1: Arch Intern Med. 2009 Apr 13;169(7):659-69.
A systematic review of the evidence supporting a causal link between dietary
factors and coronary heart disease.
Mente A, de Koning L, Shannon HS, Anand SS.
Population Health Research Institute, Hamilton General Hospital, 4-East Room 441,
237 Barton St E, Hamilton, ON L8L 2X2, Canada.
BACKGROUND: Although a wealth of literature links dietary factors and coronary
heart disease (CHD), the strength of the evidence supporting valid associations
has not been evaluated systematically in a single investigation. METHODS: We
conducted a systematic search of MEDLINE for prospective cohort studies or
randomized trials investigating dietary exposures in relation to CHD. We used the
Bradford Hill guidelines to derive a causation score based on 4 criteria
(strength, consistency, temporality, and coherence) for each dietary exposure in
cohort studies and examined for consistency with the findings of randomized
trials. RESULTS: Strong evidence supports valid associations (4 criteria
satisfied) of protective factors, including intake of vegetables, nuts, and
"Mediterranean" and high-quality dietary patterns with CHD, and associations of
harmful factors, including intake of trans-fatty acids and foods with a high
glycemic index or load. Among studies of higher methodologic quality, there was
also strong evidence for monounsaturated fatty acids and "prudent" and
"western" dietary patterns. Moderate evidence (3 criteria) of associations exists
for intake of fish, marine omega-3 fatty acids, folate, whole grains, dietary
vitamins E and C, beta carotene, alcohol, fruit, and fiber. Insufficient evidence
(< or =2 criteria) of association is present for intake of supplementary vitamin
E and ascorbic acid (vitamin C); saturated and polyunsaturated fatty acids; total
fat; alpha-linolenic acid; meat; eggs; and milk. Among the dietary exposures with
strong evidence of causation from cohort studies, only a Mediterranean dietary
pattern is related to CHD in randomized trials. CONCLUSIONS: The evidence
supports a valid association of a limited number of dietary factors and dietary
patterns with CHD. Future evaluation of dietary patterns, including their
nutrient and food components, in cohort studies and randomized trials is
recommended.
PMID: 19364995 [PubMed - indexed for MEDLINE]
Related Links
Optimal diets for prevention of coronary heart disease. [JAMA. 2002]
PMID:12444864
1: Stroke. 1984 Jan-Feb;15(1):15-23.
Epidemiologic studies of coronary heart disease and stroke in Japanese men living
in Japan, Hawaii and California: incidence of stroke in Japan and Hawaii.
Takeya Y, Popper JS, Shimizu Y, Kato H, Rhoads GG, Kagan A.
As part of the Ni-Hon-San Study, stroke incidence was compared in the Japan and
Hawaii cohorts. Stroke cases were classified in two types, intracranial
hemorrhage (ICH) and thrombo-embolic stroke (T-E). For each type the incidence in
Japan was about three times as great as in Hawaii. The ratio ICH/T-E was 1/2.2
and 1/1.6 in Japan and Hawaii, respectively. Blood pressure was the most
important risk factor, followed by age for total stroke in both Japan and Hawaii.
Proteinuria was also a risk factor in Hawaii. Conversely, an index of animal food
intake was inversely related to total stroke, significantly in Hawaii, and at a
suggestive level for total and hemorrhagic stroke in Japan. Since the levels of
blood pressure do not differ between Japan and Hawaii, one possible explanation
for the large difference in stroke incidence between the two cohorts may be the
fact that animal protein and saturated fat intake, which is inversely associated
with stroke incidence, is much greater in Hawaii than in Japan. This explanation
would support epidemiologic and experimental studies in Japan which suggest
that dietary animal protein and fat exert an inhibitory effect on the incidence of
stroke.
PMID: 6695420 [PubMed - indexed for MEDLINE]
1: JAMA. 2006 Feb 8;295(6):655-66.
Comment in:
ACP J Club. 2006 Jul-Aug;145(1):6-7. Curr Atheroscler Rep. 2007 Dec;9(6):431-3.
Curr Diab Rep. 2006 Nov;6(5):387-8. Evid Based Nurs. 2006 Oct;9(4):112-3. JAMA.
2006 Feb 8;295(6):693-5. JAMA. 2006 Jul 19;296(3):279-80; author reply 280-1.
JAMA. 2006 Jul 19;296(3):280; author reply 280-1.
Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health
Initiative Randomized Controlled Dietary Modification Trial.
Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick ML, Wassertheil-Smoller S,
Kuller LH, LaCroix AZ, Langer RD, Lasser NL, Lewis CE, Limacher MC, Margolis KL,
Mysiw WJ, Ockene JK, Parker LM, Perri MG, Phillips L, Prentice RL, Robbins J,
Rossouw JE, Sarto GE, Schatz IJ, Snetselaar LG, Stevens VJ, Tinker LF, Trevisan
M, Vitolins MZ, Anderson GL, Assaf AR, Bassford T, Beresford SA, Black HR,
Brunner RL, Brzyski RG, Caan B, Chlebowski RT, Gass M, Granek I, Greenland P,
Hays J, Heber D, Heiss G, Hendrix SL, Hubbell FA, Johnson KC, Kotchen JM.
MedStar Research Institute/Howard University, Washington, DC, USA.
barbara.v.howard@medstar.net
CONTEXT: Multiple epidemiologic studies and some trials have linked diet with
cardiovascular disease (CVD) prevention, but long-term intervention data are
needed. OBJECTIVE: To test the hypothesis that a dietary intervention, intended
to be low in fat and high in vegetables, fruits, and grains to reduce cancer,
would reduce CVD risk. DESIGN, SETTING, AND PARTICIPANTS: Randomized
controlled
trial of 48,835 postmenopausal women aged 50 to 79 years, of diverse backgrounds
and ethnicities, who participated in the Women's Health Initiative Dietary
Modification Trial. Women were randomly assigned to an intervention (19,541
[40%]) or comparison group (29,294 [60%]) in a free-living setting. Study
enrollment occurred between 1993 and 1998 in 40 US clinical centers; mean
follow-up in this analysis was 8.1 years. INTERVENTION: Intensive behavior
modification in group and individual sessions designed to reduce total fat intake
to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and
grains to at least 6 servings/d. The comparison group received diet-related
education materials. MAIN OUTCOME MEASURES: Fatal and nonfatal coronary heart
disease (CHD), fatal and nonfatal stroke, and CVD (composite of CHD and stroke).
RESULTS: By year 6, mean fat intake decreased by 8.2% of energy intake in the
intervention vs the comparison group, with small decreases in saturated (2.9%),
monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in
intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d).
Low-density lipoprotein cholesterol levels, diastolic blood pressure, and factor
VIIc levels were significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%,
respectively; levels of high-density lipoprotein cholesterol, triglycerides,
glucose, and insulin did not significantly differ in the intervention vs
comparison groups. The numbers who developed CHD, stroke, and CVD (annualized
incidence rates) were 1000 (0.63%), 434 (0.28%), and 1357 (0.86%) in the
intervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison
group. The diet had no significant effects on incidence of CHD (hazard ratio
[HR], 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI,
0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05). Excluding participants with
baseline CVD (3.4%), the HRs (95% CIs) for CHD and stroke were 0.94 (0.86-1.02)
and 1.02 (0.90-1.17), respectively. Trends toward greater reductions in CHD risk
were observed in those with lower intakes of saturated fat or trans fat or higher
intakes of vegetables/fruits. CONCLUSIONS: Over a mean of 8.1 years, a dietary
intervention that reduced total fat intake and increased intakes of vegetables,
fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD
in postmenopausal women and achieved only modest effects on CVD risk factors,
suggesting that more focused diet and lifestyle interventions may be needed to
improve risk factors and reduce CVD risk. CLINICAL TRIALS REGISTRATION:
ClinicalTrials.gov Identifier: NCT00000611.
PMID: 16467234 [PubMed - indexed for MEDLINE]
1: Lipids. 2005 Dec;40(12):1201-5.
Effects of stearic acid on plasma lipid and lipoproteins in humans.
Mensink RP.
Department of Human Biology, Nutrition and Toxicology Research Institute
Maastricht, Maastricht University, Maastricht, The Netherlands.
R.Mensink@HB.UNIMAAS.NL
More than 40 years ago, saturated FA with 12, 14, and 16 carbon atoms (lauric
acid, myristic acid, and palmitic acid) were demonstrated to be
"hypercholesterolemic saturated FA". It was further concluded that the serum
total cholesterol level would hardly be changed by isocaloric replacement of
stearic acid (18:0) by oleic acid (cis-18:1n-9) or carbohydrates. These earlier
studies did not address the effects of the various FA on the serum lipoprotein
profile. Later studies found that the hypercholesterolemic saturated FA increase
serum total cholesterol levels by raising concentrations of both the atherogenic
LDL and the antiatherogenic HDL. Consequently, the ratio of total to HDL
cholesterol will hardly change when carbohydrates replace these saturated FA.
Compared with other saturated FA, stearic acid lowers LDL cholesterol. Studies on
the effects on HDL cholesterol are less conclusive. In some, the effects on HDL
cholesterol were comparable to those of palmitic acid, oleic acid, and linoleic
acid, whereas in others a decrease was observed. This may suggest that in this
respect the source of stearic acid is of importance, which needs however further
study. From all these studies, however, it can be concluded that stearic acid may
decrease the ratio of total to HDL cholesterol slightly when compared with
palmitic or myristic acid. Without doubt, the effects of stearic acid are more
favorable than those of trans monounsaturated FA.
PMID: 16477803 [PubMed - indexed for MEDLINE]
Related Links
1: Med J Malaysia. 1991 Mar;46(1):41-50.
Effects of palm oil on cardiovascular risk.
Chong YH, Ng TK.
Palm Oil Research Institute of Malaysia, Kuala Lumpur.
A major public health concern of affluent nations is the excessive consumption of
dietary fats which are now closely linked to coronary heart disease. Against this
scenario, the tropical oils and palm oil in particular, have been cast as major
villains in the U.S.A., despite the fact that palm oil consumption there is
negligible. The unsuspecting public may not realise that the call to avoid palm
oil is nothing more than a trade ploy since in recent years palm oil has been
very competitive and has gained a major share of the world's edible oils and fats
market. Many also lose sight of the fact that, palm oil, like other edible oils
and fats, is an important component of the diet. The allegation that palm oil
consumption leads to raised blood cholesterol levels and is therefore atherogenic
is without scientific foundation. Examination of the chemical and fatty acid
composition of palm oil or its liquid fraction should convince most nutritionists
that the oil has little cholesterol-raising potential. The rationale for these
are: it is considered cholesterol free. its major saturated fatty acid, palmitic
acid (16:0) has recently been shown to be neutral in its cholesterolaemic effect,
particularly in situations where the LDL receptors have not been down-regulated
by dietary means or through a genetic effect. palm oil contains negligible
amounts (less than 1.5%) of the hypercholesterolemic saturated fatty acids,
namely lauric acid (12:0) and myristic acid (14:0). it has moderately rich
amounts of the hypocholesterolaemic, monounsaturated oleic acid (18:1, omega-9)
and adequate amounts of linoleic acid. (18:2, omega-6). It contains minor
components such as the vitamin E tocotrienols which are not only powerful
antioxidants but are also natural inhibitors of cholesterol synthesis. Feeding
experiments in various animal species and humans also do not support the
allegation that palm oil is atherogenic. On the contrary, palm oil consumption
reduces blood cholesterol in comparison with the traditional sources of saturated
fats such as coconut oil, dairy and animal fats. In addition, palm oil
consumption may raise HDL levels and reduce platelet aggregability. As with all
nutrients, there is a need to obtain a balance of different fatty acids found in
fats in edible oils and other food sources. There is no single ideal source of
fat that answers to the recent American Heart Association's call to reflect a
1:1:1 ratio of saturated, monounsaturated and polyunsaturated fats in relation to
the recommended dietary fat intake of 30% of calories or less.(ABSTRACT
TRUNCATED
AT 400 WORDS)
http://www.westonaprice.org/knowyourfats/skinny.html#9 Most of the info came from
here and his references are listed at the end of the article.