n d j o u r na l of m e dic i n e original article N Engl J Med 2013. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet ü 7447 Estruch, M.D., (55-80 años) y M (60-80 años) sem DCV, mas com Ramón Pacientes H Ph.D., Emilio Ros, M.D., Ph.D., Jordi Salas-Salvadó, M.D., Ph.D., risco cardiovascular D.Pharm., Ph.D., Dolores Corella,dos siguintes Maria-Isabel Covas, aumentado (Diabetes T2 ou 3 D.Pharm., Ph.D., factores: tabaco, HTA, LDL-C aumentado, HDL-C baixo,M.D., Ph.D., peso, Fernando Arós, M.D., Ph.D., Enrique Gómez-Gracia, excesso de Valentina Ruiz-Gutiérrez, Ph.D., Miquel Fiol, M.D., Ph.D., José Lapetra, M.D., Ph.D., história familiar de doença cardíaca coronária prematura) ü 3 dietas: Lamuela-Raventos, D.Pharm., Ph.D., Lluís Serra-Majem, M.D., Ph.D., Rosa Maria Xavier Pintó, M.D., Ph.D., Josep Basora, M.D., Ph.D., Miguel Angel Muñoz, M.D., Ph.D., 1) Dieta c/ restrição Ph.D., José Alfredo Martínez, D.Pharm, M.D., Ph.D., and José V. Sorlí, M.D., de gordura 2) Dieta Med c/ 1L de azeite /semana for the PREDIMED Study Investigators* Miguel Angel Martínez-González, M.D., Ph.D., 3) Dieta Med c/ 30g de frutos secos/día (15g de nozes+7,5g de avelãs + 7,5g de amêndoas) A bs t r ac t
- 55. The n e w e ng l a n d j o u r na l of m e dic i n e 30% A Primary End Point (acute myocardial infarction, stroke, or death from cardiovascular causes) 1.0 Control diet Med diet, EVOO: hazard ratio, 0.70 0.06 Incidence of Composite Cardiovascular (95% CI, 0.53–0.91); P=0.009 Med diet, nuts: hazard ratio, 0.70 0.05 Med diet, nuts 0.8 (95% CI, 0.53–0.94); P=0.02 0.04 0.03 0.6 Med diet, EVOO End Point 0.02 0.4 0.01 0.00 0 1 2 3 4 5 0.2 0.0 0 1 2 3 4 5 Years No. at Risk Control diet 2450 2268 2020 1583 1268 946 Med diet, EVOO 2543 2486 2320 1987 1687 1310 Med diet, nuts 2454 2343 2093 1657 1389 1031 B Total Mortality N Engl J Med 2013. 1.0 0.07 Med diet, EVOO: hazard ratio, 0.81 Med diet, nuts
- 56. Mediterr anean Dietand Cardiovascular Events the use of a separate 9-item dietary screener Table 1. Summary of Dietary Recommendations to Participants in the (Table S3 in the Supplementary Appendix). Mediterranean-Diet Groups and the Control-Diet Group. A general medical questionnaire, a 137-item validated food-frequency questionnaire,15 and Food Goal the Minnesota Leisure-Time Physical Activity Mediterranean diet Questionnaire were administered on a yearly Recommended basis.10 Information from the food-frequency Olive oil* ≥4 tbsp/day questionnaire was used to calculate intake of Tree nuts and peanuts† ≥3 servings/wk energy and nutrients. Weight, height, and waist Fresh fruits ≥3 servings/day circumference were directly measured.16 Bio- Vegetables ≥2 servings/day markers of compliance, including urinary hy- Fish (especially fatty fish), seafood ≥3 servings/wk droxytyrosol levels (to confirm compliance in the group receiving extra-virgin olive oil) and Legumes ≥3 servings/wk plasma alpha-linolenic acid levels (to confirm Sofrito‡ ≥2 servings/wk compliance in the group receiving mixed nuts), White meat Instead of red meat were measured in random subsamples of par- Wine with meals (optionally, only for habitual ≥7 glasses/wk ticipants at 1, 3, and 5 years (see the Supplemen- drinkers) tary Appendix). Discouraged Soda drinks 1 drink/day End Points Commercial bakery goods, sweets, and pastries§ 3 servings/wk The primary end point was a composite of myo- Spread fats 1 serving/day cardial infarction, stroke, and death from cardio- Red and processed meats 1 serving/day vascular causes. Secondary end points were Low-fat diet (control) stroke, myocardial infarction, death from cardio- Recommended vascular causes, and death from any cause. We used four sources of information to identify end Low-fat dairy products ≥3 servings/day points: repeated contacts with participants, con- Bread, potatoes, pasta, rice ≥3 servings/day tacts with family physicians, a yearly review of Fresh fruits ≥3 servings/day medical records, and consultation of the Nation- Vegetables ≥2 servings/wk al Death Index. All medical records related to Lean fish and seafood ≥3 servings/wk end points were examined by the end-point adju- Discouraged dication committee, whose members were un- Vegetable oils (including olive oil) ≤2 tbsp/day aware of the study-group assignments. Only end Commercial bakery goods, sweets, and pastries§ ≤1 serving/wk points that were confirmed by the adjudication Nuts and fried snacks ≤1 serving /wk committee and that occurred between October 1, 2003, and December 1, 2010, were included in Red and processed fatty meats ≤1 serving/wk the analyses. The criteria for adjudicating pri- Visible fat in meats and soups¶ Always remove mary and secondary end points are detailed in Fatty fish, seafood canned in oil ≤1 serving/wk the Supplementary Appendix. Spread fats ≤1 serving/wk Sofrito‡ ≤2 servings/wk Statistical Analysis We initially estimated that a sample of 9000 par- * The amount of olive oil includes oil used for cooking and salads and oil con- N Engl J Med 2013. sumed in meals eaten outside the home. In the group assigned to the Medi- ticipants would be required to provide statistical terranean diet with extra-virgin olive oil, the goal was to consume 50 g (ap- power of 80% to detect a relative risk reduction proximately 4 tbsp) or more per day of the polyphenol-rich olive oil supplied, of 20% in each Mediterranean-diet group versus instead of the ordinary refined variety, which is low in polyphenols.
- 57. INFLAMAÇÃO E DCV! CRP LDL Ridker PM et al. N Engl J Med 2002;347:1557-65. 2,5 2 1,5 1 0,5 0 1 2 3 4 5 Quintis de Risco Relativo para todos os Acidentes Cardiovasculares! 58
- 58. ac sa in ha op pa na co si R (C tio in th fo FIGURE 2. Diagrammatic representation of the movement of leukocytes through the endothelium and the subsequent generation of inflammatory an mediators. Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S) an
- 59. De Caterina R.N Engl J Med 2011
- 61. EPA/DHA E AA CalderPC. Am J Clin Nutr 2006;83(suppl):1505S–19S.
- 62. Time course relativoà incorporação de EPA e DHA INCORPORAÇÃO DE EPA E DHA NOS em fosfolipídios de membrana de células mononucleares FOSFOLÍPIDOS DE CÉLULAS MONONUCLEARES DHA in mononuclear cell PL (%) EPA in mononuclear cell PL (%) 4 4 3 3 2 1 2 0 1 0 4 8 12 20 0 4 8 12 20 Time (weeks) Time (weeks) Indivíduos saudáveis: 2,1 g EPA + 1,1 g DHA/dia/12 semanas Eur. J. Clin. Invest. 30, 260-‐274, 2000 Eur. J. Clin. Invest. 30, 260-274, 2000
- 63. DHA Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
- 64. DHA Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
- 65. De Caterina R.N Engl J Med 2011
- 66. 67 Gilroy DW. 2010
- 67. Serhan, CN. Annu.Rev. Immunol. 2007. 25:101–37
- 68. EPA DHA Calder PC. Biochimie. 2009 Feb 3. [Epub ahead of print]
- 69. 0.86; 9 added double Figure 3. Schema of Potential Dose Responses and Time Courses for Altering Clinical Events forme of Physiologic Effects of Fish or Fish Oil Intake reduce relativ TYPICAL DIETARY TYPICAL SUPPLEMENTAL Clinical Effect Time Course To DOSES DOSES Alter Clinical Events P = .04 Antiarrhythmia Weeks pared tality— Relative Strength of Effect analys relativ 0.92). Triglyceride-Lowering Months to Years Heart Rate–Lowering Months Neu BP–Lowering Months to Years prefere idly de and th Antithrombosis Weeks trating branes 0 500 1000 1500 2000 2500 chain EPA + DHA Intake, mg/d is unk is adeq The relative strength of effect is estimated from effects of eicosapentaenoic acid (EPA) ϩdocosahexaenoic acid the ab (DHA) on each risk factor and Mozaffarian D, Rimm EB. JAMA. 2006 Oct 18;296(15):1885-‐99. 70-72,79-84 For example, dose on the corresponding impact on cardiovascular risk. response for antiarrhythmic effects is initially steep with a subsequent plateau, and clinical benefits may occur DHA.2 within weeks, while dose response for triglyceride effects is more gradual and monotonic, and clinical benefits Effe may require years of intake. At typical Western levels of intake (eg, Ͻ750 mg/d EPAϩ DHA), the physiologic
- 70. ÍNDICE Ω3 ≥ 8%vs ≤ 4% Risco de morte por ECV 90% 71 von Schacky C, Harris WS. Cardiovasc Res. 2007 Jan 15;73(2):310-5.
- 71. BETA-OXIDAÇÃO ACTIVIDADE LIMITADA ACTIVIDADE LIMITADA
- 72. EPA DHAPOR CADA 100G PEIXE Fede lacko. n−3 PUFAs—From dietary supplenents to medicines. Pathophysiology 14 (2007) 127–132
- 73. ÓLEOS VEGETAIS RICOSEM ÓMEGA-6 DIMINUEM O RISCO DE DCV
- 78. TABLE 12 Sources of docosahexaeno Food category Poultry Shellfish Eggs Finfish Beef Game Total 1 NA, not applicable. lipids (37), presumab dietary intakes of LA account for the poten However, because LA effects may be nonlin A randomized trial t with high LA (6.7% of Blasbalg TL, et al. Am J Clin Nutr. 2011 FIGURE 8. Omega-3 tissue highly unsaturated fatty acid (HUFA) predictions over the 20th century. Solid arrows indicate the percentage of
- 79. DIET AND REDBLOOD CELL n–6 AND n–3 FATTY ACIDS LA diminui DHA na membrana dos eritrócitos N= 105 Mulheres (Canadá) Grávidas (36 semanas) LA diminui EPA na membrana dos eritrócitos Friesen RW, Innis SM. Am J Clin Nutr. 2010 Jan;91(1):23-31.
- 80. Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-‐55
- 81. non-‐fatal myocardial infarcon (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)
- 82. LYON HEART STUDY Okuyama H, Ichikawa Y, Sun Y, Hamazaki T, Lands WE. World Rev Nutr Diet. 2007;96:83-103. 83
- 83. RÁCIO N-6 /N-3 DE ALGUNS ALIMENTOS Alimento ratio Ω6 / Ω3 Ovo convencional 19,4 Ovo de Creta 1,3 Carne (músculo) bovina 5,19 alimentada com cereais Carne (músculo) bovina de pasto 2,2 Simopoulos AP. J Nutr. 2001 Nov;131(11 Suppl):3065S-73S 84 Cordain L et al. European Journal of Clinical Nutrition 2002; 56:181 – 191.
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- 85. Obrigado pedro.bastos@nutriscience.pt www.nutriscience.pt