Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health by Gary Taubes
MRFIT trial – lowering cholesterol for age 40 to 70 lowers risk of dying of heart attack by 1%…implies not really related.
WHO MONICA trial – heart disease mortality is independent of cholesterol levels, blood pressure, or even smoking habits.
Nurses Health Study – fiber consumption is unrelated to the risk of colon cancer, as is the consumption of fruits and vegetables (whole grains, fruits, and vegetables).
Diabetes – the syndrome where the body is unable to remove and store away sugar from the blood after a meal…either due to a reduced production of insulin (Type 1), or due to insulin resistance of the tissues (Type 2). One is a symptom of too little insulin. The other is a symptom of too much insulin for too long (hyperinsulinemia).
Insulin regulates the synthesis of the molecule called glycogen, the form in which glucose is stored in muscle tissue and the liver. Insulin stimulates the synthesis and storage of fats in fat depots and in the liver, and it inhibits the release of that fat. Insulin also stimulates the synthesis of proteins and of molecules involved in the function, repair, and growth of cells, and even RNA and DNA molecules as well.
Heart disease and diabetes are associated with a host of metabolic and hormonal abnormalities that go far beyond elevations in cholesterol levels and so, presumably, any possible effect of saturated fat in the diet.
Table sugar (sucrose) is half fructose (and half glucose). Fructose is found naturally only in small concentrations in fruits and some root vegetables. So the hypothesis is that the introduction of this sugar (fructose) in high concentrations chronically in the body causes these “diseases of civilization”: obesity, diabetes, heart disease, hypertension, and others.
Salt is assumed to raise blood pressure, but that’s not what happens experimentally. The thought is that salt raises water retention which will raise blood pressure (in other words, cause hypertension). Cutting salt by half (difficult to do) will drop blood pressure by 4 to 5 mmHg, but hypertension stage I is defined as 20 mmHg over what’s healthy, and stage II is defined as 40 mmHg over. So cutting salt makes little difference, and is not likely the cause of the hypertension.
Carbohydrate-rich diets can cause the body to retain water and so raise blood pressure (just as salt is alleged to do). Consequently, the weight loss in the first few weeks on a carbohydrate-restricted diet is probably water weight loss, not fat loss. Eating carbohydrates causes the kidney to hold on to salt rather than excrete it, and thus more water is retained in the body to keep the blood sodium concentration constant. Removing carbohydrates from the diet works like diuretics (the antihypertensive drugs) do, it causes the kidneys to excrete sodium, and water along with it. The insulin is what signals the kidneys to reabsorb the sodium.
Insulin contributes to high blood pressure in another way as well. Insulin stimulates the nervous system and the same flight-or-fight response incited by adrenaline. Which increases heart rate and constricts blood vessels, thereby raising blood pressure.
Because cholesterol was found in atherosclerotic plaques, cholesterol was assumed to be the agent that caused those plaques. There are 3 types of cholesterol (classes of lipoproteins): LDL (the “bad” cholesterol), HDL (the “good” cholestorol), and VLDL…the ignored cholesterol.
HDL – high density lipoprotein
LDL – low density lipoprotein
VLDL – very low density lipoprotein
John Gofman’s research showed that though the amount of LDL in the blood can indeed be elevated by the consumption of saturated fats, it was carbohydrates that elevated VLDL. And that changing the diet to a carbohydrate rich diet would increase VLDL in relation to LDL disproportionately. LDL and VLDL were good predictors of heart disease, but the single best predictor of risk was an atherogenic index, which took into account both (LDL and VLDL) measured individually and added them together. The greater the atherogenic index, the greater the risk of atherosclerosis and heart disease. Thus recommending a low fat (and consequently high carb) diet could actually do more harm than good for a patient’s risk of heart disease.
VLDL particles carry triglycerides. Pete Ahrens found that (most) patients on a high-carb diet would have high levels of tryglycerides (and hence VLDL) in their blood. The blood would look milky white when drawn. This is called lipemia. A very few patients (2 in 10 years) showed lipemia on a high-fat diet. Ahrens considered these patients to have a genetic disorder. And termed the other situation to be carbohydrate-induced lipemia. In both situations, the fat in the blood would clear up when the subjects went on a low-CALORIE diet (less food overall). This explained why the tryglycerides increase was absent in impoverished Asian populations that subsisted on bare minimums of rice.
Elevated triglyceride levels were far more common in coronary heart-disease patients than high cholesterol…only 5 percent of healthy young men had elevated triglycerides, compared with 38 percent of healthy middle-aged men, and 82 percent of coronary patients.
In the Framingham study it was found that HDL had the largest impact on risk. The higher the HDL cholesterol, the lower the triglycerides, and the lower the risk of heart disease, no matter the age, gender, or race. HDL and triglycerides have an inverse relationship.
Saturated fat increases LDL…but LDL doesn’t matter very much.
Veterans Administration funded a twenty-center drug trial. The results, published in 1999, supported the hypothesis that heart disease could be prevented by raising HDL. The drug used in the study, gemfibrozil, also lowered triglyceride levels and VLDL, suggesting that a diet that did the same by restricting carbohydrate might have a similarly beneficial effect. As of 2006, no such dietary trials had been funded.
Monounsaturated fats (olive oil, oleic acid) raise HDL and lower LDL simultaneously. This is exactly what one would want in a fat, raising the good (HDL), and lowering the bad (LDL). Turns out the principal fat in red meat, eggs, and bacon, is not saturated fat, but this very same monounsaturated fat.
Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein. Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (stearic acid is metabolized in the body to oleic acid, according to Grundy’s research) The remaining 4 percent of fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol, but will also raise HDL and will have an insignificant effect if any on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.
Ronald Krauss did research on LDL and found that LDL itself could be broken down into subtypes as well. The smallest and densest of the LDL had two significant properties: it had strong negative correlation with HDL (meaning having fewer dense LDL is better), and it was the subspecies that was elevated in patients with heart disease. The dense LDL was the indicator of heart disease.
An LDL’s structure is like a balloon. It has a single protien known as “apo B” (for short) that serves as the structural foundation for the balloon. It has an outer membrane that is composed of cholesterol and fats of yet another type, called phospholipids. And then inside the balloon, inflating it, are triglycerides and more cholesterol. Some people have large fluffy LDL with a lot of cholesterol and triglycerides inflating the balloon, and some people have mostly smaller denser LDL particles with less cholesterol and triglycerides.
So, we are able to count the number of apo B protiens (and thus the number of LDL and VLDL particles in the blood), rather than the amount of the cholesterol or triglycerides they contain. The total number of LDL and VLDL particles combined is also abnormally elevated in heart-disease patients. Whereas measuring LDL cholesterol (not the number, but the amount) has a very small correlation with heart-disease.
Small dense LDL appears to be more artherogenic (more likely to cause atherosclerosis) simply because it is small and dense. Small dense LDL can squeeze more easily through damaged areas of the artery wall to form incipient atherosclerotic plaques. The relative dearth of cholesterol in these particles may also cause structural changes in the protein that make it easier for it to adhere to the artery wall to begin with. And because small dense LDL apparently remains in the bloodstream longer than larger and fluffier LDL, it has more time and greater opportunities to do it’s damage. Finally it’s possible that LDL has to be oxidized (the biological equivalent of rusting) before it can play a role in atherosclerosis, and the existing evidence suggests that small dense LDL oxidizes more easily than the larger, fluffier variety.
(NOTE: all of the above paragraph is probably speculation. The *way* this particle causes problems does not seem to be specifically known, the above is a hypothesis on how it might. But the correlation to heart-disease is tested as noted in the previous paragraph.)
The more saturated fat in the diet, the larger and fluffier the LDL particles – a good thing.
Artherogenic Dyslipidemia – the blood profile of having higher concentrations of the dense LDL.
“Well, I would rather not get into that.” and “I’ll have to pass on that one.” – responses from LDL researchers who agree with the above and were asked to comment on the dietary implications of these findings. Perhaps they don’t want to comment outside of their fields, but it sounds a little odd.
Delipidation Cascade – this is the process by which the LDL particles are created in the liver and deliver their triglyceride cargo to the fat depots in the body. When the blood is flooded with glucose (like after we eat a carbohydrate-rich meal), the liver takes some of this glucose and transforms it into fat (triglycerides). The triglycerides are no more than droplets of oil. In the liver, the oil droplets are fused to the apo B protein and to the cholesterol that forms the outer membrane of the balloon. The triglycerides constitute the cargo that the lipo-proteins drop off at tissues throughout the body. The combination of the cholesterol and the apo B is the delivery vehicle. The triglyceride is much lighter than the cholesterol and apo B. Thus the larger the initial triglyceride cargo, the lighter (and less dense) the LDL or in this case VLDL is. As the VLDL moves through the body delivering the cargo (the triglyceride) it gets more and more dense, deflating, and becoming an LDL.
According to Krauss’s research, the rate at which triglycerides accumulate in the liver controls the size of the oil droplet packaged onto the lipoprotein. If triglycerides are hard to come by as would be the case with a diet low in calories OR low in carbohydrates, then the oil droplets packaged with the apo B and cholesterol will be small ones (more dense particles). The ensuing lipoproteins secreted by the liver will be of a subspecies known as intermediate-density lipoproteins, which are less dense than LDL, but more dense than VLDL, and these will end their lives as relatively large, fluffy LDL (the good kind of LDL to have). The resulting risk of heart disease will be relatively low, because the liver had few triglycerides to dispose of initially.
If the liver instead had to dispose of copious triglycerides, then the oil droplets are large, and the resulting lipoproteins put into the circulation will be triglyceride-rich and very low-density. These then progressively give up their triglycerides, eventually ending up, after a particularly extended life in the circulation, as the atherogenic small, dense LDL. This triglyceride-rich scenario would take place whenever carbohydrates are consumed in abundance.
Note that a study that shows a population (like southeast asian) subsisting on rice has low incidents of heart-disease is finding this because of calorie restriction. If the same diet was maintained, but the population was able to eat as much as they wanted, then it would start to show the signs of heart-disease…as developed nations do.
“High protein levels can be bad for the kidneys” “High fat is bad for your heart. Now Reaven is saying not to eat high carbohydrates. We have to eat something.” – These are statements made by Robert Silverman in 1986. Cognitive dissonance in the diabetes treating community.
The diabetic condition is associated with a host of chronic blood-vessel-related problems known as vascular complications: stroke, a stroke-related dementia called vascular dementia, kidney disease, blindness, nerve damage in the extremities, and atheromatous disease in the legs that often leads to amputation. Otherwise healthy individuals would be expected to increase their risk of all these conditions by the consumption of refined and easily digestible carbohydrates (and sugars), which inflict their damage first through their effects on blood sugar and insulin, and then indirectly through triglycerides, lipoproteins, fat accumulation, and assuredly other factors as well.
Rabbits fed high-cholesterol diets develop plaques throughout their arteries, but diabetic rabbits (Type 1 – don’t produce insulin…not insulin resistant which would be Type 2) will not suffer this atherosclerotic fate no matter how cholesterol-rich their diet. Infuse insulin along with the cholesterol-laden diet, however, and plaques and lesions will promptly blossom everywhere. Also found to be the case in chickens by Jeremiah Stamler and Louis Katz, and later in dogs too. Hence insulin itself may be a factor in the atherosclerosis of diabetic patients.
Robert Stout of Queen’s University in Belfast published a series of studies reporting that insulin enhances the transport of cholesterol and fats into the cells of the arterial wall and stimulates the synthesis of cholesterol and fat in the arterial lining. Since a primary role of insulin is to facilitate the storage of fats in the fat tissue, Stout reasoned, it was not surprising that it would have the same effect on the lining of blood vessels. Carbohydrate is disposed of in three sites adipose (aka fat) tissue, liver, and arterial wall. In 1975, Stout and Russell Ross reported that insulin also stimulates the proliferation of the smooth muscle cells that line the interior of arteries, a necessary step in the thickening of artery walls characteristic of both atherosclerosis and hypertension.
(So if you’re diabetic and injecting yourself with insulin…you’re thickening your arteries. And if you’re insulin resistant because of chronically elevated levels of insulin due to carbohydrate consumption, you’re making things even worse.)
Raising blood sugar will increase the production of what are known technically as reactive oxygen species and advanced glycation end-products, both of which are potentially toxic. The former are generated primarily by the burning of glucose (blood sugar) for fuel in the cells (note there are other fuel options, glucose is not the only one), in a process that attaches electrons to oxygen atoms, transforming the oxygen from a relatively inert molecule into one that is avid to react chemically with other molecules. One form of these are “free radicals”, and all together are known as “oxidants” because what they do is oxidize other molecules (they “rust” other molecules). This slowly deteriorates the object of oxidation…referred to as oxidative stress. Antioxidants neutralize reactive oxygen species.
The potential of advanced glycation end-products (AGEs) for damage is equally worrisome. Their formation can take years, but the process (glycation) begins simply, with the attachment of a sugar – glucose, for instance – to a protein without the benefit of an enzyme to orchestrate the reaction. That absence is critical. The role of enzymes in living organisms is to control chemical reactions to ensure that they conform to a tightly regulated metabolic program. When enzymes affix sugars to proteins, they do so at particular sites on the proteins, for very particular reasons. Without an enzyme overseeing the process, the sugar sticks to the protein haphazardly and sets the stage for yet more unintended and unregulated chemical reactions.
The glycation itself (attaching a sugar molecule to a protein) is reversible. If blood sugar levels are low enough, the sugar and protein will disengage, and no damage will be done. If blood sugar is elevated, however, the process of forming an advanced glycation end-product will move forward. The protein and it’s accompanying glycated sugars will undergo a series of reactions and rearrangements until the process culminates in the convoluted form of an advanced glycation end-product. These AGEs will then bind easily to other AGEs and still more proteins through a process known as cross-linking. The sugars hooked to one protein will bridge to another protein and lock them together. Now proteins that should ideally have nothing to do with each other will be inexorably joined.
Diabetics have high levels of an unusual form of hemoglobin, the oxygen-carrying protein of red blood cells, known as hemoglobin A1C, a glycated hemoglobin. The higher the blood sugar, the more hemoglobin that undergo glycation, and the more A1C in the bloodstream.
AGEs have been linked directly to both diabetic complications and ageing itself (hence the acronym). AGEs accumulate in the lens, cornea, and retina of the eye, where they appear to cause the browning and opacity of the lens characteristic of senile cataracts. AGEs accumulate in the membranes of the kidney, in nerve endings, and in the lining of arteries, all tissues typically damaged in diabetic complications. AGE accumulation appears to be a naturally occurring process (although it is exacerbated and accelerated by high blood sugar) we have evolved sophisticated defense mechanisms to recognize, capture, and dispose of AGEs. But AGEs still manage to accumulate in tissues with the passing years, and especially so in diabetics, in whom AGE accumulation correlates with the severity of complications.
One protein that seems particularly susceptible to glycation and cross-linking is collagen, which is a fundamental component of bones, cartilage, tendons, and skin. The collagen version of AGE accumulates in the skin with age, and again does so excessively in diabetics. (Hence the old looking skin of young diabetics…) It’s the accumulation and cross-linking of this collagen version of AGEs that causes the loss of elasticity in the skin with age, as well as in joints, arteries, and the heart and lungs.
The aorta (the main artery running out of the heart) is an example of this stiffening effect of accumulated and cross-linked AGEs. If you remove the aorta from someone who died young, you can blow it up like a balloon. It just expands. Let the air out, and it goes back down. If you do that to the aorta from an old person it’s like trying to inflate a pipe. It can’t be expanded. If you keep adding more pressure, it will just burst. This is part of the problem with diabetes and aging in general. You end up with stiff tissue: stiffness of hearts, lungs, lenses, joints. That’s all caused by sugars reacting with proteins.
AGEs and the glycation process also appear to play at least one critical role directly in heart disease, by causing oxidation of the LDL particles and so causing the LDL and it’s accompanying cholesterol to become trapped in the artery wall, which is an early step in the atherosclerotic process. Oxidized LDL also appears resistant to removal from the circulation by the normal mechanisms. LDL is particularly susceptible to oxidation by reactive oxygen species and to glycation. Both the protein portion and the lipid portion (the cholesterol and the fats ) of the lipoprotein are susceptible. These oxidized LDL particles appear to be “markedly elevated” in both diabetics and in nondiabetics with atherosclerosis, and particularly likely to be found in the atherosclerotic lesions themselves.
Recent anti-AGE compounds (or AGE breakers) have been shown to reverse arterial stiffness in lab animals…but it remains to be seen if these will work in humans.
Sugar (table sugar) is sucrose. Sucrose is half glucose and half fructose. HFCS (high fructose corn syrup) is 45% glucose and 55% fructose.
The glycemic index is a measure of how quickly carbohydrates are digested and absorbed into the circulation and so converted into blood sugar. Reaven argued that the concept of a “glycemic index” was worthless if not dangerous: saturated fat, he argued, had no glycemic index and so adding it to sugar and other carbohydrates will lower their glycemic index and make the combination appear benign when that might not be the case…like in the case of ice cream (fat and sugar). He also disparaged the glycemic index for putting the clinical focus on blood sugar, whereas he considered insulin and insulin resistance the primary areas of concern. The best way for diabetics to approach their disease, Reaven insisted, was to restrict all carbohydrates.
Carbohydrates in starches are broken down upon digestion first to maltose, then to glucose, which moves directly from the small intestine into the bloodstream. This immediately leads to an elevation in blood sugar and so a high glycemic index…higher than table sugar (sucrose). Since sucrose is half glucose, half fructose, the glucose moves into the bloodstream just as with the starch, but the fructose can only be metabolized by the liver. So most of the fructose consumed is channeled from the small intestine to the liver. As a result, fructose has little immediate effect upon blood sugar, thus only the glucose half of table sugar is reflected in the glycemic index.
An apple is roughly 6 percent fructose, 4 percent sucrose, and 1 percent glucose by weight.
Glucose goes directly into the bloodstream and is taken up by tissues and organs to use as energy; only 30-40 percent passes through the liver. Fructose passes directly to the liver, where it is metabolized almost exclusively. As a result fructose constitutes a metabolic load targeted on the liver. The liver responds by converting it to triglycerides (fat) and then shipping it out on lipoproteins for storage. The more fructose in the diet, the higher the subsequent triglyceride levels in the blood.
Peter Mayes explains our bodies will gradually adapt to long-term consumption of high-fructose diets, and so the pattern of fructose metabolism will change over time. This is why the more fructose in the diet and the longer the period of consumption, the greater the secretion of triglycerides by the liver. Moreover, fructose apparently blocks both the metabolism of glucose in the liver and the synthesis of glucose into glycogen, the form in which the liver stores glucose locally for later use. As a result, the pancreas secretes more insulin to overcome this glucose traffic-jam at the liver, and this in turn induces the muscles to compensate by becoming more insulin resistant. (The role of insulin as mentioned above is to signal the liver to synthesize the glucose into glycogen and to signal the muscles to take up that glycogen. When the pancreas sees that the glucose is not going down, it just pushes out more insulin. It yells louder. But the liver is already too busy to respond, so the louder yelling doesn’t help, and the muscles and liver start ignoring the insulin…causing insulin resistance and thus type 2 diabetes.)
Fructose is significantly more reactive in the bloodstream than glucose, and perhaps ten times more effective (bad) than glucose at inducing cross-linking of proteins that leads to the cellular junk of AGEs. It also seems that the AGEs created from fructose are more resistant to the body’s disposal mechanisms than those created with glucose. It also markedly increases the oxidation of LDL particles, which appears to be a necessary step in atherosclerosis.
Chapter 13 – Dementia, Cancer, and Aging
Alzheimer’s has a similar distribution to other “diseases of civilization”, like diabetes, which suggests that it may be related to whatever is also causing diabetes.
Study of 700 elderly members of the Sisters of Notre Dame congregation results suggest that the less vascular damage we have in our brains, the more easily we can tolerate the lesions of Alzheimer’s without exhibiting signs of dementia. It’s the extent and location of the vascular damage in the brain that appears to be the determining factor. This implies that the accumulation of damage to neurons and blood vessels is one unavoidable process of aging. And diabetics accumulate vascular damage more rapidly. So whatever dietary factors or lifestyle factors lead to Type 2 diabetes will also increase the likelihood of manifesting dementia.
AGEs are present in the amyloid plaques and tangles of Alzheimer’s. There is a theory that says that AGEs themselves are what cause the plaques in the first place.
Insulin (in a test tube) will monopolize the attention of the insulin-degrading enzyme (IDE), which normally degrades and clears both amyloid proteins and insulin from around the neurons. By this theory, the more insulin available in the brain, the less IDE is available to clean up amyloid, which then accumulates excessively and clumps into plaques. In animal experiments, the less IDE available, the greater the concentration of amyloid in the brain. Mice that lack the gene to produce IDE develop versions of both Alzheimer’s disease and Type 2 diabetes.
Richard Doll and Richard Peto published a study on cancer. The analysis stated that man-made chemicals (in pollution, food additives, and occupation exposure) play a minimal role in human cancers, and that diet played the largest role, causing 35% of all cancers, though uncertainties were so vast that the number could be as low as 10% or as high as 70%. When WHO refers to “extrinsic factors”, they mean diet and lifestyle, not man-made chemicals (the “carcinogenic soup” as the environmental movement called it).
The patterns of cancer incidence for many cancers are similar to those of heart disease, diabetes, and obesity, which suggests an association between the diseases. Those cancers apparently caused by diet or lifestyle and not related to tobacco use are either cancers of the gastrointestinal tract, including colon and rectal cancer, or cancers of what are technically known as endocrine-dependent organs (breast, uterus, ovaries, and prostate) the functions of which are regulated by hormones. (Note, insulin is a hormone.)
Warburg demonstrated that tumor cells quickly develop the ability to survive without oxygen and to generate energy by a process of fermentation rather than respiration. Fermentation is considerably less efficient, and so tumors will burn perhaps thirty times as much blood sugar as normal cells. In lab animals whose calorie intake was restricted (they were starved…or fed minimal diets), tumors were inhibited. The though being that the tumors could not get enough energy to fuel mitosis, and continue proliferating.
Howard Temin (Nobel Prize winner for cancer research) reported that cells turned malignant by a chicken virus would cease to proliferate in the laboratory unless insulin was added to the serum in which they were growing.
Malignant breast tumors had more receptors for insulin than did healthy tissue.
Cancer researchers now believe that cancer-causing mutations occur as errors in the replication of DNA during the process of cell division and multiplication. Each one of us is likely to experience some 10 thousand trillion cell divisions over the course of our lives. Over time the errors can (unluckily) build up and produce a cell that has just the right combination of errors in replication to be malignant. This suggests that cancer-causing mutations are another unavoidable side effect of aging, which is why our cells have also evolved to be exceedingly resistant to genetic damage. They have sophisticated mechanisms to search out defects in newly replicated DNA and repair them, and other mechanisms that actually prompt a cell to commit suicide (programmed cell death in technical terminology), if the repair mechanisms are incapable of fixing the damage that occurred during replication. But these programs can be disabled with the right unlucky mutation.
IGF (Insulin-like Growth Factor) is secreted both by the liver and by tissues and cells throughout the body. Most tissues require at least two growth factors to grow at an optimal rate, and IGF is almost invariably one of the two, and perhaps the primary regulator. IGF can mimic the effects of insulin as well by stimulating muscles to take up blood sugar (though not as efficiently).
Basegra says, shutting down the IGF receptor in mice will lead to what Baserga calls “strong inhibition, if not total suppression of tumor growth”. Particularly lethal to those tumors that have already metastasized from a primary site elsewhere in the body.
The working hypothesis then is that the decisive factor in malignant cancer is not the accumulation of genetic damage in cells, much of which is unavoidable, but how diets change the environment around the cells and tissues to promote the survival, growth, and then metastasis of cancer cells that do appear. IGF and insulin can be viewed as providing fuel to the fire of cancerous cells, rather than causing the cancer itself.
Chapter 14 – 20
Appetite and thus calories consumed will increase to compensate for physical activity (exercise). So although exercise can help you lose weight, it will only do so at the cost of being hungry. Being physically active “works up an appetite”.
If the diet includes less than 130 grams of carbohydrates per day, the liver increases its synthesis of molecules called ketone bodies, and these supply the necessary fuel for the brain and central nervous system. If the diet includes no carbohydrates at all, ketone bodies supply 3/4 of the energy to the brain. The rest comes from glucose synthesized from the amino acids in protein, either from the diet or from the breakdown of muscle, and from a compound called glycerol that is released when triglycerides in the fat tissue are broken down into their component fatty acids. In these cases the body is technically in a state called ketosis, and the diet is often referred to as a ketogenic diet. (Note this is different than the ketoacidosis of uncontrolled diabetes.)
Study with Stefansson and Anderson where they ate only meat (to test the Inuit diet). They consumed an average of almost 2 pounds of meat per day, or 2600 calories: 79% from fat, 19% protein, and roughly 2% from carbohydrates, which came from glycogen contained in the muscle meat. (Glycogen is the compound that stores glucose, a carbohydrate, in the liver and the muslce.)
The study produced no dramatic results. Meaning there were no bad side effects from a meat only diet. Both men lost a few pounds, even though they led pretty sedentary lives. One man’s blood pressure lowered, while the other’s stayed low. The researchers detected no evidence of kidney damage or diminished function (NOTE: this is what the vet said would happen). Nor did mineral deficiencies occur, although the diet contained only a quarter of the calcium usually found in mixed diets, and the acidic nature of a meat-rich diet was supposed to increase calcium excretion and so deplete the body of calcium.
B vitamins are depleted from the body by the consumption of carbohydrates. C vitamin may also be as well. Type 2 diabetics have roughly 30 percent lower levels of viatmin C. One explanation is that high blood sugar and/or high insulin levels work to increase the body’s requirements for vitamin C. The vitamin C molecule is similar in configuration to glucose and other sugars in the body. It is shuttled from the bloodstream into the cells by the same insulin-dependent transport system used by glucose. Glucose and Vitamin C compete in this cellular-uptake process. Because glucose is greatly favored in the contest, the uptake of Vitamin C by cells is “globally inhibited” when blood sugar levels are elevated. In effect glucose regulates how much vitamin C is taken up by the cells, according to University of Massechuesetts nutritionist John Cunningham. Glucose also impairs the reabsorption of vitamin C by the kidney, and so, the higher the blood sugar, the more vitamin C will be lost in the urine. Infusing insulin into experimental subjects has been shown to cause a “market fall” in vitamin-C levels in the circulation.
In other words, carbohydrates are flushing out the vitamin C. We might get scurvy because we don’t eat our fruits and vegetables, but it’s not the absence of fruits and vegetables that causes the scurvy, it’s the presence of refined carbohydrates. (This hypothesis has not been proven, but it is empirically evident.)
The hypothesis is that our fat tissues are storing too much fuel. This starves our other tissues (like muscle), and so we eat more. We aren’t getting fat because we eat too much…we’re eating too much because what we do eat is being stored away (as fat) where we can’t use it.
The craving for carbohydrates is akin to an addiction. Sugar (sucrose), just like cocaine, alcohol, nicotine, and other addictive drugs, appears to induce an exaggerated response in that region of the brain known as the reward center, the nucleus accumbens. Rats can be addicted to sugar, and will experience the physical symptoms of opiate withdrawal when forced to abstain.
Avoiding carbohydrates will lower insulin levels (even in the obese), and so ameliorate the hyperinsulinemia that causes the carbohydrate craving itself. “After a year to eighteen months, the appetite is normalized and the craving for sweets is lost” said James Sidbury Jr about the effects on children of his carbohydrate-restricted diet. “This change can often be identified within a specific one to two week period by the individual.”
If it’s true that easily digestible carbohydrates and sugars are addictive, then this gives a good reason that people have trouble avoiding them. It also means that if you suffer symptoms when restricting carbohydrates, they may be actual opiate withdrawal symptoms that will pass as the body readjusts and kicks the addiction.
There is also the possibility of an occasional elevation of cholesterol that will occur with fat loss, a condition known as transient hypercholesterolemia, and that is a consequence of the fact that we store cholesterol along with fat in our fat cells. When fatty acids are mobilized, the cholesterol is released as well, and thus serum levels of cholesterol can spike. The existing evidence suggests that this effect will vanish with successful weight loss, regardless of the saturated-fat content of the diet.
“Certain conclusions seem inescapable to me, based on the existing knowledge”:
1) Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.
2) The problem is the carbohydrates in the diet, their effects on insulin secretion, and thus the hormonal regulation of homeostasis – the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and well-being.
3) Sugars – sucrose and high-fructose corn syrup specifically – are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.
4) Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.
5) Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6) Consuming excess calories does not *cause* us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
7) Fattening and obesity are caused by an imbalance – a disequilibrium – in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.
8) Insulin is the primary regulator of fat storage. When insulin levels are elevated – either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.
9) By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume the leaner we will be.
10) By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.