Ray Peat: The importance of sugar and the dangers of fat (stress) metabolism

Keyhole

The Living Force
FOTCM Member
I am opening this thread up as a repository for some of the work by physiologist Dr Ray Peat. His ideas are fairly controversial and fly in the face of the paleo philosophy, but from what I can see, all of his statements are backed up by evidence. Hopefully this can pave the way for some discussion and further research.

Article no.1
Glycemia, starch, and sugar in context
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Monosaccharide -- a simple sugar; examples, glucose, fructose, ribose, galactose (galactose is also called cerebrose, brain sugar).

Disaccharide -- two monosaccharides bound together; examples, sucrose, lactose, maltose.

Oligosaccharide -- a short chain of monosaccharides, including disaccharides and slightly longer chains.

Polysaccharide -- example, starch, cellulose, glycogen.

Glycation -- the attachment of a sugar to a protein.

Lipolysis - the liberation of free fatty acids from triglycerides, the neutral form in which fats are stored, bound to glycerine.


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In the 1920s, “diabetes” was thought to be a disease of insulin deficiency. Eventually, measurements of insulin showed that “diabetics” often had normal amounts of insulin, or above-normal amounts. There are now “two kinds of diabetes,” with suggestions that “the disease” will soon be further subdivided.

The degenerative diseases that are associated with hyperglycemia and commonly called diabetes, are only indirectly related to insulin, and as an approach to understanding or treating diabetes, the “glycemic index” of foods is useless. Physiologically, it has no constructive use, and very little meaning.

Insulin is important in the regulation of blood sugar, but its importance has been exaggerated because of the diabetes/insulin industry. Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor. There probably isn't any process in the body that doesn't potentially affect blood sugar.

Glucagon, cortisol, adrenalin, growth hormone and thyroid tend to increase the blood sugar, but it is common to interpret hyperglycemia as "diabetes," without measuring any of these factors. Even when "insulin dependent diabetes" is diagnosed, it isn't customary to measure the insulin to see whether it is actually deficient, before writing a prescription for insulin. People resign themselves to a lifetime of insulin injections, without knowing why their blood sugar is high.

Insulin release is also stimulated by amino acids such as leucine, and insulin stimulates cells to absorb amino acids and to synthesize proteins. Since insulin lowers blood sugar as it disposes of amino acids, eating a large amount of protein without carbohydrate can cause a sharp decrease in blood sugar. This leads to the release of adrenalin and cortisol, which raise the blood sugar. Adrenalin causes fatty acids to be drawn into the blood from fat stores, especially if the liver's glycogen stores are depleted, and cortisol causes tissue protein to be broken down into amino acids, some of which are used in place of carbohydrate. Unsaturated fatty acids, adrenaline, and cortisol cause insulin resistance.

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“Professional opinion” can be propagated about 10,000 times faster than research can evaluate it, or, as C. H. Spurgeon said, "A lie travels round the world while Truth is putting on her boots."

In the 1970s, dietitians began talking about the value of including "complex carbohydrates" in the diet. Many dietitians (all but one of the Registered Dietitians that I knew of) claimed that starches were more slowly absorbed than sugars, and so should be less disruptive to the blood sugar and insulin levels. People were told to eat whole grains and legumes, and to avoid fruit juices.

These recommendations, and their supporting ideology, are still rampant in the culture of the United States, fostered by the U.S. Department of Agriculture and the American Dietetic Association and the American Diabetes Association and innumerable university departments of home economics, dietetics, or nutrition.

Judging by present and past statements of the American Dietetic Association, I think some kind of institutional brain defect might account for their recommendations. Although the dietetic association now feebly acknowledges that sugars don't raise the blood sugar more quickly than starches do, they can't get away from their absurd old recommendations, which were never scientifically justified: “Eat more starches, such as bread, cereal, and starchy vegetables--6 servings a day or more. Start the day with cold (dry) cereal with nonfat/skim milk or a bagel with one teaspoon of jelly/jam. Put starch center stage--pasta with tomato sauce, baked potato with chili, rice and stir-fried beef and vegetables. Add cooked black beans, corn, or garbanzo beans (chickpeas) to salads or casseroles.”

The Dietetic Association's association with General Mills, the breakfast cereal empire, (and Kellog, Nabisco, and many other food industry giants) might have something to do with their starchy opinions. Starch-grain embolisms can cause brain damage, but major money can also make people say stupid things.

In an old experiment, a rat was tube-fed ten grams of corn-starch paste, and then anesthetized. Ten minutes after the massive tube feeding, the professor told the students to find how far the starch had moved along the alimentary canal. No trace of the white paste could be found, demonstrating the speed with which starch can be digested and absorbed. The very rapid rise of blood sugar stimulates massive release of insulin, and rapidly converts much of the carbohydrate into fat.

It was this sort of experiment that led to the concept of "glycemic index," that ranks foods according to their ability to raise the blood sugar. David Jenkins, in 1981, knew enough about the old studies of starch digestion to realize that the dietitians had created a dangerous cult around the “complex carbohydrates,” and he did a series of measurements that showed that starch is more “glycemic” than sucrose. But he simply used the amount of increase in blood glucose during the first two hours after ingesting the food sample, compared to that following ingestion of pure glucose, for the comparison, neglecting the physiologically complex facts, all of the processes involved in causing a certain amount of glucose to be present in the blood during a certain time. (Even the taste of sweetness, without swallowing anything, can stimulate the release of glucagon, which raises blood sugar.)

More important than the physiological vacuity of a simple glycemic measurement was the ideology within which the whole issue developed, namely, the idea that diabetes (conceived as chronic hyperglycemia) is caused by eating too much sugar, i.e., chronic hyperglycemia the illness is caused by the recurrent hyperglycemia of sugar gluttony. The experiments of Bernardo Houssay (1947 Nobel laureate) in the 1940s, in which sugar and coconut oil protected against diabetes, followed by Randle's demonstration of the antagonism between fats and glucose assimilation, and the growing recognition that polyunsaturated fatty acids cause insulin resistance and damage the pancreas, have made it clear that the dietetic obsession with sugar in relation to diabetes has been a dangerous diversion that has retarded the understanding of degenerative metabolic diseases.

Starting with the insulin industry, a culture of diabetes and sugar has been fabulized and expanded and modified as new commercial industries found ways to profit from it. Seed oils, fish oils, breakfast cereals, soybean products, and other things that were never eaten by any animal in millions of years of evolution have become commonplace as “foods,” even as “health foods.”

Although many things condition the rate at which blood sugar rises after eating carbohydrates, and affect the way in which blood glucose is metabolized, making the idea of a “glycemic index” highly misleading, it is true that blood sugar and insulin responses to different foods have some meaningful effects on physiology and health.

Starch and glucose efficiently stimulate insulin secretion, and that accelerates the disposition of glucose, activating its conversion to glycogen and fat, as well as its oxidation. Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat. Eating “complex carbohydrates,” rather than sugars, is a reasonable way to promote obesity. Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten. The obesity itself then becomes an additional physiological factor; the fat cells create something analogous to an inflammatory state. There isn't anything wrong with a high carbohydrate diet, and even a high starch diet isn't necessarily incompatible with good health, but when better foods are available they should be used instead of starches. For example, fruits have many advantages over grains, besides the difference between sugar and starch. Bread and pasta consumption are strongly associated with the occurrence of diabetes, fruit consumption has a strong inverse association.

Although pure fructose and sucrose produce less glycemia than glucose and starch do, the different effects of fruits and grains on the health can't be reduced to their effects on blood sugar.

Orange juice and sucrose have a lower glycemic index than starch or whole wheat or white bread, but it is common for dietitians to argue against the use of orange juice, because its index is the same as that of Coca Cola. But, if the glycemic index is very important, to be rational they would have to argue that Coke or orange juice should be substituted for white bread.

After decades of “education” to promote eating starchy foods, obesity is a bigger problem than ever, and more people are dying of diabetes than previously. The age-specific incidence of most cancers is increasing, too, and there is evidence that starch, such as pasta, contributes to breast cancer, and possibly other types of cancer.

The epidemiology would appear to suggest that complex carbohydrates cause diabetes, heart disease, and cancer. If the glycemic index is viewed in terms of the theory that hyperglycemia, by way of “glucotoxicity,” causes the destruction of proteins by glycation, which is seen in diabetes and old age, that might seem simple and obvious.

Fructose 32 22
Lactose 65 46
Honey 83 58
High fructose corn syrup 89 62
Sucrose 92 64
Glucose 137 96
Glucose tablets 146 102
Maltodextrin 150 105
Maltose 150 105
Pineapple juice 66 46
Peach, canned 67 47
Grapefruit juice 69 48
Orange juice 74 52
Barley flour bread 95 67
Wheat bread, high fiber 97 68
Wheat bread, wholemeal flour 99 69
Melba toast 100 70
Wheat bread, white 101 71
Bagel, white 103 72
Kaiser rolls 104 73
Whole-wheat snack bread 105 74
Bread stuffing 106 74
Wheat bread, Wonderwhite 112 78
Wheat bread, gluten free 129 90
French baguette 136 95
Taco shells 97 68
Cornmeal 98 69
Millet 101 71
Rice, Pelde 109 76
Rice, Sunbrown Quick 114 80
Tapioca, boiled with milk 115 81
Rice, Calrose 124 87
Rice, parboiled, low amylose Pelde 124 87
Rice, white, low amylose 126 88
Rice, instant, boiled 6 min 128 90
`
GLYCEMIC LIST White Bread Glucose Based

But there are many reasons to question that theory.

Oxidation of sugar is metabolically efficient in many ways, including sparing oxygen consumption. It produces more carbon dioxide than oxidizing fat does, and carbon dioxide has many protective functions, including increasing Krebs cycle activity and inhibiting toxic damage to proteins. The glycation of proteins occurs under stress, when less carbon dioxide is being produced, and the proteins are normally protected by carbon dioxide.

When sugar (or starch) is turned into fat, the fats will be either saturated, or in the series derived from omega -9 monounsaturated fatty acids. When sugar isn't available in the diet, stored glycogen will provide some glucose (usually for a few hours, up to a day), but as that is depleted, protein will be metabolized to provide sugar. If protein is eaten without carbohydrate, it will stimulate insulin secretion, lowering blood sugar and activating the stress response, leading to the secretion of adrenalin, cortisol, growth hormone, prolactin, and other hormones. The adrenalin will mobilize glycogen from the liver, and (along with other hormones) will mobilize fatty acids, mainly from fat cells. Cortisol will activate the conversion of protein to amino acids, and then to fat and sugar, for use as energy. (If the diet doesn't contain enough protein to maintain the essential organs, especially the heart, lungs, and brain, they are supplied with protein from the skeletal muscles. Because of the amino acid composition of the muscle proteins, their destruction stimulates the formation of additional cortisol, to accelerate the movement of amino acids from the less important tissues to the essential ones.)

The diabetic condition is similar in many ways to stress, inflammation, and aging, for example in the chronic elevation of free fatty acids, and in various mediators of inflammation, such as tumor necrosis factor (TNF).


Rather than the sustained hyperglycemia which is measured for determining the glycemic index, I think the “diabetogenic” or “carcinogenic” action of starch has to do with the stress reaction that follows the intense stimulation of insulin release. This is most easily seen after a large amount of protein is eaten. Insulin is secreted in response to the amino acids, and besides stimulating cells to take up the amino acids and convert them into protein, the insulin also lowers the blood sugar. This decrease in blood sugar stimulates the formation of many hormones, including cortisol, and under the influence of cortisol both sugar and fat are produced by the breakdown of proteins, including those already forming the tissues of the body. At the same time, adrenalin and several other hormones are causing free fatty acids to appear in the blood.

Since the work of Cushing and Houssay, it has been understood that blood sugar is controlled by antagonistic hormones: Remove the pituitary along with the pancreas, and the lack of insulin doesn't cause hyperglycemia. If something increases cortisol a little, the body can maintain normal blood sugar by secreting more insulin, but that tends to increase cortisol production. A certain degree of glycemia is produced by a particular balance between opposing hormones.

Tryptophan, from dietary protein or from the catabolism of muscles, is turned into serotonin which activates the pituitary stress hormones, increasing cortisol, and intensifying catabolism, which releases more tryptophan. It suppresses thyroid function, which leads to an increased need for the stress hormones. Serotonin impairs glucose oxidation, and contributes to many of the problems associated with diabetes.

“Diabetes” is often the diagnosis, when excess cortisol is the problem. The hormones have traditionally not been measured before diagnosing diabetes and prescribing insulin or other chemical to lower the blood sugar. Some of the worst effects of “diabetes,” including retinal damage, are caused or exacerbated by insulin itself.

Antiserotonin drugs can sometimes alleviate stress and normalize blood sugar. Simply eating sucrose was recently discovered to restrain the stress hormone system (“A new perspective on glucocorticoid feedback: relation to stress, carbohydrate feeding and feeling better,” J Neuroendocrinol 13(9), 2001, KD Laugero).

The free fatty acids released by the stress hormones serve as supplemental fuel, and increase the consumption of oxygen and the production of heat. (This increased oxygen demand is a problem for the heart when it is forced to oxidize fatty acids. [A. Grynberg, 2001]) But if the stored fats happen to be polyunsaturated, they damage the blood vessels and the mitochondria, suppress thyroid function, and cause “glycation” of proteins. They also damage the pancreas, and impair insulin secretion.

A repeated small stress, or overstimulation of insulin secretion, gradually tends to become amplified by the effects of tryptophan and the polyunsaturated fatty acids, with these fats increasing the formation of serotonin, and serotonin increasing the liberation of the fats.

The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996). And the oxidation of fats rather than glucose means that the proteins won't have as much protective carbon dioxide combined with their reactive nitrogen atoms, so the real difference in the organism is likely to be greater than that seen by Fu, et al.

These products of lipid peroxidation, HNE, MDA, acrolein, glyoxal, and other highly reactive aldehydes, damage the mitochondria, reducing the ability to oxidize sugar, and to produce energy and protective carbon dioxide.

Fish oil, which is extremely unstable in the presence of oxygen and metals such as iron, produces some of these dangerous products very rapidly. The polyunsaturated “essential fatty acids” and their products, arachidonic acid and many of the prostaglandin-like materials, also produce them.

When glucose can't be oxidized, for any reason, there is a stress reaction, that mobiles free fatty acids. Drugs that oppose the hormones (such as adrenalin or growth hormone) that liberate free fatty acids have been used to treat diabetes, because lowering free fatty acids can restore glucose oxidation.

Brief exposures to polyunsaturated fatty acids can damage the insulin-secreting cells of the pancreas, and the mitochondria in which oxidative energy production takes place. Prolonged exposure causes progressive damage. Acutely, the free polyunsaturated fatty acids cause capillary permeability to increase, and this can be detected at the beginning of “insulin resistance” or “diabetes.” After chronic exposure, the leakiness increases and albumin occurs in the urine, as proteins leak out of the blood vessels. The retina and brain and other organs are damaged by the leaking capillaries.

The blood vessels and other tissues are also damaged by the chronically increased cortisol, and at least in some tissues (the immune system is most sensitive to the interaction) the polyunsaturated fats increase the ability of cortisol to kill the cells.

When cells are stressed, they are likely to waste glucose in two ways, turning some of it into lactic acid, and turning some into fatty acids, even while fats are being oxidized, in place of the sugar that is available. Growth hormone and adrenalin, the stress-induced hormones, stimulate the oxidation of fatty acids, as well as their liberation from storage, so the correction of energy metabolism requires the minimization of the stress hormones, and of the free fatty acids. Prolactin, ACTH, and estrogen also cause the shift of metabolism toward the fatty acids.

Sugar and thyroid hormone (T3, triiodothyronine) correct many parts of the problem. The conversion of T4 into the active T3 requires glucose, and in diabetes, cells are deprived of glucose. Logically, all diabetics would be functionally hypothyroid. Providing T3 and sugar tends to shift energy metabolism away from the oxidation of fats, back to the oxidation of sugar.

Niacinamide, used in moderate doses, can safely help to restrain the excessive production of free fatty acids, and also helps to limit the wasteful conversion of glucose into fat. There is evidence that diabetics are chronically deficient in niacin. Excess fatty acids in the blood probably divert tryptophan from niacin synthesis into serotonin synthesis.

Sodium, which is lost in hypothyroidism and diabetes, increases cellular energy. Diuretics, that cause loss of sodium, can cause apparent diabetes, with increased glucose and fats in the blood. Thyroid, sodium, and glucose work very closely together to maintain cellular energy and stability.

In Houssay's experiments, sugar, protein, and coconut oil protected mice against developing diabetes. The saturated fats of coconut oil are similar to those we synthesize ourselves from sugar. Saturated fats, and the polyunsaturated fats synthesized by plants, have very different effects on many important physiological processes. In every case I know about, the vegetable polyunsaturated fats have harmful effects on our physiology.

For example, they bind to the “receptor” proteins for cortisol, progesterone, and estrogen, and to all of the major proteins related to thyroid function, and to the vesicles that take up nerve transmitter substances, such as glutamic acid.

They allow glutamic acid to injure and kill cells through excessive stimulation; this process is similar to the nerve damage done by cobra venom, and other toxins.

Excess cortisol makes nerve cells more sensitive to excitotoxicity, but the cells are protected if they are provided with an unusually large amount of glucose.

The cells of the thymus gland are very sensitive to damage by stress or cortisol, but they too can be rescued by giving them enough extra glucose to compensate for the cortisol. Polyunsaturated fatty acids have the opposite effect, sensitizing the thymus cells to cortisol. This partly accounts for the immunosuppressive effects of the polyunsaturated fats. (AIDS patients have increased cortisol and polyunsaturated fatty acids in their blood.[E.A. Nunez, 1988.])

Unsaturated fatty acids activate the stress hormones, sugar restrains them.

Simply making animals “deficient” in the unsaturated vegetable oils (which allows them to synthesize their own series of animal polyunsaturated fats, which are very stable), protects them against “autoimmune” diabetes, and against a variety of other “immunological” challenges. The “essential fatty acid” deficiency increases the oxidation of glucose, as it increases the metabolic rate generally.

Saturated fats improve the insulin-secreting response to glucose.

The protective effects of sugar, and the harmful effects of excessive fat metabolism, are now being widely recognized, in every field of physiology. The unsaturated vegetable fats, linoleic and linolenic acid and their derivatives, such as arachidonic acid and the long chain fish oils, have excitatory, stress promoting effects, that shift metabolism away from the oxidation of glucose, and finally destroy the respiratory metabolism altogether. Since cell injury and death generally involve an imbalance between excitation and the ability to produce energy, it is significant that the oxidation of unsaturated fatty acids seems to consume energy, lowering cellular ATP (Clejan, et al, 1986).

The bulk of the age-related tissue damage classified as “glycation end-products” (or “advanced glycation end-products,” AGE) is produced by decomposition of the polyunsaturated fats, rather than by sugars, and this would be minimized by the protective oxidation of glucose to carbon dioxide.

Protein of the right kind, in the right amount, is essential for reducing stress. Gelatin, with its antiinflammatory amino acid balance, helps to regulate fat metabolism.

Aspirin's antiinflammatory actions are generally important when the polyunsaturated fats are producing inflammatory and degenerative changes, and aspirin prevents many of the problems associated with diabetes, reducing vascular leakiness. It improves mitochondrial respiration (De Cristobal, et al., 2002) and helps to regulate blood sugar and lipids (Yuan, et al., 2001). Aspirin's broad range of beneficial effects is probably analogous to vitamin E's, being proportional to protection against the broad range of toxic effects of the polyunsaturated “essential” fatty acids.
Article source and references can be found here
 

Hello H2O

Jedi Council Member
FOTCM Member
Ray Peat. That's cool, I started reading his articles years ago, and he was the one that really got me looking into how our knowledge base around nutrition is based on faulty evidence and studies, some going back many years. Maybe not perfect, but a good, if not technical source of information.
 

Gaby

SuperModerator
Moderator
FOTCM Member
I think his information is fascinating, especially the concepts of how toxic essential fatty acids can be when there is not enough saturated fat or antioxidants in the diet to stabilize them:

Fats and degeneration
_http://raypeat.com/articles/articles/fats-degeneration3.shtml

Cholesterol, longevity, intelligence, and health
_http://raypeat.com/articles/articles/cholesterol-longevity.shtml

It explains how the cholesterol myth has essentially wrecked our health. Saturated fat is so important and toxic PUFAs (polyunsaturated fatty acids) are so detrimental, that it explains how eating more PUFAs than your body could handle just leave you at the mercy of strokes and heart attacks:

What everyone should know about Ancel Keys' experiments
https://www.sott.net/article/335949-What-everyone-should-know-about-Ancel-Keys-experiments

We know that Keys' so-called saturated fat diet was also loaded with trans fats, and we know that trans fats cause atherosclerosis. The Nurses Health Study showed that for each 2% increase in trans fat in the diet, the risk of heart disease is doubled. And if this trans-fat loaded diet performed BETTER than a diet high in polyunsaturated fats, that suggests polyunsaturated fats from processed vegetable oils, when consumed in the amounts consumed in the study, are more unhealthy than trans fat.
The irony is that PUFAs lower your cholesterol levels and at the same time, it creates cardiovascular disease. So those who lower their cholesterol based on oxidized PUFAs will develop chronic disease including cancer, cardiovascular disease and any chronic ailment. It ages you.

From the Ancel Keys article quoted above, there is a youtube talk by Cate Shanahan that I have quoted not too long ago in the forum. She references an organic chemistry expert which has published hundreds of scientific papers. I'm attaching one to this post which in essence says that if people knew about organic chemistry 101, they would be ashamed to blame saturated fat for our cardiovascular disease epidemic. Or as the title says: "The Action of Peroxyl Radicals, Powerful Deleterious Reagents, Explains Why Neither Cholesterol Nor Saturated Fatty Acids Cause Atherogenesis and Age-Related Diseases".

Ray Peat's concepts on carbs are also interesting and there is data quoted on the attached paper which suggests that carbs don't behave as toxically as burned PUFAs. The later one can produce more glycation in your body than carbs. Burned PUFAs can also damage the carbohydrate structures in your body, making you susceptible to chronic and autoimmune disease.

Basically, the most evil thing that any person could eat is oxidized PUFAs. What we know as essential fatty acids might not be that essential after all. The one thing that seems essential is animal saturated fat. It is a fascinating concept.
 

nicklebleu

The Living Force
FOTCM Member
There is this guy Stephane Guyenet, who argues along the same lines. He is an obesity researcher and neurobiologist.

I haven't studied him yet in detail, but here is his website..
 

SeekinTruth

Ambassador
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FOTCM Member
Well the first thing to clarify for context is whether someone is keto adapted or not to be able to make sense of these claims. To say anything meaningful about carbohydrates - restriction of whatever kind - only makes sense to me in the context of nutritional ketosis; if one is keto adapted (which can take from a few weeks to a few months of very low daily carb consumption, and may be helped by certain supplements like acetyl-L-carnitine while increasing fat intake to compensate), everything is different. Second is that these claims being controversial and flying in the face of the paleo philosophy has questionable relevance for me at this point as, like so many other things, paleo has become somewhat meaningless as there are so many approaches all being labeled paleo. For example, those who consume grains on a "paleo" diet are really paleo? Going by the available evidence, agricultural grains weren't around before 8,000 to 10,000 years ago, and in other places grains and starches weren't regularly or widely available until a few centuries ago.

Third, the only way to make sense of this kind of information is to clearly differentiate the kinds of fat consumption (and again, in a ketogenic context); my ketogenic diet, for example, consists of mainly saturated animal fats which are made into ketones and burned for energy, and also take care of fat soluble vitamins and minerals, etc. It is also important to eat enough organ meats for me. PUFA's aren't used as fuel (burned for energy), but they have important functions in cell membranes, etc. On a properly formulated ketogenic diet, the percentage of PUFA's are a relatively low percentage of the fat mix ingested.

The important thing seems to be the problem of consuming a lot of carbohydrates AND fats (and especially the toxic/plastic oils so widespread for the last 80 years or so) at the same time. So, again, there has to first be a rational framework laid out of why a certain approach is being recommended. This seems to be at the heart of "metabolic derangement" of all sorts that really began with the industrial toxic oils replacing the healthy fats (lard, tallow, butter) consumed until the early part of the 20th Century in the West (and labeling the toxic fats as healthy and the healthy fats as unhealthy), then the low fat/high carb diets went into full swing a few decades later. During this same period is when health really went into a downward spiral, and the population got fatter and fatter.

The thing is that the choice is not (never was) between starches or simple sugars, and all that glycemic index blah, blah, blah, but to get over insulin resistance and other hormone/metabolism issues, as well as neuro-protective and least ROS generation approach is consistently shown to be low carb/ketogenic diets - the overwhelming amount the evidence shows this. The "importance of sugar" is pretty nonsensical when looked at in the proper context - even if it wasn't making claims about insulin and diabetes problems - but clearly the best and fastest way to address type-2 diabetes, which is now so widespread, is a sustainable low carb, keto diet. Why is sugar important at all? Will we develop health problems in the absence of sugar (e.g. sucrose, fructose)? Where's the evidence of this? Fat metabolism in a ketogenic diet context is really based on saturated and monounsaturated fats NOT PUFA's - PUFA's are not used for energy needs, but are crucial for cellular membranes, signaling, etc., so the low amounts in a good ketogenic diet are sufficient for those needs while being protected by the high amounts of saturated fat in the diet.


To give some relevant information about Peat's claims, while he is on-point in the case of a sugar burner (i.e. being in glucose metabolism), the picture changes for a fat burner. The only way to sustain a low carb diet is to be in ketosis; and for it to be healthy, it has to have 75% to 85% of daily calories in saturated animal fats. I'll quote some info from The Art and Science of Low Carbohydrate Living by Volek and Phinney (they have, between them, quite a lot of experience with formulating low carb/high fat diets for decades, for specific health issues, weight control, and for athletic performance, but I don't follow the specific recipes and foods they recommend because I don't eat cheese, yogurt, etc.; also the book is pretty well referenced, but "Citations have been held to a minimum of the key publications in each chapter (rather than the 50-100 citations per chapter we could easily conjure up).")

Until more recent years, the dogma of several decades of 'carbohydrates are necessary and good, and dietary fats are bad' wasn't being questioned with the actual data as what happened in the last several years (when it even started showing up in the mainstream media regularly). And during those decades of said dogma is when the population REALLY got unhealthy and fat in increasing numbers.

When the data was becoming overwhelming, there was finally a shift in the "consensus" about the toxic fats like trans fats/hydrogenated oils, way to much PUFA's (especially omega-6), and more recently the disastrous additional damage from high fructose corn syrup so widespread in the average diets. So the issues to be looked into with low carbohydrate diets' benefits will follow; the main approach being that carbs are replaced by fat, and protein consumption kept about the same. Oh, also the Ancel Keys Seven Countries Study of 1954, besides the "cooked data" of what kinds of fats were REALLY the problem, he omitted the 16 countries showing no correlation in saturated fat intake and heart disease, including only the 7 countries that DID show it; selective data - more than double the countries that showed no link to his"lipid hypothesis" - were excluded from the study. Same with the more recent "China Study" - the data does NOT support the conclusion and was cherry picked to support a preconceived conclusion. Whereas methodologically sound research such as that done by Weston A. Price in the 1930's, among others, showed clearly that none of the traditional diets (high fat, high in animal-based unprocessed foods) untouched by modern Western diets he found traveling globally had any of the health problems plaguing the industrialized (and now globalized) countries - not only they had pretty much perfect dental health, which was his original motivation for the research, but also health in general. Plus, Price's data was even more revealing because in certain families, some members had already started eating more westernized processed diets, showing all the same dental and general health problems as the western countries (and unlike their siblings/relatives who continued their traditional diets).

First, some of the basic contentions and background that we're familiar with here on the forum:

From the book The Art and Science of Low Carb Living (Published 2011)
Dietary saturated fat has been demonized in the media textbooks, and in national policy; whereas published scientific data shows no connection between dietary saturated fat intake and either saturated fat levels in the body or the long term risk of heart disease.

The strongest correlation between a major dietary nutrient and blood levels of saturated fat is with dietary carbohydrate -not with saturated fat intake! On average, the more carbohydrate you eat, the higher the content of saturated fats in your blood.


So the accumulated scientific data shows one of the markers of abnormality in the blood is strongly correlated with how much carbs are eaten. Abnormally high Triglycerides will go down - usually to very low levels - within a couple of months of a good low carb diet.

While keeping in mind the importance of individual variability...

... scientific evidence now supports inclusion of well-formulated low carbohydrate diets in the list of safe and sustainable dietary options to promote optimum health and wellbeing. And this is where the "art" must join the "science". Just because you decide to stop eating sugar, bread, potatoes, rice and pasta doesn't mean that you have a low carbohydrate diet suitable for long-term use. ...

...We have written this book because we are confident that a well-formulated low carbohydrate diet offers improved long-term health and well-being to people whose metabolism struggles to deal with a high carbohydrate load (aka carbohydrate intolerance). ...

... Starting two decades ago with Professor Gerald Reaven's courageous stand against the use of high carbohydrate diets in people with what we now call metabolic syndrome[4], we have become increasingly aware that some of us are 'carbohydrate intolerant'. This concept of carbohydrate intolerance is increasingly understood to be a manifestation of insulin resistance, and is associated with high blood triglycerides, high blood pressure, and in its most severe form, type-2 diabetes. These sub-groups in the population show dramatic clinical improvement when dietary carbohydrates are reduced, and thus deserve to be offered a separate path from the 'high carb, low fat' mantra promoted by national policymakers. ...
Some of the background will be covered for actual early scientific studies for low carb/high fat/ketogenic diets - and then more detail will come. Some of the following also discusses the ideas of "paleo".

Historical Perspective

Who invented the low carbohydrate diet? Was it Dr. Robert Atkins' weight loss revolution in 1972? Or Wilder and Peterman's anti-seizure diet at the Mayo Clinic in the 1920's? Or perhaps Banting's pamphlet in Britain in 1863?

The answer: none of the above. But for sure, it was long, long before these recorded efforts to codify and monetize carbohydrate restriction. This does not in any way discount the contributions of these contrarian pioneers who attempted to steer us away from our sometimes fatal romance with agricultural carbohydrates. But to understand the origins of low carbohydrate metabolism and to appreciate how deeply it is rooted in our basic human physiology, we need to go back hundreds of thousands of years, if not a million or two. ...

... And while that original African ancestral group may have developed in a tropical environment where fruit and tubers could be foraged year-round, our ability as humans to migrate into barren or temperate regions depended upon our ability to survive prolonged periods of fasting, and to adapt to hunting and gathering of less carbohydrate-rich fare. And eventually, this evoked tolerance of a low carbohydrate diet allowed some humans to become highly specialized hunters and herders, living as mobile cultures in rhythm with the animals that fed them. Recent examples of these low carbohydrate nomadic cultures were the Masai herdsmen in Central Africa[6], the Bison People of the North American Great Plains[7], and the Inuit in the Arctic[8].

But long before these last low carbohydrate cultures were finally suppressed by the agricultural imperative, much of the world's populace subsisted (if not thrived) on continuous or intermittent carbohydrate restriction. For example, agricultural carbohydrates such as wheat and rye did not come north of the Alps until brought by the Romans after the time of Christ. The Irish, Scandinavians, and Russians had no agricultural carbohydrates suitable to their climate until the potato emigrated to Europe from the Andes in the 16th century AD. What this means is that many of our ancestors had little exposure to high proportions of dietary carbohydrate until 1-2 thousand years ago; and for many aboriginal cultures, their choice of a low carbohydrate lifestyle persisted to within the last few hundred years.

Now fast forward to the present. The United States is currently re-assessing a 3-decade, uncontrolled experiment in which carbohydrates were lauded and fats demonized. Concurrently we have become one of the most obese countries in the world. And across the globe, tragically, indigenous peoples with historically low carbohydrate intakes now have extremely high prevalence rates of obesity and type-2 diabetes (e.g., the Gulf States in the Middle East, Pacific Islanders, First Nations in Canada, and Australian Aborigines).

What these observations suggest is that for many humans, from an evolutionary perspective, a high carbohydrate diet is a metabolic challenge that some find difficult as early as adolescence and many fail to meet in the middle years of life. Equally apparent is that these negative effects of a high carbohydrate intake can be forestalled or reduced by vigorous exercise, high intakes of micronutrients and/or fiber from vegetables and fruit, avoidance of simple sugars, and constant energy restriction. For many of us with severe obesity, metabolic syndrome, or overt type-2 diabetes, however, these 'healthy lifestyle' choices are not enough to fully counteract the negative effects of a substantial contribution of carbohydrate to our daily energy intake.

This condition, in which a collection of diseases characterized by insulin resistance are driven by consumption of a single nutrient class, deserves to be identified as "carbohydrate intolerance". And as with other single nutrient intolerances (e.g. lactose, gluten, fructose), the preferred intervention is to reduce one's dietary intake below the threshold level that produces symptoms.

What Does "Low Carbohydrate" Mean?

There are two ways to define the threshold below which you are eating a "low carbohydrate" diet. The first is defined by what you as an individual perceive - it is that level of carbohydrate intake (be it 25 grams per day or 125 grams per day) below which your signs and symptoms of carbohydrate intolerance resolve. At one end of this experiential range, someone with early signs of metabolic syndrome (e.g., high serum triglycerides and 10 extra pounds around the middle) might permanently banish these harbingers of ill-health by holding total dietary carbohydrate in the range of 100-125 grams per day.

At the other end of this spectrum might be a type-2 diabetic who, on a "balanced
diet" providing 300 grams per day of carbohydrates, requires 2 shots of insulin plus two other oral drugs to keep fasting glucose values even marginally controlled under 150 mg/dl. For this person to achieve an optimum initial response that allows reduction (and hopefully withdrawal) of diabetic medications, clinical experience has shown that holding dietary carbohydrate at 20-to-25 grams per day is often necessary. For many type-2 diabetics, few weeks at this level allows them to reduce or stop both insulin and oral medication while at the same time achieving better overall glucose control. A few months later, following substantial weight loss, some individuals might be able to increase daily carbohydrate intake above 50 grams per day and still maintain excellent glucose control, wheres others might need to remain below the 50 gram level to keep their type-2 diabetes in complete remission.

In either case, whether it is able to lose weight and keep it off, or putting a frank case of type-2 diabetes into remission, how much you choose to limit your dietary carbohydrate intake should be driven by your personal experience. As a result, the amount of carbohydrate that you decide to eat might vary considerably depending on your individual metabolic condition and the level of benefit you wish to derive.

Defining 'Nutritional Ketosis'

The second way to define 'low carbohydrate' is physiologic - specifically that level below which there is a fundamental shift in your body's fuel homeostasis (i.e. energy regulation) away from glucose as a primary fuel. This shift is the adaptation of the body's hormonal set and inter-organ fuel exchange to allow most of your daily energy needs to be met by fat, either directly as fatty acids or indirectly as ketone bodies made from fat. This process, which is discussed more fully in Chapter 7, begins for most adults when total carbohydrate is restricted to less than 60 grams per day along with a moderate intake of protein. After a few weeks at this level, the primary serum 'ketone' (beta-hydroxybutyrate or B-OHB) rises above 0.5 millimolar (mM). At this ketone level, which is 10-fold higher than that in someone with a daily intake of 300 grams of carbohydrate, the brain begins to derive a substantial portion of its energy needs from B-OHB, resulting in a commensurate reduced need in glucose. ...

Utility and Sustainability of Carbohydrate Restriction

Up until 150 years ago, the apparent motivation for humans to eat a low carbohydrate diet was because that was what their regional environment provided. For example, absent wild orchards and fields of waving grain, the Inuit had little choice other than meat and fat from the arctic tundra and the sea. However, some cultures with long experience and apparent choice attempted to actively defend their low carbohydrate lifestyle. Examples of this included Bison People of the North American Great Plains, who maintained their nomadic existence until the bison were virtually exterminated, and the Masai of East Africa who still avoided vegetable foods (against the vigorous advise of the British) into the 1930s. Manifestly, for these cultures, not only were their low carbohydrate dietary practices sustainable - allowing them to survive and reproduce for hundreds of generations under difficult environmental conditions - the regarded their diet of animal products as preferable to an agricultural lifestyle, despite the latter having been available to them.

In the 1920's carbohydrate restriction was employed in mainstream medical practice in the management of diabetes and in the treatment of seizures. In both these clinical situations, as there was no other effective treatment, these interventions were sustained by individual patients for years. With the advent of insulin for diabetes and anti-seizure drugs like diphenyl-hydantoin (Dilantin), these dietary interventions began to fall out of favor. However now that the practical limits and side effects of modern pharmaceutical therapy are
becoming recognized, the wheel may be again turning.


...

Recent and Future Research

The last decade has seen a dramatic increase in the volume of research publication on the topic of carbohydrate restriction. Multiple randomized, controlled trials (RCTs) have been performed comparing a variety of other diets to carbohydrate restriction. Many of these have demonstrated clear advantages in favor of low carbohydrate and ketogenic diets. ...

Getting a low carbohydrate diet "right" is not as simple as just avoiding sugars and starches. One has to decide how much and what sources of protein and fats to seek out. ...

The reason we should be motivated to undertake this effort is the inescapable conclusion that the dietary path down which industrialized cultures have wandered in the last century is clearly not leading us to health and wellbeing. And to better understand where we should be going, perhaps it would be helpful to thoughtfully examine where we have been. ...

...Such individuals included George Catlin among the Plains Indian[7], John Rae, Frederick Schwatka[10],and Vilhjalmur Stefansson among the Inuit[8], plus John Orr and J.L. Gilks among the Masai[6]

All of these observers comment on the esteem that hunting and herding peoples had for fat. ...

Putting His Life on the Line: Stefansson's Inuit Diet Experiment

In 1907, a Harvard-trained Canadian anthropologist went into the Canadian Arctic to study the Inuit culture. Whether by chance or design, he spent his first Arctic winter living among the native people of the region without any external food supply. Eight months later, he emerged speaking their language and empowered by the fact that he could live well off the available food of the region.
A decade later, Vilhjalmur Stefansson left the Arctic, having traveled where no person of European origin had gone before, sometimes for two years without any resupply. Upon his return to 'civilization', he wrote copiously about his experience among 'The People' (which is what "Inuit" means in their language).
Unfortunately for Stefansson, the decade between 1915 and 1925 was the era of vitamin discovery -the period in which scientific nutrition hit its stride. Suddenly, we had scientists to tell us what was good for us, replacing grandmothers and cultural wisdom. And scientists now said that all humans needed fruit and vegetables to prevent deficiency diseases like scurvy and beriberi.
To the newly-minted nutritionists of the 1920s, Stefansson became the proverbial buck wearing a bulls-eye. To salvage his reputation, he consented (along with an Arctic explorer colleague) to reproduce his Inuit diet under continuous observation in Bellevue Hospital in New York City. After a year, he and his colleague emerged hale and hearty, much to the disappointment of the scientists in charge.

What Stefansson's experience (and many other subsequent studies) demonstrated was that dietary carbohydrate is nutritionally superfluous in the context of a well-formulated low carbohydrate diet. ...

...we should not confuse our body's ability to maintain a normal blood glucose with our dietary carbohydrate intake. When humans are adapted to a low carbohydrate diet, blood sugar levels and one's carbohydrate intake are completely independent of one another. In fact, keto-adapted humans maintain better glucose levels across feeding, fasting, and extremes of exercise than when fed a low fat, high carbohydrate diet[23, 27]. ...


SIDEBAR - Fructose -a sugar that partitions like fat.

Most of the fructose we eat, whether as sucrose (table sugar), high fructose corn sweetener, or in natural fruits and fruit juice gets made into fat by our liver. This is because our body can't convert fructose to glucose, and the first step in cellular fructose metabolism diverts it away from the primary pathway of glucose metabolism (the MyerhoffEmbden pathway). Thus these two 6-carbon sugars, fructose and glucose, follow separate metabolic paths. In the case of fructose, it is cleaved into two 3-carbon fragments, both of which primarily contribute to fat production (lipogenesis) in the liver. ...

Energy in Foods -Fat

Most fats we get from foods are triglycerides, consisting of a glycerol "backbone" with 3 fatty acid molecules attached. An additional class of dietary fat, coming from the membranes of plants and animal, is phospholipids, which tend to be higher in essential fatty acids. Both triglycerides and phospholipids can be metabolized (burned) for energy, and they provide about 9 Calories per gram. And because many dietary fats and oils contain little or no water, fatty foods tend to be pretty energy dense (e.g., a cup of butter, olive oil, or lard contains 1600-1800 kcal).

Because fats do not dissolve in water, they are carried in the bloodstream as triglyceride droplets surrounded by emulsifying molecules like phospholipids, cholesterol, and proteins. These particles are called lipoproteins, and they are subject to much loathing because they contain cholesterol. In reality, these lipoproteins are like trucks loaded with energy traveling about in the bloodstream delivering fuel to cells. All lipoproteins contain cholesterol, and their cholesterol contents may be labeled "bad" or "good" depending on where these lipoproteins are formed and where they tend to end up. It is a simple but underappreciated fact that without cholesterol, there could be no lipoproteins, and we'd be hard pressed for an alternative method to distribute fats and fat soluble nutrients to our cells for structure and energy.

At anyone point in time in a healthy person, there is more energy as fat in the circulation than as glucose, and its exchange in and out of storage in fat cells and in the liver is every bit as dynamic and important as is glucose. In another similarity to glucose, fat is also taken up by muscles for both immediate use as well as for storage. Fat storage droplets in muscle serve as reserve fuel to support exercise (just like glycogen), dropping to low levels after prolonged exercise and building back up over the next day or two of recovery.

In addition to their role as the body's primary fuel source when insulin levels are restrained, dietary fats also contain two 'families' of essential fatty acids. Identified by their uniquely positioned double (unsaturated) bonds called omega-3 and omega-6, these two classes of fatty acids serve a wide variety of structural and signaling functions throughout the body. And because their unique structures cannot be created by human metabolism, these two classes of essential fats must be consumed from dietary sources. The metabolism of these essential fatty acids is profoundly changed in the context of carbohydrate restriction, and the implications of this for intake guidelines will be discussed in Chapter 9. ...

The primary reason we have an entire chapter about insulin resistance is that well-formulated low carbohydrate diets consistently make it better. This benefit isn't limited to just the early phase of a low carb diet when energy intake is reduced. The improved insulin sensitivity persists for months and years into carbohydrate restriction when weight loss has ceased and most of an individual's dietary energy is coming from fat. ...


Carbohydrate Increases Insulin

The primary stimulator of insulin release from the pancreas is dietary carbohydrate. In contrast, an equal amount of dietary energy as fat has virtually no effect on insulin levels. This may be obvious for educated individuals trained in nutrition and medicine, but it's worth emphasizing because it provides a theoretical construct for why a low carbohydrate diet works well in people with insulin resistance. If you consume a high carbohydrate diet, particularly one with a lot of rapidly digested sugars and refined starches, your body has an increased dependency on insulin to maintain normal metabolic homeostasis.

Specifically, the insulin released after a high carbohydrate meal is necessary to simultaneously inhibit glucose output from the liver and promote glucose uptake by skeletal muscle. Failure of insulin to perform either of these tasks, such as occurs in insulin resistance, will lead to elevated blood sugar (hyperglycemia). What this means is that when carbohydrate intake is high it puts an increased pressure on insulin to do its job effectively. If you're insulin sensitive, great -you can probably tolerate lots of carbohydrate and not run into metabolic problems. However, if insulin is struggling to perform its duties, increased consumption of carbohydrate just exacerbates an already broken system.

A low carbohydrate diet switches the body's fuel use to primarily fat. With that switch turned on, there's less need to regulate hepatic glucose output and markedly reduced surges in insulin release and glucose uptake. Thus, a low carbohydrate diet allows less dependence on insulin to maintain metabolic health. Stated another way, if we view insulin resistance as a condition of carbohydrate intolerance, dealing with dietary carbs becomes a burden, and reducing this burden allows the body to function more normally.
...

Insulin Resistance is a Hallmark of Metabolic Syndrome and Type-2 Diabetes

When diabetes was first characterized as a disease a couple of centuries ago, the diagnosis was based on the appearance of sugar in the urine. This occurs only when the blood sugar level gets so high that the kidneys can't recover all of the filtered glucose, letting some of it escape into the urine. ...

But insulin resistance does not develop suddenly, making yesterday's normal into today's type-2 diabetic. It is a slow and usually silent process occurring over years or decades. As insulin resistance develops, a number of physical and biochemical changes occur. The liver turns more blood sugar into fat so serum triglycerides go up. Fat cells spend more time in storage mode, so weight gain occurs, particularly around the center of the body, including inside the abdomen. Blood pressure also tends to rise above normal, and good (HDL) cholesterol levels go down. This combination of signs has been labeled 'metabolic syndrome', and some doctors call it pre-diabetes because a high proportion of people with 3 or more of these signs eventually develop full-blown type-2 diabetes. For more on metabolic syndrome, see Chapter 14.

Even before the signs of metabolic syndrome occur, the clever doctor/ detective can spot clues of impending diabetes. Before blood glucose and insulin start to rise; before serum triglycerides go up and HDL cholesterol goes down; before waistlines start to expand; two biomarkers of imminent trouble have been discovered. The first, a fatty acid called palmitoleic acid (POA), starts to rise in blood lipids, and it is a sign of increased conversion of carbohydrate into fat. POA is discussed in detail in Chapter 9 and also in Chapter 11. At this point, suffice it to say that an elevated level of POA in the blood is an early sign that one's body is struggling to handle whatever dose of carbohydrate is being consumed.

The second early harbinger of metabolic syndrome and type-2 diabetes is a locus of factors that we lump together under the heading 'inflammation'. Inflammation is part of what we sometimes call 'immunity' or 'host defense'. It is that complex mix of functions that our bodies use to defend against foreign substances and infections, and also how it stimulates the healing process after injury. We want inflammation levels to surge quickly when there is a threat, and retreat just as quickly when the threat is past.

About 20 years ago, it was noted that people with persistently high biomarkers of inflammation (e.g., CRP and IL-6) were at increased risk of heart attack[32, 33]. And then ten years ago this observation was extended to type-2 diabetes as well. This perspective has led us to regard inflammation as a potential underlying cause of insulin resistance and type-2 diabetes [34, 35]. Further, we now have evidence that insulin is associated with inflammation[36, 37], setting up a vicious cycle fueled by repeated ingestion of insulin-inducing carbohydrates. ...

Dietary Carbohydrate and Its Insulin Response as Stressors of Oxidative Metabolism

This is getting pretty esoteric, so we'll keep this section short. That said, however, there are some pretty interesting dots to connect here. Inflammation causes our cells (specifically our mitochondria) to increase production of molecules called 'free radicals'. Free radicals are like mini roadside bombs that interfere with normal cellular functions. So here are the dots we think can be connected: 1) dietary carbohydrate raises serum insulin; 2) insulin promotes inflammation in susceptible people; 3) inflammation increases cellular free radical generation; 4) free radicals attack any convenient nearby target; 5) ideal targets for free radicals are membrane polyunsaturated fats; 6) membrane polyunsaturated fats are important determinants of cellular function such as insulin sensitivity.

Membrane Polyunsaturated Fatty Acids and Insulin Sensitivity

In 1993, the New England Journal of Medicine published a study demonstrating that highly unsaturated fatty acids (HUFA; e.g., arachidonate and docosahexaenoate [DHA]) in muscle membrane phospholipids are tightly correlated with insulin sensitivity[38]. Specifically, this means that the more of these HUFAs there are in the muscle membrane, the more insulin sensitive the muscle. This observation subsequently has been corroborated and extended by multiple other studies. For example the significant correlation between muscle HUFA and insulin sensitivity was shown to be specific to the phosphatidylcholine phospholipids which predominate on the outer layer of the muscle membrane[39]. This is interesting from the perspective that it implies a role for the background fatty acid composition of the membrane per se, rather than the protein components inserted into it (like insulin receptors or glucose transporters). In other words, figuratively speaking, what the 'fabric' of the wall itself is made of is very important for glucose transport -it's not just about the number of switches (i.e. receptors and transporters) inserted in the wall.
How these HUFAs get into muscle membranes is a very complex process involving both diet composition and metabolism of the various essential fats after they are eaten. This process is discussed in detail in Chapter 9. For the purposes of this chapter, both dietary intakes of either the essential fatty acid precursors or their final products are important. However, there is increasing evidence that some individuals have impaired ability to convert essential fatty acid precursors into HUFA[40].

As a rule, HUFA are a bit less prone to be burned for fuel than shorter fatty acids, so on average the body tends to hang on to them. But there is another way that they can be destroyed besides being beta-oxidized (Le., burned for energy). As mentioned above, HUFA have lots of double bonds, and this makes them very susceptible to damage by oxygen free radicals (also called reactive oxygen species or ROS). The potential role of oxidative stress degrading membrane HUFA and thus promoting insulin resistance has yet to be fully explored, but it may be very relevant to this chapter. Here's why.

Low Carbohydrate Diets and Membrane HUFA

Twenty years ago, we published a couple of studies showing that very low calorie ketogenic diets raised the HUFA content in serum phospholipids (the building blocks for membranes)[41, 42]. The subjects for these studies started out pretty heavy and lost a lot of weight over a number of months. But after the weight loss diet was over, they went back to consuming more carbohydrate, and their HUFA levels went back down. [...]

Triglyceride as a Target

The reductionist focus on total LDL-C as the only valid therapeutic target has distracted us from the mounting evidence that other biomarkers may be better predictors of risk, especially if you (or your patient) have insulin resistance. If LDL-C is not the most relevant target for many people, what is? Many studies have reported that an elevated fasting plasma triglyceride level is an independent risk factor for heart disease. If you have high triglycerides after an overnight fast, there is a good chance you also have elevated postprandial lipemia (an exaggerated and prolonged increase in plasma triglycerides after a meal).

Abnormal postprandial lipemia is the driving force behind the dyslipidemia of the atherogenic lipoprotein phenotype (ALP). ALP is a term frequently used to describe a clustering of pro-atherogenic lipoprotein abnormalities including moderately increased fasting triglycerides (150 to 500 mg/dL), exaggerated postprandial lipemia, decreased HDL-C <40 mg/dL), and a predominance of atherogenic small dense LDL particles (pattern B).

These lipid disorders have also been referred to as the 'lipid triad' or 'atherogenic dyslipidemia: The prevalence of ALP varies depending on the criteria used (i.e., triglyceride, HDL level, or LDL size). When defined as peak LDL particle diameter <25.5 nm, ALP has been estimated at a prevalence of 30-35% in middle-aged men in the United States. So what makes having high post-prandial triglycerides harmful? Increased hepatic triglyceride production precipitates formation of highly atherogenic small LDL particles and a reduction in HDL cholesterol, all of which indicate a causal role for elevated triglycerides in the pathogenesis and progression of heart disease.

Carbohydrate is the Major Driver of Plasma Triglycerides

An increase in fasting triglyceride levels is an early signal that your body is struggling to metabolize carbohydrate. Therefore the weapon of choice for managing elevated triglyceride levels is carbohydrate restriction. ...

How then does a person with insulin resistance deal with a high carbohydrate meal? Whereas the conversion of glucose to glycogen is self-limiting, there is an almost unlimited capacity to convert carbohydrate to fat (aka, de novo lipogenesis). The fatty acids derived from carbohydrate-induced hepatic de novo lipogenesis are made into triglycerides, packaged into large VLDL particles, which then released into the circulation contributing to elevated plasma triglycerides. Alternatively, if they are not released from the liver, these triglycerides can build up to cause fatty liver (hepatic steatosis). ...


The Polyunsaturated Fatty Acid Response to Carbohydrate Restriction

Most serious scientists avoid the topic of polyunsaturated fatty acid (PUFA) metabolism like a plague. Why? Because it's a tangle of obscure names and symbols, parallel metabolic pathways, and positional isomers with conflicting functions. And besides, there are so many of them! In a single serum fraction, we typically identify about 20 different fatty acids with two or more double bonds (the definition of a polyunsaturate) belonging to 3 different metabolically distinct families (for details, see post-script below).

So again, it is fair to ask, what's the upside of opening this metabolic can of worms? The answer, simply, is that the dramatic changes in PUFA associated with adapting to a low carbohydrate diet can help explain the underlying physiology of its benefits.

First, we'll offer you an overview of why that might be. Then we'll tell you how we stumbled into this understanding over the last 20 years.

Point 1. Low carbohydrate diets cause the physiologically important endproducts of essential fatty acid (EFA) metabolism in membranes to go up sharply[29, 41, 42]. EFA end-products in muscle membranes are positively correlated with insulin sensitivity[38]. Thus these membrane composition changes can explain the improved insulin sensitivity that occurs when an insulin resistant individual adopts a low carbohydrate diet.

Point 2. Increased EFA end-products in liver membranes shut down expression ofthe enzymes that drive lipogenesis[72]. The consensus experts assume that human lipogenesis is inconsequential, however, they see no reason to explain how it stops when dietary carbs are reduced. But from the perspective offered by POA, something clearly puts the brakes on lipogenesis when a person transitions to a low carbohydrate diet, and our observation of increased EFA end-products offers an elegant mechanism. In addition, this helps explain the dramatic reduction in serum triglycerides that we see in individuals with metabolic syndrome who go on a low carbohydrate diet.

Point 3. A simple explanation for increased EFA end-products might be that the body makes more of them on a low carb diet. But unfortunately it isn't that simple. All of the data (levels of metabolic intermediates and enzyme activities) point in the opposite direction -that production of EFA end-products goes down! So if they go up without more being made, this indicates that the body must be destroying them more slowly. And since the arch-enemy of PUFA is a group of molecules we call free-radicals (or more precisely, reactive oxygen species - ROS), perhaps the rate of ROS generation is reduced when dietary carbohydrates are restricted. {**This is in fact established in many studies posted in the Ketogenic Diet, Life Without Bread and other threads on the forum - more ATP is produced in fat burning mode and less ROS compared to glucose metabolism (AKA sugar burning mode)**} The mainstream consensus still regards this as an 'outside the box' (or should we say "radical") fantasy, but it is also consistent 'with our multiple observations that a host of biomarkers of inflammation (known inducers of ROS generation) go down when a low carb diet is adopted[29].

So there you have it. It's really kind of elegant. Inflammation driven by the forced metabolism of carbohydrate drives up the production of ROS in mitochondria. ROS damage membrane EFA end-products, which at some point can't be replaced fast enough. The resultant reduction in membrane EFA end-products unleashes the genes (e.g. fatty acid synthase) that control liver lipogenesis, and at the same time the loss of membrane HUFA causes increased insulin resistance in muscles. Insulin resistant muscles take up less glucose, resulting in more of it being diverted to the liver for lipogenesis. Take away the high levels of ROS and membranes suffer less damage, their content of EFA end-products rises, and both dyslipidemia and insulin resistance improve. The trigger for this set of metabolic dominos -the switch that controls this process -is dietary carbohydrate.

Summary

Clearly there is much more to dietary fats and health than is contained in simplistic edicts like "saturated fats are bad for you': We have shown you that our bodies respond to saturated fats very differently when we are keto-adapted, such that they are rapidly burned for fuel rather than being stored. By contrast, people eating higher levels of dietary carbohydrates, even when they are not over-eating total calories, have higher blood levels of saturated fats. As illustrated by the elevated levels of POA associated with higher proportions of dietary carbohydrate, some individuals are particularly prone to dispose of dietary carbohydrates via lipogenesis, which creates a lot of saturated fatty acids as well as POA.

The other new and important insight into the fatty acid response to carbohydrate restriction comes from examining the changes in EFA endproducts in phospholipids. Keto-adaptation results in marked changes in how our bodies are able to construct and maintain optimum membrane composition, and this appears to be due to less production of ROS and inflammatory mediators. There is much more for us to learn about this process, but at the very least, this observation helps explain the improvement in insulin sensitivity that occurs when you become keto-adapted. [...]

Why We Respond More Acutely to Carbohydrate than to Fat Intake

Depending on dose and timing of dietary carbohydrate, blood glucose can exhibit large and rapid excursions. However failure to maintain an adequate supply of glucose can have dire consequences; thus our bodies ardently defended a minimum blood glucose level. Falling below this minimum (in the absence of blood ketones) triggers prompt physiological responses to maintain glucose levels necessary for brain. In contradistinction, blood fat levels (either as triglycerides or free fatty acids) are neither sensed nor monitored to the same degree or in the same way as glucose. The need to sense fatty acid levels is not as vital for minute-to-minute functioning. ...


From the Chapter on METABOLIC SYNDROME

As the definitions imply, metabolic syndrome describes a collection of metabolic abnormalities. These derangements in combination are a harbinger of type 2 diabetes and cardiovascular disease. With any collection of symptoms, a good scientific detective asks whether there is a common cause. In the case of metabolic syndrome the common thread linking an ever growing constellation of abnormalities is insulin resistance. Insulin resistance is defined as a diminished response to a given concentration of insulin. While insulin resistance may be doing the dirty work at the cellular level, the ringleader of the metabolic syndrome crime syndicate is dietary carbohydrate. Since the inability to properly metabolize dietary carbohydrate is the direct result when insulin action is impaired, from a functional perspective, insulin resistance can be more accurately described as carbohydrate intolerance. When viewed in this context, carbohydrate restriction is a fully rational approach to treating the diverse factors that congregate in metabolic syndrome. Restricting carbohydrate is akin to arresting the crime boss -once you put the correct perpetrator in jail, everything else falls into place.

Syndrome X, Insulin Resistance Syndrome, and Metabolic Syndrome
Dr. Gerald Reaven is generally credited with making the observation that individuals with insulin resistance (as evidenced by hyperinsulinemia) showed common metabolic disturbances that significantly increased their risk of cardiovascular disease. In 1988 he termed this locus of symptoms 'syndrome X' [4]. Later he used the term 'insulin resistance syndrome: which more accurately reflected the underlying metabolic problem. The related term 'metabolic syndrome' was introduced by the Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program. Reaven viewed the metabolic syndrome as a diagnostic tool to identify people at increased cardiovascular disease (CVD) risk based on the presence of specific criteria (see side bar). Regardless of the term used, the presence of insulin resistance is accepted as the underlying physiologic construct. Interestingly, Reaven recognized that the favored diet of the time -a low fat/high carbohydrate diet -would exacerbate the syndrome. This was self-evident from the title of his 1997 review paper[ 104J entitled "Do high carbohydrate diets prevent the development or attenuate the manifestations (or both) of syndrome X? A viewpoint strongly against". Reaven was cognizant that " .. .low fat/high carbohydrate diets should be avoided in the treatment of syndrome X.", but few took heed of such warnings amidst the tsunami-like forces advocating in favor of fat restriction.

Metabolic Syndrome Defined[105]

• You have metabolic syndrome if at least three of the following are present:

• Waist circumference: ~40 inches (men) or ~35 inches (women)

• Fasting triglycerides: ~150 mg/dL

• HDL-C: <40 mg/dL (men) or <50 mg/dL (women)

• Blood pressure: ~130/85 mm Hg or use of hypertensive medication

• Fasting glucose: ~1 00 mg/dL or use of hyperglycemia medication

[...]

Carbohydrate Restriction -The Elephant in the Room

Over the last 20 years there have been tens-of-thousands of studies, review papers, and international scientific conferences focused on metabolic syndrome. How often can the words carbohydrate restriction be found in the thousands of peer-reviewed papers on metabolic syndrome? How often are these words uttered by researchers/clinicians at seminars about innovative treatment options for metabolic syndrome? Truthfully? Hardly ever!
[...]
 

Laura

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Hyperinsulinism runs in my family. It's pretty nasty. If I eat carbs for a period of time (not exclusively, just normally), usually about two weeks, I start having severe hypoglycemia as a result of the hyperinsulinism. That usually results in an episode of insulin shock. This is a very bad thing. I have learned through my life that eating carbs in what would be called a normal way always ends in this result. The only thing that prevents it is avoidance of carbs as much as possible or, at the very least, only "slow carbs". I can get away with playing around a little but I can tell when I start skating on thin ice by the way I feel.

So, anybody trying to tell me that sugars are okay - or even good - just isn't going to win points. I've lived with this 64 years now, watched elder members of my family suffer with it and now, a younger generation: my own children. I've said it before, I think that some people who are really sensitive to some things are like canaries in a mine. The carbs may not bother some people for a very long time, but one day that silent but deadly heart attack or stroke will get them. There is no such thing as an essential carbohydrate. Yeah, some slow carbs are helpful because epigenetics has made it so, and we can survive on what is less than optimal, but who wants less than optimal?
 

Oxajil

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I also don't respond too well on carbs, and I have to be careful about them. In my case, (most) fruits are the worst.

Keyhole said:
the experiments of Bernardo Houssay (1947 Nobel laureate) in the 1940s, in which sugar and coconut oil protected against diabetes, [...]

In Houssay's experiments, sugar, protein, and coconut oil protected mice against developing diabetes.
Here's the thing though, if sugar helped protect against diabetes in rats, it can't be said that it will have the same effect in humans (or something to that effect). I don't think his experiments as mentioned above can give insight into how humans would react to fats, sugar, etc. See this article by Nora Gedgaudas, where she writes:

Even if the diet fed to these mice in the Melbourne study consisted of actual food, mice are largely herbivorous creatures (read: naturally eat a high carb diet) and are poorly equipped to make much use of significant dietary fat. Dr. John Briffa wrote an excellent article titled, “Why Human, Not Mice, Studies are the Most Appropriate for Judging the Effects of Diet on Human Health” following a similarly ridiculous mouse study a few years ago.

In it he points put that “these researchers chose an inappropriate animal model to test their theory on, and then fed the animals an inappropriate diet to boot. These actions suggest that the researchers were doing what they could to design an experiment to produce a desired outcome.”
Quickly going through Houssay's paper, though, I didn't notice him trying to link his findings to people. As far as I understand from his paper, he was clear that this experiment says something about how the rats reacted. However Dr Ray Peat is using his experiments as a reference to support her view that "the dietetic obsession with sugar in relation to diabetes has been a dangerous diversion", and that's not really credible, as I assume she refers to people. FWIW.
 

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Nienna

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Laura said:
Hyperinsulinism runs in my family. It's pretty nasty. If I eat carbs for a period of time (not exclusively, just normally), usually about two weeks, I start having severe hypoglycemia as a result of the hyperinsulinism. That usually results in an episode of insulin shock. This is a very bad thing. I have learned through my life that eating carbs in what would be called a normal way always ends in this result. The only thing that prevents it is avoidance of carbs as much as possible or, at the very least, only "slow carbs". I can get away with playing around a little but I can tell when I start skating on thin ice by the way I feel.

So, anybody trying to tell me that sugars are okay - or even good - just isn't going to win points. I've lived with this 64 years now, watched elder members of my family suffer with it and now, a younger generation: my own children. I've said it before, I think that some people who are really sensitive to some things are like canaries in a mine. The carbs may not bother some people for a very long time, but one day that silent but deadly heart attack or stroke will get them. There is no such thing as an essential carbohydrate. Yeah, some slow carbs are helpful because epigenetics has made it so, and we can survive on what is less than optimal, but who wants less than optimal?
Thank you for that, Laura. I thought, maybe, I had wandered into bizarro world. I don't feel good when eating more than a few carbs. My back becomes inflamed sooner than any other indicators.

It makes me wonder if Big-Ag/Big Food are trying to get things back to people eating a lot of carbs again for their profit margin by having research come out in their favor?
 

Keyhole

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SeekinTruth, the points you bring up here do not necessarily conflict with the information Ray Peat presents. They are simply approaching the topic from a different angle. I believe that both arguments are equally as valid, but what is missing here is an examination of details with an approach which factors in information and places it in environmental context. Has anyone considered the possibility that poly-unsaturated fats (not carbohydrates) are the environmental trigger for insulin resistance - as an evolutionary survival mechanism? Let me explain further

The northern and southern hemispheres experience harsh winters. Low-carbohydrate/Ketogenesis is the way in which animals survive these periods. A ketogenic metabolism produces more ATP per amount of substrate and burns it slowly and steadily. This is clearly to preserve energy stores when there is little substrate available in the environment. This considered, it would be fatal to increase metabolic rates and run through all energy reserves via glucose metabolism. Nature’s answer to living in long, dark, cold winters is to preserve all energy through burning energy slowly and more efficiently.

Twenty years ago, we published a couple of studies showing that very low calorie ketogenic diets raised the HUFA content in serum phospholipids (the building blocks for membranes)[41, 42]. The subjects for these studies started out pretty heavy and lost a lot of weight over a number of months. But after the weight loss diet was over, they went back to consuming more carbohydrate, and their HUFA levels went back down. [...]
Let’s examine this extremely relevant and important piece of information. The degree by which a membrane’s fatty acids are saturated is dependent upon two things it seems:1.temperature/light/environment and 2.diet. Both of which act as information for the body system. It is well known that mammalian cell membrane fatty acid composition changes to a more unsaturated state just before entering hibernation:

During mammalian hibernation, cellular membranes continue to function at temperatures approaching 0 C. The molecular mechanisms that confer this capacity to the membranes are unknown but may be related to the fluidity of the membrane and to the level of unsaturated fatty acids. The basic tenets of membrane fluidity and the contribution of cholesterol, polar head groups, and fatty acids toward maintaining a fluid membrane in a liquid-crystalline state are examined in this review. It is shown that although unsaturated fatty acids can enhance membrane fluidity at low temperatures, there does not appear to be a consistent trend toward increased levels of unsatruated fatty acids during hibernation in all tissues of hibernators. Consequently, there may be some other role for the alterations in the composition of membrane fatty acids found during the hibernating cycle other than increasing membrane fluidity to permit continued activity at reduced temperatures.
link:https://www.ncbi.nlm.nih.gov/pubmed/6998741
After hibernation, the fatty acid composition of membranes changes again to saturated fatty acids. The same is seen in fish, fish living in cold water have less saturated fats, whereas fish living in warm waters have a higher degree of saturated fats. Again, the same cycle is seen in chill resistant plants.

What is the function of unsaturation here? Researchers speculate that maintaining fluidity in cold temperatures may be reason for this. Michael Crawford speculates whether unsaturated fatty acids (specifically DHA) has the ability to capture photons to compensate for the lack of seasonal light in winter.

Either way, we see from the above research that both temperature/light and food (actually, lack of food) exerts an influence on the body and provides information regarding the external environment. Cold environments and low carbohydrate diets seem to contain this information.

This sends the signal that substrate is scarce, that the body must revert to a slower, more efficient metabolism for a period (winter), and to make the necessary structural alterations to survive (one example is to change the degree of saturated fats in cell membranes). Naturally, winter is a period in which less-energy is expended and overall activity is drastically reduced for most organisms.

All life on either side of the hemisphere exhibits fluctuations between high levels of activity and low levels of activity. We call this Spring/Summer and Autumn/Winter.

If we look at this from a biochemical level, winter is a less stressful state for our physiology. As you stated:
but to get over insulin resistance and other hormone/metabolism issues, as well as neuro-protective and least ROS generation approach is consistently shown to be low carb/ketogenic diets - the overwhelming amount the evidence shows this.
Ketogenic metabolism produces less Reactive Oxygen Species in the mitochondria, thereby produces a less stressful internal environment. Hence, antioxidants are required in significantly less quantities and anti-stress factors are not required. Jack Kruse has numerous pieces of evidence supporting the existence of an evolutionary pathway that is common to all mammals, called the “leptin-melanocortin pathway”. Overall, it is a mechanism by which the body survives through the winter.

So, where does insulin-resistance fit into this?

Let’s consider that animals such as the grizzly bear enter into a period of physiological insulin-resistance in preparation for hibernation. This is not considered to be a disease, but is actually the only way that they manage to survive:
As an alternative approach, we explored hibernation where obesity is a natural adaptation to survive months of fasting. Here we report that grizzly bears exhibit seasonal tripartite insulin responsiveness such that obese animals augment insulin sensitivity but only weeks later enter hibernation-specific insulin resistance (IR) and subsequently reinitiate responsiveness upon awakening. Preparation for hibernation is characterized by adiposity coupled to increased insulin sensitivity via modified PTEN/AKT signaling specifically in adipose tissue, suggesting a state of "healthy" obesity analogous to humans with PTEN haploinsufficiency. Collectively, we show that bears reversibly cope with homeostatic perturbations considered detrimental to humans and describe a mechanism whereby IR functions not as a late-stage metabolic adaptation to obesity, but rather a gatekeeper of the fed-fasting transition.
Basically, what this suggests is that insulin resistance is a tool that animals use to accumulate excess fat tissue, so that they have enough energy to be able to revert to a ketogenic metabolism and survive while hibernating. Note that these animals become insulin-sensitive when they come out of hibernation in time for spring.

So with this information in mind, let’s question what the trigger is that initiates this state of insulin resistance? Recall that, both animals and plants naturally alter their cell membranes in response to environmental influences: light, temperature, and food. In lower light cycles and colder temperatures, polyunsaturated fats become abundant. Also consider that in the context of the grizzly bear, the cold-water salmon-run occurs in Autumn, in preparation for winter.

What does this essentially mean? It means that poly unsaturated fatty acids are environmental signals that winter is coming, and all that comes with it! (low metabolic rate, lowered immunity, lowered state of physiological stress).

It also means that Polyunsaturated fats cause insulin resistance as designed by nature.
This is something that Peat cites in numerous studies, and provides adequate biochemical explanation for. Let’s not forget that the mass-distribution and consumption of vegetable oils was pretty much at the same time that carbohydrate consumption increased. But carbohydrates seem to have taken the blame for all of man's ills. Peat argues for the benefit of saturated fats, but just not a state of low-carb ketosis.

Considering the information cited earlier about low-carb diets inducing phospholipid fatty acid changes to unsaturated fats, what does this suggest about the information contained within that dietary template? When we review all of this in an environmental context, it seems clear that ketosis represents a semi-hibernation state that is not suited to a high-activity-level metabolically-stressful environment. It’s clinical application is undisputed for conditions such as diabetes. But is this surprising? If insulin resistance is a pre-hibernation state, then ketosis is nature’s answer for reversing insulin resistance.
Similarly, it can be used successfully for obesity and many other specific diseases. But as a long-term solution for average people? This is questionable.

We live in a stressful environment, in heated houses, with artificial light on all year round. This is essentially summer, 24/7. Peat’s delves further into how he views sugar as an “anti-stress molecule” which is suited to high stress (summer) environments. He also explains that glucose metabolism produces much more Co2, which also acts as an “anti-stress molecule”. These are to protect against the stresses of high-activity-level environments. He also cites extensive evidence to support his conclusions.

Laura said:
Hyperinsulinism runs in my family. It's pretty nasty. If I eat carbs for a period of time (not exclusively, just normally), usually about two weeks, I start having severe hypoglycemia as a result of the hyperinsulinism. That usually results in an episode of insulin shock. This is a very bad thing. I have learned through my life that eating carbs in what would be called a normal way always ends in this result. The only thing that prevents it is avoidance of carbs as much as possible or, at the very least, only "slow carbs". I can get away with playing around a little but I can tell when I start skating on thin ice by the way I feel.

So, anybody trying to tell me that sugars are okay - or even good - just isn't going to win points. I've lived with this 64 years now, watched elder members of my family suffer with it and now, a younger generation: my own children. I've said it before, I think that some people who are really sensitive to some things are like canaries in a mine. The carbs may not bother some people for a very long time, but one day that silent but deadly heart attack or stroke will get them. There is no such thing as an essential carbohydrate. Yeah, some slow carbs are helpful because epigenetics has made it so, and we can survive on what is less than optimal, but who wants less than optimal?
With all due respect, Laura, this is your individual circumstance. Similar for others who suffer from long-term health conditions and probably benefit from low-carb template. However, this doesn't apply to everyone. So to say that sugar is "bad" is pretty black and white IMO. I also wonder whether the consumption of PUFA's like fish oil may also contribute to the issues in some case which are attributed to sugar.

Oxajil said:
I also don't respond too well on carbs, and I have to be careful about them. In my case, (most) fruits are the worst.
FWIW, maybe some people simply don't get on well with it for whatever reason. It is probably multi-faceted. But it certainly not as simple as saying that fruit and sugars are detrimental as a rule.

Oxajil said:
Quickly going through Houssay's paper, though, I didn't notice him trying to link his findings to people. As far as I understand from his paper, he was clear that this experiment says something about how the rats reacted. However Dr Ray Peat is using his experiments as a reference to support her view that "the dietetic obsession with sugar in relation to diabetes has been a dangerous diversion", and that's not really credible, as I assume she refers to people. FWIW.
The reference list can be found at the bottom of the page, and it is pretty extensive. From what I could find, there were plenty of human studies in the list. On the topic of studying rats, I agree with the point made. All things considered though, many of the biochemical studies could not be done on humans because it would be seen as unethical. So, whether we can transfer the results or not, I'm not sure.
 

hlat

The Living Force
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Keyhole said:
Oxajil said:
Quickly going through Houssay's paper, though, I didn't notice him trying to link his findings to people. As far as I understand from his paper, he was clear that this experiment says something about how the rats reacted. However Dr Ray Peat is using his experiments as a reference to support her view that "the dietetic obsession with sugar in relation to diabetes has been a dangerous diversion", and that's not really credible, as I assume she refers to people. FWIW.
The reference list can be found at the bottom of the page, and it is pretty extensive. From what I could find, there were plenty of human studies in the list. On the topic of studying rats, I agree with the point made. All things considered though, many of the biochemical studies could not be done on humans because it would be seen as unethical. So, whether we can transfer the results or not, I'm not sure.
I thought it was clear that animal testing results provide no information about humans?

The Health & Wellness Show: The Quackery and Cruelty of Animal Medical Research
https://www.sott.net/article/322259-The-Health-Wellness-Show-The-Quackery-and-Cruelty-of-Animal-Medical-Research
 

nicklebleu

The Living Force
FOTCM Member
hlat said:
I thought it was clear that animal testing results provide no information about humans?

The Health & Wellness Show: The Quackery and Cruelty of Animal Medical Research
https://www.sott.net/article/322259-The-Health-Wellness-Show-The-Quackery-and-Cruelty-of-Animal-Medical-Research
I think that this blanket statement cannot be accurate. Mammals all share certain aspects of genetic and metabolic functions and control.

The problem is to make sense of the correlation between animal and human organisms, which is admittedly very difficult. Modern science is developing techniques on a cellular level that may be more accurate than animal models, but only at the cellular level. When it comes to the interplay of cellular mechanisms with the overall control of these, there is no substitute for animal models as or yet.

I am not advocating animal tests nilly-willy as they are done nowadays, but if they are done with the right frame of mind, taking animal welfare seriously, in cases where there is no alternative, and not misused for propaganda purposes, as so often happens nowadays, it still might be something that needs to be done.

Anyway, my 2 centavos.
 

Laura

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I think that animal dietary studies can only be transferable to humans IF the animals in question naturally eat a more or less omnivorous diet with emphasis on meats/proteins.
 

Altair

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Nienna said:
It makes me wonder if Big-Ag/Big Food are trying to get things back to people eating a lot of carbs again for their profit margin by having research come out in their favor?
I have the same impression and I don't tolerate carbs, as well. I saw how type 1 diabetes was killing my grandma (she eventually died from it) and how my mother was suffering from type 2 diabetes until she switched to ketogenic diet which allowed her to drop all her medications.

So, I'm a bit skeptical about all this new "research".
 

Joe

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White, refined sugar = bad for me. Far too immediately bio available. I can handle some 'slow sugars' in carbs, but even then there's a pretty low tolerance. Trial and error goes a long way to determining what is right for an individual's body. In line with the Keyhole is saying, I don't see any point in trying to uncover 'research' that 'proves' that something is always good or bad for everyone. But put it this way, the individual responses of hundreds of people on this forum to cutting back on sugar and increasing dietary saturated animal fat is a testimony to the fact that more fat and less sugar IS, in a general sense, beneficial for many people.
 
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