There is a lot of information out there about the best foods to help us lose weight, prevent cancer, fight inflammation – the list goes on. In fact, for everything about our health we try and improve, there’s someone out there with a new theory on how to do it. But what does the science say?
Welcome to the Nutrition Facts Podcast. I’m your host Dr. Michael Greger. And I’m here to give you the evidence-based approach to take the mystery out of the best way to live a healthier, longer life.
Today, it’s saturated fats. Go online and there appears to be controversy over whether or not saturated fats are bad for you. It butter back or not? Let’s see what the science says:
Time magazine famously exhorted people to “Eat Butter,” no doubt selling lots of magazines, but perhaps selling the public short. They followed up with an article doubling down, saying that “The case for eating butter just got stronger,” based on this study: “A Systematic Review and Meta-Analysis of Butter Consumption.” “Pooling all the studies, each daily serving of butter was associated with only a 1 percent higher risk of death.” Wait, this is the study making the case stronger to eat butter? Further, the study suggests that swapping like a spoonful of oil in place of butter every day might drop the risk of diabetes 8 percent. “Thus, even with the absence of major health associations in the present investigation, healthier alternatives may be available.” But a 1 percent increase in risk is pretty tiny; why didn’t they find a larger effect? Well, it is just a tiny part of people’s overall diets. It’s illustrative to review the candy literature.
The National Confectioners Association is fond of contracting with scientists-for-hire, like Exponent Inc., infamous for shilling for Big Tobacco and chemical companies, encouraging people to eat candy every day in moderation, you know, like 15 to 25 jelly beans a day. Parents who restrict foods in an attempt to moderate a child’s intake of calories are just going to make their kids fat.
See, parents use “coercive practices to limit children’s access to palatable, energy-dense, or low-nutrient foods.” Parents have the gall to tell their kids when, how often, or how much candy can be consumed. Don’t they know butterscotch is back? See, “evidence suggests that candy is not associated with adverse health effects.” Don’t believe me? Here you go: ten thousand kids surveyed, asked if they had eaten candy within the last 24 hours, compared to those who said no, and they concluded that “candy consumption was not associated with adverse health parameters in children or adolescents.” And, this, a study in which the authors declared, “no conflicts of interest.” I mean, yeah, it was a study about candy funded by the candy industry, but “no conflicts of interest” here.
Do you see how with such a blunt instrument, it would be hard to tease out the specific health effects of candy? But we don’t need a study, since we already know what candy is. It’s candy. It’s mostly pure sugar. We already eat too much sugar; we don’t need more. You don’t need to pay off researchers to come up with a study like this. We already know what butter is. It’s butter. It’s mostly pure saturated fat. We already eat too much saturated fat; we don’t need more. Anyway, it gets even crazier. Candy consumers were “less likely to be overweight and obese than non-candy consumers.” So hey, maybe the candy company was right. Pass the Peeps!
“Is candy eating really a way to control body weight?” Who can name me an alternative explanation of why obese children eat less candy? Right, reverse causation. Perhaps it’s not cutting down on candy that led to obesity, but rather obesity led to cutting down on candy. In other words, the “reported candy consumption reflects consequences of obesity, not causes,” just like people with heart disease may cut down on butter, clouding the association. And remember, it was “reported” candy consumption, which brings up the specter of reporting bias. “In other words, overweight kids may guiltily under report their intake of candy to a greater extent than do those of normal weight.”
I mean, otherwise, “what would the implications of such a finding be?” Do we want to randomize kids to eat more candy to see if it makes them lose weight? “It is doubtful that any ethical committee would be happy about that kind of a proposal.” But you don’t know until you put it to the test. Feed folks extra candy or peanuts same number of extra calories, and surprise, surprise: those that ate all that extra candy gained more weight.
But what about that interventional trial showing that candy can improve ADHD symptoms? If you’re the Mars candy bar company, and you want to fund a study showing candy bars help kids focus, what would you do? The “parents were sent a formal letter instructing them to send their kids to school hungry without breakfast” and then gave them a candy bar or, basically nothing, an aspartame beverage, and, what do you know, feeding kids something rather than nothing “enhanced their ability to stay on task.” That reminds me of the famous Frosted Mini-Wheats ad, “clinically shown to improve kids’ attentiveness by nearly 20 percent,” with the really fine print explaining that this was compared to kids that ate nothing at all.
Butter’s been put to the test, too. Give people a single meal with butter, and you get a boost of inflammatory gene expression within just hours of consumption, significantly more than the same amount of fat in olive oil, or particularly walnut, form. You can randomize people to foods made with all sorts of different fats, and butter was shown to be the worst in terms of LDL cholesterol. Yeah, but these were short-term studies. It’s not like you can randomize people to eat or avoid butter for years, unless they’re locked up in a mental hospital, where by switching diets, you can raise or lower their cholesterol and cut coronary events by about 40 percent; though they also cut down on meat and eggs; so, it wasn’t just butter.
Yeah, but it’s not like you can get a whole country to cut down on butter. Oh, but you can: a 75 percent drop in butter consumption in Finland helped create an 80 percent drop in heart disease mortality, which was driven largely by the countrywide drop in cholesterol levels, which was largely driven by the countrywide dietary changes to lower saturated fat intake, like the move away from butter.
The bottom line is that researchers have put it to the test: randomized, controlled trials involving more than 50,000 people, and the more you decrease saturated fat content, the more your cholesterol drops, “the greater the protection.” “Lifestyle advice to all those at risk for cardiovascular disease,” to lower the risk of our #1 killer of men and women, population groups should continue to be advised to permanently reduce their saturated fat intake. The American Heart Association got so fed up with industry attempts to confuse people, they released a Presidential Advisory in 2017 to make it as clear as they could: “The main sources of saturated fat to be decreased include butter.”
Next up, we look at the reason those eating plant-based diets have less fat buildup in their muscle cells and less insulin resistance.
The association between fat and insulin resistance is now widely accepted; so-called ectopic fat accumulation: the accumulation of fat in places it’s not supposed to be, like within our muscle cells. But all fats don’t affect muscles the same. The type of fat, saturated or unsaturated is critical. Saturated fats like palmitate, found mostly in meat, dairy, and eggs, cause insulin resistance, but oleate, found mostly in nuts, olives, and avocados may actually improve insulin sensitivity. What makes saturated fat bad? Saturated fat causes more of those toxic breakdown products and mitochondrial dysfunction, and increases oxidative stress, free radicals, and inflammation, causes a vicious cycle of events in which saturated fat-induced free radicals cause dysfunction in the little power plants within our muscle cells, which causes an increase in free radical production and the impairment of insulin signaling.
Fat cells filled with saturated fat activate an inflammatory response to a far greater extent. This increased inflammation, along with eating more saturated fat, has been demonstrated to cause insulin resistance through free radical and ceramide production. Saturated fat has also been shown to have a direct effect on skeletal muscle insulin resistance. Accumulation of saturated fat increases the amount of diacylglycerol in the muscles, which has been demonstrated to have a potent effect on muscle insulin resistance. It doesn’t matter if the fat in our blood comes from our own fat, or from their fat.
You can take muscle biopsies from people and correlate the saturated fat buildup in their muscles with insulin resistance.
While monounsaturated fats are more likely to be detoxified or safely stored away, saturated fats create these toxic breakdown products, like ceramide, that cause lipotoxicity. Lipo, meaning fat, as in liposuction, and toxicity. This fat toxicity in our muscles is a well-known concept in the explanation of the trigger for insulin resistance.
I’ve talked about the role saturated and trans fats contribute to the progression of other diseases, like autoimmune diseases, cancer, and heart disease, but they can also cause insulin resistance, the underlying cause of prediabetes and type 2 diabetes. In the human diet, saturated fats are derived from animal sources while trans fats originate in meat and milk, in addition to partially hydrogenated and refined vegetable oils.
That’s why experimentally shifting people from animal fats to plant fats can improve insulin sensitivity. Insulin sensitivity was impaired on the diet with added butterfat, but not on the diet with added olive fat.
We know prolonged exposure of our muscles to high levels of fat leads to severe insulin resistance, with saturated fats demonstrated to be the worst. But they don’t just lead to inhibition of insulin signaling, the activation of inflammatory pathways, and the increase in free radicals. They cause an alteration in gene expression, leading to a suppression of key mitochondrial enzymes, like carnitine palmitoyltransferase which finally solves the mystery of why those eating vegetarian have a 60% higher expression of that fat-burning enzyme. They’re eating less saturated fat.
So do those eating plant-based diets have less fat clogging their muscles and less insulin resistance too? There hasn’t been any data available regarding the insulin sensitivity or inside-muscle cell-fat of those eating vegan or vegetarian, until now.
Researchers at the Imperial College of London compared the insulin resistance and muscle fat of vegans versus omnivores. Now those eating plant-based diets have the unfair advantage of being so much slimmer, so they found omnivores who were as skinny as vegans to see if plant-based diets had a direct effect, as opposed to indirectly pulling fat out of the muscles by helping people lose weight in general.
They found significantly less fat trapped in the muscle cells of vegans compared to omnivores even at the same body weight. They found better insulin sensitivity, better blood sugar levels, better insulin levels, and, excitingly, significantly improved beta-cell function, the cells in the pancreas that make the insulin in the first place. They conclude that eating plant-based is not only expected to be cardioprotective, helping prevent our #1 killer, heart disease, but that it may be beta cell protective as well, helping also to prevent our seventh leading cause of death, diabetes.
Finally today, we ask how might Big Butter design a study to undermine global consensus guidelines to reduce saturated fat intake?
Where did these consensus guidelines to dramatically lower saturated fat consumption come from? From literally hundreds of metabolic ward experiments, which means you don’t just ask people to change their diets, you essentially lock them in a room, for weeks if necessary, and have total control over their diet. You can then experimentally change their level of saturated fat intake however you want and see the corresponding change in their cholesterol levels. And the results are so consistent you can create an equation, the famous Hegsted Equation, where you can predict how much their cholesterol will go up based on how much saturated fat you have them eat. So if you want your LDL cholesterol to go up 50 points all you have to do is eat like 30% of your calories from saturated fat. When you plug in the numbers, the change in cholesterol shoots up, right as predicted. The experiments match the predictions. In fact, you can do it at home with one of those home cholesterol testing kits, eat a stick of butter every day and watch your cholesterol climb. It’s not rocket science. And look at this, this was 1965; we’ve known about this for 50 years that even if you keep calorie intake the same, increases in saturated fat intake are associated with highly significant increases in LDL bad cholesterol. Now your good cholesterol goes up a bit too, but that increase is smaller than the increase in bad, which would then translate into increased heart disease risk overall.
So if you feed vegetarians meat even just once a day, their cholesterol jumps nearly 20% within a month. To prevent heart disease, ideally we would need to get a total cholesterol under 150, which you can see these vegetarians were, but then even just once a day with the meat and their cholesterol shot up 19%. But the good news is that within just 2 weeks of returning to their meat-free diet, their cholesterol dropped back down into the safe range. Note that their HDL good cholesterol hardly moved at all, so their ratio went from low risk of heart attack to high risk in a matter of weeks with just one meat-containing meal a day. And indeed randomized clinical trials show that dietary saturated fat reduction doesn’t just appear to reduce cholesterol levels, but subsequent cardiovascular events like heart attacks as well.
So we have randomized clinical trials, controlled interventional experiments. These are our most robust forms of evidence, no wonder there’s a scientific consensus to decrease saturated fat intake. You’ll note, though, that the Y-axis here is not cholesterol, but change in cholesterol. That’s because everyone’s setpoint is different. Two people eating the same diet, the same amount of saturated fat, the same number of chicken nuggets a day can have very different cholesterol levels. One person can eat 10 chicken nuggets a day and have an LDL cholesterol of 90; another person eating 10 a day could start out with an LDL of 120. It depends on your genes. But while our genetics may be different, our biology is the same, meaning the rise and drop in cholesterol is the same for everyone. So if both folks cut out the nuggets, the 90 might drop to 85, whereas the 120 would be expected to drop to 115. Wherever you start, we can lower our cholesterol by eating less saturated fat, but if I just know what your saturated fat intake is, how many nuggets you eat. I can’t tell you what your starting cholesterol is. All I can say with certainty is that if you eat less, your cholesterol will likely improve.
But because of this extreme “interindividual variation,” this wide variability in baseline cholesterol levels for any given saturated fat intake, if you take a cross-section of the population, you can find no statistical correlation between saturated fat intake and cholesterol levels, because it’s not like everyone who eats a certain set amount of saturated fat is going to have over a certain cholesterol. So there’s like three ways you could study diet and cholesterol levels: controlled feeding experiments, free-living dietary change experiments, or cross-sectional observational studies. As we saw, there is a clear and strong relationship between change in diet and change in serum cholesterol in the interventional designs, but because of that interindividual variability, in cross-sectional designs, you can get zero correlation. In fact, if you kind of do the math, that’s what you’d expect you’d get. In statistical parlance, one would say that a cross-sectional study doesn’t have the power for detecting such a relationship. Thus because of that variability, these kinds of observational studies would seem an inappropriate method to study this particular relationship. So since diet and serum cholesterol have a zero correlation cross-sectionally, an observational study of the relationship between diet and coronary artery disease incidence will suffer from the same difficulties. So again, if you do the math, observational studies would unavoidably show nearly no correlation between saturated fat and heart disease. These prospective studies can be valuable for other diseases, but the appropriate design demonstrating or refuting the role of diet and coronary heart disease is a dietary change experiment. And those dietary change experiments have been done; they implicate saturated fat, hence the lower saturated fat guidelines from basically every major medical authority. In fact, if we lower saturated fat enough, we may even be able to reverse heart disease, opening up arteries without drugs, without surgery. But wait a second. Let’s put our Big Cheese and Chicken hat back on. Observational studies would show no correlation, mathematically could show no correlation. We’ve known since 1979 that observational studies simply don’t have the power to show the relationship. Bingo!
All we need now is a friendly researcher. How about Ronald M. Krauss? Funded by the National Dairy Council since 1989, also the National Cattlemen’s Beef Association, as well as the Atkins Foundation, perfect. Then you just combine together all the observational studies that don’t have the power to provide significant evidence and what do you know, no significant evidence was found.
This 2010 meta-analysis was basically just repackaged for 2014, using the same and similar studies. As the chair of Harvard’s nutrition department put it, their conclusions regarding the type of fat being unimportant are seriously misleading and should be disregarded, going as far as suggesting the paper be retracted, even after the authors corrected a half dozen different errors.
But it’s not like they falsified or fabricated data. They didn’t have to. They knew beforehand the limitations of observational studies; they knew they’d get the “right” result, and so they published it, helping to “neutralize the negative impact of milkfat by regulators and medical professionals.” And it’s working, brags the dairy industry: “Perceptions about saturated fat in the scientific community are changing. This is a welcome message to consumers, who may be tired of hearing what they shouldn’t eat.” They don’t have to convince consumers, just confuse them. Confusion may easily be misused by the food industry to promote their interests.
It’s like that infamous tobacco industry memo that read “doubt is our product.” “Doubt is our product since it’s the best means of competing with the body of fact that exists in the mind of the general public.” They don’t have to convince the public that smoking is healthy to get people to keep consuming their products. They just need to establish a controversy. Some science says its bad, some science says it’s not bad. Conflicting messages in nutrition cause people to become so frustrated and confused they may just throw their hands up in the air and eat whatever they want, which is exactly what saturated fat suppliers want, but at what cost to the public’s health?
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