German epidemiologist Dr. Karin Michels of the University of Freiburg recently declared coconut oil a “pure poison” because of its saturated fat content, re-igniting the perceived controversy about this oil. This inevitably gets major media (you know, the industry now largely run by Big Pharma, given the extraordinary dominance of direct-to-consumer drug ads) in a tizzy, doing things like resurrecting American Heart Association (AHA) advice to limit saturated fats, interviewing dietitians and mainstream doctors who, like Freiburg, declare saturated fat a scourge on health.
Funny, because the data never did associate saturated fat nor total fat with cardiovascular risk. There were a handful of flawed studies, misrepresented studies, and data that demonstrated no connection between saturated fat and heart disease that was unpublished because it was contrary to prevailing opinion in the 1960s, 1970s, and onward. Think Ancel Keys’ notorious Seven Countries Study in which he cherry-picked the data to “prove” that, the greater the saturated fat intake in a country, the more heart disease deaths occurred . . . until it was revealed that he left out the data on 15 other countries that would have disproven the association. (The breathtaking blunders have been recounted in excruciating detail by authors Nina Teicholz in her The Big Fat Surprise and Gary Taubes in Good Calories, Bad Calories. And several reanalyses (“meta-analyses”) of the combined data, including more recent studies, such as this review, conclude that there is no association between saturated fat intake and cardiovascular risk.
Despite this, the AHA reiterated its stand on saturated fat, basing their opinion on the (flawed) studies from the 1960s and more recent observational data that did indeed suggest that saturated fat was associated with increased cardiovascular risk. After all, lead author on the AHA position paper was Dr. Frank Sacks, an author of numerous observational studies. (And the AHA has gotten their dietary message so wrong so many times in the past—use Crisco for heart health, the AHA Check-Mark stamp of approval on Cocoa Puffs, Pop Tarts, and Count Chocula—why should we believe ANYTHING they say in diet?)
Let me talk for a moment about observational studies. An observational study is typically conducted like this: I have you fill out a dietary questionnaire that asks you to recall what you ate for, say, the last 3 days. I then recontact you 5, 10, or 20 years later and see what happened to you: healthy, heart attack, dead. Problem: filling out a questionnaire at one moment in time is a lousy way to assess diet, people change diets for a variety of reasons over the years—to lose weight, financial troubles, diet fads, etc. Another problem: confounding factors. If you say, for instance, that you are a vegetarian, it also means that you don’t drink much, don’t smoke, don’t engage in other high-risk behaviors, probably take nutritional supplements, eat more whole foods over processed foods. In other words, eating a certain way means that there are other behaviors attached to that way of eating; any effect on outcomes cannot be assumed to be due to vegetarianism per se, but to the entire collation of behaviors. There are other sources of bias in observational studies that muddy the results. Bottom line: Observational studies cannot establish cause-effect relationships; they can only suggest an hypothesis. To prove whether or not saturated fat does or does not cause heart disease cannot be based on questionnaires; a randomized prospective study in which people are randomly assigned to an eating style are compared. This has indeed been done and has shown NO association between saturated fat consumption and heart disease. The huge National Institutes of Health Mr. Fit Study (Multiple Risk Factor Intervention Trial), for example, that compared a low-fat, low-saturated fat, low-cholesterol diet (skim milk, butter replaced with margarine, no more than two eggs per week, minimized red meats, etc.) versus people who stayed on their higher-fat and cholesterol diet. 12,000 participants over 7 years: no difference in outcome.
Observational data is like having no data at all. Time after time, the conclusions drawn from observational studies (and falsely reported by researchers like Sacks or the media as definitive conclusion) have fallen apart in prospective studies like Mr. Fit. My favorite example is Premarin, horse estrogens prescribed to women for years. Observational data suggested that Premarin (that looks and acts NOTHING like human estrogens) reduced breast cancer, reduced endometrial cancer, and reduced heart disease. This was responsible for making Premarin the most widely-prescribed drug in the world for about a decade. Then the prospective, randomized HERS and Women’s Health Initiative trials were conducted. Conclusion: Premarin INCREASED breast cancer, INCREASED endometrial cancer, INCREASED cardiovascular death, even accelerated dementia. And this has been the story over and over again: Conclusions drawn in observational studies have proven to be flat wrong about 4 times out of 5. This hasn’t stopped people like Frank Sacks, through his observational Physicians’ Health Study and Nurses’ Health Study to, time and again, declare observational findings as fact. Unfortunately, even the USDA buys this observational fiction, incorporating the findings of observational studies in their dietary guidelines.
Conventional thinkers also claim that saturated fat raises total and LDL cholesterol. Is that true? Yes, it is . . . but who cares? Let’s be clear: Cholesterol does not cause heart disease. And total and LDL cholesterol are lousy predictors of heart disease. Lipoproteins, inflammation, and phenomena such as postprandial (after-eating) lipoproteins cause heart disease. Cholesterol is a crude and indirect index of lipoproteins. Why not measure the lipoproteins themselves that are far superior predictors of cardiovascular risk. If you do, you will see that saturated fat:
- Raises HDL (“good”) and shifts it towards larger, more protective, HDL particles
- Reduces triglycerides—that would otherwise contribute to lipoprotein distortions (via triglyceride-rich VLDL particles that influence the composition of other particles, increasing small LDL particles, for instance)
- Shifts LDL particles towards less harmful large with less small LDL particles
And, in the context of grain and sugar elimination that markedly reduces, often eliminates, small LDL particles, you will see that total and LDL cholesterol become wildly inaccurate reflections of REAL measures such as total low-density lipoprotein number. In other words, the crude total cholesterol and calculated LDL cholesterol derived via a crude, outdated equation no longer reflect lipoprotein composition.
Back to coconut oil. Eat it, enjoy it, use it to cook and bake, make Fat Blasters or Fat Bombs out of it. It is satiating, an excellent cooking oil, and the medium-chain triglyceride that comprises nearly half of its content by weight (lauric acid) improves cognition in people with cognitive impairment and dementia. It is rich in saturated fat that does not increase risk for cardiovascular disease.