The main problem that mainstream medicine and cardiologists have with low carb high fat diets is concern that “eating all that fat” will increase risk for heart disease. This concern was so great that Atkins was called before a senate committee where witnesses said that his diet was malpractice and was like mass murder. The problem is that the “cholesterol, diet, heart” hypothesis was adopted without any substantiating proof. What lead to the diet heart hypothesis was that there is cholesterol in the atherosclerotic lesion in arteries so researchers therefore believed that dietary cholesterol caused these lesions. In 1915 a researcher named Nikolai Anitschkow did a study where he fed rabbits diets high in cholesterol and they developed atherosclerotic lesions in their arteries. The problem was that rabbits are herbivores and not physiologically adapted to eating cholesterol since plants don’t contain. When they fed high cholesterol diets to dogs/wolves which are carnivores, they do not develop atherosclerosis. In the 1950’s a physiologist named Ansel Keys also believed that dietary fat and cholesterol caused heart disease. To “prove” this he documented the diet patterns of seven countries and concluded that the people in the countries that had the highest total and saturated fat intake also had the highest incidence of heart disease. The problem was that he chose to exclude those countries that had the opposite findings, namely France and Switzerland which had the highest saturated fat intake also had the lowest incidence of heart disease. At the same time a physician named John Yudkin in England theorized that dietary sugar was the real cause of vascular disease and when he looked at Keys’ own data he showed that sugar tracked more closely to heart disease than fat did in the countries Keys picked. Keys went on a mission, however, to convince the world that eating fat, and saturated fat in particular should be limited to avoid heart disease. He apparently was very persuasive as he had little trouble convincing the US government of his theory So, 1980 with the first USDA dietary guidelines for Americans, total fat, cholesterol, and saturated fat were advised to be avoided and complex carbohydrates were recommended to be eaten preferentially. No mention was made for sugar restriction. At this same time, besides Yudkin warning about sugar as the cause of heart disease, the leading lipidologists in the US including Pete Ahrens of Rockefeller University were studying lipid patterns and heart disease and discovered that triglycerides and HDL were more strongly correlated with heart disease than LDL cholesterol, and that diets low in fat and high in carbohydrate, although they might lower LDL cholesterol, worsened triglycerides and HDL and worsened risk for heard disease. Plus they found that LDL cholesterol itself had very little correlation with heart disease. When they presented this argument to George McGovern’s senate committee looking into diet and health, Senator McGovern said to Ahrens, “You mean I can eat all fat and cholesterol I want and it won’t hurt me?” When Ahrens said, “Yes,” McGovern said “Well that’s not what my cardiologist says.” Unfortunately the government bought the “cholesterol, diet, heart hypothesis” as well as the American Heart Association and it has been the mainstay of dietary guidelines ever since.
AFTER the government decided to adopt these guidelines, they then went about funding studies that they felt would prove it correct with three large studies totaling nearly a billion dollars in tax payer money, LRC-CPPT, MRFIT, and Women’s Health Initiative. They failed. None showed convincing evidence of benefit of the diet. The largest, the women’s health initiative, followed 50,000 women for 8 years, half followed a low cholesterol, low fat diet. After 8 years there was no benefit in any parameters of weight, heart disease, or cancer. Nonetheless the government and AHA stuck to their belief.
The reason that diets that lower cholesterol failed to prevent heart disease is because total cholesterol has nothing to do with causing heart disease. Numerous studies have failed to show a correlation between total cholesterol or even total LDL and heart disease, in fact in women over 50, all studies show that the higher the cholesterol, the longer they live. A large study done at UCLA found that the average LDL of acute heart attack patients was less than 100 and a third were less than 70. The national average LDL cholesterol at the time was 140. So why did these studies fail? It turns out Yudkin was correct. It is sugar via the metabolic syndrome that is the cause of heart disease along with basically all the other chronic diseases of civilization namely obesity, diabetes, hypertension, heart disease, stroke, and cancer. As Gary Taubes so eloquently illustrates in his recent book, “The Case Against Sugar,” excess sugar and in particular the fructose part of sugar induces a physiologic state called insulin resistance which causes insulin levels to rise, both at baseline and especially after consuming glucose containing food. This state of fructose induced insulin resistance with high insulin levels is called metabolic syndrome and is a precursor of diabetes and is the substrate for the chronic diseases of modern civilization. It was first described by a Stanford diabetologist, Gerald Reaven. It is associated with numerous physiologic changes in the body including high insulin levels, truncal and visceral obesity, elevated blood pressure, high triglycerides, low HDL levels, elevated blood sugar, change in size of LDL particles to small dense character, increased leptin level from leptin resistance as well. It is this metabolic syndrome with it’s elevated insulin level which is associated with vascular disease, coronary artery disease, stroke, as well as cancer, not cholesterol. There is much debate going on as to what feature or features of the metabolic syndrome actually cause vascular disease. Most researchers are still focused on lipids so they are studying the various lipid particles, LDL, large vs small, Apo B particles, Apo A particles, HDL, large vs small HDL, trying to see which particles “cause” vascular disease as well as what change in the lipid particles associated with the metabolic syndrome are responsible for vascular disease. The fact that metabolic syndrome is associated with a higher LDL particle count and that those LDL particles are smaller and more dense leads some to believe that the high number of small dense LDL particles overwhelm the vascular endothelium and cause plaque to form. The trouble is that some studies show that the total number of these particles actually doesn’t correlate with incidence of heart disease any more than the fact that they are small and dense as caused by metabolic syndrome (1). Looking at individuals and groups there is no more evidence that various lipid particles “cause” vascular disease beyond being markers that an individual has insulin resistance and metabolic syndrome and that that something about insulin resistance, metabolic syndrome itself is the actual cause of the vascular lesions of atherosclerosis. I personally believe it is the high insulin level itself that does the damage to the walls of vessels that makes them vulnerable to plaque formation and that various lipid particles and their sizes are nothing more than markers of insulin resistance and metabolic syndrome with it’s chronic elevated insulin levels. There is data to suggest this. When rabbits are fed cholesterol they do develop atherosclerosis as stated above. However when researchers make rabbits diabetic by treating the pancreas to not make insulin, and these rabbits are fed high cholesterol diets, they don’t get atherosclerosis until they are given high doses of insulin. Studies by Robert Stout, in England, showed insulin enhanced transport of cholesterol and fat into cells of the arterial wall just as insulin enhances transport of fat into fat cells in adipose tissue. Insulin is also induces tissue growth including stimulating growth of arterial smooth muscle cells.
As Gary Taubes argues in The Case Against Sugar, dietary sugar appears to be the main culprit in causing metabolic syndrome and the diseases associated with it namely obesity, diabetes, hypertension, heart disease, stroke, and cancer. Societies that don’t or didn’t have sugar, don’t have any of these diseases. This includes the Inuit in the arctic where the diet was all animal products which included mostly cariboo, fish, and marine mammal blubber. Their diet was 80% fat and 20% protein. They had none of those diseases of western society including obesity, diabetes, hypertension, heart disease, and cancer. After the first explorers studied the Inuit and made these observations, they were studied closely and observed for the development of these diseases. The first case of breast cancer didn’t appear until 1966 and by 1975 there were only two more. Now the Inuit have the same incidence of all these diseases as they have adopted the modern western diet with it’s high sugar consumption. The same goes for the native peoples in America where early military physicians noted the same thing, as well as Albert Schweitzer in Africa where he worked with native peoples for 40 years. He noted the remarkable absence of those diseases. George Campbell, another physician who came after Schweitzer worked with the Zulu in South Africa. He had clinics in the bush where the Zulus ate their natural diet as well as an urban clinic in Durban. He noted again none of the above diseases of western civilization in the clinic in the bush but all of them in the city where the diet was western type. In his meticulous records, he noticed that it took a diet containing 70 lb of sugar per year for 20 years for the above diseases to start showing up. This appears to be holding up in current observations. The current average per capita sugar consumption in the US now is 120 lb per person per year. In all societies where sugar consumption has been tracked, there have been a dramatic increases in consumption after they became westernized or from the general dramatic increase in world consumption the past 140 years. In the US annual per capita sugar consumption rose from 10 lb per capita per year in the early 1800’s to, to 80 lb per year in 1900, to 100 pounds per year in 1920. It peaked at 150 lb per person per year in 1995. Now it is about 120 lb per person per year. In every case the dramatic rise in sugar consumption was associated with a similar dramatic rise in obesity and diabetes in all societies.
I believe atherosclerosis is “caused” by disruption of the endothelial lining of arteries where there is injury which leads to the cascade of lipid deposition and atherosclerosis, but there has to be injury to the endothelium first. High cholesterol alone won’t cause this. In the vast majority of individuals that injury is caused, I believe, by high insulin levels caused by metabolic syndrome. Once the injury has occurred, high LDL may contribute to accelerating the process, possibly. The next most common cause of endothelial injury leading to atherosclerosis is hypertension and artery wall stress. An example of this is patients with coarctation of the aorta who have hypertension from a purely mechanical basis ie narrowing of the aorta above the heart, without any metabolic syndrome component to their hypertension. If not caught early and treated with surgery, they die in their 30’s of MIs. Again artery wall stress injures the artery lining and then inflammation sets in with atherosclerosis formation.
There are two more points to be covered in the argument that lipid particles don’t cause heart disease. First, proponents of the theory like to point to familial hypercholesterolemia where individuals have a genetic variation that causes high cholesterol levels. Homozygous individuals with two copies of the gene do indeed have extremely high cholesterol levels over 1,000 and die of myocardial infarctions early in life in their 30’s. But their cholesterol levels are extremely high and fortunately this is very rare. Homozygous individuals have high cholesterol, usually in the 300-500 range and have higher incidences of heart disease compared to the general population, before age 50, but no increase in heart disease rates after 50 despite still having the same high cholesterol levels (2). Ok, so if high cholesterol levels cause heart disease in these individuals why doesn’t it carry through their whole lives. Another interesting observation was made about heterozygote FH’s. Familial hypercholesterolemia can be traced back genetically through families. Such a study was done in a family pedigree in Holland. They traced the gene in a family back to the early 1800s. It turned out that FH heterozygotes had lower mortality rates in all decades of life through the 1800’s, but in the 1900’s they started showing increased mortality, right when the sugar/ diabetes epidemic started to take off (3). So it appears again that without the injury to the lining of the artery caused by sugar and the metabolic syndrome, high cholesterol in these FH heterozygotes was harmless.
There is an animal model for this as well. Back to dogs. Researchers fed dogs high cholesterol diets plus removed their thyroid glands to make them hypothyroid which also raises cholesterol even higher. They didn’t develop coronary atherosclerosis until they were made hypertensive by creating surgical coarctations of their aortas (4). Again it took the endothelial injury of the hypertension before the hypercholesterolemia could induce coronary artery disease, just as the hypercholesterolemic rabbits who were made diabetic didn’t develop vascular disease until they were given insulin to injure the the endothelial lining of their arteries.
The final argument in the cholesterol heart disease hypothesis is the reduction in cardiac events in patients given cholesterol lowering therapy. The most common such drug is the statin class which does lower cholesterol and is associated with lower incidence of cardiac events but dubious data on total all cause mortality. With statins, however the degree of LDL lowering does not correlate with the degree of cardiac event reduction suggesting it is some other action of statins that lowers cardiac events other than LDL lowering. Some attribute it to coronary plaque stabilizing effects of statins rather than LDL lowering. The new class of cholesterol lowering drugs the PCSK9 blockers lower cholesterol dramatically and a recent study showed that getting further LDL lowering with one of these drugs caused a whopping 15% lowering in cardiac events from 11.3 % of patients having events to 9.8 % of individuals in each group having events, an actual absolute lowering of only about 1%. However, there was no reduction in total all cause mortality (5). Same goes for statins. A recent study looked at 100,000 patients who were treated with statins after a heart attack. Those who could tolerate statins ie who stayed on them had a similar reduction in cardiac events compared to those who did not tolerate statins, however total all cause mortality was higher in those who stayed on statins than those who weren’t and came off them (6). To me these studies suggest that if you have a condition that CAUSES vascular disease by injuring endothelium such as hyperinsulinemia via metabolic syndrome, or hypertension, then a high LDL level particle count MIGHT accentuate the atherosclerotic process at best. But again aggressively lowering LDL in these individuals doesn’t bestow total all cause mortality benefits.
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