We have all been told that eating fat “clogs your arteries.” What are your thoughts on this?
In short, there’s really no scientific proof of that. The story is one of “associations,” meaning this is linked to that, which is linked with that, which is linked with that, therefore it causes it. This is really not logical. What I was taught in the 1980s when I was in training, was that eating fat raises the blood cholesterol and the blood cholesterol causes the arterial damage, atherosclerosis and heart disease, and all those problems. Many people are still teaching that today, but to use a metaphor, we’re using smartphones today, not phones with cords like back then. There’s new knowledge that shows there’s actually another way to go about it. I do the diplomatic, “Well, maybe that might be true, but there’s another way to go about it now.” There are other scientists who are not so diplomatic and will just come out and say that was flatly wrong, that we were taught that fat causes the fat on the arteries. I’m very skeptical of that even though we were taught that.
One of the pioneering books that was helpful for me as a researcher and as a physician was Gary Taubes’s book, called Good Calories, Bad Calories. I mentioned this book in a recent talk I gave and some of the researchers said I can’t believe you talked about a book. Well, this is a book about science. Gary Taubes spent five years reading papers and has more knowledge about these papers than even the people who did the studies, because he read other people’s papers. In the book he tells the story of how this notion that fat in food causes arterial damage and atherosclerosis really has never been proven. That was important for me. His article in the New York Times Magazine was in 2001 and his book came out in 2006 or so, but it’s still an important read if you’re struggling with the idea, “but we were taught that.” This is the weak, observational science that was being used to say that we knew cause and effect. That’s just not possible. You can’t prove cause and effect without an experiment.
On that talk panel I was on recently with the American Society of Nutrition, the story was told by a different presenter about the low fat diet and Ancel Keys and all that. And in an evidence-based medicine program that I’m in at Duke, we used those studies as critiques. We critique them and say, “Don’t use those studies; they’re not good enough!” When you say there’s controversy, I think there’s a perpetuation of the weak science, because perhaps it works in some people. Cord phones still work; that doesn’t mean smartphones can’t work. I can accomplish a lot using a low-carb diet and having people eat fat, but it’s almost emotionally ingrained. You wouldn’t go over that center line on the road because you know the consequences are bad. The fear of eating fat goes a long way back and the science is weak.
What about if you eat a high-carb diet and fat? How does that affect cardiovascular health?
The science doesn’t prove that fat is bad in that context. We know the typical American diet that has sugar, starch, carbs, fat, and protein together is a bad diet in terms of creating diabetes and obesity. How you tease out what component is the cause is not so easy. People often see what they want to see. I’ve heard that as sort of the diplomatic, “Well, fat’s bad … if you’re eating carbs.” It’s an easier logical step for a lot of people to take to say, ”Okay, I was taught correctly: fat’s bad when you eat carbs, but now I’m not eating carbs, so eating fat is fine.” In a clinical setting I’ll use that, but purely scientifically, fat is not proven to be the bad guy even when you eat carbs. It may be that it was the carbs all along! I don’t think we have solid evidence of that, but there has been a sort of taboo or a limit on the research in this direction. Now it’s becoming unearthed that the industry prevented studies about products that had sugars and starches in them, almost to the extent that the tobacco industry suppressed information.
Science is known as sort of a self-writing discipline, if you will. Eventually you’ll find the answer, you’ll find the truth if you have science. But if you don’t allow all things to be studied, then you won’t ever really find the truth. Our study came out in 2002; from 1980 to 2002, you couldn’t study a high-fat diet, because everyone thought that eating fat was bad. There was a constraint on being able to study a high-fat diet even though there were doctors that were using it at the time. Now, 20 years have passed and a lot of other studies have been done on high-fat diets and it looks good. We’re struggling with emotionally ingrained beliefs that eating fat is bad, so now you can’t even study it, but clinically, there are lots of different benefits that occur. We’ve seen that in our clinics, in the research, in the Adapt events. It’s pretty amazing what can happen.
What is good cholesterol and bad cholesterol?
Traditionally we were taught that LDL was “bad,” low-density lipoprotein. We’d say L is for “lousy,” to make you remember, or L is for “lethal.” It turns out, there’s a good LDL and a bad LDL. The small LDLs are the bad guys; large LDLs are not as bad. Dr. Nadir Ali, a cardiologist at the University of Houston has some great videos on what LDL does. In fact, it’s not there to cause heart disease. It actually has beneficial effects. The deep dive is that LDL even helps you fight bacteria and fight infections. In some clinical trials—we published our paper on what happens to the large and small LDLs many years ago—in general what happens on a low-carb diet is the small LDLs turn to large LDLs. That’s thought to be a beneficial effect when you think about changes in cholesterol. Now, that’s not a hundred percent. Not everyone on a low-carb diet has the small LDL gone. I think the consensus is eroding, it’s changing.
I helped write the book Cholesterol Clarity — Jimmy Moore asked me to help write it and it’s basically a summary of the podcasts that he did with cholesterol experts who are doing the research but not getting their information beyond the clinical barrier or buffer. The cholesterol scientists for a long time have said it’s not about LDL, it’s about inflammation. So, the science about cholesterol is changing to look at inflammation, which sets the scene for cholesterol. Going back to “good cholesterol,” that’s thought of as the HDL. H being “healthy.” But, there’s a good HDL and a not-so-good HDL. It gets ever more complicated as you look at this. There are some skeptics who have looked at the data in a different way and basically said none of this matters. I’m more and more open to the idea that we’re talking about the wrong thing—that cholesterol is not the most important thing for cardiac risk, even though most doctors believe it is. I have even had doctors who have ignored diabetes and obesity and they treat the cholesterol by not treating the underlying cause of the cholesterol problem. It gets very complicated. I can see eyes glaze over pretty quickly in my clinic patients. So a lot of times I’ll just say, “Hey, don’t worry about that.”
Are triglycerides a good measure of cardiovascular risk?
Yes. There are good studies showing the fasting triglyceride or even the random triglyceride during the day correlating with heart disease. It doesn’t get a whole lot of attention. More attention has been paid to the idea of a low HDL. The way I explain it is that the total cholesterol and LDL is the old way to look at things. I want to look at the triglyceride and the HDL, and even the ratio – triglyceride divided by HDL – which is a great predictor of insulin resistance. More and more studies are now coming out looking at that ratio correlating with outcomes. It didn’t hit the research world until very recently, so now, larger studies are incorporating that number, and it does correlate pretty well. It correlates with insulin resistance, which is thought to be one of the underlying factors toward heart disease and diabetes—diabetes being a strong risk for heart disease.
If someone does want me to explain the lipid profile, I’ll cover the triglyceride and HDL and say the old way would be to look at the total and the LDL, and actually, on a low-carb diet it goes down (the favorable change) and then I’ll cover up the total and LDL and say, “Well, the new way is to look at the triglyceride and the HDL.” We look at those trends over time, triglyceride almost always going down and HDL almost always going up. For the most part, that reassures people. If not, then I go to a website which has a calculator, called CV Risk Calculator. It’s an American College of Cardiology and American Heart Association guideline where you can input your numbers and get your heart disease risk for the next ten years. Interestingly, when you go through inputting your numbers, they don’t even ask for LDL anymore. I’ll use that if someone really wants to go further and to look at the total, the LDL, the older way, and triglyceride and HDL, the new way.
Do you typically see that triglycerides improve on a low-carb diet?
Absolutely, yes. This still doesn’t make sense even to a lot of doctors. Triglycerides are in the family of fats. Doctors who think of the old way don’t make the connection that it’s actually sugar and starch in food that creates the triglyceride in the blood. Where that happens is in the liver. So, fatty liver is actually from sugar and starch, not from fat in food. In my area, doctors still make the mistake of thinking that if you have fatty liver disease, you should cut the fat from your food. No, it’s the sugar and starch in the food that creates the fatty liver. Fatty liver makes the triglyceride in the blood go up, so I can understand why this is confusing. It’s confusing to the general public; it’s confusing to doctors. We just teach how it works and show by example, by having someone try it, and by measuring all of these things in a clinic, show that these things do change in a favorable way.
What other tests are good for predicting cardiovascular risk?
There was an old saying, “How do you know something? Is it by teaching?” No, not really, because you can just put up a PowerPoint and talk through it. It’s by writing. By reading and then writing something new is how you really learn something. In the book, Cholesterol Clarity, I had to make a call regarding this question. What do you measure? Well, don’t measure the predictors; measure whether you have the disease or not. The disease you’re trying to prevent by looking at cholesterol in the blood is arterial disease in the neck, the heart, the artery of the abdomen called the aorta. In our area you can get these measurements by ultrasound. It’s non-invasive; it’s the same technique used to look at babies growing. It’s safe, no radiation. I advise people to follow their own arteries, not the prediction of whether you have it or not. It works really well for those who are in the prevention mode. If your arteries are clear, you don’t have the disease, then you don’t have to prevent the disease that you don’t have. Another guideline in the US, the coronary calcium score, will give you an idea of whether you have coronary disease, but it doesn’t show you the artery directly. It’s a predictor of whether you have it. These ultrasound measurements show you the artery directly. This concept falls down if you do have moderate disease. Whatever you’ve done, if it’s smoking, it’s blood pressure, it’s diabetes, it’s diet as well—if you don’t have the disease, don’t change what you’re doing. If you do have a disease, then you might want to consider making some changes. Monitor the disease, not just treat risk factors.
There’s a whole intellectual approach to treating cholesterol in the blood. In fact, a lot of doctors will resist checking the arteries, because they think there’s a perfect correlation between the predictor in the blood and the disease, and there isn’t. It’s not a perfect correlation. And then drug companies get involved with selling products that have some benefit, but not much. It turns out you have to treat a hundred people to save one person from having a stroke, for example, so most people who take a pill don’t really have any benefit from these things. We have doctors who are taught that that’s the right way to do things, and there are guidelines that say if you don’t do it you’re out of line, so that gets complicated. I just teach, “Here’s what you’re trying to prevent, and that’s what you should follow, not predictors.” Twenty, thirty years ago when I was in training, we didn’t really have access to these types of measurements so easily, so widespread, so it would make sense that you would only use a predictor of it. Now that you have access to measuring the disease directly, why wouldn’t you?
Can a low-carb diet cause heart palpitations and arrhythmia?
I think that may come from a study from a year or two ago, a big epidemiology study where they categorized people by what they say they eat: low-carb, moderate carb, and there was a slight increase in people who said they ate 30% carbs or less—30%. Keto is about 5%. So there was a broad range of what “low-carb” meant.
There are some people who get what’s called palpitations, meaning some skipped heartbeats, the first week or two, and it’s part of the keto adaptation, the “keto flu.” (I wish it was called “keto cold,” because it’s pretty mild and most people don’t get it.) But some people do get palpitations. I’ll get an occasional email and I just reassure people. Unless they have heart disease, then I get more worried, but I reassure people that it’s the transition of the fluid shifts that are occurring. When you stop eating carbs, your body gets rid of the fluid; you have a diuresis (water loss) that can cause temporary transient skipped heartbeats and I don’t worry about it. It’s something that is temporary. I’ve treated a lot of people with heart disease through the years, and on low-carb diets and on high-carb diets, people get atrial fibrillation, so I have to say this is not the perfect cure for atrial fibrillation. People get into car accidents whether they eat carbs or not—it doesn’t mean the low-carb diet caused the car accident! We’re at that stage where if you have something that happens, regardless of the diet, to know if it’s more common, we’re going to have to have a comparative study—study people who are eating carbs versus not, in a controlled way, to see if the occurrence of it is any more frequent.
In my experience, I don’t think this is the cause of it. I think life causes these things, whether you eat carbs or not. That’s a good place to shine more research on. If I had a magic wand that could do all sorts of research, one of the first studies I would do is in people with heart disease and diabetes. To follow them and compare them to a group that’s not doing a low carb diet, maybe a Mediterranean or other type of diet, and see what happens, if these things happen at a greater frequency than other types of diets.
Darrell asks: “Is it a fallacy that eating red meat daily is bad for you? Is this being debunked in today’s science?”
It is a fallacy that eating red meat daily is bad for you. The same kind of epidemiology science that led toward the restriction of fat in food is what led people to saying you shouldn’t eat red meat. There’s an interesting new epidemiology study being done at McMaster University in Canada, they’re doing a big epidemiology study of diet and health and they’re not finding the same findings that the Harvard nutritional epidemiologists have found, which is causing a stir. So, if you do give value to that type of information, it’s now contradictory. You can see what you want to see in those kinds of studies, so I don’t worry about eating red meat every day. I tell my patients it’s okay if you like it. You don’t have to eat red meat on a keto diet, but you certainly can.
Thomas asks: “If I had plaque in my arteries, would a low-carb diet be able to minimize future risks or even be able to reverse it?”
The best study we have so far is a two-year study out of Israel, where several different types of diets were used, including a low-carb diet. It wasn’t as low as keto, so I hold out that it (keto) might do even better, but a low-carb diet led to a reduction in arterial thickness in the neck, called “carotid arterial thickness.” When you look at it, all of the diets worked, as long as people lost weight, their blood pressure went down, and they followed a particular diet program. I think there are lots of ways to do it. A low-carb diet is another appropriate way, although studies like this don’t tell you what will happen to you, so I still believe in the clinical assessment of people. There’s no one-size-fits-all. It’s possible that if you followed a low-carb diet that it wouldn’t get better. With any kind of disease or prevention of the disease, you want to still measure things that we typically measure. Don’t just put your head in the sand and say, “Dr. Westman said it was fine.” I still believe that we should monitor these things, how you feel and then metabolic and blood or imaging as needed.
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