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 source and references can be found hereGlycemia, starch, and sugar in context
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.
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.
“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.