Replacing saturated fat with healthier fats can lower your risk of cardiovascular disease. That may seem like old news, but given the popularity of coconut oil and headlines like “Butter is Back,” it bears repeating.
Frank Sacks is professor of cardiovascular disease prevention at the Harvard T.H. Chan School of Public Health and professor of medicine at Harvard Medical School. He has led groundbreaking clinical trials on diet and blood pressure, lipids, and weight loss. Sacks spoke with Nutrition Action’s Bonnie Liebman in 2017.
The case against sat fat
Q: How strong is the evidence that saturated fat in foods like meat, butter, and cheese is harmful?
A: The evidence that saturated fat causes atherosclerosis and heart disease is compelling. It’s consistent across randomized trials, large observational epidemiologic studies, and animal studies.
Saturated fat increases LDL—or low-density lipoprotein—cholesterol. And LDL cholesterol is a cause of heart disease. It’s not a risk factor. It’s a direct, absolute cause.
It all fits very, very well. And that builds a powerful case that saturated fat causes heart disease, and it is healthful to replace it with unsaturated fat, especially polyunsaturated fats like those in soybean oil, mayo, nuts, and fish.
Q: Why have some people heard that the evidence on saturated fat has gotten weaker?
A: Some of the more recent studies take a standard epidemiologic approach, which is inadequate. Saturated fat seems to be harmless in those studies because it’s being compared, by default, to the typical American diet, which is high in refined, junk-food carbohydrates. They’re also linked to a higher risk of heart disease.
Q: Why inadequate?
A: Let’s say you give someone advice to reduce their saturated fat. Well, what do they eat instead? If they just reduced their saturated fat, they’d lose weight, because they’d be getting fewer calories. That’s unlikely. So what do they actually do? In many cases, people who eat less saturated fat eat more refined carbohydrates.
Q: Like white bread, pasta, rice, sweets, and sugary drinks?
A: Yes. But Walter Willett and Frank Hu—my colleagues at Harvard—devised a new epidemiology based on food substitutions that would occur in real life. And that’s really innovative.
Q: Because they look at what’s replacing the saturated fat?
A: Yes. They’ve designed a method where, with everything else being equal, they can compare people who have, say, high saturated and low unsaturated fat intakes with people who have low saturated and high unsaturated fat intakes.
When they do that, it’s clear that higher saturated fat and lower unsaturated fat is a bad dietary pattern.
Q: Can a lower-fat diet be healthy?
A: Yes, if the foods are healthful, such as whole grains, vegetables, fruits, and beans. But not if they’re rich in refined, junk-food carbohydrates.
[Click here for more information on what should be included in a healthy diet.]
Q: Didn’t you re-examine the clinical trials from the 1960s that assigned people to diets with different fats and then measured heart disease rates?
A: Yes. We separated them into core and non-core trials, because some were superb in quality, and some were kind of dreadful. So we set out uncontroversial criteria for a good clinical trial.
For example, core trials had to keep people on diets for at least two years and had to use a biomarker like blood cholesterol to show that people were sticking to their assigned diets.
Q: What did the core trials find?
A: The risk of heart disease was about 30 percent lower in people who ate polyunsaturated fats instead of saturated fats. If you include the non-core trials, you see only about a 20 percent lower risk of heart disease, but that is still statistically significant.
LDL & Beyond
Q: How do we know that LDL cholesterol causes heart disease?
A: We know that LDL is the main carrier of cholesterol in the blood, and it enters into the walls of major arteries and deposits cholesterol there. And that sets off a chronic inflammatory reaction, which helps lead plaque to build up in arteries.
Also, people who inherit genes that raise their LDL have a higher risk of heart disease. That’s not true for people with genes that lower HDL, which is sometimes called good cholesterol.
And pretty much any class of drugs that reduces LDL—like statins, ezetimibe, PCSK-9 inhibitors, or resins like cholestyramine—also reduces heart disease.
Q: How do the drugs work?
A: They vary, but statins and PCSK-9 inhibitors increase the number of LDL receptors. Many people have high LDL levels because they have too few LDL receptors, which clear LDL from the blood.
Q: Is large LDL safer than small LDL, as some people argue?
A: No. It’s basically a non-issue. If you have a lot of big LDL, it’s no better than a lot of little LDL. In fact, big LDL is probably worse, because it’s loaded up with more cholesterol.
Q: Do high triglyceride levels cause heart disease?
A: We don’t have proof with triglycerides the way we have proof that LDL cholesterol causes heart disease. But the evidence linking triglycerides to heart disease is getting stronger.
A high level of triglycerides means a high level of VLDL—very-low-density lipoproteins. Like LDL, VLDL can get into the artery wall, deposit cholesterol, and set off an inflammatory reaction.
And Apo C-III, a protein that’s part of VLDL, damages the artery wall.
But triglycerides have less influence on heart disease than LDL cholesterol. That’s partly because VLDL carries much less cholesterol.
Q: Is low HDL a risk, since HDL takes cholesterol out of arteries?
A: We know that people who have low levels of HDL cholesterol have higher rates of heart disease. That’s incontrovertible. As a risk factor, it’s totally solid. But if you raise HDL levels, can you increase cholesterol removal from the artery wall and reduce heart disease? That’s where the HDL story breaks down. We’ve got several instances where that doesn’t occur.
Q: HDL-raising drugs haven’t protected against heart disease?
A: Right. HDL is a hot area of research. We’re in the early stages of trying to understand it. My lab is focused on HDL because there’s so much to learn.
Which fats are best?
Q: Why recommend polyunsaturated fats over monounsaturated fats?
A: The data are stronger for polyunsaturated fats—not just the omega-3 fats in fish oil but the omega-6 fats in soybean and other oils—than for the monos in olive oil and canola oil. And polyunsaturated fats lower LDL more than monos and have anti-inflammatory effects.
[Interested in which oils are rich in polyunsaturated, monounsaturated, or saturated fat? Check out our handy, printable graphic.]
Q: What about coconut oil?
A: Coconut oil comprised about 3 percent of the American Heart Association’s advisory and generated about 95 percent of all the press coverage and criticisms.
But the evidence is straightforward. Some of the short-chain saturated fatty acids in coconut oil don’t raise LDL cholesterol. But they don’t counteract the effects of the oil’s longer-chain fatty acids, which do increase LDL cholesterol. So coconut oil raises LDL cholesterol in the same way that, say, butter does.
Q: Have large trials tested coconut oil’s impact on heart disease?
A: No. So, in the absence of any 10,000-person study, we have to go on the best available evidence, which shows that coconut oil raises LDL cholesterol. Coconut oil has no demonstrated benefits to offset the rise in LDL.
Q: What about dairy fat?
A: Butter increases LDL cholesterol just as you’d expect from its saturated fat. It’s like coconut oil, except there’s a lot more data linking dairy fat to heart disease because it was pitted against polyunsaturated fats in clinical trials. And dairy comprises much of the fat eaten by people who have a high saturated fat intake.
Q: How can people avoid confusion?
A: If you want to sort out what is good scientific knowledge and what is speculation or biased, look at guidelines produced by the American Heart Association, American Diabetes Association, or American Cancer Society. Those well-established organizations carefully vet their advice. Individual studies that have contrarian implications don’t come close to the scientific merit of their advice and guidelines.
For the media, established knowledge is boring. The media wants something new. But that’s not necessarily good for your health. You’re better off with established scientific knowledge, and if it’s boring, that’s fine. You won’t be healthier because the media sells more newspapers.
The information in this post first appeared in the November 2017 issue of Nutrition Action Healthletter.
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