1. MITOS EM NUTRIÇÃO
Pedro Carrera Bastos

2. RECOMENDAÇÕES NUTRICIONAIS

3. PIRÂMIDE
AMERICANA
USDA, 1992

4. NOVA RODA
PORTUGUESA
Cereais e 4 a 11 doses
derivados,
tubérculos
Hortaliças 3 a 5 doses
Fruta 3 a 5 doses
Lácteos 2 a 3 doses
Carnes, peixe e ovos 1,5 a 4,5 doses
Leguminosas 1 a 2 doses
Gorduras e óleos 1 a 3 doses
Instituto do Consumidor, 2003

6. HARVARD SCHOOL OF PUBLIC HEALTH, 2005
http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/pyramid/

8. PIRÂMIDE VEGETARIANA

9. PIRÂMIDE MEDITERRÂNICA

11. PIRÂMIDE LATINO-AMERICANA

13. VÁRIAS DIETAS

14. VÁRIAS DIETAS

16. LENDAS
Battle Creek
S. Graham J.H. Kellogg
M. Bircher-Benner W. Arbuthnot-Lane
D. Burkitt

17. DINHEIRO

18. COMO CHEGAR A CONCLUSÕES

19. Estudos com Humanos:
Estudos Metabólicos de curto prazo
RCTs
CAUSA/EFEITO
Estudos com Animais
Epidemiologia
Estudos In vitro
Cordain L. Dietary implications for the development of acne: a shifting paradigm. In: U.S. Dermatology Review II 2006, (Ed.,Bedlow, J).
Touch Briefings Publications, London, 2006.

20. RECOMENDAÇÕES BASEADAS EM
LENDAS E EPIDEMIOLOGIA

21. CONTROVÉRSIAS

23. COLESTEROL DIETÉTICO < 300 MG/DIA
Dietary Guidelines for Americans, USDA, 2005

24. 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

26. EFEITOS NO CURTO PRAZO
INCREMENTO DE 100 MG/D DE COLESTEROL DIETÉTICO AUMENTOU:
ü CT: 2.2 mg/dl
ü C- HDL: 0.3 mg/dl
26
Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

27. EFEITOS A LONGO PRAZO
3 grupos de Consumo de ovos por semana (Framingham Heart Study)
27
Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

28. EFEITOS A LONGO PRAZO
Colesterol Total nos 3 grupos
28
Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

29. of each
that th
Dietary cholesterol The
changes
1.4 1 trolling
models
1.2 statistica
erate
1.0
0)
a manipul
I
0.8 more
a
0) function
-C
E 0.6 reduction
in dieta
0.4
shown
0.2 tions
35.43
. Confined Inst meals Free : :ii- mg/dL;
Location of subjects mmol/L
0.6%
FIGURE 2. Regression WH, et al. Am J Clin Nutr. 1997 Jun;65(6):1747-64.
Howell coefficients of saturated fatty acids, poly- On
unsaturated fatty acids, and &holesterol for studies of subjects free-living
analysis

30. US NATIONAL HEALTH AND NUTRITIONAL
SURVEY (1984–1994)
30
Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

31. 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-

33. 826 HERRON ET AL
Table 1. Distribution of Cholesterol in LDL Subclasses and LDL Peak Diameter of Hypo- and Hyper-responders
During the EGG or SUB Periods
LDL Peak
LDL-1 (mg/dL) LDL-2 (mg/dL) LDL-3 (mg/dL) Diameter (nm)
Women
Hyper-responders (n ϭ 14)
EGG 31.7 Ϯ 12.2a 22.1 Ϯ 10.7b 5.1 Ϯ 5.5a 26.90 Ϯ 0.25a
SUB 28.1 Ϯ 10.4b 16.6 Ϯ 7.8a 4.1 Ϯ 5.5a 26.99 Ϯ 0.33a
Hypo-responders (n ϭ 13)
EGG 21.8 Ϯ 7.8c 19.4 Ϯ 10.5ab 4.5 Ϯ 5.5a 26.58 Ϯ 0.57b
SUB 21.9 Ϯ 8.0c 19.1 Ϯ 11.5ab 4.6 Ϯ 6.8a 26.67 Ϯ 0.62b
Men
Hyper-responders (n ϭ 12)
EGG 23.3 Ϯ 8.4c 19.6 Ϯ 8.2ab 16.6 Ϯ 16.2c 26.24 Ϯ 0.58b
SUB 20.0 Ϯ 7.9c 25.6 Ϯ 5.6b 9.9 Ϯ 10.4bc 26.40 Ϯ 0.53b
Hypo-responders (n ϭ 13)
EGG 18.2 Ϯ 8.8d 20.5 Ϯ 5.6ab 6.8 Ϯ 6.1ab 26.75 Ϯ 0.35a
SUB 20.5 Ϯ 9.0c 20.5 Ϯ 9.0ab 7.8 Ϯ 7.5b 26.67 Ϯ 0.52b
Sex effect P Ͻ .05 NS P Ͻ .01 P Ͻ .01
Response effect P Ͻ .05 NS NS NS
Diet effect NS NS P Ͻ .05 NS
Interaction sex ϫ response NS NS NS P Ͻ .001
Interaction sex ϫ diet NS NS NS NS
Interaction response ϫ diet P Ͻ .001 P Ͻ .05 P Ͻ .001 NS
Interaction sex ϫ diet ϫ response NS P Ͻ .01 P Ͻ .05 NS
NOTE. Values are presented as mean Ϯ SD for the number of subjects indicated in parentheses. Values in the same column with different
superscripts are significantly different as determined by 3-way ANOVA and LSD as post hoc test.
Abbreviations: EGG, egg; SUB,KL, Lofgren NS,Sharman M, Volek JS, Fernandez ML. Metabolism. 2004 Jun;53(6):823-30.
Herron substitute; IE, not significant.
consumption, while hyporesponders experienced no change for contrast, plasma LCAT and CETP activities were significantly

34. 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

35. LDL PEQUENAS E DENSAS
ü sdLDL:
ü Tamanho da partícula <
25.5nm
ü Densidade > 1.04g/ml
ü Aumenta
significativamente o
risco de DCV
ü TG elevados e HDL-C
baixo é um bom preditor
de sdLDL
Griffin BA. Proc Nutr Soc 1999;58:163-69

37. Cordain, 2009
FLUXO DE LDL PARA A INTIMA É > PARA LDL PEQUENAS E DENSAS
UMA VEZ NA INTIMA, LDL PEQUENAS E DENSAS SÃO SUSCEPTÍVEIS DE SOFRER
OXIDAÇÃO
37

38. • 1.
Células
espumosas

40. 214 Esrey et al.
TABLE 3. Cox regression estimates of the effect of dietary intake measured at baseline on coronary heart disease death among
3925 men and women 30 to 59 years of age after 12.4 years foIIow-up in the North American Lipid Research Clinics Prevalence
FoIIow-Up Study
Model 3
Model 1 Modei 2 (adjusted for age, sex,
(adjusted for age, sex, (adjusted for age, sex, energy intake, serum lipids,
energy intake) energy intake, serum lipids”) and other risk factorsb)
Variable Estimate RR (95% CI) Estimate RR (95% CI) Estimate RR (95% CI)
% Fat
Total 0.044" 1.04 (1.01-1.08) 0.043" 1.04 (1.01-1.08) 0.043' 1.04 (l.Ol-1.08)
Saturated 0.104” 1.11 (1.04-1.18) 0.095" 1.10 (1.03-1.17) 0.103" 1.11 (1.04-1.18)
Monounsaturated 0.095" 1.10 (1.03-1.17) 0.094' l 1.10 (1.03-1.18) 0.080' 1.08 (1.01-1.16)
Polyunsaturated -0.040 0.96 (0.88-1.05) -0.027 0.97 (0.89-1.07) -0.014 0.99 (0.90-1.08)
% Carbohydrate -0.034" 0.97 (0.94-0.99) -0.040" 0.96 (0.93-0.99) -0.036' 0.96 (0.94-0.99)
% Protein 0.020 1.02 (0.97-1.08) 0.013 1.01 (0.96-1.07) 0.011 1.01 (0.95-1.07)
% Alcohol + alcohol’ -0.019 0.98 (0.92-1.05) 0.001 1.00 (0.94-1.06) 0.0001 1.00 (0.95-1.07)
Cholesterol (10 mg) per 5000 kJ 0.004 1.00 (0.99-1.02) 0.006 1.01 (0.99-1.02) 0.004 1.00 (0.99-1.02)
?Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins.
bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m*), and glucose
intolerance (present/absent).
‘p < 0.05.

41. ?Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins.
bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m*), and glucose
intolerance (present/absent).
‘p < 0.05.
“p < 0.01.
RR = Relative risk for coronary heart disease mortality, defined as exp(@, associated with a I+unit increase in the dietary variable; 95% CI = 95% confidence
interval, defined as exp@ 2 1.96 SE)(z, - q), where SE is the standard error of /3, and 7, and Q represent the two levels of the dietary variable being
compared; % =percentage of total energy provided by the dietary variable.
(total cholesterol and HDL) were added to the regression model and none approached statistical significance. The magnitude and direc-
(model 2), the estimated relative risks for the dietary variables re- tion of some estimates changed between the three models evaluated,
mained stable. The magnitudes of these relationships were also unaf- but within a small range. When a quadratic alcohol term was included
fected by the addition of other known coronary risk factors (model 3). in the Cox model, percentage of energy intake as alcohol was signifi-
cantly associated with risk of coronary disease death within this older
Among the older age group, no relationships between dietary fat or age group.
its fatty acid components, carbohydrate, or protein, and coronary heart None of the dietary components examined were significantly associ-
disease death were identified (Table 4). The estimares of the regression ated with total mortality within either the young or the older age
coefficients were al1 smaller than those among the younger age group groups.
TABLE 4. Cox regression estimates of the effect of dietary intake measured at baseline on coronary heart disease death among
621 men and women 60 to 79 years of age after 12.4 years follow-up in the North American Lipid Research Clinics Prevalence
Follow-Up Study
Model 3
Model 1 Model 2 (adjusted for age, sex,
(adjusted for age, sex, (adjusted for age, sex, energy intake, serum lipids,
energy intake) energy intake, serum lipids”) and other risk factorsb)
Variable Estimate RR (95% CI) Estimate RR (95% CI) Estimate RR (95% CI)
% Fat
Total -0.0004 1.00 (0.96-1.04) -0.002 1.00 (0.96-1.04) -0.011 0.99 (0.95-1.03)
Saturated -0.031 0.97 (0.89-1.05) -0.026 0.97 (0.90-1.06) -0.038 0.96 (0.88-1.05)
Monounsaturated 0.025 1.03 (0.95-1.11) 0.019 1.02 (0.94-l. 11) -0.005 1.00 (0.91-1.08)
Polyunsaturated 0.006 1.01 (0.91-1.11) -0.004 1.00 (0.90-l. 10) -0.004 1.00 (0.90-1.10)
% Carbohydrate 0.004 1.00 (0.97-1.04) 0.003 1.00 (0.97-1.04) 0.016 1.02 (0.98-1.05)
% Protein 0.017 1.02 (0.94-l. 10) 0.015 1.02 (0.94-1.10) 0.0002 1.00 (0.93-1.08)
% Alcohol + alcohol’ -0.114" 0.89 (0.84-0.94) -0.116** 0.89 (0.83-0.95) -0.124” 0.88 (0.83-0.95)
Cholesterol (10 mg) per 5000 kJ 0.011 1.01 (0.99-1.03) 0.011 1.01 (0.99-1.03) 0.006 1.01 (0.98-1.03)
“Serum lipids (mmoliliter) included total serum cholesterol and high-density lipoproteins.
bOther risk factors were systolic blood pressure (mmHg), cigarette smoking status (current smoker/nonsmoker), body mass index (kg/m’), and glucose
intolerance foresent/absent).

42. 37,851 H seguidos por 8 anos
80.082 M seguidas por 14 anos
Baseado em Hu Fb, et al. JAMA. 1999;281:1387-1394 e adaptado por Okuyama H, et al. World Rev Nutr Diet. 2007;96:1-17.

43. NUTRITION MYTHS

44. REDUZIR GORDURA DIETÉTICA DIMINUI
RISCO DE DCV

45. “DIMINUIR GORDURA REDUZ O RISCO
CARDIOVASCULAR”

46. 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

47. dicated an increase in the plasma very low density lipopro- factory because the conditions of this experiment were ca
n (VLDL) level and a decrease in both the plasma HDL and fully controlled and the statistical power of the protocol 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

48. ENTRE 1968-1978, NA GRONELÂNDIA
ü Nenhum caso de
morte por DAC
ü Nenhum caso de
enfarte agudo
do miocardio
(População = 2,600)
Bang HO, Dyerberg J. Adv Nutr Res 1980 3:1-22.

49. ALIMENTOS VEGETAIS / ANIMAIS EM 13 SOCIEDADES
PRIMITIVAS!
Cordain L et al. Eur J Clin Nutr 2002; 56 (suppl 1):S42-S52. !

50. misnomer. The countries around the Mediterranean basin have differe
differ in the amount of total fat, olive oil, type of meat andamount of total fat, olivemilk vs. cheese;intake;
differ in the wine intake; oil, type of meat and wine frui
the rates of coronary heart disease and cancer, with the lower death ra
the rates of coronary heart disease and cancer, with the lower death rates andof Greece (the diet e
Greece. Extensive studies on the traditional diet longer life be
The Greece. Extensive studies on So Special about the ofGreece (the high intake of fruits, vegetables (particularly wildt
Mediterranean Diets: What Is the traditional diet ofDiet of Greece? before 1960) indicate Greeks consists of a
diet
1 of sourdough bread rather than pasta; more olive oil and olives; less m
The Scientific Evidence
of Greeks consists of a high intake of fruits, vegetables (particularly wild plants), nuts and cer
and moderate amounts of wine, more so than other Mediterranean coun
diet of Crete shows a number of protective substances, such as s
of sourdough bread rather than pasta; more olive oil and olives; less(EFA), high amounts of fiber, antioxid
Artemis P. Simopoulos2 (n-6):(n-3) essential fatty acids milk but more cheese
polyphenols from olive oil), vitamins E and C, some of which have been
and Center for Genetics, Nutrition and Health, Washington, DCthan othercancer, including cancer ofcountries. Analyses of th
The moderate amounts of wine, more so Mediterranean the breast. These findings should serve
intervention trials that will test the effect of specific dietary patterns in t
diet of Crete shows a diet,” implying that all Mediterranean people with cancer. J. diet, is131:as selenium, glutathione
ABSTRACT The term “Mediterranean
number of protective substances, sucha 3065S–3073S, 2001.
have the same
Nutr.
(n-6):(n-3) countries around the Mediterranean basin have different diets, religions andWORDS: Their antioxidants (especially resv
misnomer. The essential fatty acids (EFA), high amounts of fiber, diets
KEY
cultures.
diet of Crete (n-3) fatty acids
c wild plants
c a c c
differ in the amount of total fat, olive oil, type of meat and wine intake; milk vs. cheese; fruits and vegetables; and
polyphenols from olive oil), vitamins E and C, some of which have been shown to be assoc
the rates of coronary heart disease and cancer, with the lower death rates and longer life expectancy occurring in
The health of thedietary pattern the population in general
individual and intake and
cancer, including the traditionalvegetables (particularly wild These indicate that the should serve as aa strong incenti
of Greeks consists of a high intake of fruits, of the breast. plants),is thefindings
Greece. Extensive studies on
cancer diet of Greece (the diet before 1960) and cereals mostly in the form genetics and number of diet” is a m
nuts result of interactions between
intervention trials that will testoil and olives; less of specificofdietarypattern of the an in the prevention but in facb
of sourdough bread rather than pasta; more olive the effect milk but environmentalmore fish; less meat;
more cheese; factors. Nutrition is
major importance (1– patterns
environmental factor of
and moderate amounts of wine, more so than other Mediterranean countries. Analyses the dietary 4). Our genetic profile has not changed
and m
surprising
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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 isIETÉTICA: during evolutionENERGIA TrateinCrete, according to data compiled by the
(n-6) to (n-3) fatty
GORDURA D and16.74:1, whereas 37% DA aasdecrease as (n-3)
it was 2–1:1 (Table 1, Fig. 1).trans fatty acids and low a death OTAL CONSUMIDA Although Greece and th on.
United Nations in their demographic yearbook for 1948. Nutritional Sciences.
It
fatty status of intake; 3) the dietary Mediterranean basin was 11.3–13.7 per0022-3166/01 $3.00 © beforeusually IIforand
acid the countries surrounding the patterns complex carbohydratesinhabitants 2001 American Society considered to be area
Recent investigations ofa decrease inand health
1000 and World War
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
and 1946 –1948 many (14.0 –18.0 3065S
fruit and vegetable intake; and 5) a decrease in protein,Greece before 1960.Crete have been below this l
anti-
United States as in Crete (19). The diet of Crete represents
the traditional diet of The Seven Coun-
oxidant and calcium intake (5–17). Furthermore, was theratio establish credible data on cardio-
tries Study the first to of
1
Presented as part of the 11th Annual Research Conference on Diet, Nutrition
and Cancer held in Washington, DC, July 16 –17, 2001. This conference was
sponsored by the American Institute for Cancer Research and was supported by 1930 (19). No other area in th
(n-6) to (n-3) fatty acids is 16.74:1, whereas during evolution in contrasting populations
vascular disease prevalence rates
the California Dried Plum Board, The Campbell Soup Company, General Mills,
goslavia, Japan and Greece), with differences low a death rate as Crete, acc
as found on the
(United States, Finland, The Netherlands, Italy, former Yu-
Lipton, Mead Johnson Nutritionals, Roche Vitamins Inc. and Vitasoy USA. 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,

51. n’s Health Initiative Randomized Controlled
Health Initiative Randomized Controlled
cation TrialTrial epidemiologic studies and some trials have linked diet with car-
dification Multiple
Context
diovascular disease (CVD) prevention, but long-term intervention data are needed.
Linda Objective To test the hypothesis thatsome trials have linked diet with car- diet be low in
Context Multiple epidemiologic studies andstudies and intervention, intended to with car-
Context Multiple epidemiologic a dietary some trials have linked
Hsia, MD; fat and high in vegetables, fruits, but long-term intervention data are needed.
D;
diovascular disease (CVD) prevention, and grains to long-term intervention data are CVD risk.
. diovascular disease (CVD) prevention, but reduce cancer, would reduce needed.
L.arcia L.
D; Design, Setting, To test the hypothesis that a dietary intervention, trial of 48 835low in
Objective and Participants Randomized controlled intended
Objective To test the hypothesis that a dietary intervention, intended to be low in to be post-
s; H.
Lewis H. menopausal women aged 50 tograins to reduce cancer, would reduce would reduce CVD risk.
fat and highand high in vegetables, fruits, and grains to reduce cancer, CVD risk.
fat in vegetables, fruits, and 79 years, of diverse backgrounds and ethnicities, who
PhD; , PhDDesign,Design, Setting, and Participants Randomized controlled trial ofWomenpost-
Croix participated in the Women’s Health Initiative controlled trial of 48 835 Trial. 48 835 were
; Setting, and Participants Randomized Dietary Modification post-
menopausal women aged 50 to 79 years, of diverse541 [40%])and ethnicities, whogroup (29 294
L. menopausal to an aged 50 to 79(19 backgroundsbackgrounds
orman L. randomly assignedwomeninterventionDietary Modification Trial. Womenand ethnicities, who
years, of diverse or comparison
s, MD;
;L. [60%]) participated in the Women’s(19 541 [40%]) orDietary Modification were Women were
participated in the Women’s Health Initiative
in a free-living setting. Study enrollment occurred between Trial. and 1998 in
randomly assigned to an intervention
Health Initiative comparison group (291993 294
40 US clinical centers; mean follow-up in this 541 [40%]) or8.1 years. in group (29 294
randomly assigned to an intervention (19 analysis was comparison
Karen L. [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998
MD;
.ysiw 40 US clinical centers; mean follow-up in Study enrollment occurred between 1993 and 1998 in
[60%]) in a free-living setting.
D; , MD; Intervention Intensive behavior this analysis this in group and individual sessions de-
was 8.1 years.
modification analysis was 8.1 years.
40 US clinical centers; mean follow-up in
PhD; M. signed to reduce total fat intake to 20% of calories and increase intakes of vegetables/
inda Intervention Intensive behavior modification in group and individual sessions de-
Perri, PhD;fruits toInterventionand grains behavior modification inintakescomparison group received
signed to5 servings/d intake to 20% of calories and increase group of vegetables/ sessions de-
reduce total fat Intensive to at least 6 servings/d. The and individual
D; L.
oss fruits to 5 servings/d and grains to at intake servings/d. The comparison group received of vegetables/
signed to reduce total fat least 6 to 20% of calories and increase intakes
diet-related education materials.
bins, MD; diet-related education materials.
fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received
RISCO
0%
5%
10%
15%
20%
25%
DAC
Total
DCV
RELATIVO
E.
nda G. E. Main Outcome Measures Fatal and nonfatal coronary heart disease (CHD), fatal (CHD), fatal
GloriaG. Main Outcome Measures Fatal and nonfatal coronary heart disease
Linda diet-related education materials.
PhD;
ns, MD; ;Linda G.nonfatal stroke, andand CVD (composite of CHD and stroke). disease (CHD), fatal
z, PhD and nonfatal Outcome Measures Fatal and nonfatal coronary heart
and Main stroke, CVD (composite of CHD and stroke).
Stevens, PhD;
Resultsand nonfatal stroke, and CVD (composite of CHD and stroke). intake
Results By year 6, mean fat intakeintake decreased byenergy intake in the inter- in the inter-
By year 6, mean fat decreased by 8.2% of 8.2% of energy
DrPH;
PH;
aurizio
ouise R. ventionvs(3.3%),comparisonmean fatwith fat; increases occurred inof energy veg- in monoun-
vention the comparison group, with small decreases in saturated (2.9%), monoun-
saturated
Results By year 6, group, intake decreased by 8.2%
vs the and polyunsaturated (1.5%) small decreases in saturated (2.9%), the inter-
intakes of
intake
tolins, DrPH;
se ;R.
D saturated (3.3%),the comparison group, with small decreases in saturated (2.9%), monoun-
vention vs and polyunsaturated (1.5%) fat; increases occurred in intakes of veg-
; Annlouiseetables/fruits (1.1(3.3%), and grains grains (0.5 serving/d). Low-density lipoprotein cholesterol
etables/fruits (1.1 servings/d)
R. (0.5 serving/d). Low-density lipoprotein cholesterol
enry R. levels, diastolic blood pressure, and factor VIIc levels(1.5%) fat; increases occurred in intakes of veg-
saturated servings/d) polyunsaturated were significantly reduced by 3.55
and and
ord,; MD;
y R.
PhD mg/dL, 0.31 mm Hg, and 4.29%, respectively; levels serving/d). Low-density lipoprotein cholesterol
etables/fruits (1.1 servings/d) and grains (0.5 levels were lipoprotein cho-
levels, diastolic blood pressure, and factor VIIcof high-densitysignificantly reduced by 3.55
D; ; Henry mg/dL, triglycerides,Hg,blood 4.29%, respectively; levels of in the intervention
hD R.
lesterol, levels, mm glucose, and insulin did not significantly differ high-density lipoprotein 3.55
0.31 diastolic and pressure, and factor VIIc levels were significantly reduced by cho-
unner, PhD;vs comparison groups. mm numbers who developed CHD, stroke, of high-density lipoprotein cho-
ski, MD;
ette;
MD lesterol,mg/dL, 0.31 The Hg, and BV, et al. JAMA. 2006 Febsignificantly differ in the intervention
Howard 4.29%, respectively; levels and
triglycerides, glucose, and insulin did not 8;295(6):655-66CVD (annual-
, MD; , vs comparison groups. 1000glucose, and insulin(0.88%) 1357 (0.86%)differ in the intervention
hlebowski MD;
lesterol, triglycerides, (0.63%), 434 (0.28%), and significantly in the in-
ized incidence rates) were did not
The numbersand 2088 developed CHD, stroke,and CVD (annual-
tervention and 1549 (0.65%), 642 (0.27%), who developed the comparison group. CVD (annual-
in CHD, stroke, and
vs comparison groups. The numbers who

52. RISCO RELATIVO
25% EM MULHERES QUE
TINHAM DCV
20%
15%
RISCO
0%
5%
10%
15%
20%
25%
DAC
Total
DCV
RELATIVO
10%
5%
0%
DAC Total DCV
Howard BV, et al. JAMA. 2006 Feb 8;295(6):655-66

53. DIMINUIÇÃO DA GORDURA TOTAL
DE 35% PARA 32.3%
AUMENTO DO RÁCIO PUFA/
SAFA EM 100%
Burr ML, Fehily AM, Gilbert JF, et al. Lancet 1989; 2:757-761.

55. ÁCIDOS GORDOS SATURADOS
USDA, AHA: < 10% DO TOTAL CALÓRICO
Dietary Guidelines for Americans, USDA, 2010

56. Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

57. SAFA EM ALGUNS ALIMENTOS
Alimento AG Saturados AG AG AG AG
(100 g) (g) Laúrico Mirístico Palmitico Esteárico
12:0 14:0 16:0 18:0
Manteiga 51 3 7 2 10
Óleo de 86,5 44,6 16,8 8,2 2,8
Coco
Cacau 8,07 0 0,02 3,69 4,25
Óleo de
49,3 0,1 1 43,496 4,3
palma
Leite gordo 1,865 0,077 0,297 0,829 0,365
57 Fonte: USDA food database

58. Mensink RP, Zock PL, Kester AD, Katan MB. Am J Clin Nutr. 2003 May;77(5):1146-55

59. 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

60. CHINA RURAL: < 5% EUA: 11-12% CRS: 4-18%
KITAVA: 17% MAASAI: 30-35% TOKELAU: 40%

62. A meta-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.

63. NUTRITION MYTHS

64. ÓLEOS VEGETAIS RICOS EM ÓMEGA-6
DIMINUEM O RISCO DE DCV

65. with omega-6 PUFAs on
follow that decreasing omega-6 levels will do the same.
re present for each trial,
Indeed, the evidence considered here suggests that it would
es and the observational
cing saturated fatty acid have the opposite AHA Science Advisory PUFA intakes
effect. Higher omega-6
ars, white bread, white can inhibit the conversion of ␣-linolenic acid to eicosa-
As reduces CHD risk. On pentaenoic Fatty 79 but and Risk for Cardiovascular Disease
Omega-6
acid, Acids such conversion is already quite
A Science Advisory From the American Heart Association Nutrition
a-6 PUFAs used in the low,80 and whether additional Nutrition, Physical would have
Subcommittee of the Council on small changes Activity, and
ies, and nonhuman pri- net effects on Council on Cardiovascular other benefits of on
Metabolism; CHD risk after the Nursing; and Council LA
Epidemiology and Prevention
eductions in CHD risk consumption are taken into account is not clear. The focus
William S. Harris, PhD, FAHA, Chair; Dariush Mozaffarian, MD, DrPH, FAHA;
PUFA intakes of 10% to on Eric Rimm, ScD, FAHA; Penny Kris-Etherton, PhD, FAHA; Lawrence L. Rudel, PhD, FAHA;
ratios, rather than on levels of intake of each type of
Lawrence J. Appel, MD, MPH, FAHA; Marguerite M. Engler, PhD, FAHA;
lower intakes, with no PUFA, has many B. Engler, PhD, FAHA; Frank Sacks, MD, FAHA
Mary conceptual and biological limitations.
81
nts.
A large body of literature suggests that higher intakes of
Conclusions
omega-6 (or n-6) polyunsaturated fatty acids (PUFAs)
reduce risk for coronary heart disease (CHD). However, for
levels,5 may have physiological sequelae.6 – 8 LA comes
primarily from vegetable oils (eg, corn, sunflower, safflower,
soy). The average US intake of LA, according to National
s of Omega-6 This advisory was undertaken to summarize the current
the reasons outlined below, some individuals and groups have
recommended substantial reductions in omega-6 PUFA in-
Health and Nutrition Examination Survey 2001 to 2002 data
for adults Ն19 years of age, is 14.8 g/d.9 On the basis of an
ds evidence on the consumption of omega-6 PUFAs, partic-
take.1– 4 The purpose of this advisory is to review evidence on
the relationship between omega-6 PUFAs and the risk of
average intake of 2000 kcal/d, LA intake is 6.7% of energy.
AA (Ϸ0.15 g/d) is consumed preformed in meat, eggs, and
ega-6 PUFAs tradition- ularly LA, and CHD risk. Aggregate data from randomized
CHD and cardiovascular disease. some fish.
of essential fatty acid trials,PUFAs are characterized by the presence of at least Arguments for reduced LAandlong-term the
Omega-6
case-control and cohort studies,PUFAs intakes are based on
Omega-6 PUFAs Omega-6 and Inflammation
ngly seeking to define animal thedouble bonds, with the first bond at(LA), an assumptionthatbecause CHD has an inflammatory is the
2 carbon-carbon
carbon from
feeding experiments indicate andthat the omega-6 fatty acid, AA, com-
methyl terminus. Linoleic acid
the sixth
ponent 10 because the
consumption
k for chronic disease, of primaryleastomega-6 PUFA. LA (18:2 omega-6),energy from synthesisintakes shouldofreduce tissue AA
at dietary 5% to 10% be synthe- substrate forreducing LA of a variety PUFAs
18-carbon fatty acid with 2 double bonds
the cannot
of is molecules, the omega-6 proinflammatory
of Medicine’s Food and reduces established for healthyCHD relative content, which lower the risk the inflammatory evidence,
the risk of adults, estimates de- and therefore should reduce for The The potential
sized by humans, and although firm minimum requirements
have not been
to lower intakes. CHD. data
Reference Intake Report also suggest thathospitalized patients receiv- appear istofrom human studies, regarding this line
rived from studies in infants and
higher intakes derived primarily be safe and may
ing total parenteral nutrition suggest that an LA intake of of reasoning examined below.
67 defines an adequate be LA can be more and elongated to form(as part of a low–saturated-fat,proin-
tion,
even desaturated beneficial other eicosanoids (20-carbon AA metabolites). Some are of
Ϸ0.5% to 2% of energy is likely to suffice. After consump- AA is the substrate for the production of a wide variety
d 12 g/d for women (5% low-cholesterol the metabolically␥important flammatory, vasoconstrictive, and/or proaggregatory, such as
acids. The latter is converted to diet). In summary, the , AHA supports anHow-
omega-6 PUFAs such as ␥-linolenic and dihomo- -linolenic
prostaglandin E thromboxane A , and leukotriene B .
2 2 4
f age, approximately the omega-6 PUFA intake of at least 5% to 10% and epoxyeicosatrienoic acids.
omega-6 PUFA arachidonic acid (AA; 20:4 omega-6), the
substrate for a wide array of reactive oxygenated metabolites. prostacyclin, lipoxin A , 4
of energy in
ever, others are antiinflammatory/antiaggregatory, such as
11 12
the Dietary Reference the context focusesother on this fattylifestyle AA by a cytochrome P450recommen-
PUFA, this advisory of primarily AHA acid,
Because LA accounts for 85% to 90% of the dietary omega-6
from and dietary epoxygenase. Epoxyeicosa-
Epoxyeicosatrienoic acids are fatty acid epoxides produced
ry Guidelines for Amer- dations. To reduce omega-6 PUFA also have important vasodilatortheir via
recognizing that dietary AA, which can affect tissue AA trienoic acids
intakes from properties
acronutrient distribution current Heart Associationwouldeffort to avoid any actual or potential conflicts of interest that may arise than oftooutside
The American
levels makes every be more likely to increase as a result an
relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are
particular energy source decrease risk for CHD. showing all such relationships that might be perceived as real or potential conflicts
required to complete and submit a Disclosure Questionnaire
of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on November 6, 2008. A copy of the
statement is available at http://www.americanheart.org/presenter.jhtml?identifierϭ3003999 by selecting either the “topic list” link or the “chronological
Downloaded from circ.ahajournals.org by on July 26, 2010
list” link (No. LS-1966). To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.
Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development,
visit http://www.americanheart.org/presenter.jhtml?identifierϭ3023366.
Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express

69. Simopoulos AP, Cleland LG (eds): Omega–6/Omega–3 Essential Fatty Acid Ratio:
The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 74–80
Effects of an Indo-Mediterranean
Diet on the Omega–6/Omega–3 Ratio
in Patients at High Risk of Coronary
Artery Disease: The Indian Paradox
Daniel Pellaa, Gal Dubnovb, Ram B. Singhc, Rakesh Sharmad,
Elliot M. Berryb, Orly Manor b
a
2nd Interna Klinika,Safaric University, Kosice, Slovakia;
b
Department of Human Nutrition and Metabolism, Hebrew University, Hadassah
Medical School, Jerusalem, Israel;
c
Subharti Medical College, Medical Hospital and Research Centre, Moradabad, India;
d
Department of Medicine, Columbia University, New York, N.Y., USA

70. > PREVALÊNCIA DE DAC NOS INDIVÍDUOS DA REGIÃO
URBANA
Pella D et al. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 74-80.

71. Simopoulos AP, Cleland LG (eds): Omega–6/Omega–3 Essential Fatty Acid Ratio:
The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 81–91
Omega–6/Omega–3 Fatty Acid Ratio:
The Israeli Paradox
Gal Dubnov, Elliot M. Berry
Department of Human Nutrition and Metabolism, Hebrew University,
Hadassah Medical School, Jerusalem, Israel
ü ÓLEO MAIS CONSUMIDO: ÓLEO DE SOJA
While the amount of fat is very important in terms of public health in
dealing with the current epidemic of obesity, an equally significant issue is the
ü R ÁCIO P/S = 0,9 – 1,2
type of fat consumed. As polyunsaturated fatty acids (PUFA) have long been
shown to possess cholesterol-lowering effects [1], increasing their consumption
has been promoted in the management of coronary artery disease (CAD) [2].
ü Á L : 10% E
CIDO INOLEICO recommendations followed bothOTAL IÁRIA
These
T
DA NERGIA experimental and population based
studies that showed decreasing rates of CAD in countries with increasing
D
polyunsaturated/saturated fat (P/S) ratios over the past years.
The dietary habits in Israel appear to be as recommended: low in total
ü % LA : 25%
NO ADIPÓCITO in total fat and in saturated fat, while high in hypolipidemic omega–6
calories,
fatty acids (␻6) as compared with other western countries [3, 4]. Unexpectedly, the
rates of modern-world illnesses are about the same as they are in the USA and
RÁCIO N-6/N-3 > 20/1
Europe [3, 5, 6]. The reason for this is not clear. Recent evidence suggests that
a high intake of omega–6 fatty acids may prove harmful [2, 7–9]: these fatty
acids may elevate the risk of hyperinsulinemia and its associated metabolic dis-
orders, atherogenesis, and cancer. Another group of PUFA, the omega–3 fatty
PREVALÊNCIA DE DAC É COMPARÁVEL À DE
acids (␻3), have demonstrated cardioprotection in observational [10–15] and
intervention studies for both secondary [16–18] and primary [18] prevention.
An example for this is shown in figure 1: an Indo-Mediterranean diet, rich in
OUTROS PAÍSES OCIDENTAIS
the plant-derived omega–3 fatty acid alpha-linolenic acid, markedly decreased
the risk for a cardiac event among both those with established coronary artery
disease, or those only with risk factors [18]. A recent meta-analysis showed that
both dietary and non-dietary sources are equally beneficial [19], and the health
benefits of plant- derived or fish- derived omega–3 fatty acids now seem to
have a sound basis [20]. As the omega–6 and omega–3 fatty acids compete for

72. non-fatal myocardial infarction (MI) + CHD death.
n-6 specific PUFA trials non significantly increased the risk of
non-fatal MI + CHD death by 13%
(risk ratio (RR) 1·13; 95% CI 0·84, 1·53; P=0·427)