# Lipid Hypothesis

Category: Theories & Frameworks

Also known as: diet-heart hypothesis, cholesterol hypothesis

The lipid hypothesis, also known as the diet-heart or cholesterol hypothesis, is the theory that cholesterol in the blood causes atherosclerosis, and that consuming polyunsaturated oils lowers blood cholesterol while saturated fats raise it, thereby preventing heart disease…

10 passages · 3 authors · 2011–2023 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/lipid-hypothesis

## Synthesis

The **lipid hypothesis**, also known as the diet-heart or cholesterol hypothesis, is the theory that cholesterol in the blood causes atherosclerosis, and that consuming polyunsaturated oils lowers blood cholesterol while saturated fats raise it, thereby preventing heart disease. [Source 1] Ray Peat argued that this hypothesis was constructed without valid evidence, serving instead to create a market for the seed oil industry after their products were displaced from paints and plastics by petroleum-based compounds. [Source 1] He noted that the hypothesis left behind any concept of nutritional essentiality, allowing industry and academic supporters to promote polyunsaturated oils as having *drug-like therapeutic properties*, with larger amounts supposedly being more protective. [Source 1] Peat maintained that there was no basis for a connection between high cholesterol, saturated fat, and heart disease, a position he adopted after reading John Yudkin’s work in 1972, which showed that sugar, not fat, increased blood lipids. [Source 2]

Peat and others have detailed how the lipid hypothesis was refuted by multiple lines of evidence. Uffe Ravnskov demonstrated that none of the hypothesis’s arguments—linking dietary saturated fat to blood cholesterol, blood cholesterol to atherosclerosis, or atherosclerosis to heart disease mortality—had evidential support. [Source 4] A veterans’ study in the 1960s found that replacing saturated fats with liquid oils caused more deaths from heart disease and significantly more from cancer, creating early problems for the theory. [Source 4] Danny Roddy notes that Chris Masterjohn and others have thoroughly picked apart the flaws in the hypothesis, vindicating saturated fats in the process. [Source 7] Georgi Dinkov has pointed out that the association between high cholesterol and cardiovascular disease is not causative, and that only **oxidized cholesterol** is problematic, with oxidation occurring only under conditions of excessive reactive oxygen species. [Source 9] Peat emphasized that cholesterol is actually a protective substance, increasing at locations of injury and being necessary for healthy cell division, DNA replication, nerve function, and learning, functioning as the body’s most basic *anti-stress protective substance*. [Source 4]

Peat’s framework reinterpreted elevated cholesterol as an adaptive response to stress and low thyroid function rather than a dietary pathology. He observed that cholesterol increases during stress to provide the raw material for steroid synthesis, with levels rising before exams and normalizing afterward. [Source 3, 6] Elevated cholesterol is closely related to **low thyroid function**, and together with thyroid hormone and vitamin A, it is used to synthesize the “youth-associated” steroid precursor **pregnenolone**. [Source 3, 6] In this context, Peat saw cholesterol not as a toxin to be lowered, but as a crucial structural and functional molecule. He described protoplasm as a complex solution in which cholesterol acts as both a *lubricant* and a *stabilizer*, decreasing cell rigidity by increasing protein mobility. [Source 5, 10] Experimentally, lowering the cholesterol content of red blood cells makes them more rigid and fragile, while restoring normal cholesterol restores their flexibility, directly contradicting the membrane fluidity arguments of the lipid hypothesis. [Source 10]

The actual drivers of atherosclerosis, in Peat’s view, are the polyunsaturated fats that the lipid hypothesis promoted as protective. He documented that **lipid peroxidation** products from polyunsaturated fats, such as hydroxynonenal, malondialdehyde, and acrolein, attract macrophages that accumulate in plaques, while the age pigment **lipofuscin**, derived largely from PUFA, accumulates iron and catalyzes oxidation, creating local hypoxia and inflammation. [Source 5] Furthermore, polyunsaturated fatty acids degrade the protein ABCA1, which is responsible for removing excess cholesterol from arteries, thereby impairing the cholesterol secretory pathway in macrophages. [Source 5] Peat traced the origins of the “essential fatty acid” concept that underpinned the lipid hypothesis to the flawed 1929 experiments of George and Mildred Burr, whose fat-free diet produced a condition that was actually a **vitamin B6 deficiency** caused by the diet’s high sugar content accelerating metabolic rate and nutritional requirements. [Source 2, 7, 8] He noted that animals fed a diet lacking these so-called essential fatty acids consumed oxygen at a very high rate, had unusually stable mitochondria, resisted immunological rejection of transplanted tissues, and were extremely hard to kill by trauma and toxins. [Source 8]

## People also ask

### What did Ray Peat believe actually causes atherosclerosis?

Peat argued that polyunsaturated fats drive atherosclerosis through lipid peroxidation products that attract macrophages and degrade the protein responsible for removing cholesterol from arteries, while cholesterol itself is a protective substance.

### How does thyroid function relate to cholesterol levels?

The corpus describes elevated cholesterol as closely related to low thyroid function, with Peat observing that cholesterol rises during stress to provide raw material for steroid synthesis and is used with thyroid hormone to produce pregnenolone.

### What was the original basis for the essential fatty acid concept?

Peat traced the concept to the Burrs' 1929 experiments, arguing their fat-free diet actually caused a vitamin B6 deficiency because its high sugar content accelerated metabolic rate and nutritional requirements.

## Related concepts

- [Age Pigment (Lipofuscin)](https://bioenergeticoracle.com/md/concepts/age-pigment-lipofuscin/index.md)
- [Arachidonic Acid](https://bioenergeticoracle.com/md/concepts/arachidonic-acid/index.md)
- [Atherosclerosis](https://bioenergeticoracle.com/md/concepts/atherosclerosis/index.md)
- [Benign Prostatic Hyperplasia (BPH)](https://bioenergeticoracle.com/md/concepts/benign-prostatic-hyperplasia-bph/index.md)
- [Bohr effect](https://bioenergeticoracle.com/md/concepts/bohr-effect/index.md)
- [Cholesterol](https://bioenergeticoracle.com/md/concepts/cholesterol/index.md)

## Cited passages

Passage numbers match the `[Source N]` markers in the synthesis above.

### Source 1 — Fats and degeneration

Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/fats-degeneration3.shtml

> Although "Burr's disease" clearly turned out to be a B-vitamin deficiency, probably combined with a mineral deficiency, it continues to be cited as the basis justifying the multibillion dollar industry that has grown up around the "essential" oils.
>
> Two years before Burr's experiment, German researchers found that a fat-free diet prevented almost all spontaneous cancers in rats. Later work showed that the polyunsaturated fats both initiate and promote cancer. With that knowledge, the people who kept claiming that "linoleic, linolenic, and maybe arachidonic acid are the essential fatty acids," should have devoted some effort to finding out how much of that "essential nutrient" was enough, so that people could minimize their consumption of the carcinogenic stuff.
>
> Between the first and second world wars, cod liver oil was recommended as a vitamin supplement, at first as a source of vitamin A, and later as a source of vitamins A and D.
>
> But in the late 1940s, experimenters used it as the main fat in dogs' diet, and found that they all died from cancer, while the dogs on a standard diet had only a 5% cancer mortality. That sort of information, and the availability of synthetic vitamins, led to the decreased use of cod liver oil.
>
> But around that time, the seed oil industry was in crisis because the use of those oils in paints and plastics was being displaced by new compounds made from petroleum. The industry needed new markets, and discovered ways to convince the public that seed oils were better than animal fats. They were called the "heart protective oils," though human studies soon showed the same results that the animal studies had, namely, that they were toxic to the heart and increased the incidence of cancer.
>
> The "lipid hypothesis" of heart disease argued that cholesterol in the blood caused atherosclerosis, and that the polyunsaturated oils lowered the amount of cholesterol in the blood. Leaving behind the concept of nutritional essentiality, this allowed the industry (and their academic supporters, such as Frederick Stare at Harvard) to begin promoting the oils as having drug-like therapeutic properties. Larger amounts of polyunsaturated fat were supposed to be more protective by lowering the cholesterol, and were to be substituted for the saturated fats, which supposedly raised cholesterol and increased heart disease, producing atherosclerotic plaques in the blood vessels and increasing the formation of blood clots.

### Source 2 — Sugar Myths 1 – Sugar and the Link Between Cholesterol.

Ray Peat · Transcript · 2011

> **Ray Peat:** Yeah they form in the brain and on the skin, everywhere and they tend to get formed faster and faster, the more stress you’re under and pretty soon, if you’re under the influence of unopposed estrogen they can eat all the oxygen and not leave any for the cell functions. That was what really started getting me interested in the unsaturated fat metabolism. I did that dissertation in 1972 and that was the year that John Udkin published his book, ‘Pure White & Dangerous’ or something. I read that and was so impressed by his argument that sugar increases blood lipids, saturated fats and cholesterol that, that was what started me on the idea of recommending increased sugar for people who are under stress, because I had already become convinced that there was no basis at all for the connection between high cholesterol and saturated fat and heart disease and so on. And so when I would see someone deficient in progesterone, having too much estrogen and age pigment, they would often recover if they could increase their cholesterol production and the simplest way to do that is to have them eat some extra sugar. That started me seeing the therapeutic possibilities of sugar and from there I worked backwards, understanding where the lipid hypothesis had come from and especially the doctrine that essential fatty acids are essential nutritionally, and since they’re what lipofuscin is made from, it seemed increasingly important to understand how that theory came about. I saw that George and Mildred Burr were the ones who created that idea in the 1929 and 30. In their experiment they didn’t, at that time, know about most of the essential nutrients, vitamins and minerals, so they fed what they thought was a complete diet.

### Source 3 — Hair Like a Fox: A Bioenergetic View of Pattern Hair Loss

Danny Roddy · Book · 2013

> Uffe Ravnskov, Dr. Chris Masterjohn, and others have refuted the lipid hypothesis in finding that there’s no connection between saturated fat, cholesterol, and heart disease. However, elevated cholesterol is closely related with low thyroid28 and along with vitamin A the three substances are used to synthesize the "youth-associated" steroid-precursor, pregnenolone. In an adaptive process, cholesterol increases during stress to provide the raw material for steroid synthesis. For example, in an experiment with college students, cholesterol levels went up before exams, and returned to normal shortly after the exam.29 If cholesterol levels were too low, common among violent criminals and those with depression and suicidal tendencies, the most efficient way to normalize cholesterol levels would be to consume more fructose, “the most lipogenic carbohydrate.” The most common criticism launched at fructose is that fructose is shunted directly to the liver where it is converted to fat, setting the stage for fatty liver disease (NAFLD), diabetes and obesity. While it is true that the liver rapidly uses fructose, it does so primarily to refill the liver's sugar supply in the form of glycogen. In one study, an infusion of fructose resulted in about 360 percent more hepatic glycogen than a glucose infusion.30 The liver's glycogen storage capacity is very large. One study suggested that “de novo lipogenesis [DNL] is not an important pathway in humans” and that chronic overfeeding on carbohydrates increased glycogen stores of about 500 grams before DNL became significant.31 To clarify, only with chronic overfeeding and saturated glycogen stores does the conversion of carbohydrate to fat become significant. While usually mentioned in the context of athleticism, hepatic glycogen is an important health factor for everyone. Adequately "stocking" the liver's reserve of glycogen is central in resisting maladaptation to long-term adaptive "stress" hormones like adrenaline, glucagon, and cortisol. For instance, cortisol levels in wild monkeys who consume a diet of primarily fruit, increase when their diets contain less sugar.32 Similarly, sugar lowers the main pituitary hormone, ACTH, which signals the production of cortisol.33 In contrast to the beneficial effects of fruits, starchy carbohydrates (e.g., grains, breads, pastas and legumes) are a problematic carbohydrate source.

### Source 4 — Sugar Myths 1 – Sugar and the Link Between Cholesterol.

Ray Peat · Transcript · 2011

> **Ray Peat:** They convinced doctors, by a huge campaign that cholesterol was found in the wall of arteries that were developing atherosclerosis, and since you could lower the cholesterol in the blood, they argued that you would lower the cholesterol in the wall of the artery and that would prevent heart disease. Ravenschoff much later showed that none of those arguments had any evidence to support them. Atherosclerosis didn’t have a direct connection to heart disease, mortality, cholesterol in the blood didn’t have a connection directly with the formation of atherosclerosis and dietary fats, saturated fats didn’t create the cholesterol in the blood. But there was a slight back sliding in the ability to sell doctors on the ideas of eating unsaturated fats to lower cholesterol. There was a study with veterans in which putting them on the liquid oil diet eliminating saturated fats caused more of them to die of heart disease, and a lot more of them to die of cancer. There was some problem with that lipid theory already in the 1960s and John Udkin came out, he had been doing research since the mid 50s, 1972 he published this book arguing that sugar caused heart disease because it increased cholesterol! Already since I knew that cholesterol didn’t have anything to do with heart disease, except protecting against it to some extent. That was when I realised that he was right on the issue that sugar would increase cholesterol in some people.

### Source 5 — Cholesterol in Context: Part I

Ray Peat · Newsletter · 2018

> When a drop of water is on an oily surface it doesn’t spread, because of its strong cohesive forces, and the oil’s lack of those forces. When a drop of oil falls onto water, it spreads, becoming extremely thin. Benjamin Franklin estimated that a teaspoonful of olive oil spread over about half an acre of a pond. Oil has very weak cohesive forces, and effectively no tensile strength. The fact that cholesterol strengthens cells, keeping them from disintegrating under stress, obviously has nothing to do with a lipid bilayer membrane. That membrane doctrine has made it seem paradoxical that the loss of cholesterol should make cells stiffer, while weakening them. Gilbert Ling has, for 65 years, pointed out the numerous “paradoxes” confronted by the advocates of the lipid boundary membrane, but the membrane doctrine continues to govern most biomedical thinking, including theories of cholesterol’s role in the diseases of aging.
>
> About 40 years ago, someone noticed that the commercial cholesterol used for research was contaminated by oxidation, and that pure cholesterol didn’t produce the same toxic effects. Lipid peroxidation was observed in atherosclerotic plaques, and the breakdown products of polyunsaturated fats such as hydroxynonenal, malondialdehyde, and acrolein (from EPA, arachidonic acid, and other highly unsaturated fats in the affected blood vessel) are known to attract white blood cells such as macrophages, which accumulate in the plaques. The age pigment, ceroid or lipofuscin, that’s derived largely from PUFA and associated with the macrophage “foam cells” in the plaque, accumulates iron (Lee, et al., 1998), and by catalyzing oxidation, creates local hypoxia, leading to lactic acid production, contributing to an inflammatory process. The products of lipid peroxidation, such as azelaic acid (Riad, et al., 2018), along with lactate, lead to the calcification of tissue.
>
> Several observers have demonstrated that a protein that can remove excess cholesterol and other lipids from arteries, ABCA1 (ATP-binding cassette transporter or CERP (cholesterol efflux regulatory protein)), is degraded by polyunsaturated fatty acids.

### Source 6 — Casualties of The Nutritional Dark Ages, Part II: Fructose

Danny Roddy · Article · Jul 23, 2013

> Although, he spent a considerable amount of time linking the consumption of sucrose to the lipid hypothesis (i.e., high cholesterol causes heart disease), explaining that fructose produces an unfavorable increase in blood lipids.
>
> Uffe Ravnskov and many others have refuted the lipid hypothesis finding that there’s no connection between blood lipids and disease, however, elevated cholesterol is closely related with low thyroid (Sundaram, et al. 1997). Cholesterol, thyroid hormone, and vitamin A are used to synthesize the "anti-stress" steroid-precursor, pregnenolone. In an adaptive process, cholesterol seems to increase during stress to provide the raw material for steroid synthesis. For example, in an experiment with college students, cholesterol levels went up before exams, and returned to normal after (Grundry and Griffin, 1959).
>
> In this context, an excess of cholesterol could suggest maladaptation. However, If cholesterol is too low, which is popular among the depressed (Morgan, et al., 1993), the suicidal (Golier, et al., 1995), and violent criminals (Golomb, et al., 2000), one of the best ways to increase it, would be to consume more fructose, which as John Yudkin demonstrated, is highly lipogenic.
>
> A Bioenergetic View of Fructose
>
> A dozen or so years ago, a religious friend told me "If I stood for nothing, I would fall for anything." While this statement is lost on me in a religious context, I often think about it in a nutritional one. For instance, in my almost decade-long nutrition journey I've seen many substances that were originally thought to be therapeutic, only later found to be harmful. Changing one's mind in the face of better evidence is great, however, when this happens repeatedly, a problem may exist in the broader context.
>
> As I mentioned in Casualties of The Nutritional Dark Ages, Part I: Calcium, after many failed health experiments, I began studying the work of Ray Peat, Hans Selye, Broda Barnes, Roger J. Williams, Albert Szent-Györgyi, Gerald Pollack and more recently Gilbert Ling. After shedding pounds of cognitive dissonance, my 'wellness context' evolved and I adopted the idea that health problems were likely the result defective energy metabolism.

### Source 7 — Hair Like a Fox: A Bioenergetic View of Pattern Hair Loss

Danny Roddy · Book · 2013

> Chris Masterjohn and others have thoroughly picked apart the flaws in the "the lipid hypothesis," vindicating saturated fats in the process (for many of the same reasons that are discussed in this chapter). Even more controversial than the role of unsaturated and saturated fats in human physiology is the role of the so-called "essential fatty acids," or EFAs, which include
>
> - Omega-6 linoleic acid (LA)
> - Omega-6 arachidonic acid (AA)
> - Omega-3 alpha-linolenic acid (ALA)
> - Omega-3 docosahexaenoic acid (DHA)
> - Omega-3 eicosapentaenoic acid (EPA)
>
> Found predominantly in oily fish such as salmon, halibut, and sardines, and in dietary supplements derived therefrom (e.g., fish oil, cod liver oil, salmon oil, krill oil), these fats, now universally believed to be beneficial, have been elevated to the status of vitamins. Especially when viewed in our bioenergetic context, however, the early research that deemed certain polyunsaturated fatty acids as “essential” seems, in my estimation, to have been presumptuous.
>
> ### A Brief History of EFAs
>
> The idea that some fats were essential began in 1929 when George and Mildred Burr published a paper claiming that a variety of diseases including dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration were cured when their rodents were supplied with adequate linoleic acid (LA).5 The experimental diet used to support this finding consisted of purified casein (a milk protein) and purified sucrose, aligned with supplemental vitamins and minerals. Besides being deficient in several nutrients that hadn’t been discovered yet (e.g., zinc, copper, manganese, molybdenum, and selenium) the fat-deficient high-sucrose diet caused the rats to consume oxygen at an extremely high rate (i.e., increase their metabolic rates). Some wondered if rather than a deficiency of LA, the rats’ nutritional requirements were simply higher due to their higher rates of metabolism. The suspicions of these few skeptical individuals were proven to be justified when the purported essential fatty acids deficiency was cured with the addition of vitamin B6,6 suggesting that rather than curing a deficiency, the addition of LA was simply decreasing the rate of metabolism and therefore the nutritional requirements.

### Source 8 — Fats and degeneration

Ray Peat · Article · 2013 · https://raypeat.com/articles/articles/fats-degeneration3.shtml

> Larger amounts of polyunsaturated fat were supposed to be more protective by lowering the cholesterol, and were to be substituted for the saturated fats, which supposedly raised cholesterol and increased heart disease, producing atherosclerotic plaques in the blood vessels and increasing the formation of blood clots.
>
> Since all ordinary foods contain significant amounts of the polyunsaturated fats, there was no reason to think that, even if they were essential nutrients, people were likely to become deficient in them. So the idea of treating the seed oils as drug-like substances, to be taken in large amounts, appealed to the food oil industry.
>
> Prostaglandins, which are produced in the body by oxidizing the polyunsaturated fatty acids, provided an opportunity for the drug industry to get involved in a new market, and the prostaglandins offered a new way of arguing for the nutritional essentiality of linoleic and related acids: A whole system of "hormones" is made from these molecules.
>
> Since some of the prostaglandins suppress immunity, cause inflammation and promote cancer growth, some people have divided them into the "good prostaglandins" and the "bad prostaglandins." PGI2, or prostacyclin, is considered to be a good prostaglandin, because it causes vasodilatation, and so drug companies have made their own synthetic equivalents: Epoprostenol, iloprost, taprostene, ciprostene, UT-15, beraprost, and cicaprost. Some of these are being investigated for possible use in killing cancer.
>
> But many very useful drugs that already existed, including cortisol and aspirin, were found to achieve some of their most important effects by inhibiting the formation of the prostaglandins. It was the body's load of polyunsaturated fats which made it very susceptible to inflammation, stress, trauma, infection, radiation, hormone imbalance, and other fundamental problems, and drugs like aspirin and cortisone, which limit the activation of the stored "essential fatty acids," gain their remarkable range of beneficial effects partly by the restraint they impose on those stored toxins.
>
> Increasingly, the liberation of arachidonic acid from tissues during stress is seen as a central factor in all forms of stress, either acute (as in burns or exercise) or chronic (as in diabetes or aging). And, as the fat stores become more toxic, it seems that they more readily liberate the free fatty acids.

### Source 9 — [Ep.4]How To Accomplish Metabolic Flexibility: The Key to a Longer Life

Georgi Dinkov · Interview · Oct 9, 2023

> **Dr. Joel Rosen:** right? No, thank you so much for that explanation. So that’s all things created equal, not considering the quality of the sugar, the quality of the fat, um, but just from a from a, I guess, a genesis of how we got here, because now we’re, I could see as a listener might be thinking okay, perhaps because we vilified sugars, and we’ve gotten into getting into ketosis fast and fast doing these intermittent fasting and increasing our fat intake. But I would argue that it started before that when we vilified fat, and we started so maybe it kind of got us to how we got here from from having this whole Randle cycle, which is saying we’re preferentially we’re not preferentially too much demand to have to do beta oxidation. And then when you combine that with getting carbohydrates or unhealthy sugars, that creates a load on the system where metabolic flexibility breaks down, and insulin resistance ensues, or it’s anyways, kind of gets us to how maybe the evolution of how this came from when we started off with, with having low fat diets and going from there.
>
> **Georgi Dinkov:** I think it started in the early 20th century. If you look at some of the older publications and how people ate back in the day, they didn’t worry that much about macronutrients or how much fat or sugar they were taking, they were eating, you know, according to taste. If you look at some of the older commercials from the 1940s, and 50s, these housewives were geared to housewives and saying, You need to feed your children at least five or six meals a day. We did milkshakes, ice cream, drinking several bottles of Coke a day, old, and people were not obese back in the day, at least per capita, which is the reason that we’re seeing today. Something happened I will say in the 1950s, where I think that’s when the cholesterol hypothesis first started forming. Were basically the the outset, Big Pharma really started that. But for whatever reason, medical professionals shifted towards limited lipid-like molecules and started with cholesterol, saying that, yes, cholesterol and high cholesterol are associated with cardiovascular disease. And that is true, but associated, does not mean causative. And there have been several cases that have demonstrated that it’s only oxidized cholesterol, but it’s problematic. But oxidized cholesterol only happens when you have a normal amount of reactive oxygen species that generate other ones. Cholesterol by itself is absolutely crucial for the cell. It’s part of the bilayer. The bilayer lipid membrane is a precursor to all steroids, right. So it’s clearly something that the body definitely needs. But I think a lot of cholesterol gurus think that if you eat too much fat, you will get fat.

### Source 10 — Cholesterol in Context: Part I

Ray Peat · Newsletter · 2018

> For example excitotoxicity (Fang, et al., 2014), and other forms of energy depletion can stiffen cells, and prolonged energy depletion and inflammation lead to degenerative changes—tissue calcification, fibrosis, and invasive, disorganized cell movement, for example. These stress related stiffenings of the cell substance and matrix have nothing directly to do with the local quantity of cholesterol.
>
> Hypothyroidism, leading to energy depletion and increased stress hormones, causes increased rigidity of various cells that have been examined, including red blood cells and brain cells (Tacconi, et al., 1991). The stiffer cells are also more fragile and disintegrate more easily. The stiffness of red blood cells in hypothyroidism increases the viscosity of the whole blood, and changes in blood proteins contribute to this. The fact that hypothyroidism usually involves an increase in cholesterol along with the increased rigidity and viscosity often leads the “lipid bilayer” people to explain those changes as a result of the increased absorption of cholesterol by the red cells, reducing the “fluidity of the membrane.” The experiments that showed the protective anti-hemolysis effect of cholesterol conflict with this, because stiffer red cells are more fragile. When the cholesterol content of red blood cells is experimentally lowered, they become more rigid, and restoring the normal amount of cholesterol restores their flexibility (Murphy, 1962). The in vitro behavior of simple mixtures of cholesterol with fats simply doesn’t correspond with the way cholesterol affects living cells.
>
> One of the strangest things about cholesterol research is that there have been so few studies of the general physical interactions of cholesterol with proteins, in contrast to the obsessive study of its in vitro interactions with fats. In the body, the adipose tissues with a high fat content maintain a much lower cholesterol content than the muscle tissues. This is partly because muscles produce more cholesterol than fat tissue does, but also because the structural proteins of cells have a high affinity for cholesterol. In effect, fat and proteins are mutually soluble. I think it’s correct to think of protoplasm as a complex kind of solution of proteins, water, cholesterol and other lipids, nucleic acids, ATP, and smaller amounts of other substances, with a viscosity that varies as small changes of solutes modify the balance of cohesive forces.

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