The Rhetoric of Health


by Charles Berezin


I am not a scientist, and I do not intend to write a scientific treatise. Rather, my academic background is in rhetoric. I am trained to recognize how patterns of thought emerge into stories. In my reading of nutritional texts, I have seen egregious rhetoric crowd out some very interesting stories. I intend to reveal the bad rhetoric I have seen and tell some interesting stories along the way.

Rhetoric is about knowing the difference between a good argument and a bad argument. While it is possible to make a bad argument for a good idea, it is not possible to make a good argument for a bad idea. Somewhere along the line, a rat will have crept in. So when we see a bad argument, it is important to know whether the problem is the idea or the argument. The great enemy of good argument is the idée reçue, the received idea, the thing that must be true because everyone believes it but which has never been truly investigated or understood. The received idea behaves like a virus. Just as a virus causes an infected cell to make copies of itself, so the received idea distorts whatever rhetorical pathway it infects into self-justification.

We can understand the scientific method as a kind of rhetorical pathway. As long as we stick close to the path, the belief goes, we will arrive at some truth. But as we shall see, in nutrition and health, that pathway is littered with received ideas. Too often, what appears as truth is really a version of the received idea that threw the researcher off course. Chief among those received ideas is the lipid hypothesis, the belief that dietary fat and cholesterol are the culprits in the majority of disorders of the human species. To read nutritional literature is to see myriad specious justifications for the lipid hypothesis.

For a good discussion of the lipid hypothesis, I refer the reader to Gary Taubes’ excellent book, Good Calories Bad Calories, in which Taubes not only soundly refutes the scientific rationale, but also explains the historical and political circumstances that allowed an unproven idea to become nutritional dogma for thirty years.

I was originally much taken with Protein Power, by the Drs. Eades, since it made eminent sense while turning upside down everything I thought I knew about health. I was fascinated by their step-by-step dismantling of the lipid hypothesis, which I had blithely accepted as background for all my decisions about health and nutrition. It's been a quest for more information since then. What's exciting is discovering how much of what I'm learning corroborates other pieces until a coherent story starts emerging. The more I find out, the more I feel that nutrition is a social justice issue since people are being denied the information that would enable them to make appropriate decisions about one of the most important areas in their lives and are being left vulnerable to the predations of the pharmaceutical industry and what I will call the medical-pharmaceutical-health insurance complex. I see an obese person, at least partially, as someone who has been victimized by bad information and limited choices.

Besides the Eades, I am much beholden to Dr. Ron Rosedale, whose remarkable speech to a nutritionists' symposium prompted many of these speculations, as well as to the excellent work of Dr. Richard Feinman at SUNY Downstate and his colleagues at Nutrition and Metabolism who have taught me much.

What I have learned about nutrition has ignited my passions for storytelling and social justice. I have come to see that there is a rhetoric of health which exists apart from whatever technical information might support it and which helps us understand the technical information by putting it in context.


The basis of that rhetoric of health comes from some suggestive remarks by Rosedale. He points out, although it is common knowledge, that in evolution, nothing is ever thrown away; rather, adaptations are built upon existing processes, so that all our bodily processes are compilations of what has gone before: ontogeny recapitulates phylogeny, as the saying goes. This idea explains why our bodily processes are so unbelievably complex, one process built upon another. (This complexity, for what it’s worth, undermines the idea of intelligent design. The value in engineering design is in elegance: simplicity, straight lines, few moving parts. Had we been intelligently designed, our bodily processes would be far more elegant. They are not elegant.)

Rosedale also points out that our bodies are communities of cells in communication with one another. Disease can be understood as a breakdown in communications, cells acting on bad information with destructive results. The endocrine system, which controls hormones, enzymes, and the like, is the communication system, sending chemically coded messages to the cells telling them how to behave, how to cooperate with other cell communities, and what to do next. Everything that happens in our bodies happens as the result of complex metabolic pathways, in which hormones, enzymes, proteins, and fats interact in ways that produce varying effects.

These metabolic pathways can be understood as archeological accretions. Archeologists know that human settlements tend to get built on top of the ruins of previous settlements, so if you want to find out what happened previous to the level you're working on, dig deeper. In metabolism, new hormones and enzymes get added onto the previous mix in ways that modify existing pathways to produce adaptive results. Nothing gets thrown away. In metabolism, unlike archeology, however, those previous accretions still exert their effects. That is why insulin is so important.

Once again, Rosedale points out that insulin is the first hormone, the ur-hormone present in almost all animal organisms. All other hormones are directly or indirectly derived from insulin.

As such, it is the basis for almost everything that happens in our bodies, which is why it has such powerful effects. When one of these metabolic pathways goes awry and produces a disease state, we need to find out what has disturbed that metabolic pathway to produce that undesired effect. Chances are that insulin has had a hand in it.

Most know only that insulin controls blood sugar levels, but that is only a minor component of its many roles. We know that there is a vicious cycle in which chronically high insulin levels cause insulin resistance, a condition in which cells shut down their insulin receptors to avoid insulin overload. When that happens, insulin can no longer drive glucose into the cells, so blood glucose levels remain high. The continuing high glucose levels stimulate the pancreas to release even more insulin until there is finally enough to overwhelm the diminished receptor activity, bully glucose into the cells, and lower blood sugar levels. Meanwhile, the increased insulin levels are wreaking havoc on many of the crucial metabolic pathways that keep us healthy.

Metabolic pathways do not alter themselves. Something coming in from the environment is doing it. The substance from the environment that has the most immediate and massive effect on the endocrine system is carbohydrates, which stimulate insulin, the ur-hormone, which, we have seen, is positioned to affect all the metabolic pathways in the body. The key to maintaining health, then, is to control insulin levels and prevent insulin resistance, which magnifies the deleterious effects of insulin. The key to controlling insulin levels is to control carbohydrates in the diet; nothing could be clearer.


Why should insulin have such destructive propensities? We need insulin to live, but anything above the minimal levels is going to wreak havoc on our health. Our health depends on achieving the necessary insulin reactions with the least amount of insulin possible. Rosedale has pointed out that in many organisms, the chief role of insulin is to control life span, the higher the insulin level, the shorter the life span. It would be reasonable to assume that it plays a similar role in human beings.

Insulin most likely plays a role in our survival strategy. Every species has strategies for survival based on leveraging its environment. Does a species develop fangs and claws to take advantage of abundant animal protein, or flat teeth and a long digestive system to take advantage of abundant grasslands, etc.?  Human beings have different strategies based on whether the environment is rich in resources or poor in resources. The genus homo has existed for about two million years. Our species, homo sapiens, has existed for about two hundred thousand years. We inherited our diet and digestive equipment from the genus homo, and they have remained fairly constant for the last two million years.

Our Paleolithic ancestors were hunter-gatherers, and their diet was low carbohydrate, based on animal protein and fat. Recent speculation is that our earliest ancestors gained an advantage by going to a kill after all the predators and scavengers had finished, smashing open the large bones and skulls with rocks, bones that even large animals could not crack with their jaws, and eating the marrow and brains, high in life-sustaining fat. Whatever roots, greens, and fruits they also ate were seasonal and much lower in sugar and starch than the hybridized fruits and vegetables available year round in our supermarkets. They certainly had no grains. This diet did well for us for two million years. The fossil evidence shows that Paleolithic homo sapiens were larger and had higher bone density than modern people.

Human beings, as a species, have one strategy when resources are plentiful and another strategy when they are not. We know that the preferred macronutrients for the human body are protein and fat. So resource-rich conditions means lots of available protein and fat. When protein and fat were less available, the proportion of carbohydrates in the diet would rise, so resource-poor conditions would mean less protein and fat and more carbohydrates. The evidence suggests that Paleolithic people had, for the most part, a resource rich environment. But all that changed with the advent of agriculture, some scant ten or twelve thousand years ago. A diet based on processed grains meant that carbohydrates were now the largest portion of the diet. Despite having abundant food, agriculturists created, in essence, an artificial resource poor environment.

Strategy #1

The important thing from the point of view of species' survival is to defend the strength and diversity of the gene pool. Under resource-rich conditions, the species can defend the gene pool with fewer, long-lived, larger individuals with high metabolism rates. Bodies have little need for long-term fat storage, since fat is plentiful. There is less survival pressure for individuals to reach reproductive maturity early and less pressure for these same individuals to expire soon after reproduction.

Strategy #2

Under resource poor conditions, this strategy makes no sense. Defending the gene pool under resource poor conditions would require a larger number of smaller individuals with lower metabolism rates so that more people could get to the age of sexual maturity using fewer resources. Our bodies would need to create and store fat since dietary fat is less available. Not only would people would reach sexual maturity earlier, thet would die sooner to conserve resources for those who have not yet passed on their genes.

Insulin, stimulated by the higher carbohydrate level of the resource-poor diet, is the toggle switch between these two strategies. We know that pre-agricultural hunter-gatherers had a low carbohydrate diet and low insulin levels, while agriculturists dramatically increased their insulin levels with their grain-based diet. Everything that happens to us in strategy #2 is spurred directly or indirectly by insulin resistance and the accompanying hyperinsulinemia. Metabolic syndrome caused by hyperinsulinemia is an efficient way of culling those of us who have already passed on our genes and so are no longer necessary to the survival of the species. So after ten thousand years of artificial resource poor conditions, we have massive overpopulation and massive misery. The idea is not to recreate the Paleolithic diet; that would be impossible. Rather, the Paleolithic diet tells us what a resource rich nutritional environment looks like. It's up to us to use politics, economics, and technology to assure a resource rich environment for the world's population.


Ontogeny recapitulates phylogeny means that the embryonic development of the individual mimics the evolutionary development of the species.  Just as life on earth started as a single celled organism, so do we.  At one point in our gestational development, we have gills.  Then we lose the gills and develop lungs and feet, etc.  But the relationship between ontogeny and phylogeny doesn’t stop at birth.  Throughout our lives, our bodies go through both ontogenetic and phylogenetic processes: ontogenetic processes being those that promote the survival of the individual; and phylogenetic processes being those that support the survival of the species. 

We saw that in strategy two, the strategy for an environment poor in resources, phylogenetic processes tend to predominate.  For instance, scientists now suggest that exposure to estrogen is a contributing factor to female cancers.  We know that within historical time, the age of menarche has been decreasing, while the age of menopause has been getting later, thus increasing women’s exposure of estrogen and the susceptibility to female cancers.  It is possible, then that early menarche and late menopause are related phylogenetic processes that promote more individuals to defend the gene pool and early death to conserve resources.

The tension between ontogenetic and phylogenetic processes starts at birth and continues until the foreordained victory of phylogeny, super-long lived individuals not being in the interest of our species.  In this view, aging can be seen not so much as a process itself, but as a sharpening of the conflict between these two sets of processes.  It is also true that ontogenetic processes tend to mute phylogenetic processes and vice versa, although there is no causal relationship here.  Rather, what we do to promote one set of processes tends to suppress the other.  An irony of modern medicine is that it is primarily an attempt to control the effects of phylogenetic processes while doing almost nothing to promote ontogenetic processes.  A more reasonable approach might be to promote ontogenetic processes first, note the effects, and then deal with whatever symptoms have not cleared up.

As we have noted, insulin is the toggle switch: high insulin promotes phylogenetic processes; low insulin promotes ontogenetic processes. 


The official response to this low carbohydrate narrative has ranged from the vitriolic to the pathological. There are many reasons for this response. Chief among the naysayers has been the American Heart Association. Even when their own studies show the superiority of low carbohydrate diets in controlling the factors leading to heart disease, they deny the results. When we consider that every box of insulin-stimulating Cheerios contains the AHA seal of approval, we can begin to understand the powerful forces linked to the lipid hypothesis and the threat posed by the low carbohydrate narrative.

I do not want to go into all of the reasons for official hostility here. Rather, I would refer the reader to Gary Taubes  book, Good Calories, Bad Calories for an account of the history and politics of the predominance of the lipid hypothesis. For another scientific refutation of the contentions of the American Heart Association, I recommend "High Protein Weight Loss Diets and Purported Adverse Effects: Where is the Evidence?" (Sports Nutrition Review Journal 1(1) 45-51, 2004)

As a review of nutritional dogma, here's a sampling of what nutritionists have told us over the past forty years.

To lower cholesterol, we should eat low cholesterol foods. We now know this is wrong. The liver regulates the level of cholesterol in the blood and makes eighty percent of it. When you eat low cholesterol foods, the liver compensates by making more; when you eat high cholesterol foods, the liver makes less. You cannot control serum cholesterol levels by controlling dietary cholesterol.

The benefits of low cholesterol are also highly questionable. In fact, recent research has shown that there is no connection between cholesterol levels and atherosclerosis. There is some evidence that oxidized particles of the smaller, denser type of LDL associated with high triglycerides can get stuck in endothelial tissue and cause inflammations that stimulate plaque, but there is no correlation between LDL levels and levels of oxidized LDL. Atherosclerosis is more highly correlated with triglyceride levels, inflammation markers, and anti-oxidant status than cholesterol.

Cholesterol is very important to our overall health. Lowering cholesterol could be detrimental. Almost all the studies that show a decrease in mortality from CHD in a low cholesterol group also show an increase in mortality from all causes in that same low cholesterol group, so where's the benefit of lowering cholesterol?

We should eat margarine instead of butter. This is also wrong. The trans fats in margarine are a serious threat to health as they deform the lipid bilayer so important to the structure and proper functioning of the cell. On the other hand, the short and medium chain saturated fatty acids in butter are beneficial.

Use polyunsaturated vegetable oil and avoid saturated fat. Wrong again! This is bad advice for at least two reasons. Polyunsaturated vegetable oils are high in omega-6 fats and low in omega-3s. Optimal functioning of the eicosanoid system requires at least a 2:1 ratio, which researchers on the Paleolithic diet say our hunter-gatherer forebears achieved. The modern diet, full of polyunsaturated fats has about a 20:1 ratio of omega 6 to omega 3. As a result, our eicosanoid systems tend to be compromised, leading to a number of conditions requiring the intervention of prescription drugs.

Polyunsaturated fats heated to frying temperature form lipid peroxides, which challenge the anti-oxidant system. We also now know that seventy percent of the lipid content of arterial plaques consists of polyunsaturated fats. It's best to avoid them.

On the other hand, saturated fats are generally beneficial. There are actually seven or so saturated fatty acids in our bodies, grouped as short, medium, or long chain fatty acids. The short and medium chain fatty acids play a role in cell construction and in other bodily processes. The long chain fatty acids tend to get burned for fuel or stored as adipose tissue. Only two of these SFAs have a direct effect on cholesterol and tend to raise LDL and HDL equally, which would improve even the traditional CHD risk ratios.

The greatest source of long chain SFAs is de novo lipogenesis, which means the creation of new fat from glucose derived from carbohydrates. Insulin stimulates de novo lipogenesis and also prevents the body from burning fat for fuel. So if you have high insulin levels, your body has no choice but to store these long chain SFAs as adipose tissue. High insulin levels can make you fat.

Eat lots of whole grain products. More questionable advice! Whole grains contain very few essential nutrients, and those they do contain are readily available in vegetables and fruits that are much lower in insulin-stimulating carbohydrates. There is a lot more fiber in a serving of berries than in a couple of slices of whole grain bread. Cereal fiber contains phytates, which bond with minerals. So if you combine your fortified bran cereal with milk and think you're doing yourself a favor, think again. The calcium will bond with the phytates and pass through your system with the fiber. You will absorb very little of the mineral. There is no need for grains in the human diet. The genus homo did very well for two million years with no grains of any kind in the diet. It's hard to see what has happened in the last thirty years to make them an essential nutrient.

Given that nutritionists have such a sorry record, why does anyone listen to them? No one notices that they are wrong because their pronouncements are part of a narrative that accompanies the lipid hypothesis and is supported by many other elements of the scientific and commercial environments. Taken singly, each pronouncement's being wrong is never enough to sink the lipid hypothesis.

Part of the problem is simply bad science. In a recent interview, the science writer, Gary Taubes, was asked how he became involved in the question of low carbohydrate nutrition. He answered that he had been assigned a story that involved interviewing nutritional researchers and ended up feeling that these were the worst scientists he had ever encountered and that there had to be another story here. He was right.


Many nutritional recommendations come from epidemiological studies. Reading through these studies, one notices a persistent confusion among nutritional researchers about causality and correlation. Here's a typical example that shows how questionable research affects doctors' recommendations. Sifting through masses of data, nutritional researchers noticed that pregnant women who drank coffee suffered more miscarriages than women who did not drink coffee. So the word went out: pregnant women should avoid coffee to prevent miscarriages.

The facts are a little more complicated. It seems that when an embryo is firmly implanted in the uterus, the uterus sends a strong pregnancy signal to the brain, which then sets in motion the endocrinological changes which support the pregnancy. If the embryo is not firmly implanted in the uterus, no strong pregnancy signal is sent to the brain, and the pregnancy does not get well supported by the endocrine system. These women tend to have a greater number of miscarriages. It turns out that those endocrinological changes associated with the strong pregnancy signal also cause a chemical change in the taste buds, leading to disliking coffee. So those pregnant women who drink coffee tend not to like it anymore and stop drinking it. Women who tend to miscarry for these reasons never develop a dislike of coffee, since there is no strong pregnancy signal, and continue to drink it. While there is a strong correlation between miscarriages and coffee, there is no causal relationship.

One can imagine, however, that doctors, motivated by defensive medicine, will continue to tell pregnant women to avoid coffee even though there's no scientific basis for saying so. If a pregnant woman in their care did drink coffee and did have a miscarriage for whatever reason, they could be liable for malpractice. Such is the dynamic conservatism of the medical business. A correct understanding of the link between coffee and miscarriages would help doctors identify those women at greater risk for miscarriages. But accepting the false conclusions of an epidemiological study has prevented a more effective level of medical care.


Nutritionists' primary interest is that the foods that we eat contain essential and appropriate nutrients. They are concerned with what you put in your mouth. What happens to it after you swallow is outside their department. But how your body manages what you eat is equally as important as what you eat. Nutritionists recommend, for instance, that women should supplement calcium to avoid osteoporosis, but whether that added calcium promotes bone density or kidney stones depends on the milieu into which you introduce that calcium.  Similarly, nutritionists tell us to supplement vitamin D.  But they don’t tell us is that vitamin D is fat soluble, not water soluble, and unless your body is metabolizing fat, all that Vitamin D will remain sequestered in your adipose tissue and you will absorb very little of the vitamin.  Unfortunately, most nutritionists, who are still in thrall to the lipid hypothesis, will recommend that you eat a low fat/high carbohydrate diet that will generate an insulin level that shuts down fat metabolism, also shutting off the absorption of vitamin D.

Most micronutrients are fat soluble and require fat metabolism to be absorbed.  The major exception is vitamin C, ascorbic acid, which is water soluble.  But vitamin C is sufficiently chemically similar to glucose that it shares a cellular receptor with glucose.  The higher the ratio of glucose to vitamin C in your bloodstream, the less vitamin C you will absorb. So nutritionists tell you to drink orange juice because it is high in vitamin C, important to the functioning of your immune system, but orange juice is also high in glucose which will impede the absorption of vitamin C and compromise your immune system.  But you won't get that information from nutritionists or from the Florida Orange Juice Commission.

This nutritional compartmentalism affects the quality of nutritional research. We have numerous studies telling us that red meat and animal fat are bad for us. Usually this information comes from epidemiological studies in which researchers sift through masses of data looking for the effects of particular variables. Usually, they find what they're looking for. It's not difficult to justify a pre-existing bias with an epidemiological study. The problem is that we have no idea what else those red meat-eaters were eating. If you combine your meat and fat with potatoes, as many do, they're going to behave differently in your body than if you had skipped the potatoes and eaten some broccoli instead. High insulin levels prevent the burning of fat for fuel and promote fat storage.  They also promote de novo lipogenesis, a process by which excess glucose that you cannot burn gets returned to the liver and converted into saturated fat.  So any fat you take in with your red meat will, most likely, in the presence of insulin stimulated by the potato, get added to the fat which the liver makes from glucose. Insulin resistance will only exacerbate this effect.

So naturally, red meat and animal fat come off poorly in these kinds of studies. But the researchers have no idea whether the fat they're complaining about is dietary fat or de novo lipogenesis from carbohydrates. Any epidemiological study that demonizes red meat and fat and doesn't control for insulin levels or carbohydrate content of the diet is inconclusive. 


Nutritionists are fond of telling us that carbohydrates are a preferred nutrient because the body burns carbohydrates before it burns far or protein, and burns it efficiently, with no by-products. There is a metaphor buried in this argument that warrants closer examination. Those who make this claim are placing a value on efficiency. Where does this idea come from? In a mechanical system, which cannot renew itself, efficiency is definitely a good thing. A mechanic will keep a supply of spare parts on hand for those parts that wear the fastest. The more efficient the mechanism, the less often those spare parts will be needed.

But the human body is not a mechanism; it is an organism, which works on very different principles. If efficiency were a value to the body, then any nutrient that gets burned efficiently would be a preferred nutrient, like carbohydrates, in this argument. However, there is one substance that the body burns even before carbohydrates and  more efficiently and completely than carbohydrates: alcohol. Alcohol is a toxin. Clearly, there’s something wrong with this efficiency argument.  Perhaps the principle is that the body burns most efficiently those substances that it wants to get rid of the fastest, those nutrients that it doesn't want to keep around. There are many substances in the body that are useful and necessary in certain amounts and toxic in slightly larger amounts. Oxygen and iron fall into this category. Perhaps glucose does as well.

A mechanism works on the principle of redundancy of parts. Because a mechanism cannot renew itself, its longevity is determined by replacement parts. An organism works on the principle of redundancy of function. If one system fails, another can do the job. Cholesterol is a good example. Cholesterol has multiple functions: it forms part of the cell structure; it is the substrate for sex hormones; it plays a role in the permeability of the skin, where it also aids in the synthesis of vitamin D from sunlight; it helps in the transmission of nerve impulses; and it helps fight infection. Because cholesterol is so important for maintaining health, your body has multiple ways of getting it. The liver makes most of it, but you can also use dietary cholesterol, and, if all else fails, every cell in your body has the ability to manufacture the cholesterol it needs. When something is important, your body has multiple ways of doing it or getting it.

Insulin is interesting in this regard. While there are a number of hormones that will raise blood sugar, only one hormone, insulin, will lower it. This lack of redundancy shows that, in evolutionary terms, lowering blood sugar was never terribly important, more evidence that carbohydrates were never a large part of the human diet until the advent of agriculture some scant ten thousand years ago.

If we look at nutrients from the point of view of the multifunctional principle, a clear picture emerges. There are two reasons we must eat, to provide fuel and building blocks for renewing tissues. Protein is capable of both jobs. It provides amino acids for building new tissues and can be burned for fuel, if needed. It provides the chemical basis for gluconeogenesis, in which the liver synthesizes glucose from amino acids or fat for those tissues which use glucose. In fact, all the glucose your body actually needs can be provided in this manner.

Fat also does both jobs. It forms part of the structure of the cell and is an important component of a number of key metabolic pathways. It also gets burned for fuel and stored as adipose tissue for future energy generation. Carbohydrates, on the other hand, serve no other purpose than to be burned for fuel, and what doesn't get burned gets stored as fat because your body doesn't want all that glucose sticking around for too long. Fat and protein are the body's preferred nutrients, not carbohydrates.

Nutritionists tell us that you need carbohydrates for energy, but it's not true. Your body will happily burn fat for energy, or the ketone bodies that fat metabolism produces. There is no need to burn carbohydrates. If you ate zero protein, you would sicken and die, the same with fat. If you ate zero carbohydrates, your body would hardly notice.


Here's another typical example of medical research gone awry in which we see the lipid hypothesis operating in a more sinister fashion. Recently, a researcher isolated an enzyme called ACAT2, which, he claimed, is the cause of atherosclerosis. When he eliminated this enzyme in mice that had been bio-engineered to have hardened arteries, their atherosclerosis cleared up to a remarkable degree. Now, all that was needed, according to this researcher, was to develop a drug that would have the same effect in humans, and atherosclerosis would be a thing of the past.

If we understand the idea of metabolic pathways, we know enough to smell a rat, here. We are told the function of ACAT2 is to modify cholesterol to enable it to move about the bloodstream. So far, it sounds like a beneficial enzyme enabling tissues to get the cholesterol they need. Then we are told that the "molecularly altered cholesterol then takes up residence in blood vessel walls, clogging arteries and leading to cardiovascular disease." Here is a logical leap here that beggars the imagination, the received idea at work. Cholesterol moving around the bloodstream does not automatically clog arteries unless a bunch of other conditions are present. If those conditions are present, then lowering ACAT2 to prevent cholesterol from flowing freely in the bloodstream may diminish arterial plaque, but it may also prevent the cells from getting the cholesterol they need, leading to all kinds of other problems. It would be like starving a person to prevent indigestion. If we remove ACAT2 its metabolic pathway, what other effects will we trigger?

We are led to believe that ACAT2 is the evildoer here, and that if we can control it, then we've conquered atherosclerosis. But ACAT2 does not exist in a vacuum. It does its job as the result of complex interactions with hormones and other enzymes in the metabolic pathway in which it resides. It got its role in its metabolic pathway through an adaptive mechanism that contributed to the survival of our species. A successful adaptation does not suddenly turn around and start causing disease states. If ACAT2 is, in fact, contributing to a disease state, then something is altering that metabolic pathway that causes ACAT2 to behave in this way. Since the body is an open system, whatever is stimulating this problem is probably coming in from the environment. I'd put my money on carbohydrates since they have the largest and most immediate effect on the endocrine system, and they stimulate insulin, the ur-hormone that affects almost all the metabolic pathways in our bodies.

Isolating ACAT2 and identifying it as the cause of atherosclerosis is bad science. A more reasonable approach would be to ask what is disturbing that metabolic pathway to produce atherosclerosis and then look for a way to make it whole again. Our researcher is remarkably uninterested in what might be disturbing the metabolic pathway in which ACAT2 resides. Instead, he wants to disturb it even further by eliminating a key component of that pathway. What would cause a supposedly trained scientist to distort basic science to such an intolerable degree? The answer . . . the desire to produce a saleable drug. If we can twist and pull our research to point to a single substance as the cause of a disease state, then we can design a molecule to impede that substance and make billions by patenting it. The rewards of bad science are enormous.

To be fair, our researcher may believe that he's benefiting mankind even while he's checking his stock portfolio. But he ascribes to the disease management model of health care in which the two appear as conjoined twins. According to this model, atherosclerosis is a disease which requires a treatment, and finding a treatment usually means designing a molecule which a drug company can patent. The researcher can hardly be blamed if a disease is also a marketing opportunity.

But atherosclerosis is not a disease. It is a symptom of a metabolic pathway gone haywire. Unfortunately, this view is drowned out by the quest for the designer molecule. The problem is that anyone with enough knowledge and authority to put a stop to this kind of meretricious foolishness is also out there looking for designer molecules to patent. Our health care system has denigrated into a disease management system because of the quest for the designer molecule. And there's the entire medical-pharmaceutical-health insurance complex to support it.


In my work as an organizational consultant, I participated in a project in a large pharmaceutical company that taught me a lot about how the medical-pharmaceutical-health insurance complex works. The project was called "Global Value Planning." The idea was to insert economic information early enough into the development cycle so that they could be sure they were designing a molecule that would get paid for. To the pharmaceutical company, the world appeared as various "payer environments." The UK, with its National Health Service, was one kind of payer environment that called for a particular strategy to enter. The US, with its private health insurers was another kind of payer environment. There, the strategy was to get on the formulary of a few large insurers and the rest would follow suit. The project was supposed to assure that whatever molecule was designed would have a value proposition that worked in multiple payer environments.

Payers and drug companies play an elaborate game in which payers throw up obstructions to new molecules and companies take down these obstructions. Part of the game is for the drug companies to enlist the aid of "Key Opinion Leaders," prominent doctors and researchers who could be counted on to give company products a good review. Then the idea is to get as much on the label as possible to give the sales force as much leeway as possible in pitching the drug to doctors and to sponsor free continuing education sessions for doctors which are nothing more than pitch sessions for company products.

Medical education reinforces the disease management model of health care so that doctors are continually clamoring for more and better treatments and see the designer molecules pushed by the drug companies as the answer. The three components of this complex, the medical establishment, the pharmaceutical companies, and the health insurers share the same set of assumptions and have become reflections of each other in a fun-house hall of mirrors. The whole thing is fueled by the search for the designer molecule because that's where the money is. That's how our health care system has become a disease management system run for the benefit of the pharmaceutical companies.


The medical-pharmaceutical-health insurance complex comes together with the disease management system and the lipid hypothesis to form a powerful narrative that dominates the scientific and popular imagination in health and nutrition. The power of that narrative comes from its ability to generate billions in profits for those poised to take advantage of it. So when NIH researchers were caught taking "consulting fees" from pharmaceutical companies, they couldn't understand what people were upset about and vigorously protested the new rules designed to keep them honest. They were unable to see the ethical contradictions in their behavior because they had bought into that dominant narrative in which the whole point of research is to produce drugs for disease management. And since someone was going to make money from those drugs, why shouldn't they?

Hardly anyone notices that that narrative is based on a received idea with no validity. And those who do notice are relegated to the fringes. However, there is a change in the air. Slowly, another narrative is developing that can compete with the lipid hypothesis. According to that narrative, insulin resistance and hyperinsulinemia are the prime factors in the disorders clustered as "metabolic syndrome," obesity, heart disease, hypertension, and type 2 diabetes, as well as many other disorders and conditions. The first order of business in controlling these disorders is to lower insulin levels, which can only be accomplished by restricting carbohydrates. The point of medical practice is less to manage disease than to study and maintain the metabolic pathways that keep us healthy, to help patients restore those metabolic pathways which have gone awry, and to help them avoid drugs that deform metabolic pathways.

At the moment, the competition between these two narratives is still terribly lopsided in favor of the lipid hypothesis, despite the growing evidence that it is wrong. But its days are numbered. Consider the following statement from the August 2005 issue of the Journal of Internal Medicine from a recent study on the role of dietary fat:

Over the last decades evidence from large-scale epidemiological studies has been emerging, partly defying the previously believed hypotheses, with voices rejecting the fat-disease hypotheses becoming more prominent. Most researchers today agree on total fat intake not being a risk factor for cardiovascular disease or cancer. The role of dietary fat in the development and treatment of obesity has also been under question.

Such statements are the death knell of the lipid hypothesis as well as recent discoveries of hyperinsulinemia playing a role in other serious disorders, like Alzheimer's, breast cancer, and colorectal cancer.

This low carbohydrate-insulin control narrative is supported by good science, but good science cannot do the job alone. There needs to be some organizational support for this new narrative in the same way that powerful groups like the American Heart Association and the American Diabetic Association support the lipid hypothesis. We might call such a group the International Association for the Advancement of Metabolic Medicine. Such a group would, among other things, sponsor continuing medical education for MDs, showing them how to practice according to this new narrative.



The recent bankruptcy of Atkins Nutritionals, Inc. set off paroxysms of joy in the halls of purveyors of high carbohydrate foods. The news was received with high fives, cheers, and celebration. This reaction seems disproportionate. Clearly, they felt as though some terrible threat had been lifted. Why should powerful interests feel threatened by a tiny, undercapitalized company?

The demise of Atkins Nutritionals is really quite meaningless. Low carbohydrate diets stress whole, unprocessed foods: animal protein, vegetables and fruits. Fortunately for our species, those vegetables and fruits highest in micronutrients tend to be lowest in carbohydrates. Biased reporting on low carbohydrate diets leaves out the vegetable and fruit part and equates low carb with no carb, but it's not true. Atkins Nutritionals, Inc. went against this grain by making low carbohydrate substitution products: bread, muffins, pasta, cereal, etc. Those who understand the principles of low carbohydrate eating consider these products processed junk food and avoid most of them. They're expensive and taste funny, to boot. Anyone who tried to maintain a low carbohydrate diet using these products was doomed to failure. The bankruptcy of Atkins Nutritionals, Inc. is the failure of a company with a bad product and a bad business plan. Nothing more.

The real threat to those who celebrated the Atkins bankruptcy is the demise of the lipid hypothesis as represented by the growing popularity of low carbohydrate diets. They think they have won the battle, but they are doomed to lose the war. Good science will eventually win. In Galileo's day, powerful forces made Galileo recant his belief in the heliocentric universe. Was that recantation a victory for the forces supporting the geocentric hypothesis?

Lipid Numbers

This article was stimulated by a friend who knew of my studying nutrition and asked me to interpret his lipid numbers from a recent blood test from my point of view


Not being an MD, I would never be so bold as to offer advice.  Having studied these issues, what I can offer is something for you to take up with your doctor, if you so choose.  With that demurral, here’s what I see in the numbers you gave me.

The important numbers here are the triglycerides and the HDL level.  The risk factor for heart disease is triglycerides/HDL>3.  Your risk ratio is 1, well below the risk factor despite the flags on your report indicating high numbers.  To understand why, we need to understand what triglycerides are and exactly how cholesterol is implicated in heart disease.

Triglycerides are a storage form of saturated fat, mostly palmitic acid, created by the liver from carbohydrates.  When you eat carbohydrates, your body wants to get rid of them as fast as possible, so the first thing it does is burn off as much as it can.  What can’t get burned gets shunted to the liver which turns the carbohydrates into saturated fat in a process known as de novo lipogenesis.  The next step is to move these triglycerides to the adipose tissue for storage and later use.  Here’s where the lipoprotein comes in.  The only way to move fat from one place to another is through the bloodstream; the problem is that fat is not water soluble.  So the liver creates a water soluble envelope for transporting non-water soluble compounds through the bloodstream, the lipoprotein.

Another non-water soluble compound that travels through the bloodstream in the lipoprotein is cholesterol.  There is no such thing as good cholesterol or bad cholesterol; there is only cholesterol, an important substance for which your body has many uses.  Every cell in your body requires cholesterol on a constant basis.  Most cholesterol is made in the liver and sent through the bloodstream in the same lipoprotein as the triglycerides.  LDL takes cholesterol to the cells that need it; HDL picks up any unused cholesterol and takes it back to the liver for recycling.  Never does your body excrete cholesterol; it is too precious a substance to waste.

When there are problems with lipoproteins, it is with the LDL profile.  There are about seven different sub-fractions of LDL grouped into two profiles: LDL A is a large, fluffy particle, while LDL B is a smaller denser particle.  The small, dense LDL B particle can get stuck in the endothelium, the inner surface of the artery, whereupon it oxidizes and causes an inflammatory reaction from the immune system.  The immune system creates a plaque under the injured endothelium which can constrict the artery if it gets big enough or break off and form an embolism.

Every lipoprotein starts out from the liver as a very low density lipoprotein, or VLDL.  We can think of the VLDL as something like an airport shuttle, ferrying various passengers to various parts of the city.  The two most important passengers in the VLDL are triglycerides and cholesterol.  The first stop the VLDL makes is to offload the triglycerides into the adipose tissue, at which point the VLDL becomes a low density lipoprotein, or LDL, filled mostly with cholesterol.  The more carbohydrates you eat, the more triglycerides your liver makes; the more triglycerides, the higher the ratio of triglycerides to cholesterol in the lipoprotein.  Most of the seats in this airport shuttle will be taken up by triglycerides, and there will be little room left over for cholesterol.  When this VLDL offloads its crowd of triglycerides into the adipose tissue, the resultant LDL, because of the small amount of cholesterol in it, will be a small, dense particle of LDL B, the troublemaker.

If you eat low carbohydrate, and, subsequently, have low triglycerides, there will be more cholesterol in the VLDL, and the resultant LDL particle will be the larger, fluffier LDL A.  So the overall number for LDL is meaningless unless we know the LDL profile.  If your LDL is primarily profile A, a high number is not harmful.  If your LDL is primarily profile B, a low number will not help you; you’re in trouble.  Profile A is always correlated with high HDL and low triglycerides, so the only important risk ratio is triglycerides/HDL.  Your HDL level is unusually high.  This is good.  Ignore the flag on that number in the report.

The protein that comprises the lipoprotein is known as apolipoprotein B100.  If you eat a low fat diet, your total LDL will likely go down , as will your level of HDL, but the level of apoB 100 will remain unchanged, which, of course, means that there is less cholesterol in each particle of LDL.  Your LDL profile will have shifted to profile B.  When you eat a low carbohydrate diet, your LDL will either stay the same or could even rise a little, but HDL will also rise.  However, the level of apoB 100 will go down, signifying larger particles of LDL profile A.  I see nothing but good news in your lipid panel, but don’t take my word for it; take it up with your doctor.