So in part I, I discovered that the American Heart Association (AHA) based their claims on research that is likely not applicable to my diet, and that of other health-conscious individuals who consume animal food products. The research they cited involved replacing saturated fatty acids (SFAs) in the diet with polyunsaturated fatty acids (PUFAs). The saturated fat diet in those studies included margarine, a lot of milk, butter, and most likely a sedentary lifestyle (exercise wasn’t as trendy back then in the 50s and 60s). While the AHA excluded studies that found an increased risk of cardiovascular events in the high PUFA group because they consumed margarine, they happily included studies when margarine was present in the diets of the SFA group.
Furthermore, the only study (out of the four core trials supporting their hypothesis) that listed amounts of various foods consumed in the two diet groups took place in a hospital where patients were on drugs that negatively affect the heart (phenothiazine, thoridazine, and TCA antidepressants); and in the SFA group patients took more drugs on average, confounding the results. Yet the AHA concluded that “lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD.”
I also discovered that numerous papers published in the AHA’s journal, Circulation, report an increased incidence of CVD and cardiovascular mortality with higher saturated fat intake whereas other journals like BMJ and ACJN do not. In fact it seems that every paper in Circulation points to the idea that LDL cholesterol is bad, HDL is good, and lowering cholesterol through pharmacological means or by reducing saturated fat intake is protective for CVD. But perhaps there is an observer effect at play here; maybe the AHA’s bias and bottom line indirectly cause them to see such results, whereas in the BMJ, results vary.
Nevertheless, in this post, I want to discuss three systematic reviews and meta-analyses the AHA cited in their Presidential Advisory. These papers do not support the AHA’s viewpoint, however they were cited because they evaluated trials that the AHA included as “core” evidence. How these types of publications work is they search the literature for studies addressing a specific research question. Then, they pick the studies that match their criteria the best. Their search criteria may have identified hundreds of studies, but only a handful make the cut usually. Then they pool the results and conduct one analysis as if the results came from one big study.
The disadvantage of this technique is that the studies identified likely use different methods, and cannot be compared exactly. But if there is a true effect (of saturated fat in this case), it shouldn’t matter.
So the AHA kind of did their own analysis, identifying four trials that made their cut, because they replaced polyunsaturated fat with saturated fat, from three separate meta-analyses. They disagreed with the conclusion in these meta-analyses because they didn’t think that studies where people consumed more PUFA could substitute for studies where PUFA directly replaced SFA.
This is getting confusing so let’s briefly sum up the conclusions from three separate meta-analyses below.
1. Mozaffarian et al. Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
This systematic review and meta-analysis included eight studies, including the four that constitute the AHA’s “core” trials. One of the included studies (Minnesota Coronary Experiment) found the complete opposite that the other studies did. In the high PUFA group, cholesterol decreased, but heart attacks went up. This was also seen in the Sydney Diet Heart Study. The AHA ignored these studies because margarine was consumed in the high PUFA group. Yet it was also consumed in high SFA groups in at least one of the core trials they cited (and likely the other ones too as it was a common product back then), yet they felt that those studies were adequate in supporting their hypotheses.
Another paper by this lead author (with a slightly different research question) came to a different conclusion that they did here. In post-menopausal women, it was found that increasing saturated fat intake reduced the progression of atherosclerosis. I highly doubt that this is due to the nature of the participants. The AHA isn’t talking about that study.
2. Hooper et al. Reduction in saturated fat intake for cardiovascular disease.
The Cochrane meta-analysis included a total of fifteen trials. Some of them weren’t even about cardiovascular disease, but followed up with participants after a long enough period of time where cardiovascular events occurred. These researchers found that when pooling total cardiovascular events in all fifteen trials, there was a 17% reduction in mortality. But specifically for cardiovascular mortality or all-cause mortality, there was no association. Another major flaw to these trials is that they rely on populations that due to a variety of factors, already have an increased incidence of inflammatory diseases. It’s called being modern. These diseases are lower in incidence in rural/traditional populations, even if those populations consume animal products rich in saturated fat like milk (like the Maasai tribe).
One of their studies, the Rose Corn Oil study, saw twice as many cardiovascular events in the group consuming corn oil relative to the control group, but the overall number of events was too small to be statistically significant. Drinking oil every day probably is not healthy anyway.
3. Chowdhury et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis.
I don’t think it’s necessary to pore through the details anymore. Eventually, something gets critically lost. We could evaluate each individual study, but the fact remains that there is not one single study that I am aware of that examines the relationship between saturated fat in the diets of people who consume animal products along with vegetables, and exercise moderately. There is NO CONCEPT of SYNERGY in medical research. Everything has to be isolated and factored with statistical analyses. I’ve long believed that this process is completely useless when it comes to understanding nutrition.
The question is, is saturated fat inherently disease promoting. Multiple meta-analyses say no. Yet some, but not all trials that attempted to reduce saturated fat among a modern population who may already have an increased risk show that there is a protective effect. What if movement, a natural prerogative, has a synergistic relationship with saturated fat? Maybe after exercise, saturated fat is good for us? This question has never been addressed to my knowledge by the literature. The possibilities for synergy are endless.
This study concluded “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.” It’s a headache to look through all these studies. It’s non-intuitive, unnatural, and makes no sense after a while, unless you have a bias, like the AHA, or even people who are die-hard saturated fat fans.
Red meat typically has more monounsaturated fat than saturated fat. Grass-fed red meat, and pasture-raised eggs have more omega-3 fatty acids than the crap people ate in these old-school trials. There are synergistic components to healthfully raised animal products that are cardioprotective. L-carnitine is cardioprotective and it’s only found in animal products. The type of reductionist thinking used by the medical community alienates us from what’s in front of us.
In sum, focusing on saturated fat only helps the AHA promote statin use, as increasing the amount of saturated fat in the diet can reliably increase serum cholesterol, and if it can be shown that this increase is associated with increased mortality from cardiovascular disease, statins sound like a good idea.
What’s also interesting in the original studies the AHA cited is that for whatever reason, participants tended to have pretty high cholesterol levels (above 250 ng/dl). This may be caused by being sedentary…who knows. Eating energy-dense foods while being sedentary is the condition of the modern man and has nothing to do with saturated fat intake. But I could care less. I’m done.