Folks, hold your horses; I know just what’s going on here.
My friendly adherents (thank you; I love you, too) are here for another refreshing installment of “stuff I already knew was right and love to Tweet.” My detractors (back at ya’, bub) are here knowing in advance they will disagree with everything, in eager anticipation of throwing up all over this column and me (I always carry an umbrella) in social media.
So, for starters, let’s establish this: the “I only consider information I already know to be true” mentality, in either direction, is far more toxic to us than even our most egregious forays into the realm of Frankenfood. If your brain is mired in such gunk, saturated fat is unlikely to hurt you further, although it certainly won’t help.
Stated differently, the relentless pursuit of confirmation of the opinion you already own- be you reader or writer, seller or buyer- is not even in the same part of the animal kingdom as the pursuit of truth.
Believe it or not, there is a discernible truth about saturated fat, hard to perceive through the smoke of all the overcooked arguments though it may be. Let’s give it a go.
We have known for a long time- many years- that all saturated fat is not created equal with regard to health effects. The details of a discussion encompassing, for instance, just stearic acid, lauric acid, palmitic acid, and myristic acid- to say nothing of caprylic, caproic, butyric, enanthic, and so on- could take many interesting pages. Suffice to say: some saturated fatty acids are quite convincingly established to be harmful, and others are not.
This is not a place to go into great detail about diverse sources of evidence, although I do spend considerable time in just such places. Here, it’s appropriate to note that “convincingly established” refers not to one favored study, not the latest spate of hyperbolic headlines, and not someone’s effort to sell the newest book of dietary revelation- but the weight of evidence. As someone who has contributed to and reviewed the literature in question, and written extensively about assessment of evidence, I find the weight of evidence most compelling when it in turn is a product of hybrid vigor. Specifically, we know what we know most reliably when mechanistic studies in cell culture and animal models align with biomarker studies in people, and when those in turn align with outcome studies and intervention trials in people, and when those in turn align with observational epidemiology at the level of whole populations.
Our knowledge of saturated fat is informed by just such evidence, spanning species, decades, methods, and populations.
Regarding mechanisms of effect, there is one especially salient refrain among those championing saturated fat for health: it tends to raise HDL levels. Yes, that is true. But does that actually validate the agenda of the “eat more meat, butter, and cheese” crowd? No, for two reasons.
First, the obvious one. You can have low HDL but feel fine and never get heart disease; or have enviably high HDL, but have a massive MI. Which would you prefer?
The point is that none of us really cares about our blood levels of HDL, or any other moiety for that matter, other than as proxies for health outcomes that actually affect our lives. High HDL is desirable only if and when it signifies a lower risk of cardiovascular disease. That’s what actually matters.
But doesn’t a higher HDL reliably guarantee lower heart disease risk? Absolutely not, and for a reason that is all but intuitive with a simple analogy.
Consider, for instance, an argument that good urine output is an indicator of healthy kidneys, vitally important for control of blood volume and consequently, blood pressure (an established fact). Now, consider that a high intake of, let’s say, pickles, increases urination. The obvious argument by the International Confederation of Pickle Pushers is: See! Good urine output is good for blood pressure, and pickles increase urine output- so pickles are good for blood pressure!
But don’t sign up for the pickle-juice diet just yet. You see what’s going on, right? The rather massive sodium load from pickles is actually prone to raise blood pressure, and blood volume, and the urine output is simply the body attempting to keep up, and compensate.
I don’t know for sure if that applies to the effects of saturated fat on HDL, but I find no clear indications in the scientific literature that it does not. In other words, maybe a rise in HDL from saturated fat intake is a genuinely good thing, and attenuates the rather obvious harms of excess saturated fat intake from the usual sources. But we can’t reliably reach that conclusion. Maybe HDL goes up because confronted with more saturated fat, the body NEEDS more HDL. Maybe “saturated fat raises HDL” actually translates to: saturated fat stresses the body, and the body does what it can to compensate.
That is conjecture at this point, but so is the contention that higher HDL automatically means that saturated fat is doing us “good.” The far more important issue is: what happens to heart disease risk?
That question has been answered, at least in the real world where most of our saturated fat does, indeed, come from variations on the theme of meat, butter, and cheese, and not from cacao beans and coconut.
Mechanistic studies suggest less inflammation and atherogenesis when saturated fat intake is reduced, and replaced by unsaturated fats. Intervention studies show similar benefits when a baseline diet with many liabilities, a high load of saturated fat among them, is replaced with either a Mediterranean diet high in unsaturated fats, or a diet low in total fats. Dramatic declines in cardiovascular disease at the population level over a span of decades, have been observed in North Karelia, Finland, where a reduction in saturated fat intake was among the priority interventions.
Also in the real world, the longest-lived, most vital populations on the planet vary widely in their intake of total fat, but none has a high intake of saturated fat. The idea that a diet high in saturated fat “could” be as good is a leap of faith. The call to “jump” is more often than not issued by those with something to sell you.
Another crucial, and often neglected matter- with regard to saturated fat specifically, and nutritional epidemiology in general- is the “instead of what?” question. We are, for example, hearing these days that “butter is back.” Instead of what?
Push on that issue, and you are told: instead of stick margarine. Well, that was tossed on the rubbish heap of bad ideas over 20 years ago! Or, maybe we are told: instead of the bagel. But who ever actually chooses between a bagel and butter? The bagel, a generally dubious idea in its own right, invites the butter.
What this really distills down to is the simplest of marketing ploys: use a sound bite to tell people what they want to hear, and then only acknowledge the subtleties of truth in the fine print. Is butter back relative to olive oil? Hell no! Is it back relative to apples?
While routinely ignored, or willfully neglected, this “instead of what?” question was the particular focus of a study in about 85,000 people. When members of this group reduced their intake of saturated fat over time, the health results varied directly with the replacements. When saturated fat calories are supplanted by trans fat calories, things go from bad to worse. When they are replaced with refined starch or added sugar, things are equally bad both times. While some point to such data to say, “see, raising saturated fat intake does not raise heart disease rates!” they actually show: excesses of saturated fat and sugar seem to be almost exactly, comparably bad for us.
Notably, when saturated fat calories from the customary sources- bacon-cheeseburgers, Reuben sandwiches, and pepperoni pizza come to mind- are replaced with either unsaturated fat (from nuts, seeds, olives, avocado, and fish), or with calories from whole grains- rates of cardiovascular disease decline significantly.
The truth about saturated fat is not unsettled. What is unsettled is: can we handle the truth?
Saturated fat need not be exonerated, let alone canonized, to make the case that excess sugar is bad for us, too. Our appetite for sound bites and hyperbolic promises, and our antipathy for the more measured character of reliable truth, does nothing to advance our health. It does encourage us to keep fixating on nutrients while neglecting foods; to argue over foods while neglecting overall dietary patterns; and to keep inventing new ways, and reinventing old ones, to eat badly.
Until we decide to change it, that, sadly, is the truth.
David L. Katz, MD, MPH, FACPM, FACP, FACLM, is the Founding Director (1998) of Yale University’s Yale-Griffin Prevention Research Center, and current President of the American College of Lifestyle Medicine. He has published roughly 200 scientific articles and textbook chapters, and 15 books to date, including multiple editions of leading textbooks in both preventive medicine, and nutrition. He has made important contributions in the areas of lifestyle interventions for health promotion; nutrient profiling; behavior modification; holistic care; and evidence-based medicine. David earned his BA degree from Dartmouth College (1984); his MD from the Albert Einstein College of Medicine (1988); and his MPH from the Yale University School of Public Health (1993). He completed sequential residency training in Internal Medicine, and Preventive Medicine/Public Health. He is a two-time diplomate of the American Board of Internal Medicine, and a board-certified specialist in Preventive Medicine/Public Health. He has received two Honorary Doctorates.