The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.

Abstract

"A fat diet, rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA), is said to be an important cause of atherosclerosis andcardiovascular diseases (CVD). The evidence for this hypothesis was sought by reviewing studies of the direct link between dietary fats and atherosclerotic vascular disease in human beings. The review included ecological, dynamic population, cross-sectional, cohort, and case-controlstudies, as well as controlled, randomized trials of the effect of fat reduction alone. The positive ecological correlations between national intakes of total fat (TF) and SFA and cardiovascular mortality found in earlier studies were absent or negative in the larger, more recent studies. Secular trends of national fat consumption and mortality from coronary heart disease (CHD) in 18-35 countries (four studies) during different time periods diverged from each other as often as they coincided. In cross-sectional studies of CHD and atherosclerosis, one group of studies (Bantu people vs. Caucasians) were supportive; six groups of studies (West Indians vs. Americans, Japanese, and Japanese migrants vs. Americans, Yemenite Jews vs. Yemenite migrants; Seminole and Pima Indians vs. Americans, Seven Countries) gave partly supportive, partly contradictive results; in seven groups of studies (Navajo Indians vs. Americans; pure vegetarians vs. lacto-ovo-vegetarians and non-vegetarians, Masai people vs. Americans, Asiatic Indians vs. non-Indians, north vs. south Indians, Indian migrants vs. British residents, Geographic Study of Atherosclerosis) the findings were contradictory. Among 21 cohort studies of CHD including 28 cohorts, CHD patients had eaten significantly more SFA in three cohorts and significantly less in one cohort than had CHD-free individuals; in 22 cohorts no significant difference was noted. In three cohorts, CHD patients had eaten significantly more PUFA, in 24 cohorts no significant difference was noted. In three of four cohort studies of atherosclerosis, the vascular changes were unassociated with SFA or PUFA; in one study they were inversely related to TF. No significant differences in fat intake were noted in six case-control studies of CVD patients and CVD-free controls; and neither total or CHD mortality were lowered in a meta-analysis of nine controlled, randomized dietary trials with substantial reductions of dietary fats, in six trials combined with addition of PUFA. The harmful effect of dietary SFA and the protective effect of dietary PUFA on atherosclerosis and CVD are questioned."

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Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

Abstract

"BACKGROUND:

A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.

OBJECTIVE:

The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.

DESIGN:

Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.

RESULTS:

During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.

CONCLUSIONS:

A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietarysaturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat."

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Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet.

Abstract

"We recently showed that a hypocaloric carbohydrate restricted diet (CRD) had two striking effects: (1) a reduction in plasma saturated fatty acids (SFA) despite higher intake than a low fat diet, and (2) a decrease in inflammation despite a significant increase in arachidonic acid (ARA). Here we extend these findings in 8 weight stable men who were fed two 6-week CRD (12%en carbohydrate) varying in quality of fat. One CRD emphasized SFA (CRD-SFA, 86 g/d SFA) and the other, unsaturated fat (CRD-UFA, 47 g SFA/d). All foods were provided to subjects. Both CRD decreased serum triacylglycerol (TAG) and insulin, and increased LDL-C particle size. The CRD-UFA significantly decreased plasma TAG SFA (27.48 ± 2.89 mol%) compared to baseline (31.06 ± 4.26 mol%). Plasma TAG SFA, however, remained unchanged in the CRD-SFA (33.14 ± 3.49 mol%) despite a doubling in SFA intake. Both CRD significantly reduced plasma palmitoleic acid (16:1n-7) indicating decreased de novo lipogenesis. CRD-SFA significantly increased plasma phospholipid ARA content, while CRD-UFA significantly increased EPA and DHA. Urine 8-iso PGF(2α), a free radical-catalyzed product of ARA, was significantly lower than baseline following CRD-UFA (-32%). There was a significant inverse correlation between changes in urine 8-iso PGF(2α) and PL ARA on both CRD (r = -0.82 CRD-SFA; r = -0.62 CRD-UFA). These findings are consistent with the concept that dietary saturated fat is efficiently metabolized in the presence of low carbohydrate, and that a CRD results in better preservation of plasma ARA."

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Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women.

Abstract

"BACKGROUND:

The influence of diet on atherosclerotic progression is not well established, particularly in postmenopausal women, in whom risk factors for progression may differ from those for men.

OBJECTIVE:

The objective was to investigate associations between dietary macronutrients and progression of coronary atherosclerosis among postmenopausal women.

DESIGN:

Quantitative coronary angiography was performed at baseline and after a mean follow-up of 3.1 y in 2243 coronary segments in 235 postmenopausal women with established coronary heart disease. Usual dietary intake was assessed at baseline.

RESULTS:

The mean (+/-SD) total fat intake was 25 +/- 6% of energy. In multivariate analyses, a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up. Compared with a 0.22-mm decline in the lowest quartile of intake, there was a 0.10-mm decline in the second quartile (P = 0.002), a 0.07-mm decline in the third quartile (P = 0.002), and no decline in the fourth quartile (P < 0.001); P for trend = 0.001. This inverse association was more pronounced among women with lower monounsaturated fat (P for interaction = 0.04) and higher carbohydrate (P for interaction = 0.004) intakes and possibly lower total fat intake (P for interaction = 0.09). Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high. Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein. Monounsaturated and total fat intakes were not associated with progression.

CONCLUSIONS:

In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression."

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