I've got all these posts on coconut oil if you want to decide for
yourself. Or you can trust your doctor to have read all these and more.
I'm doing some, way too many pros vs. cons for me. But I'm not medically
trained like that professor that called it pure poison with no research
to back up her opinion.
Frank M. Sacks, MD
Departments of Nutrition and Molecular Metabolism, Harvard T.H. Chan School of Public
Health, Boston, MA
Address for Correspondence: Frank M. Sacks, MD Nutrition Department Harvard T.H. Chan School of Public Health 677 Huntington Avenue, Boston, MA 02115 Tel: 617-432-1420 Fax: 617-432-3101 Email: fsacks@hsph.harvard.edu
That coconut oil contributes to cardiovascular disease would appear non-controversial because
its saturated fat content increases plasma LDL-cholesterol concentration.1 Cholesterol-rich LDL
is a major cause of atherosclerosis because it delivers its cholesterol load to the arterial wall and
causes obstruction and inflammation. Nonetheless, coconut oil has been accorded much attention
in the popular media as a potentially beneficial food product. In fact a survey in 2016 found that
72% of Americans viewed coconut oil as a “healthy food”. 2 This represents a remarkable
success in marketing by the coconut oil and related industries calling coconut oil a natural,
healthful product, despite its known action to increase LDL-cholesterol, an established cause of
atherosclerosis and cardiovascular events. A systematic review, published in 2016, identified 7 trials that tested the effect of coconut oil on LDL-cholesterol. In these trials, coconut oil was compared to oils that had high content of unsaturated fats.3 Significant detrimental effects were found in six of them. The present study by Neelakantan, Seah, and van Dam is an important advance over this systematic review in that it includes a total of 17 published trials, takes a quantitative rather than a descriptive approach, and includes a range of outcomes relevant to assessing cardiovascular and metabolic health.4 This meta-analysis found that coconut oil significantly increased plasma LDL-cholesterol and HDL cholesterol, and had no effect on triglycerides, body weight, body fat, and markers of glycemia and inflammation as compared with non-tropical vegetable oils. Overall, this meta-analysis is rigorously conducted and reported, putting the results in the context of CVD prevention. Coconut oil is composed mainly of the saturated fatty acid, lauric acid (12 carbon atoms), but also of other long-chain saturated fatty acids, myristic (14 carbon atoms), and palmitic acids (16 carbon atoms).5 Mensink carried out a comprehensive systematic review with meta
regression of each of these fatty acids on plasma LDL-cholesterol and other lipoproteins.1
3
Mensink’s review considered all sources of lauric, myristic and palmitic acids, not only from
coconut oil, but in other foods such as dairy fat, palm kernel and palm oil. All of these saturated
fatty acids increased LDL-cholesterol. Lauric acid, the most prevalent fatty acid in coconut oil,
had a significant linear effect on LDL-cholesterol. Mensink used carbohydrate as the direct
comparator nutrient for the fatty acids. His approach found even more of an effect on LDL
cholesterol of these saturated fatty acids compared against mono- and polyunsaturated fatty
acids, combining the two estimates (coconut oil minus carbohydrate) + (carbohydrate minus
unsaturated fats). This is a practical way to illustrate the dietary application of the present meta
analysis since unsaturated oils like soybean, corn, olive or peanut oils are practical replacements
for coconut oil. Lauric acid is often classified as a medium-chain fatty acid, lumped with shorter chain fatty acids that have 6, 8 or 10 carbons.6 However, lauric acid, with its 12 carbon atoms, acts
biologically like a long-chain fatty acid absorbed by packaging into chylomicrons. This mechanism increases LDL-cholesterol. True medium-chain fatty acids are absorbed directly into the portal circulation, and do not affect LDL-C. Coconut oil is not an oil that acts as if its main components are medium-chain fatty acids. Coconut oil has about 13% true medium-chain fatty acids having 6, 8 or 10 carbon atoms. Thus, classifying lauric acid as a medium-chain fatty acid is a misnomer, going against its biological action as a long-chain fatty acid. Neelakantan and colleagues wrote a well-reasoned section in the introduction that rebuts this argument, and stands by the well established absorption of lauric acid to form chylomicrons, like other long-chain saturated fatty acids. The database includes small numbers of trials that could be used in analyses of effects on LDL-cholesterol of specific dietary comparisons, such as coconut oil vs. butter, or coconut oil vs. individual nontropical vegetable oils. Although not the primary aim of the present study, these comparisons could be used to form a hierarchy of health effects of cooking oils. However, the effect on LDL-cholesterol of additional dietary comparisons may be estimated well by the meta regression analysis on the component fatty acids. While coconut oil increases plasma HDL-cholesterol, it is impossible to know if this is a
beneficial mechanism in cardiovascular disease. 7 Although HDL-cholesterol is a robust risk
marker for cardiovascular disease, genetic studies and HDL-raising drugs have not so far
supported a causal relationship between HDL-cholesterol and cardiovascular disease. HDL, the
lipoprotein, is composed of a huge array of subparticles that may have adverse or beneficial
actions. 7,8 It is unknown which, if any, foods or nutrients that raise HDL-cholesterol do so in a
way that reduces atherosclerosis and coronary events. Thus, effects on cardiovascular disease of
foods or nutrients cannot be judged from changes in HDL-cholesterol. There is no randomized clinical trial that determined the effect of coconut oil on cardiovascular events such as myocardial infarction, heart failure, or stroke. Such a trial is unlikely to be attempted due to high cost of hundreds of millions of dollars, large numbers of participants, and many years of treatment with coconut oil and an appropriate control fat. The inevitable rise in LDL-cholesterol sustained over years in those assigned to coconut oil will create an ethical concern of harm, and may stop the trial before a definitive result is obtained. This situation is relevant to much of nutrition research. This limitation can be countered with evidence from effects of foods on established cardiovascular risk factors, such as LDL cholesterol, and on incident cardiovascular events in large prospective, observational cohorts. Advertisements give the impression that purportedly beneficial constituents other than
saturated fat compensate for its adverse effects on LDL-cholesterol. Yet, controlled trials in humans are not available that support beneficial actions of components of coconut oil on cardiovascular disease risk factors or mechanisms. Coconut oil may be viewed as one of the most deleterious cooking oils that increases risk for cardiovascular disease. Even in comparison with palm oil, another tropical oil with high saturated fat content, coconut oil increased LDL-cholesterol. Replacing coconut oil with nontropical unsaturated vegetable oils, especially those rich in polyunsaturated fat, will have a health benefit. We believe that the results from the present meta-analysis can inform the development of nutrition recommendations and USDA dietary guidelines. In culinary practice,
coconut oil should not be used as a regular cooking oil although it can be used sparingly for
flavor or texture.
No comments:
Post a Comment