Questions on key nutrition topics, the latest science & nutritional information

Where does the data now stand on saturated fats?

Since 2014 when my book was published, the data exonerating saturated fats has grown even stronger. There are now more than 17 systematic reviews and meta-analyses of scientific studies looking at the relationship between saturated fats and heart disease. These studies include randomized, controlled clinical trials on more than 50,000 people, which is an enormous amount of the most rigorous kind of data available.

Nearly all of the analyses reviewing this data have concluded that:

  • Saturated fats have no effect on cardiovascular mortality and/or
  • Saturated fats are not associated with heart disease.
  • Don’t these studies conflict with our official nutritional advice?

They do. To understand why, one needs to know the history of why we believe these fats are bad for health.

Beginning in the 1950s, University of Minnesota pathologist Ancel Keys, launched the so-called “diet heart” hypothesis, which states that saturated fats and dietary cholesterol cause heart disease. Largely due to his outsized personality, Keys was able to get this idea implanted in the American Heart Association, which in 1961, became the first group in the world to recommend that the public cut back on saturated fat and cholesterol to prevent cardiovascular disease.

In subsequent decades, Governments and public health groups around the world spent billions of dollars on clinical trials (the “gold standard” of scientific evidence) trying to ‘prove’ this hypothesis, but all of these trials had “null” results—which is to say, they could not show that Keys was correct. In some cases, trials showed that reducing consumption of saturated fat and cholesterol (and replacing them wiht polyunsaturated vegetable oils) actually caused harm, including increased death rates from cancer and suicides.

Rather than respond to this ‘inconvenient’ data, however, scientists instead persevered in their belief that saturated fats must somehow be bad for health. These scientists, together with their funders at the National Institutes of Health, the American Heart Association, and elsewhere, ignored or even buried inconvenient data for decades. My book tells this story.

The story is largely one of politics: the influence of the food industry, the inability of large public health institutions, including our own federal government, to back out of a failed hypothesis, and the reality of nutrition experts who are unable or unwilling to change their minds, despite an overwhelming amount of evidence to the contrary.

Recently, however, there has been change. Beginning in 2010 with the work of Ron Krauss, scientists around the world have begun to unearth and reexamine the long-ignored literature on saturated fats, resulting in the 17 meta-analyses and reviews listed above.

Note that in response to this evidence, the Canadian Heart and Stroke Association in 2015 dropped its previous % limits on saturated fats.

Is there a short, non-book-length version of this story?

A short piece I wrote on how we came to believe that saturated fats are bad for health is “The Questionable Link Between Saturated Fat and Heart Disease,” in the Wall Street Journal (behind a paywall; also available here), which is adapted from my book. When it came out, it was the most emailed piece in the newspaper’s recent history.

Another option is an article that I wrote for Men’s Health magazine, “What if Bad Fat is Actually Good for You?” way back in 2007.

  • Given this enormous reevaluation of the literature on saturated fats over the past five years, why do the 2015-2020 U.S. Dietary Guidelines continue their caps on saturated fats?

The answer is that the expert committee for those Guidelines did not adequately or comprehensively review the recent data on these fats. This fact, which I reported for a 2015 article in The BMJ, was controversial and thus highly contested, yet it has stood up to multiple rounds of peer review, and is now confirmed as correct.

Another important paper on this subject is: “Evidence from randomised controlled trials does not support current dietary fat guidelines: a systematic review and meta-analysis,” BMJ Open Heart, 2016.

Why, then, do I keep seeing studies saying that saturated fats cause heart disease?

These studies are being published by epidemiologists and in particular, the nutrition department at the Harvard School of Public Health, which has published about one paper roughly every six months, based on data from its two epidemiological databases. These studies are flawed in numerous ways, and critiques of them can be found on pubpeer, here, here and here. More importantly, the Harvard studies are contradicted by the earlier clinical trial data reflected in those 17 reviews. That trial data (unlike Harvard’s epidemiological findings) can actually demonstrate cause and effect. It is therefore more definitive.

Indeed, the usual process in science is to start with an epidemiological association, which suggests a hypothesis, and then move on to test that hypothesis in clinical trials. Once properly tested in trials, there is no point in going back to look at hypothesis-generating epidemiological data again. It’s therefore not clear why Harvard keeps publishing these epidemiological associations or why informed reporters keep citing them.

In sum: the question of whether saturated fats cause heart disease has repeatedly been tested in large clinical trials, with null results. There is no need to go back to epidemiological data, which re-suggests a hypothesis that has already been thoroughly tested.

If I eat saturated fats, won’t my cholesterol go up?

The short answer is: Maybe, but not in a way that will increase your risk for heart disease. Saturated fat was originally demonized for its ability to raise total cholesterol. However, researchers in the 1980s discovered that total cholesterol did not turn out to be a reliable predictor of heart attack risk. The conversation then shifted to saturated fat’s tendency to raise LDL-cholesterol (the “bad” kind). However, yet again, clinical trials could not confirm LDL-C’s ability to predict heart attack risk. In many large clinical trials, LDL-C did not turn out to be correlated with the risk of dying from heart disease.

Also, it turns out that LDL-C has sub-fractions: some are small and dense, while others are light and buoyant. The small, dense ones have been found to predict increased risk, whereas the light, buoyant ones predict reduced risk. The kind of LDL that saturated fats cause to increase is the light, buoyant kind. Therefore, saturated fats actually appear to reduce heart-disease risk, not increase it.

Moreover, saturated fats are the only foods known to increase your HDL-C, the “good” cholesterol. When your doctor tells you to raise your HDL, s/he will recommend drinking red wine or getting more exercise, but a far easier way to raise HDL is simply to eat more saturated fats. Saturated fats reliably boost the “good” HDL cholesterol.

The first succinct publication of all this information was in an article that I wrote for Men’s Health magazine, “What if Bad Fat is Actually Good for You?” way back in 2007.

So, in sum, the effects of saturated fat on blood lipids can be said to be positive. Further explanation and references on all of the above can be found in my book.

Doesn’t it depend on what is eaten to replace saturated fats?

This is an argument promoted by defenders of the diet-heart hypothesis, and it is odd, because these same experts talk about other foods as simply being “good” or “bad” without insisting on a discussion about “what replaces them.” This discrepancy in approach leads me to believe that the “replacement” argument against saturated fats is probably a rhetorical maneuver aimed at creating confusion over the the data on saturated fats.

However, because this argument is being promoted by experts at the highest level, including those directing the review of saturated fats for the 2015-2020 Dietary Guidelines, it deserves a response.

Saturated fats vs. carbohydrates. All reviews agree that replacing saturated fats with “refined carbohydrates” leads to poorer cardiovascular outcomes. This position was confirmed by the expert committee for the US dietary guidelines as well as the latest American Heart Association “Presidential” advisory on saturated fats. However, if you look at data from randomized controlled clinical trials, saturated fats have never been replaced by “refined carbohydrates.” E.g., In no trial did researchers say: reduce saturated fats (in meat/dairy) and replace these foods with cookies, crackers, chips, and white flour. Instead, large clinical trials, including the Women’s Health Initiative (WHI) and the “Boeing Studies” counseled subjects to reduce the fats in meat/dairy and replace these with whole grains, fruits, and vegetables. The WHI, which measured “hard endpoints” (heart attacks and death) found no benefit of this diet. The Boeing Studies, which measured “soft endpoints,” found that the low-fat diet had mixed cardiovascular benefit (it lowered LDL-C but also lowered HDL-C and raised triglycerides).

Thus, the data show that replacing fats with total carbohydrates, including fruits, vegetables and whole grains, does not improve cardiovascular outcomes. Implication: It is healthier to eat a breakfast of eggs rather than whole-grain cereal or
oatmeal; cheese is a better snack option than crackers or fruit.

On sat fats vs. polyunsaturated vegetable oils. Remember that the original advice by the American Heart Association in 1961 was to replace saturated fats with polyunsaturated vegetable oils, so that hypothesis was tested on a massive scale. Thus, we have a huge volume of rigorous data, from government-funded, randomized, controlled clinical trials, conducted in the 1960s and 70s (which I describe in Ch. 2 in my book). This trial data has been reviewed in at least 9 meta-analyses and systematic reviews. These reviews universally conclude that replacing saturated fats with polyunsaturated vegetable oils has no benefit for cardiovascular or total mortality. Those studies that separately analyze strokes and heart attacks conclude that saturated fats have no effect on these outcomes. Only by ignoring that data and looking instead at the less definitive composite endpoint of “cardiovascular events,” a category that combines heart attacks with more subjective events such as angina, could the AHA arrive at its negative findings for saturated fats. For a full discussion of this issue including a table of the 9 meta-analyses, see this article that I co-authored with cardiologist Eric Thorn for the medical website Medscape.

This is the clinical trial data, which is the most rigorous and is the only kind of data that show cause and effect. There are multiple recent papers, mostly by the Harvard School of Public Health concluding that swapping saturated fats for polyunsaturated vegetable oils, but these studies are based on weak epidemiological data and involve complex modeling involving multiple assumptions. This kind of data can suggest hypotheses but not prove them. Because we have rigorous clinical trial data on this topic, that is far more definitive.

It is not clear why Harvard persists in publishing data on a topic that has already been tested in clinical trials, but one clue is that members of that group report receiving funds from vegetable oil companies, and the Harvard team appears to work closely with Unilever, one of the largest vegetable-oil manufacturers in the world. (Indeed, in one recent Harvard analysis, nearly half the authors were actually employees of Unilever.)

In sum, the extensive clinical trial data on this topic have concluded that saturated fats have no effect on heart attacks, stroke, cardiovascular mortality or total mortality.

Are there positive arguments for eating butter, meat and cheese?

Yes, there are the three major ones:

  1. These foods are far more nutrient dense than plant foods, and their nutrients have been shown to be more bio-available than those in plant foods. For instance, vitamin B12 is not available in plant foods. Fat-soluble Vitamins A, D, E and K need fat to absorb properly—and this fat comes naturally in animal foods. (The current USDA diet is inadequate in D vitamins without fortified foods.) Choline, lutein, and heme iron are scare in plant foods while abundant in animal foods–and so on. (I will post more links and information on this later.)
  2. Protein and fat have been shown, in clinical studies, to be far more satiating than carbohydrates. These satiating qualities mean that people are far less likely to “overeat” on these foods. For instance, most people, when they eat bacon and eggs for breakfast, are not hungry until lunch, whereas a breakfast of cereal and low-fat yogurt often has people starving by mid-morning. And as we all know, people “overeat” quite easily on carb-based foods like cookies, crackers, chips, bread, etc. Because protein and fat are found naturally paired together in animal foods, these are the most easily accessible, whole foods that make up this healthy and satiating diet.
  3. Finally, the historical record supports a diet higher in animal foods: One hundred and fifty years ago, we ate far more red meat, cheese, butter and lard than we do today (butter and lard were the principal fats that Americans used for cooking before 1900). We ate this way before the epidemics of heart disease, obesity and diabetes. I provide data on these facts in in my book and also debunk the myth that pre-1900, we just didn’t live long enough to suffer from the chronic diseases that appear later in life.

Where does the data stand on total fat?

It’s clear that a low-fat diet, defined in the scientific literature as between 20 and 35% of calories as fat, is not a healthy diet. This diet has been tested in multiple, NIH-funded clinical trials, on more than 55,000 people, all of which found that the low-fat diet was completely ineffective for combatting obesity, diabetes, heart disease, or any kind of cancer.

Worse than that, the low-fat diet has been shown to worsen various disease risk factors. According to the expert report for the 2015 US Dietary Guidelines, low-fat diets are “associated with dyslipidemia”—meaning that the low-fat diet is linked to heart disease. Worse than that, rigorous evidence shows that the low-fat diet actually causes these harmful effects. Low-fat diets reliably cause HDL-C (the “good” cholesterol) to drop and triglycerides to rise, both signs of increased heart-disease risk. These factors also signal the onset of the metabolic conditions that cause obesity and diabetes.

Given this data, the low-fat diet is no longer officially recommended by our major nutrition authorities. The American Heart Association (AHA) dropped its longstanding limits on total fat in 2013, and the US Dietary Guidelines (DGAs) followed suit by eliminating any reference to limits on total fat in 2015. This doesn’t mean that low-fat caps don’t still exist in the fine-print of the DGA report, but the official, topline advice, to eat a low-fat diet, recommended by the AHA since 1970 and the DGAs since 1980, is gone.

Even so, the government has yet to announce this important change to the public. There have been no press releases to let the American public know that the major dietary policy for disease prevention of the last 35+ years is now over.

Where does the science stand on dietary cholesterol?

The American Heart Association dropped its caps on dietary cholesterol in 2013. The US Dietary Guidelines followed suit in 2015. Why? Because since the 1950s, rigorous scientific evidence has shown that dietary cholesterol has little marginal effect on blood cholesterol. The more cholesterol you eat, the less your body itself produces. The back story and science on this subject is covered in my book, with references.

Is sugar uniquely unhealthy?

In his latest book, The Case Against Sugar, science journalist Gary Taubes makes the case that sugar has always been at the “scene of the crime” when populations have become obese/diabetic.

However, as Taubes acknowledges, even if sugar has the unique ability to cause obesity and diabetes, the cure is not the same as the cause. In other words, for people who are already obese or diabetic, many will not be able to manage conditions simply by eliminating sugar–because those people have already tipped over into an unhealthy metabolic state, quite different from that of a healthy person. A metabolically unhealthy person has conditions known as insulin resistance and hyperinsulenemia, which means that s/he can no longer effectively process carbohydrates. A large body of rigorous scientific evidence demonstrates that for these people to recover, they must reduce the total amount of carbohydrates they eat. For these people, even too many “healthy” whole grains cannot be tolerated. The science on this may change, with regard to what type of carbs can be tolerated (glucose vs. fructose, refined, unrefined, and so on), but currently our state-of-the-art understanding of how to reverse these diseases is that total carbohydrates must be restricted.

It is also true that there is not, currently, an adequate body of rigorous (clinical trial) evidence to conclude that sugar is a unique driver of metabolic diseases. As a result, population-wide recommendations limiting sugar intake are questionable. I reviewed this issue for a piece in The Atlantic, “The Limits of Sugar Guidelines.”

No doubt a major reason that the science is still lacking on sugar is that the sugar industry has manipulated the science in a number of ways. To learn more on this issue, you can read work by:

Nevertheless, I think it would be a mistake to blame the sugar industry for everything that has gone wrong in nutrition science and policy over the past 60 years. Having researched the history and politics of this field for more than a decade now, I know that many industries have played a role in manipulating nutrition science, including the vegetable oil industry, Big Pharma, the soy, grain and corn industries, as well as many manufactured food companies.

I made this point in an op-ed for the L.A. Times, “Don’t scapegoat Big Sugar. Lots of food producers profited from the demonization of fat.”