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What’s Good to Eat? Fat, Cholesterol and Health

December 26, 2011

Fresh eggs, excellent source of cholesterol!

My brother Phil remarked to me last year that he didn’t know what to believe about diet, one day cholesterol is the root of all evil, another day it’s something else. Well, that’s not precisely what he said, but the question is an important one: how do you know what to believe on the all important question of what to eat?

I had a lot of answers for him, but didn’t know where to start. I knew that too much information at the wrong time or presented poorly is as useless as the wrong information.

To illustrate the conflicting dietary claims the world is awash in, nothing is better than the topic of cholesterol and saturated fat, the causes, we’ve been told, of heart disease. A contributor to the Healthy Food Coalition, an open group on Facebook, tackles just that issue, far more succinctly than any other source I can think of. The author of the post, Annette Hunsberger Presley, gave me permission to reproduce it here. I’ll update with the references once I fix the formatting, which disappeared when I copied it.

I was very familiar with these studies cited by Annette, but I couldn’t have put this together myself. If you’re ready to tackle even more depth on the topic, I recommend Gary Taubes’s  masterpiece, Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health. I confess I haven’t finished the book, but I consider reading the first half an achievement nevertheless. So, on to Annette’s post:

The paper I sent to the American Dietetic Association

Thank you for this opportunity to delve into the science behind hyperlipidemia and its effect on health. The advice we give the American public will affect their longevity and quality of life and, therefore, I believe we need to be diligent in seeking the facts about cholesterol, saturated fat, and heart disease so that our advice reflects the most up-to-date and accurate science.

From the Evidence Analysis Library, I was able to obtain the following facts: 1) Saturated fat raises both LDL and HDL so it appears not to have a deleterious effect on the Total cholesterol/HDL ratio; 2) There is no evidence to support or not support a high carbohydrate diet or a high fat diet in the treatment of elevated triglycerides; 3) Polyunsaturated fats lower LDL cholesterol; 4) Fiber lowers LDL cholesterol; 5) Omega-3 fats lower LDL cholesterol; and 6) Trans fat raise both LDL and HDL and is, therefore, worse than saturated fat in its effects on cholesterol. 

The above facts are all well and good, but I was unable to find any science connecting blood cholesterol levels to heart disease or the lowering of blood cholesterol to the prevention of heart disease. I also did not find any discussion on the effects of LDL particle size (even though this has been a significant focus in cholesterol research since the 1980s) in the prevention or causation of heart disease. I think it is essential to have these questions addressed. After all, why are we trying to lower cholesterol? We need to have sound science behind the why in order to be truly science-based and in order to be sure that we are giving out the right advice.

Because my questions were not addressed in the Evidence Analysis Library, I also read The Cholesterol Wars: The skeptics vs. the preponderance of evidence by Daniel Steinberg, a supporter of the lipid hypothesis, and The Great Cholesterol Con: Why everything you’ve been told about cholesterol, diet and heart disease is wrong! by Anthony Colpo. After reading these books, I have a good idea of the beliefs on both sides of the cholesterol question and I believe both sides have some merit.

What is the lipid hypothesis? According to Daniel Steinberg, the lipid hypothesis “postulates that hypercholesterolemia is a major causative factor in atherosclerosis and coronary heart disease.” The hypothesis “relates to blood lipids, not dietary lipids, as the putative directly causative factor.”

Others interpret the lipid hypothesis as “saturated fat and cholesterol in the diet raise blood cholesterol levels which leads to atherosclerosis and heart disease.” There are two factors to consider: A blood lipid-heart relationship and a diet-heart relationship. There are actually two different hypotheses, the lipid hypothesis and the diet-heart hypothesis. What evidence do we have to support either of these two hypotheses?

Autopsy evidence  

In 1936, Landé and Sperry autopsied 123 individuals ranging in age from eleven to eighty and wrote, “No relationship was evident, and it is concluded that the incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.” (1)

In 1961, an Indian study also showed no correlation between serum cholesterol levels and the amount or severity of atherosclerosis (2). Autopsies conducted on war veterans in 1963 showed no correlation between serum cholesterol and atherosclerosis and even found that those with blood clots and other features of CHD had lower mean cholesterol levels than those who did not have any CHD features (3).

The 1968 International Atherosclerosis Project examined plaques in the arteries of 22,000 corpses in 14 nations and found that populations in all parts of the world had the same degree of atheroma whether they were meat eaters or vegetarians or whether they suffered a great deal of heart disease or very little to no heart disease (4).

A few studies have claimed a relationship between serum cholesterol and atherosclerosis, but the best correlation coefficient was only 0.36 which is rather weak and certainly would not support any claims of ‘significant’ association (5-8).

Autopsy studies do not appear to support the blood lipid-heart hypothesis, instead pointing to atherosclerosis as a normal, unavoidable process. Also, the degree of plaque build-up does not appear to be related to the incidence of heart disease. We cannot prove or disprove a diet-heart relationship with autopsy studies since we do not have adequate data on what these people ate.

Animal evidence  

Nikolai Anitschkow (9) fed rabbits a high cholesterol diet and found that they developed atherosclerosis similar to that found in humans, but they also developed plaque in organs and other tissues, unlike humans, probably due to the fact that rabbits are herbivores and do not have any way to process cholesterol. Feeding cholesterol to rabbits also raises blood cholesterol levels to an astronomically high level not seen in humans. Studies on other mostly herbivorous animals such as guinea pigs, chickens, goats and parrots also showed plaque build up with cholesterol feeding.

Carnivorous animals, on the other hand, do not respond the same as herbivores to cholesterol feeding. Dogs can take in a large quantity of cholesterol without developing plaque or high blood cholesterol levels, but they will suffer elevated blood cholesterol levels and atherosclerosis if the thyroid is removed or suppressed with medication (10). Several studies also showed that rabbits fed high cholesterol diets along with iodine or thyroid gland did not develop atherosclerosis (11, 12).

When rabbits develop atherosclerosis, their plaques never rupture and they don’t get heart attacks like humans. Many other animals are the same way and it may be due to the fact that rabbits and other animals make their own vitamin C, whereas humans do not. The balance between collagen degradation and collagen synthesis is one of the main determinants of plaque rupture (13) and vitamin C is essential for the synthesis of collagen.

Animal studies, alone, are unable to prove or disprove anything for humans due to differences in physiology, but, they can provide some data that may be useful to look at in humans. Animal studies do show that elevated cholesterol levels in the blood produce atherosclerosis, and we also know that people with familial hypercholesterolemia have elevated blood cholesterol levels and a higher rate of heart disease. What animal studies can’t tell us is what causes the elevated cholesterol in humans, whether it is the mere presence of elevated cholesterol in the blood stream or the combination of elevated cholesterol and some other factor such as iodine or vitamin C deficiency that causes atherosclerosis or whether there is something entirely different going on that may be the cause.

Epidemiological studies:  

We have Ancel Key’s Seven Countries Study (14) where he picked seven countries and plotted on a graph mean cholesterol levels for each country and the number of coronary deaths in that country.  He was able to show that Japan, which had the lowest cholesterol levels, also had the lowest rates of coronary death while Finland, with the highest cholesterol levels, had the highest rate of coronary death. The other five countries fit neatly in a line on this graph. The rate of coronary death appeared to relate to the level of blood cholesterol. The countries with higher rates of heart disease also had higher saturated fat intake.

There are several problems with this study. At the time, data was available for 22 countries and if all 22 countries are put on the graph, there is no correlation between blood cholesterol levels and coronary death. In fact, if Keys had chosen to use Finland, Israel, Netherlands, Germany, Switzerland, France and Sweden instead of Italy, Greece, Yugoslavia, Netherlands, Finland, USA and Japan, he would have shown the exact opposite effect; the higher the blood cholesterol levels, the lower the incidence of coronary death. Researchers also found a significant difference in iodine intake between Eastern and Western Finland with no significant difference in saturated fat or cholesterol intake. Eastern Finland had higher rates of heart disease and lower iodine intake (15).

I don’t believe we can use this study to support the lipid hypothesis or the diet-heart hypothesis as it is so clearly biased and manipulated. A study like this would never be taken seriously by today’s scientific standards and there is good evidence that it is not blood cholesterol or saturated fat that is the issue. Inadequate iodine intake is associated with CHD. The Japanese diet happens to be high in iodine, so is it the iodine that offers protection, the low saturated fat diet, or some other factor?

We also have the Japanese migration studies (16) where the Japanese from native Honshu were compared to Japanese who had migrated to Hawaii and San Francisco. The results showed higher cholesterol levels in the Japanese from Hawaii and San Francisco as well as higher rates of heart disease. The assumption is that a higher saturated fat diet was the cause of the elevated cholesterol, but in a follow-up study (17), one of the researchers, Dr. Marmot, found that the Japanese Americans who retained their traditional culture, but ate higher fat American foods were much better protected from heart disease than the Japanese Americans who adopted the American lifestyle but ate the lower fat Japanese diet.

The Japanese migration studies seem to indicate that it is not saturated fat or elevated cholesterol levels, but lack of social ties that increase heart disease risk. While the Japanese enjoy the longest average life expectancy in the world, they got to that point while increasing saturated fat intake. Life expectancy in Sweden is only 2 months shy of life expectancy in Japan, yet the Swedes have a high saturated fat intake (18).

Daniel Steinberg claims that the Framingham study “provided the first solid and unarguable evidence that individuals with higher blood cholesterol levels at the time of the baseline examination were more likely to experience a myocardial infarction in the subsequent years of follow-up.” Researchers found that elevated baseline cholesterol was associated with increased mortality in people under 50, but found no relationship between cholesterol and CVD in those over 50. Researchers also had to admit; “There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years…” The study found that for every 1mg/dl per year drop in cholesterol levels during the first 14 years, there was a 14% increase in CVD and an 11% increase in overall mortality during the subsequent 18 years (19).  However, this fact was reported as, “a 1% reduction in cholesterol corresponds to a 2% reduction in CHD risk.” (20) 

If we look at the facts from Framingham, we find an association between cholesterol levels taken at baseline and myocardial infarction years later in people under 50. We also find that lowering cholesterol levels increases the risk of all cause mortality and heart disease. What we don’t know is 1) why a high baseline cholesterol level appears to increase the risk for heart disease as opposed to high cholesterol later on; 2) what other factors were present that might contribute to heart disease; or 3) whether the people with high initial cholesterol died because they tried to lower their cholesterol. From Framingham, it does not appear that lowering cholesterol is beneficial.

Professor John Yudkin analyzed data from 15 countries and found extreme variations in heart disease and fat intake. Some countries with high fat intakes had low rates of heart disease, while other countries with identical fat intake had very different rates of heart disease. Yudkin examined more than dietary fat; he also included fat as a percentage of calories, different types of fat, carbohydrates and protein in his analysis and found that sugar intake showed the strongest association with CHD (21). Yudkin also found higher rates of CHD in countries with the most TV, radio and car ownership.

The Pukapuka and Tokelau people in the South Pacific have a high saturated fat diet due to coconut intake, but researchers note a complete lack of CVD in these populations despite an average blood cholesterol level of 240 mg/dl in Tokelau (22).

The Masai in Africa live on fat-rich milk, meat and blood with an average intake of 300 grams of animal fat daily. Professor George Mann found the Masai to be slim and fit and virtually free of heart disease (23) and despite their very high saturated fat intake, most of them had blood cholesterol levels below 160 mg/dl (24).

Of twenty-five prospective studies examining a link between saturated fat and CHD between 1963 and 2005, six (25-30) found an increased risk of CHD with saturated fat intake, though in two of the studies (29, 30), after adjusting for confounders, such as age and smoking, there was no significant association between saturated fat intake and incidence of CHD. The other nineteen (31-49) studies found no link between CHD and saturated fat. If we take a close look at the four (25-28) that found a connection, one would increase their risk for heart attack by increasing their saturated fat intake by a mere 0.5 to 1.7 percent of calories.

On a 2000 calorie diet, that amounts to 1.1 to 3.8 grams of saturated fat. In the Honolulu Heart Program, the difference between saturated fat intake between those who remained free from CHD and those who died of a heart attack was only half of one gram.

I don’t believe we are being scientifically objective if we believe that the microscopic differences in saturated fat intake in a few studies is proof of the lipid hypothesis or the diet-heart hypothesis. Not only is that quite a stretch to believe, but we would also have to ignore nineteen studies that showed no association between saturated fat and CHD.

Epidemiological studies, of course, cannot prove causation, only association, and many of these studies measured more than one dietary component, so we can’t be sure which dietary component was more significant. But, the epidemiological evidence does not appear to support either the lipid hypothesis or the diet-heart hypothesis, unless the dietary component is sugar or, perhaps, a lack of iodine or unless we are to believe that 1 to 4 grams of extra saturated fat per day is the difference between life and death. 

Dietary Intervention Trials  

Out of seventeen trials (50-66) conducted between 1946 and 2006; there are six trials (50, 53, 59, 60, 64, and 65) that found a statistically significant mortality benefit with intervention. Morrison (50) placed 50 heart attack patients on a low-fat, high protein diet with supplemental calcium, phosphorus, wheat germ and brewer’s yeast (treatment group). Another 50 patients were on their typical diet (control group). At the end of the study, thirty-eight patients in the control group had died compared to twenty-two in the treatment group. The problem here is that multiple interventions were used. Was it the low-fat diet, the high protein diet, the calcium, or B-vitamin containing brewer’s yeast or a combination of all of them or several of them that were responsible for the results? We don’t know, so we cannot say with certainty that it was the low-fat diet.

Hood et. al. (53) conducted a non-randomized, non-blinded trial with 460 patients. The dietary intervention group was put on a low saturated fat, high polyunsaturated fat diet and received close medical supervision whereas the control group was not supervised at all. The researchers found a significant decrease in total mortality in the intervention group, but the control group had a significantly higher number of high-risk, CHD-prone patients. This study clearly has some serious flaws. Was the higher death rate in the control group due to the lack of medical supervision, the diet or the fact that more people prone to CHD were in this group? 

The Oslo Diet Heart Study (59) randomized over 400 men to a diet or control group. The diet group lowered saturated fat and margarine intake and ate a high polyunsaturated fat diet. They experienced a significant reduction in blood cholesterol, CHD incidence and mortality, so this would appear to support the lipid hypothesis and the diet-heart hypothesis. However, those in the diet group were also told to increase nut, fruit and vegetable intake which would increase antioxidants and other cardio-protective nutrients. In addition, the men in the diet group were told to eat more fish and were supplied with sardines canned in cod liver oil.  Fish has been shown to be cardio-protective and cod liver oil contains vitamin D which is now being recognized as an important nutrient for heart health. The diet group did contain more hypertensive men, but the control group had more overweight men and more men over the age of sixty. Though both groups started out with the same number of smokers, the control group ended up with significantly more heavy smokers. I don’t believe we can objectively state that a decrease in saturated fat is responsible for the lowered CHD incidence and mortality. It could be the sardines in cod liver oil, the increase in nut, fruits or vegetables or the decrease in trans fat. There are too many variables to single out one as “the” culprit.

The Finnish Heart Study (60) was very poorly designed and received a lot of criticism. Patients in two different hospitals were studied.  For six years, hospital K received a high polyunsaturated diet and hospital N received their normal diet and then it was reversed.  Patients were included in the study even if they were admitted for a month or if they were discharged and readmitted a year later. The study was also not randomized or blinded. A significantly lower number of CHD deaths were found in those on the experimental diet, though in women, it was only significant for those in hospital N. Because of the poor design, we could hardly use this study as proof positive of the lipid hypothesis or the diet-heart hypothesis.

The STARS trial (64) involved sixty people. Half were told to lower intake of saturated fat, vegetable oils, margarine and refined carbohydrate-rich junk foods. They were to limit meat, fish and dairy products and increase fruit, vegetable and complex carbohydrate intake. The treatment group did have higher DHA levels indicating that not all of them decreased their fish intake as instructed. At the end of the study, there was 1 death in the treatment group and 3 deaths in the control group and 10 treatment subjects had widening of the arteries compared to only one in the control group. This study is used to declare decisive proof that saturated fat and trans fat cause coronary occlusion. Again, the problem is that the treatment diet involved several different variables, so we cannot objectively say that saturated fat was the culprit. It may have been the decrease in refined carbohydrate or trans fat or the increase in fruit and vegetable intake or a combination of the above. The prescribed diet, which included lowering saturated fat, worked, but was it because of the lowered saturated fat intake? We can’t answer that question, scientifically.

The Lion Diet Heart Study (65) randomly assigned 605 recent heart attack patients to one of two groups. The control group did not receive any specialized dietary instruction other than what may have been given by their physician or hospital dietitian. Those in the treatment group were advised to eat a Mediterranean type diet with increased vegetables, bread and fish. Chicken was to replace red meat, olive oil or a high omega-3 fat canola oil based margarine was to replace butter. Fruit was to be eaten daily. The study was cut short at twenty-seven months because CHD was slashed by 81% and total mortality by 60% in the treatment group. However, the differences between the treatment and control group could not be explained by blood cholesterol levels since both groups had identical total cholesterol and LDL-C levels during the entire study. This study would not support the lipid hypothesis since blood cholesterol levels were the same in both groups. Nor does it support the diet-heart hypothesis, as once again, there are too many dietary variables to declare with certainty that it was the lowering of saturated fat that caused the favorable results.

Rose et. al. (51) compared the effect of corn oil, olive oil and saturated fat on CHD. The corn oil group had significantly increased CHD incidents, deaths and total deaths despite the fact that they had a lower blood cholesterol level than the saturated fat group.  The olive oil group didn’t do much better than the corn oil group. Those in the saturated fat group lived the longest. 

The DART trial (63) had three different groups; a group that ate more fish, one that lowered fat intake while increasing the ratio of polyunsaturated to saturated fat and a group that ate more cereal fiber. They found no mortality change in the low-fat group, a slight increase in mortality in the fiber group and a significantly lowered mortality in the fish group, despite the fact that blood cholesterol levels went up in the fish group.

Recently, the Women’s Health Initiative (66) showed no benefit to lowering total fat or saturated fat in the diet in preventing heart disease. In fact, those with existing heart disease were at increased risk for events on the lower fat diet.

The Multiple Risk Factor Intervention Trial (MRFIT) (67) tested several variables such as a low fat diet, smoking, exercise and blood pressure on heart disease risk but was unable to find any significant decrease in coronary artery disease. Steinberg points out that the difference in cholesterol levels between the control and test group was only 2%, so there wasn’t enough cholesterol lowering in the test group to make a difference. To me, this would indicate that saturated fat and cholesterol intake does not significantly raise blood cholesterol levels and a low fat, low cholesterol diet doesn’t significantly lower blood cholesterol levels and therefore does not support a diet-heart hypothesis. Since the difference in cholesterol levels was minor, it is possible that lowering cholesterol further may provide protection, so we can’t say with certainty that MRFIT does not support the lipid hypothesis, but MRFIT clearly does not support a diet-heart relationship.

The most widely used study to prove the lipid hypothesis is the Lipid Research Clinics Coronary Primary Prevention Trial (LRCCPPT) (68, 69). Both the treatment and control groups were put on a low saturated fat and low cholesterol diet and instructed on that diet by a dietitian. The treatment group also received a cholesterol reducing drug. The trial participants were all middle aged men with cholesterol levels higher than 95% of the population (they all, most likely, suffered from familial hypercholesterolemia). The treatment group experienced 19% fewer CHD events than the control group which was barely significant. Both non-fatal and fatal coronary events had to be added together to get a barely significant finding. Taken separately, there is no significant difference between the treatment and control groups. The original design of the study was to use the more stringent significance level of .01 as opposed to the normal .05 because they wanted to make sure there was a real difference. They ended up using the less stringent .05 level because they could not find any significant differences with the .01 level. But just for argument sake, lets say this study offers proof of the lipid hypothesis. What about all the other studies that don’t show any proof and in fact contradict it? We cannot objectively use one study that shows a barely significant result in people with a genetic defect as proof positive. This study also does not prove the diet-heart hypothesis since both groups were put on the exact same diet. We cannot make any objective statements about diet from this study.

In 2006, after examining all the available clinical evidence, Hayward et. al. reported that,”…current clinical evidence does not demonstrate that titrating lipid therapy to achieve proposed low LDL cholesterol levels is beneficial or safe.”(70)

Overall, the dietary intervention trials do not support the diet-heart hypothesis. There are more studies showing no correlation between saturated fat and cholesterol intake and heart disease than studies showing a correlation and several studies show a health benefit for saturated fat intake. Those that do show a correlation are flawed or contain too many variables to give us any definite answers. I do not see how we can objectively or scientifically reject the numerous negative studies to support the few positive studies. The evidence is, at best, extremely weak to support the advice to lower saturated fat and cholesterol in the diet.

The lipid hypothesis is another matter. I do believe enough evidence exists from the above data and from studying people with familial hypercholesterolemia to look at blood cholesterol a little more thoroughly. What we don’t know, at this point, is to what extent blood cholesterol matters or if it is solely blood cholesterol or a combination of factors that present health problems. So far, simply lowering blood cholesterol levels has not produced significant results across the board, so maybe we need to do something in addition to lowering cholesterol, or something else entirely. 

We know that people with familial hypercholesterolemia have higher rates of heart disease. We also now know that they have a defective LDL receptor gene so that they have difficulty getting cholesterol from the blood into the cells. That is why they have higher than average blood cholesterol levels. 

Statin trials have shown that coronary events are reduced even if LDL is not lowered (71-76). In the PROSPER trial, those with the highest LDL cholesterol levels lived the longest (77). In the Japanese Lipid Intervention Trial, the highest death rate was seen among those with cholesterol levels below 160 mg/dl. The lowest overall mortality rate was seen in those who had blood cholesterol levels between 200-259 mg/dl and LDL between 120-159 mg/dl.  In humans, 20 mg/day for 9 days of atorvastatin administration reduced oxidized LDL, but did not reduce blood levels of LDL (78).

Based on the evidence, statins appear to exert a positive effect on CHD through some other mechanism besides cholesterol lowering which would imply that the lipid hypothesis is incorrect in its present form. It appears that the presence of oxidized LDL is more important than the amount of cholesterol in the blood. Steinberg also points out very clearly in chapter 5 of his book that it is oxidized LDL that leads to atherosclerosis. When cholesterol cannot make it into the cells, it has to “wait” in the blood stream.  While “waiting” it is exposed to free radical damage which changes native LDL (large, fluffy particles) into oxidized LDL (small, dense particles). References 79 through 83 explain the development of and atherogenic properties of oxidized LDL. What we need to do is find a way to get cholesterol into the cells and a way to prevent LDL from becoming oxidized.

Are there dietary measures we can take to prevent LDL from becoming oxidized?

The component of LDL that is the most likely to become oxidized is the polyunsaturated fatty acids (PUFA). LDL from people who consume more PUFA from vegetable and fish oils oxidizes more easily and vitamin E does not help to minimize that oxidation (84).  It is the linoleic acid component of oxidized LDL that leads to atherogenesis (85). A 2004 study by Mozaffarian et. al. showed that postmenopausal women who ate more PUFA, had worsening atherosclerosis over time, but for those who ate more saturated fat, the less their atherosclerosis progressed. In the highest intake of saturated fat, atherosclerosis actually reversed over time (86). Herron et. al., in 2004, noted that a high cholesterol diet protects LDL from becoming oxidized (87) and yet another study showed egg consumption to be protective of LDL (88). Milk fat has also been shown to be negatively associated with CVD (89, 90). Polyunsaturated fats have also been shown to increase cancer risk (91-93) and to play a role in acute respiratory distress syndrome (94). Antioxidants have been shown to protect LDL from oxidation (95-96). 

After all this research, I have come to the conclusion that both proponents and adversaries of the lipid hypothesis have blind spots. Proponents have recognized the role oxidized LDL plays in atherogenesis and the role the LDL receptor gene plays in getting cholesterol into the cells, but still insist that we should control cholesterol production to reduce the amount in the blood. They still insist on lowering LDL even though studies show it is not the amount of LDL but the amount of oxidized LDL that is the problem. They insist on a low saturated fat and cholesterol diet even though they admit that diet does not play a role in the lipid hypothesis. Adversaries of the lipid hypothesis insist that cholesterol does not play a role in heart disease, despite evidence that oxidized LDL promotes atherosclerosis.

It appears to me that we may be doing more harm than good in recommending a diet high in vegetable oils and low in saturated fat and cholesterol. After all, we developed heart disease, cancer, diabetes and obesity while decreasing saturated fat intake and increasing vegetable oil intake. It seems ridiculous to blame a fat that has been around for thousands of years for diseases that have only been around for the past 100 years. Vegetable oils have also only been used in the past 100 years. The currently accepted low-fat, food-guide-pyramid diet may be causing the very disease we are prescribing the diet to prevent. Based on the evidence, I cannot with a clear conscious recommend a diet high in vegetable oils and low in saturated fat. There is just no good science to support that recommendation and a good deal of science that would contradict that recommendation. I believe it is more important to be scientifically correct than politically correct. And politics has played a more significant role than science in our dietary recommendations whether we choose to believe that or not.

Dietitians are promoted as “the nutrition expert.” How can we possibly make that claim if we do not abide by what the science actually says? How can we claim to be science-based when we ignore every piece of science that contradicts the view we want to take? Our view should be based on the actual science, not the politics behind the science. The science that has come out in the last twenty to thirty years clearly contradicts the diet-heart hypothesis and the lipid hypothesis in its present form. So, trying to lower total cholesterol and LDL cholesterol is a waste of time because it does nothing to prevent LDL from becoming oxidized and, therefore, is not helpful in preventing atherosclerosis.

Based on all the evidence so far, I believe the following:

There is no scientific support for the diet-heart hypothesis, the belief that saturated fat and cholesterol in the diet cause atherosclerosis and heart disease. The lipid hypothesis is not true in its present form. It is not the amount of cholesterol in the blood that matters, but the amount of oxidized LDL, so I would support the oxidized lipid hypothesis. I support diet recommendations that prevent the oxidation of LDL.Reduction of PUFA intake Increase in cholesterol and saturated fat intake Increase in antioxidant intake I support looking into ways to increase LDL receptor function. A recent study shows that curcurmin may be beneficial here (97) and thyroid hormone and iodine may play a role as well.  

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