Rethinking Saturated Fat
This blog is connected to yesterday’s blog about red meat. Red meat has been vilified for decades now because of its content of saturated fatty acids. The mainstream advice has been and still is to keep off foods like red meat and eggs and switch to the omega-6 polyunsaturated fats. It’s never been my advice as lowering cholesterol can have disastrous effects on health and well being. And I’ve always recommended red meat as an important part of your diet – see here for my article on red meat.
The mantra that your cholesterol can never be low enough found strength in the fact that increasing dietary omega-6 linoleic acid in the place of saturated fat has been shown to lower both total cholesterol and LDL cholesterol (low density lipoprotein cholesterol), both of which if elevated are widely thought to increase the incidence of heart disease.
This myopic stand should have died long ago but influential stalwarts such as the American Heart Association have kept it alive and well. However, a new study analyzing old data may just be a significant nail in that mantra’s coffin. (See abstract below – for the full paper go here.)
Calling the Mantra Into Question
In this study the researchers did an in-depth analysis of the data on effects of linoleic acid on deaths from coronary heart disease and cardiovascular disease from the Sydney Diet Heart Study — a randomized controlled trial conducted from 1966 to 1973 in which 458 men aged 30-59 years who had recently had a coronary event, such as a heart attack or an episode of angina, were randomly divided into two groups.
The intervention group was instructed to reduce saturated fats (from animal fats, common margarines and shortenings) to less than 10% of energy intake and to increase linoleic acid (from safflower oil and safflower oil polyunsaturated margarine) to 15% of energy intake. It should be noted that safflower oil is a concentrated source of omega-6 linoleic acid and provides no omega-3 polyunsaturated fatty acids (PUFAs).
The control group received no specific dietary advice. Both groups had regular assessments and completed food diaries for an average of 39 months. All non-dietary aspects of the study were designed to be equal in both groups.
The study found that the omega-6 linoleic acid group had a higher risk of death from all causes, as well as from cardiovascular disease and coronary heart disease, compared with the control group.
At the very least this study has to have you wondering about the validity of the universally espoused but misguided information about polyunsaturated and saturated fats and the risk of heart disease.
What We Don’t Know Matters
The backbone of science is a two fold process – first to come up with a theory/hypothesis and second to test it out using the scientific method. Basically you try and prove that the hypothesis is wrong and if you and others fail to do so, then that hypothesis is provisionally accepted with the understanding that ongoing studies may modify it or even prove it wrong. You shouldn’t skip the ongoing studies and jump from a hypothesis to a truism, like has happened with linking the cholesterol group of fats with heart disease and mortality.
What we know about total, HDL, LDL and other cholesterols is open to both interpretation and to corrections. For example the idea that HDL, the so called “good” cholesterol is to be heart protective may or may not be true. In fact a recent study identified two types of HDL, with one of those types increasing the risk of cardiovascular disease (see abstract below).
A significant part of the problem is Big Pharma, the rich and influential pharmaceutical industry that pushes its own financial agenda in both research and marketing. A blatant example is their unbending faith that cholesterol has to be lowered and controlled and as such push to have everyone on statin drugs, regardless of their cholesterol levels or risk of developing heart disease.
Their facile statements that universal statin use would be beneficial for everyone ignores the significant adverse effects of statins, and the lack of valid, impartial evidence that statins in fact can reduce morbidity and mortality in anyone that uses them.
Statins are not innocuous drugs and studies have shown that they can adversely affect health in many ways, including loss of muscle and strength, muscle pain, erectile problems, decreased libido, increased risk or cataracts, and kidney and liver damage.
It’s About Time
The time has come to question the cholesterol “truths” and this study is part of the answer but there’s still much more we have to know before we can make such blatant and misguided statements about good and bad foods.
Professor P. Calder, the author of the accompanying editorial says that the findings of the study argue against the “saturated fat bad, omega 6 PUFA good” dogma and suggest that the American Heart Association guidelines on omega-6 PUFAs may be misguided. They also “underscore the need to properly align dietary advice and recommendations with the scientific evidence base.”
Good for him and the authors of the study. And it’s about time that the tide turned to facts and caution, instead of partial truths and manipulation.
Abstracts Cited In Blog
BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707.
Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis.
Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR.
Laboratory of Membrane Biophysics and Biochemistry, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA.
To evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death.
Evaluation of recovered data from the Sydney Diet Heart Study, a single blinded, parallel group, randomized controlled trial conducted in 1966-73; and an updated meta-analysis including these previously missing data.
Ambulatory, coronary care clinic in Sydney, Australia.
458 men aged 30-59 years with a recent coronary event.
Replacement of dietary saturated fats (from animal fats, common margarines, and shortenings) with omega 6 linoleic acid (from safflower oil and safflower oil polyunsaturated margarine). Controls received no specific dietary instruction or study foods. All non-dietary aspects were designed to be equivalent in both groups.
All cause mortality (primary outcome), cardiovascular mortality, and mortality from coronary heart disease (secondary outcomes). We used an intention to treat, survival analysis approach to compare mortality outcomes by group.
The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).
Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.
The full version of the study is available at: http://www.bmj.com/content/346/bmj.e8707.
J Am Heart Assoc. 2012 Apr;1(2). pii: jah3-e000232. doi: 10.1161/JAHA.111.000232. Epub 2012 Apr 24.
Apolipoprotein C-III as a Potential Modulator of the Association Between HDL-Cholesterol and Incident Coronary Heart Disease.
Jensen MK, Rimm EB, Furtado JD, Sacks FM.
Department of Nutrition, Harvard School of Public Health, Boston, MA (M.K.J., E.B.R., J.D.F., F.M.S.).
High-density lipoproteins (HDL) are structurally and metabolically heterogeneous and subclasses with differential effects on coronary heart disease (CHD) might exist. Apolipoprotein (apo) C-III, a small proinflammatory protein that resides on the surface of lipoproteins, enhances the atherogenicity of VLDL and LDL particles, but little is known about the role apoC-III on HDL. We investigated whether the presence or absence of apoC-III differentiates HDL into subtypes with nonprotective or protective associations with risk of future CHD.
METHODS AND RESULTS:
High-density lipoprotein cholesterol (HDL-C) levels were measured in plasma separated according to apoC-III (by immunoaffinity chromatography) in two prospective case-control studies nested within the Nurses’ Health and the Health Professionals Follow-Up Studies. Baseline was in 1990 and 1994, and 634 incident CHD cases were documented through 10 to 14 years of follow-up. The relative risk of CHD per each standard deviation of total HDL-C was 0.78 (95% confidence intervals, 0.63-0.96). The HDL-C subtypes were differentially associated with risk of CHD, HDL-C without apoC-III inversely and HDL-C with apoC-III directly (P=0.02 for a difference between the HDL types). The relative risk per standard deviation of HDL-C without apoC-III was 0.66 (0.53 to 0.93) and 1.18 (1.03 to 1.34) for HDL-C with apoC-III. HDL-C with apoC-III comprised ?13% of the total HDL-C. Adjustment for triglycerides and apoB attenuated the risks; however, the two HDL-C subgroups remained differentially associated with risk of CHD (P=0.05).
Separating HDL-C according to apoC-III identified two types of HDL with opposing associations with risk of CHD. The proatherogenic effects of apoC-III, as a component of VLDL and LDL, may extend to HDL.