The Cholesterol Hypothesis
I’ve been thinking quite a bit about the recent news of the latest celebrity heart attack victims. Even my own mother had to go to the hospital to get a stent for a “serious blockage.” Unfortunately for her, the pain that she went in for still remained when she returned home. She feels better now but it makes me wonder if the procedure was really necessary. A co-worker at my job was concerned about heart disease because other members in her family died as a result. She went in for a check and the doctor found a major blockage and she required a stent. Through all of this, I couldn’t help but remember the quote from Gary Taubes’s book, Good Calories, Bad Calories, that the Masai of Kenya have copious atherosclerosis (hardening of the arteries) but no heart attacks. Of course that would suggest that it’s quite natural for atherosclerosis to form but that doesn’t necessarily mean that the person will have a heart attack. In fact, the only way we “know” that atherosclerosis is to blame is usually due to an autopsy after the fact. The person has the attack and then the autopsy reveals blockages and thus the consensus is that the person died of a heart attack “caused” by atherosclerosis. Sounds reasonable, right? Just like eating fat makes you fat, and eating cholesterol clogs your arteries, which leads to a heart attack. These stents and angioplasties are fairly routine these days and perhaps that explains why we live a little longer, but the incidence of heart disease and attacks goes on unabated. So where did this notion (that a blockage causes a heart attack) originate?
From Taubes’s book, I learned that cholesterol is a primary component of atherosclerotic plaques. Proponents of the cholesterol hypothesis envisioned the human circulatory system as a kind of plumbing system. Dr. Jeremiah Stamler referred to the accumulation of cholesterol in lesions on the artery walls as “biological rust” that can “spread to choke off the flow of blood, or slow it just like rust inside a water pipe so that only a dribble comes from your faucet.” This imagery was so compelling that we still talk and read about artery-clogging fats and cholesterol, as though the fat of a greasy hamburger were transported directly from stomach to artery lining.
Researchers went on to conduct myriad studies on every type of animal they could find — even those that were vegetarian who would never eat a high-fat diet, but none of these studies did much to implicate either animal fat or cholesterol. Researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream than those who didn’t. Since 1950, it’s been really tough to show any real benefit from lowering cholesterol either through drugs or diet. Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol.
Taubes relates that in 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death. They autopsied more than a hundred very recently deceased New Yorkers (who died violent deaths) and measured the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic illness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.” GCBC, at 21.
This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. Even if high cholesterol was associated with an increased incidence of heart disease, this begged the question why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.
I’m still begging the question today. This CNN article claims that heart attacks can happen at any age and makes the situation sound rather hopeless. “Heart attack risk goes up in men older than 45 and women older than 55, but it can happen even earlier. While lifestyle modifications help reduce risk — eating a healthy diet, maintaining good blood pressure and normal weight, not smoking — sometimes it’s not enough.” It’s especially not enough when we truly don’t understand the mechanism for the heart attack to begin with. I find it very interesting that when they tell these stories, they often miss little details, like this one from the article: “One evening in 2000, he and his buddies decided to snowshoe up Vail Mountain and ride the gondola down. Bender complained of indigestion on the way up, which was odd because his last meal had been lunch. He told his friends he needed to sit down before getting on the gondola. After the group got in the cable car, he lost consciousness.” It is only odd if you don’t consider the role of diet in heart disease. Many newbies to low carb diets tell me how much the diet improved their Gastroesophageal reflux disease (GERD). One woman told me how her acid reflux was so bad that she had to prop herself up with pillows at night in order to get some sleep. After low carb, she was able to sleep through the night for the first time in over 10 years. Now imagine coupling that with atherosclerosis and perhaps we’re onto something. It’s the sudden rise and fall of blood sugar that embarasses the heart muscle in most cases, though not all. Owing to the fact that Masai have no heart attacks despite atherosclerosis, it’s safe to presume that if one achieves stable and steady blood sugar, they can eliminate or severely reduce their risk of heart disease. It has nothing to do with the fact that they walk so much. As you’ll see below, if you make the changes that are suggested below, you too will have the energy to walk.
The carbohydrate hypothesis is the only one that makes any sense. It is the simple hypothesis that needs to be refuted if possible. Right now, we blame cholesterol for mere presence. An autopsy is performed and we say that there were blockages caused by cholesterol and that must be why the patient died. But that doesn’t explain why so many people exist for many years with such blockages and don’t have a heart attack. That also assumes that cholesterol was responsible for the blockage in the first place. Perhaps it showed up to “fight the fire” so to speak.
On Page 76 of Good Calories, Bad Calories, we find that in 1955, Pete Ahrens at Rockefeller University found out why those who eat carbohydrates tend to have so much more fat in their blood. Ahrens was specifically studying triglycerides, rather than the VLDL particles that carry the triglycerides. Ahrens was considered by many investigators to be the single best scientist in the field of lipid metabolism. He had observed how the triglycerides of some patients shoot up on low-fat diets and fall on high-fat diets. This led Ahrens to describe a phenomenon that he called carbohydrate-induced lipemia (an excessive concentration of fat in the blood). When he gave lectures, Ahrens would show photos of two test tubes of blood serum obtained from the same patient—one when the patient was eating a high-carbohydrate diet and one on a high-fat diet. One test tube would be milky white, indicating the lipemia. The other would be absolutely clear. The surprising thing, Ahrens would explain, was “that the lipemic plasma was obtained during the high-carbohydrate period, and the clear plasma during the high-fat regimen.” ([Elliot] Joslin had reported the same phenomenon in diabetics thirty years earlier. “The percent of fat” in the blood, he wrote, “rises with the severity of the disease…and is especially related to the quantity of carbohydrate, which is being oxidized, rather than with the fat administered.”)”
According to Ahrens’s research, a high carbohydrate diet would actually elevate the levels of fat in the blood and that would perhaps explain why carbohydrate-eaters have so much cholesterol blocking their arteries. Now, when Ahrens says “fat”, what is he talking about? He’s talking about triglycerides, which are three fatty acid molecules joined to one glucose molecule. Our bodies must make triglycerides when glucose is present in order for it to travel through the blood stream in and out of fat tissue. When you get you bloodwork done, pay special attention to the number of triglycerides you have in your bloodstream.
If the number is above 150, you’re in danger. I can assure you that if you eat like I do, your triglyceride number will plummet.
By the early 1970s, several researchers independently confirmed what Ahrens was looking for. First by Peter Kuo of the University of Pennsylvania, then by Lars Carlson of the Karolinska Institute in Stockholm, and by the future Nobel laureate Joseph Goldstein and his colleagues from the University of Washington. All three reported that high triglycerides were considerably more common in heart-disease victims than was high cholesterol. In 1967, Kuo reported in The Journal of the American Medical Association that he had studied 286 atherosclerosis patients, of whom 246 had been referred to him by physicians who thought their patients had the genetic form of high cholesterol. This turned out to be the case for fewer than 10 percent. The other 90 percent had carbohydrate-induced lipemia, and, for most of these patients, their sensitivity to carbohydrates had elevated both their triglyceride levels and their cholesterol. When Kuo put his patients on a sugar-free diet, he reported, with only five to six hundred calories of starches a day, both their triglyceride levels and their cholesterol lowered. Two months later,JAMA published an editorial in response to Kuo’s article, suggesting that the “almost embarrassingly high number of researchers [who had] boarded the ‘cholesterol bandwagon’” had done a disservice to the field. “This fervent embrace of cholesterol to the exclusion of other biochemical alterations resulted in a narrow scope of study,” the editorial said. “Fortunately, other fruitful approaches have been made possible in the past few years by identification of the fundamental role of such factors as triglycerides and carbohydrate metabolism in atherogenesis.” GCBC at 77.
We know that when insulin is high in the bloodstream, fatty acids are low; meaning, that they are shuttled into fat tissue. If there is a low blood sugar drop, it may be that the heart cannot get enough of what it needs in order to keep pumping. I realize that the heart can also use fatty acids and perhaps ketones but during high insulin, they would not be available per the Krebs cycle. A high-carbohydrate diet is common to all these cases of heart attack. Yes, I’m aware of a couple of other ways that a heart attack might occur but the jury is still out.
From Taubes, we learned that in 1957, the American Heart Association (AHA) opposed Ancel Keys on the diet-heart issue (his hypothesis that dietary fat led to blocked arteries). The AHA’s fifteen-page report castigated researchers, including Keys, presumably—for taking “uncompromising stands based on evidence that does not stand up under critical examination.” Its conclusion was unambiguous: “There is not enough evidence available to permit a rigid stand on what the relationship is between nutrition, particularly the fat content of the diet, and atherosclerosis and coronary heart disease.”
But just three years later, this committee reversed itself in a tersely-written recommendation citing no references, that suggested that Americans reduce the fat in their diets. There was no evidence to support this position but it didn’t stop them from putting it out there. It seems pretty clear that they were under pressure from some source to concede to the conventional consensus despite any evidence to rely on. And this is the part that should anger you.
And finally, from Taubes’s book, we find that the Masai nomads of Kenya in 1962 had blood-cholesterol levels among the lowest ever measured, despite living exclusively on milk, blood, and occasionally meat from the cattle they herded. Their high-cholesterol diets supplied nearly three thousand calories a day of mostly saturated fat. George Mann, an early director of the Framingham Heart Study, examined the Masai and concluded that these observations refuted Keys’s hypothesis. In response, Keys cited similar research on the Samburu and Rendille nomads of Kenya that he interpreted as supporting his hypothesis. Whereas the Samburu had low cholesterol—despite a typical diet of five to seven quarts of high-fat milk a day, and twenty-five to thirty-five hundred calories of fat—the Rendille had cholesterol values averaging 230 mg/dl, “fully as high as United States averages.” “It has been estimated,” Keys wrote, “that at the time of blood sampling the percentage of calories from fats may have been 20–25 percent of calories from fat for the Samburu and 35–40 percent for the Rendille. Such diets, consumed at a bare subsistence level, would be consistent with the serum cholesterol values achieved.” Keys, however, had no reason to assume that either the Samburu or the Rendille were living at a bare subsistence level. To explain away Mann’s research on the Masai, Keys then evoked more recent research suggesting that the Masai, living in nomadic isolation for thousands of years, must have somehow evolved a unique “feedback mechanism to suppress endogenous cholesterol synthesis.” This mechanism, Keys suggested, would bestow immunity on the Masai to the cholesterol-raising effects of fat. GCBC at 26.
This is similar to what people say about my diet. How can I eat all of this meat and fat and not be worried about a heart attack? It must be that I have developed some “feedback mechanism” in my 44 years that suppresses endogenous cholesterol synthesis. This bestows upon me, the ZC guru, immunity to the cholesterol-raising effects of fat. Sigh!
It’s pretty simple, folks. If you want to avoid a heart attack, avoid carbohydrates of any source. Don’t gamble with your health and say that perhaps only a little bit won’t help. A little bit often leads to a lot so don’t go there. Make this change once and for all and own it. You’ll be very glad you did eventually.Share on Twitter
In: Cholesterol, Diet, Heart Disease, Hypertension