"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."
You hear low-carbers freaking out about raising blood sugar because it causes glycation of proteins similar to what grilling does to a juicy steak. Of course, eating carbohydrates does not raise blood sugar significantly in a healthy person – and all the focus should be on restoring insulin sensitivity and not avoiding glucose. In fact, one person contacted me last week to share with me a dramatic lowering of blood glucose levels and complete conquering of pretty severe insulin resistance after quadrupling carbohydrate intake – a result of eating a high-starch, low polyunsaturated fat diet. Several years of low-carbing gave her extremely high insulin levels (14-18 iu/M), which dropped to 4.7 in four months of RRARF.
Anyway, that aside, Peat points out that polyunsaturated fatty acids are a much more major culprit in protein glycation than glucose. That rings true for me, as I reversed many signs of aging years ago on a high sugar diet, but seemed to age much more quickly during my years on a low-carb diet, which featured lots of high-PUFA pork, poultry, and total polyunsaturated fat intake (hard to avoid when eating 200-300 grams of fat per day).
"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."
Basically the polyunsaturated fats, because they are more heat, oxygen, and light sensitive – degrade much more quickly in the human body. Although certainly better, in the grand scheme of things it probably doesn’t matter if you eat your PUFA with a bunch of vitamins, minerals, and antioxidants or not. When tissues are comprised of polyunsaturated fats they will simply deteriorate and age you more quickly. That’s just how it goes. And because of the byproducts of their degradation, glucose metabolism is eventually impaired – leading to insulin resistance, metabolic syndrome, and type 2 diabetes.
"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."
Peat is very controversial when it comes to fish oil. While we know that there are countless anti-inflammatory benefits to mega-dosing fish oil in the short-term, Peat seems unfazed. He knows that the more fish oil you have in your tissues, the more quickly you will deteriorate. I think Peat would look at fish oil as a get-health-quick scheme that is a terrible long-term investment.
"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."
When I talk about polyunsaturated fat, I usually focus on the anti-metabolic effects of the fats. Peat’s research goes far beyond this to include the various ways they can do damage to tissues, blood vessels, and so forth.
"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."
Like I’ve said before, loading up the tissues with polyunsaturated fat is like giving a sniper a nuclear bomb to take out threats in which a simple long range rifle would have been sufficient. Collateral damage. Yes that's the name of an Arnold movie, and no his love of fairly unattractive maids cannot deter me from worshipping the Sperminator. I know Maria probably eats nothing but salad, and consequently has the sex drive of a panda. She knew what she was getting into. Arnold needs to be coming day and night! This video is even funnier given the recent fiASSco…
"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."
This translates to resting up and eating a high-carb, high-calorie, low-PUFA diet with a little added fat and protein and frequent feedings. It’s amazing what something so simple can do for glucose metabolism and subsequent health improvements that stem from an impairment in glucose metabolism.
"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."
The lack of glucose is one reason metabolism falls so sharply on low-carbohydrate diets, and why it takes a common root problem (hypothyroidism) and makes it worse. You can also see why having a higher metabolic rate would prevent insulin resistance and keep glucose oxidation firing on all cylinders. Type 2 diabetes could be described as an inability to use glucose properly, not a disease of consuming too much sugar. In fact, eating more carbohydrate improves the ability of your body to use glucose properly – generally-speaking.
"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."
The vendetta that the mainstream has against sodium could be very inappropriate considering the low metabolic rate of the masses. In fact, eating more salt and more carbohydrate could be a more appropriate recommendation to give to a hypothyroid population. When looking at the origins of many of our common diseases with an open mind as Peat and I have, a very different picture emerges.
"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."
Aside from his controversial statement about Houssay’s experiments, Peat is basically saying that human biology – and all mammalian biology with maybe the exception of hibernating animals that derive a massive benefit from the anti-metabolic polyunsaturated fats in autumn, favors saturated fats over polyunsaturated fats – or at the very least a high ratio of saturated to unsaturated fat. That is the case with virtually all mammalian milk and also the type of fats that are produced inside the body as well. While many adhere stubbornly to a simple-minded “if it’s natural it HAS to be good” philosophy, it could very well be that there are natural things that are more congruent, and natural things that are less congruent, with our general and individual physiological makeup. There can be better and worse options. Not all things are created equal.
"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."
In other words, polyunsaturated fats interfere with normal hormone action, including impairing the effectiveness of the thyroid hormones. This is significant, as you could have normal or even above-normal thyroid hormone production (or other hormones) and still be deficient at the cellular level.
"Unsaturated fatty acids activate the stress hormones, sugar restrains them."
That is the crux of Peat’s belief system right there.
"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)."
While Mark Sisson is calling excessive “fat metabolism” a paradigm shift – claiming it is superior, I don’t know if anything could convince me of this after my experience with a slow and steady degradation of health on a high-fat, near-zero sugar diet. Peat claims that it is recognized in “every field of physiology” that glucose oxidation is superior to fat. I don’t know about this.
"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."
Once again, Peat is casting the blame of glycation on decomposition of polyunsaturated fats more so than exposure to high levels of glucose.
"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."
I had hoped to talk more about gelatin, but there’s really not that much to say about it other than the amino acid profile of gelatin, because it lacks methionine, cysteine, and tryptophan, tends to have a more anti-inflammatory effect. I’m not sure it is clear what the right kind and amount of protein truly is. It probably is very different for each species, and is highly dependent on activity levels, gender, age, and the context of the rest of the diet. But in the interest of improving glucose oxidation I don’t think there’s any question that eating more calories and more of those calories as carbohydrates – sugar, starch, or a blend of the two, achieves that effect in addition to reducing the overall protein requirement. “Animal” protein is fantastic for muscle-building and during the growth and development phases of life – which is why dairy and eggs for example are so rich in growth-promoting proteins. But otherwise plant proteins seem to keep inflammation much lower. I haven’t found a faster way to reduce inflammation personally or with my own family members than to reduce animal protein ingestion.
Anyway, we’ll let that conclude our month of Ray Peat. You should be pretty sick of Ray Peat by now and ready to move on. But it is important to see where he is coming from, particularly as it pertains to polyunsaturated fat.
When nearly every disease state we know of is being increasingly linked to inflammation, free radical production, and low mitochondrial activity – and the links between each one of the “Big 3” you might call them are clearly negatively impacted by excess polyunsaturated fat intake (which also happens to be the most dramatic dietary change that took place in the 20th century), Peat’s smear campaign against them becomes incredibly valuable and timely. There is no doubt that he is one of the greatest contributors to the understanding of the nutrition-health interaction of any researcher that has come before him. I hope we can continue to learn from him, while also building on his work – better refining and individualizing it in the future. Yay Ray!
www.raypeat.com
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