The Demonization of Cholesterol
In the swamp of modern nutrition advice,
one particular villain has been thrust into the spotlight — cholesterol. The demonization of cholesterol allowed for the subsequent rise of low-fat diets, statin prescriptions, and an unjustified fear of cholesterol-rich foods.
This was no accident. This was an orchestrated campaign, propelled by industry interests. Through influenced studies and altered public perception, this was undoubtedly intentional.
It’s clear that humans have not only survived but thrived on diets that included ample amounts of cholesterol-rich foods.
That’s enough of me preaching to the choir, now to the story of how the very foods that were painted as the prize on cave walls have been painted as the enemy in our minds.
Nutritional guidelines
In 1972, the National Board of Health and Welfare in Sweden developed guidelines for "basic foods" (cheap + mass-produced), and "supplemental foods" (nutrient-dense + less affordable) due to high food prices. The model was redone by Anna-Britt Agnsäter to showcase appropriate amounts. The basic foods at the base included margarine, bread, cereals, potato, and dairy. There was a large section of supplemental vegetables and fruit. Finally, the apex of supplemental foods were meat, fish and eggs.
While Sweden did this out of scarcity, we were told to do this for better health. In 1977, D. Mark Hegsted (we’ll talk about him again later) helped draft the Dietary Goals for the United States. Also called the “McGovern Report”, it suggested an increased consumption of carbs from grains and vegetables to cut the risk of heart attacks and other diseases.
Over the years, more guidelines were released that fell along the lines of the aforementioned. The one that really stuck was the low-fat, grain-based food pyramid introduced by the United States Department of Agriculture (USDA) in 1992. This had placed bread, cereals, rice, and pasta (6-11 servings!) at the base of the pyramid, encouraging people to limit animal products.
The Cholesterol Myths
Years before the food pyramid, the cholesterol hypothesis was instilled. When cholesterol was first discovered as early as 1834, it was recognized as a principle of the nervous system because so much was found localized in the brain and in the myelin around nerve cells. If fact, cholesterol is vital to ensure proper fluidity, thickness, compressibility, water penetration and intrinsic curvature of biological membranes.
It’s essential for the health and function of our cell membranes, which allow for every known intra- and extra-cellular reaction to take place. This goes to show that dietary cholesterol is not some foreign pathogen to our bodies when consumed.
The initial idea came up that an elevated blood cholesterol concentration was the sole cause of cardiovascular disease through a study giving rabbits, which are herbivores, cholesterol. The study was in 1908 by Nikolai N. Anitschkow, a Russian experimental pathologist, purified cholesterol from egg yolks, dissolved it in sunflower oil, and fed it to rabbits. Their blood cholesterol levels increased and their arteries were soon covered in yellow intimal lesions. In terms of lipoprotein metabolism, this rabbit study was flawed for many reasons.
It’s known that rabbits are overly sensitive to dietary cholesterol. They can rapidly develop hypercholesterolemia and aortic atherosclerosis. (PMID: 25277507) After all, they are herbivores. This fact alone should be enough to throw out the idea. With a diet of just 2% cholesterol, rabbits show a rapid elevation in plasma cholesterol, exceeding upward of 2,000 mg/dl. (PMID: 5504967) We know that human consumption of dietary cholesterol has little-to-no effect on blood concentration of cholesterol. (PMID: 16596800)
Rabbit plasma doesn't contain apoAII, which is a multifunctional protein, involved in cholesterol traffic in humans. (PMID: 31374929) Rabbit HDL only contains contains only apoAI. (PMID: 19778946)
Rabbit hepatic lipase activity (which contributes to HDL regeneration) is naturally very low. About 1/10th the activity as that of rats. (PMID: 25277507) If a human has a hepatic lipase deficiency, they have an inability to properly break down fats (lipids) and this reflects in their blood concentration of triglycerides and cholesterol. (condition)
Side note – in the study they “purified cholesterol from egg yolks, dissolved it in sunflower oil, and fed it to rabbits”…. enough said. (PMID: 23975896)
The diet-heart and lipid hypothesis
Later, John Gofman laid the foundation for the diet-heart and lipid hypothesis. Ancel Keys is often accredited for this, but Gofman has the smoking gun here. Gofman discovered three classes of plasma lipoproteins, which are molecules that carry cholesterol, and other important molecules, in the blood. He later was the first to propose the role of lipoproteins in the causation of heart disease in 1950. (PMID: 15403115)
He became known as the father of clinical lipidology as he ultimately gave birth to the field. Few know that he left the field while blaming carbohydrates in the diet, unlike others involved in the theory:
“What is solidly established is that the Sf° 20-400 lipoprotein levels [i.e., blood triglyceride or VLDL concentrations] on the average, can be raised by increasing the dietary carbohydrate intake and can be lowered by decreasing it. … Furthermore, many individuals who are characterized habitually by some type of error in their metabolism that makes their Sf° 20-400 lipoproteins habitually extremely high will experience a marked reduction in the blood levels of these lipoproteins when the carbohydrate intake is lowered.” (here)
In a 1960 editorial (one of his final publications) he emphasized his concern about carbohydrates because the topic was being ignored:
“Several investigators have shown that a low-fat high-carbohydrate diet produces opposite trends in the blood cholesterol and the blood lipid levels. The cholesterol level falls because the low fat diet depresses the level of the cholesterol rich Sf° 0-20 lipoproteins. The triglyceride level rises because the high carbohydrate intake elevates the level of the triglyceride-rich Sf° 20-400 lipoproteins. Both the triglyceride-bearing and cholesterol-bearing lipoproteins have been associated with the development of coronary disease. It therefore behoves the physician utilizing the dietary approach to understand the likelihood that a focus on the fat intake without an appreciation of the effect of carbohydrate intake will not lower all the blood lipids associated with the development of coronary heart disease.” (here)
When he switched the blame to carbs, he even wrote a book that contained recipes for carbohydrate reduction. It’s no wonder Gofman switched fields to study low-level radiation instead… the lipidology field was not in favor of inconvenient truths. Gofman was, however, looking to truly help. In his 1996 book, Preventing Breast Cancer, Gofman showed that medical x-rays were responsible for upwards of 75 percent of breast cancers in the United States.
The Seven-Countries Study
Goffman’s thrown-out idea was later recycled (without credit) by Ancel Keys who was quickly given the spotlight. (PMID: 13085148 + here) He claimed that saturated fat was the sole cause of cardiovascular disease. He was a Minnesota physiologist who brought together researchers from all over the world to study heart and vascular diseases among countries with varied traditional, eating patterns in lifestyles.
Their main hypothesis was that the rate of coronary disease and populations varied, depending on the fat composition of their diet and their serum cholesterol levels. With the data, they enforced the concept that saturated fat causes cardiovascular disease by raising serum cholesterol. However, while the researchers had FAO & WHO data from twenty-two countries, they only used supporting data from seven countries for the study.
It’s no secret that the seven-country study cherry-picked supporting countries. Countries consuming high saturated fat with low rates of heart disease (i.e. France) were excluded. Diets in Greece at the time were temporarily low in saturated fat. The data was collected during Lent.
The researchers also ignored concerns at the time suggesting sugar was better correlated with heart disease than saturated fat. The data used from the Food and Agriculture Organization of the United Nations showed the amount of food available for consumption (production, imports, exports, and the proportion of available food used for purposes other than human nutrition) in each of the countries, instead of how much food was consumed by individuals of the population.
Four years later in 1957, researchers Jacob Yerushalmy and Herman Hilleboe, published a paper titled “Fat in the Diet and Mortality from Heart Disease; A Methodologic Note” that was critical of the SCS graph. They found the SCS graph overly simplistic and misleading.
They conducted their own statistical analysis of data. Keys used FAO & WHO data from 1948-1949 and Yerushalmy and Hilleboe use FAO & WHO data from 1951-1953. They don’t exclude any countries from the analysis, for any reason, choosing instead to include all the countries for which the FAO & WHO had data, which was 22 countries.
Jacob Yerushalmy and Herman Hilleboe went a step further to find out if dietary fat was really the best correlation. This data showcases the relationship between heart disease and other elements of diet, using the same data Keys used:
Table IV findings: Deaths of all causes except of the heart to rule out high ill-defined coders due to insufficient diagnostics (middle column)
Total calories from fat: strongest negative association with mortality (-0.674)
Percent of total calories from fat (-0.657)
Percent of total calories from carbohydrate had the strongest positive association mortality with morality (0.671)
Animal fat and animal protein strong negative association with mortality
The "All Causes" column is statistically insignificant (Significant values are those of (+/-) 0.43), nonetheless, animal fats/protein have a negative association with mortality. Carbohydrates are positive.
"Table IV shows that fat calories and animal protein calories, which were seen above to be positively associated with heart disease, are here negatively associated with noncardiac diseases. A … plausible explanation is that the dietary components which according to the rank correlation coefficients appeared to be positively related to heart disease are indices of the various countries. That is, it may be that the amount of fat and protein available for consumption is an index of a country’s development, industrially, nutritionally, medically, and no doubt in other respects as well." (here)
Despite this ground-breaking find, Jacob Yerushalmy and Herman Hilleboe still concluded that we can't affirm a cause-and-effect relationship to this type of information. Correlation ≠ Causation.
Harvard and The Sugar Research Foundation
From here, we had the Harvard scientists paid by the sugar industry. That’s right. The Sugar Research Foundation, known today as the Sugar Association, paid Harvard scientists the equivalent of about $50,000 in today’s dollars to publish research on heart disease in the New England Journal of Medicine. The studies used in the review were handpicked by the sugar group to push the blame onto fat.
This political influence on our diet policies and research is something to be made known. D. Mark Hegsted (one of the paid Harvard scientists) went on to become the Administrator of the Food and Nutrition Service at the USDA. (here)
In 1977, he helped draft the Dietary Goals for the United States. This report suggested that increased consumption of fruits, grains and vegetables could help cut the risk of heart attacks and other diseases. (here)
Another paid scientist, Dr. Fredrick J. Stare, founded the Department of Nutrition at Harvard's School of Public Health. (here) Stare rejected the idea that the Standard American diet was harmful.
From an article in The Saturday Review from 1978 about him titled “Harvard's Sugar-Pushing Nutritionist” he had a major influence on the general public: (here)
“He reaches the general public directly through a syndicated radio program, a syndicated newspaper column, and a series of popular books. All feature, in addition to standard nutritional advice, the special Stare message, as carried on the jacket of his widely read book Panic in the Pantry: "Eat your additives; they're good for you."
Knowing that these two have such a corrupt background and later went on to shape the world of nutrition into what we know it to be today is frightening. They kicked off this “plant-based agenda”. They effectively convinced millions that replacing animal foods with industrial grains was a wise health decision.
The star of that era (in my eyes): Weston A. Price
Weston A Price's research on Nutrition and Physical Degeneration showed the effects of industrial foods on isolated groups. Tooth decay, facial deformities, and bone loss were evidence to point to the lack of nutrients and minerals in the diet.
Top half: primitive Polynesians with broad facial and dental structures;
Bottom half: modernized Polynesian boy with narrowed arches causing the crowding of teeth
Plant anti-nutrients from grains, we now know, is one of the reasons for this. Phytic acid, high in grains, seeds, and nuts, is a tightly bound storage form of phosphorus shaped like a snowflake. The arms essentially bind to minerals like calcium and iron, these strip your body of nutrients.
Lectins are another antinutrient to consider. These are going to negatively affect our intestinal permeability, lead to a leaky gut and from there, we're looking at auto-immunity.
This plant-forward movement also led to the huge push for margarine and vegetable oils high in unsaturated fats rather than animal fats high in saturated fat. These inferior fats are more susceptible to oxidation being higher in unsaturated fatty acids.
Even monounsaturated fats (touted as the healthiest fat) are not as resilient as saturated fats are. Neglecting saturated fats is not the best thing you can do for your health.
Turning my head to all mainstream advice, I prioritize saturated fats from animal sources. When I do consume plant fats, they are highly saturated like that of coconut oil.
Plant fats also lack the nourishing nutrients found in animal fats like fat-soluble vitamins in their proper forms, many trace minerals, and unique fatty acids. And cholesterol. Yes – it is a nutrient with characteristics generally ascribed to antioxidant molecules.
What about all of the present studies?
When it comes to dismantling the idea that animal fats lead to CVD, there are a few major points to be made.
When studies point to “risk” in the consumption of a food, they will generally use the premise that an increase in LDL-C concludes an increased risk for cardiovascular disease.
But in this case, if high LDL-C is what causes CVD, the LDL-C of untreated patients with CVD should be higher than normal… right?
“However, in a large American study [Citation] including almost 140,000 patients with acute myocardial infarction (AMI), their LDL-C at the time of admission to hospital was actually lower than normal. In another study with the same finding [Citation], the authors decided to lower the patients’ LDL-C even more, but at a follow-up 3 years later, total mortality among those with LDL-C below 105 mg/dl (2 mmol/l) was twice as high compared to those with a higher LDL-C, even after adjustment for confounding variables (14.8% vs. 7.1%, p = 0.005).” (here)
The idea that a high LDL-C is any risk at all is misrepresented. In a systematic review of 19 cohort studies which included 68,000+ elderly people (>60 years of age), they found an inverse association between all-cause mortality and LDL-C. Cardiovascular mortality was highest in the lowest LDL-C quartile.
You might be asking…
…what’s up with this big push and why would they wrongfully demonize cholesterol as they do? One conflict of interest comes down to selling statin drugs. Statin treatment has been widely promoted for cardiovascular prevention. These drugs are successful in lowering LDL-C… however, they are not successful in lowering the incidence of the disease.
To prove this, there would need to be a definite systematic exposure–response relationship, comparing the degree of cholesterol lowering in patients in single trials and the total reduction of their risk. True exposure–response has been calculated in these three clinical trials, yet it was absent in all three. (1, 2, 3)
Statins don’t come without their risks. Cholesterol is a vital substance to our bodies due to it’s role within cell membranes. Because statins block the production of this molecule necessary for normal cell function, this comes to no surprise.
“Furthermore, case–control and cross-sectional studies have shown that statin use is observed significantly more often among patients with cataracts [76], hearing loss [77], suicidal ideation [78], peripheral neuropathy [79], depression [80], Parkinson’s disease [81], interstitial cystitis [82], herpes zoster [83], impotency [84], cognitive impairments [85–88], and diabetes [89,90]. In some of these studies, the side effects disappeared with discontinuation of the statins and worsened with rechallenge [74,84,85].”
Statin drugs can start a domino effect of more prescriptions to treat the side effects. As much as I hate to say it – this medical model is incredibly profitable.
Concluding words
If you read this far, I’m applauding you. I know I carried you through barrels, over walls, and upstream a river to tell this history and to show that cholesterol is not the boogeyman.
This is why following the ways of time-tested health is key. No industry influence. It’s much wiser to study voluntary ways of living from the past.
In times when choices were made based on what works.
When choices were made based on what made people thrive.
When choices were made based on the care for the health of the people they loved.
Lucky for you, you’re right where you should be. It’s never too late to get back these ways.
Appreciatively, Mia
