Saturated fat, does it matter?

Recommendations to reduce saturated fat consumption have pervaded our media since the AHA published its first dietary guidelines for the American public in 1961. The AMA at first opposed the recommendations but the AHA pushed on. The guidelines encouraged substitution of polyunsaturates for saturated fat. The guidelines were presented in a two page report with 1/2 page of references. A subsequent independent review of those references revealed that 1/2 of them did not support the recommendations, details, details.

My last blog looked at a meta-analysis of the major studies subsequently published on this topic and found that implementation of that recommendation does not reduce heart attacks or cardiac deaths and in fact there was a trend (not statistically significant) for worse outcomes associated with substituting PUFA (polyunsaturated fatty acids, primarily linoleic acid) for SFA (saturated fatty acids).

Please note that we are talking hard endpoints here, death and heart attack. So much of the literature that consumes this issue only looks at the effect on so called risk factors. When you actually look at the clinical outcomes (death, heart attack, stroke)  there is no benefit demonstrated when saturated fats are reduced.

In 1966 the makers of Mazola Corn Oil and Mazola Margarine sponsored publication of Your Heart Has Nine Lives, a book advocating the substitution of vegetable oils for butter and other “artery clogging” saturated fats.

The history of this campaign to demonize SFA and glorify PUFA is well described in Gary Taubes Good Calories, Bad Calories, as well as in Mary Enig’s essay The Oiling of America. I would encourage you to read both.  The latter is available on line as is Gary Taubes’ famous essay What if its all a big fat lie?

In 2010 a highly respected lipid research group published what should have been a wake-up call study for the medical profession.

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

The data included 5 to 23 years follow up on 347,747 subjects. 11,006 developed coronary heart disease or stroke. Intake of saturated fat was not associated with an increased risk of coronary heart disease (CHD), stroke, or  cardiovascular disease (CVD =CHD plus stroke).

“there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

To be clear, association (statistical correlation) does not prove or disprove causation, but if such a large amount of data from prospective studies shows no statistically significant correlation, than a causative theory should be rejected until and unless randomized controlled clinical trials suggest otherwise.

This study should have created a tsunami in the media and in the medical community but it hardly caused a ripple in the pond. Michael Eades explains why in an excellent post here.

The editors of the journal published a scathing rebuke of the authors but could not find anything wrong with the data and conclusions except that the data refuted their belief system. Busy physicians tend to read the editorials and place more credence in an editorial than in a study that questions or refutes a major thesis.

Lets look at some other studies that considered hard clinical endpoints.

Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial.

The objective of this study was:

“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.”

This study was a randomized controlled trial of 48,835 postmenopausal women aged 50-79 years of diverse backgrounds and ethnicity.

“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).”

Did this decrease heart attacks or strokes? NO

“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).”

Now lets look at a study where women were followed after a heart attack to see if reducing saturated fat helped.

Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84.

In this study quantitative coronary angiography was performed at baseline and after mean follow up of 3.1 years. 2243 coronary artery segments in 235 women were studied.

Here is what they found.

  • 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
  • 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 (of coronary atherosclerosis) when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein
  • Monounsaturated and total fat intakes were not associated with progression. (extra virgin olive oil and macadamia nuts are rich in monounsaturated fat)

The P values cited demonstrate unequivocal statistical significance for all of these associations.

So intake of carbohydrate and polyunsaturated fat was positively associated with progression of coronary atherosclerosis. Conversely, saturated fat intake was associated with less progression of coronary stenosis.  Again, I must point out that association does not prove or disprove causation. Nevertheless, there have been no prospective studies that demonstrate an association between saturated fat consumption and cardiovascular events (real clinical endpoints). Here we have data that show a negative association with saturated fat but positive association with carbohydrate and polyunsaturated fat consumption.

The logic has always been that substituting PUFA for SFA reduces cholesterol levels (short term studies) and therefore it should reduce heart attacks and strokes. But if you search the medical literature you find that the overwhelming body of data shows no reduction in hard clinical outcomes by reducing saturated fat, in fact just the opposite is true as in the two Ramsden studies cited in my previous post.

Uffe Ravnskov has pointed out that the proponents of the dietary  saturated fat-cholesterol theory often times misrepresent the data from published studies and cite those studies in support of the theory when in fact the data actually refute the theory. (as was the case for the AHA’s first dietary recommendations demonizing saturated fat in 1961) Uffe’s letters to the editor have been a nuisance to the proponents of that theory for decades.

An exhaustive review of the literature by Ravnskov was published in 1996. The summary deserves a complete quotation here.

J Clin Epidemiol. 1998 Jun;51(6):443-60.

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



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 and cardiovascular 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-control studies, 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.

That was published in 1998, since then the evidence remains as Uffe described it 15 years ago. More studies show no relationship between saturated fat consumption and cardiovascular death, heart attack, or stroke.

Finally, multiple autopsy studies around the world have been conducted to investigate an association between diet and atherosclerosis. None of these studies have demonstrated a positive association between degree of atherosclerosis and saturated fat intake.

Yet the AHA continues to recommend lower levels of saturated fat consumption while showing little concern for the problem of sugar and refined carbohydrates.

In my next post I will discuss why sugar and refined carbohydrates are major players in the physiology of atherosclerosis. Future posts will address the China Study, Forks Over Knives, the Ornish Diet and related topics. Additionally I will discuss why an egg a day keeps the doctor away.

Go in peace.

Bob Hansen MD.

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