Les AG essentiels dépriment le métabolisme

Ray PEAT PhD. a écrit:Polyunsaturated fats profoundly interfere with the function of the thyroid hormone and the cellular respiratory apparatus (mitochondria). Without the toxic fats, respiratory energy metabolism was very intense.

The reason linseed oil and fish oil were used for making varnishes and paints was that they are "drying oils," reacting with oxygen to polymerize and harden. The physical and chemical propertiess of the oils are fairly well understood, and among the polyunsaturated fatty acids (PUFA) the omega -3 fatty acids react most easily with oxygen. Heat, light, and moisture increase their spontaneous interactions with oxygen, and besides polymerizing, these oils produce a variety of reactive particles, including acrolein, which combine with other substances, such as cellular proteins and DNA, with highly toxic effects. At low temperatures and low oxygen concentrations these oils are not highly reactive. Fats that harden at low temperatures (as saturated fats do) wouldn't be convenient for organisms that live in a cool environment, and so organisms regulate the type of fat they synthesize according to the temperature of their tissues. The fact that certain types of polyunsaturated fatty acids function nicely in fish, worms, and insects, doesn't mean that they are ideal fats for mammals.

The fact that vitamin E prevented or cured some of the major diseases in farm animals caused by excessive PUFA, and that it could retard the development of rancidity in stored oils, led quickly to the persistent belief that lipid peroxidation is the only toxic effect of the vegetable oils. However, the oils were being seen to cause other problems, including accelerated aging and obesity, but those problems weren't of interest to farmers, who wanted to sell plump young animals as cheaply and quickly as possible. Even fresh oils have toxic effects, and the oxidative damage they do is often the consequence of these other toxic actions.

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In the early 1930s George Burr had discovered that animals on a fat free diet had an extremely high rate of metabolism, but he didn't investigate the important ramifications of that observation, such as their increased need for vitamins and minerals, in accordance with their rate of metabolism. The PUFA slowed metabolism, and that effect was good for agriculture.
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By 1920, the polyunsaturated fatty acids were recognized to inhibit proteolytic enzymes.
Scattered studies have found that polyunsaturated fats inhibit the proteolytic enzymes involved in the digestion of food, in the removal of clots, in the formation of thyroid hormone, and many other essential physiological processes.
Since the organism consists mainly of proteins, there are complex innate systems for regulating the proteolytic enzymes, activating or inactivating them as needed, and such complexity isn't likely to depend on variable, unstable dietary factors. Exogenous substances that inhibit some proteases could create an unlimited variety of functional and anatomical irregularities.
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The inhibition of detoxification enzymes by PUFA (Tsoutsikos, et al., 2004) affects many processes, such as the elimination of estrogen, contributing to the positive feedback between estrogen and the oils. The meaning of this tends to be lost, because of the estrogen industry's effective campaigns.
Another situation in which fatty acids participate in a positive feedback system is the stress reaction, in which the released fatty acids impair mitochondrial energy production, increasing the stress and leading to further release of fatty acids.
One of the perennial theories of aging that has remained viable is the metaplasm / lipofuscin / age pigment theory, the idea that a toxic material accumulates in tissues over time. The age pigment contains proteins, cross-linked PUFA, and metals. The inhibition of proteolytic enzymes is involved in its accumulation, and the ratio of PUFA to saturated fatty acids is an important factor in its formation. Estrogen is one of the factors that can promote the formation of age pigment, probably partly because its lipolytic action increases the cells' exposure to free fatty acids. The lipofuscin contributes to inhibition of proteolysis, probably partly through increased production of free radicals and hydrogen peroxide.
The proteolytic enzymes are an essential part of innate immunity, and the highly unsaturated fatty acid, EPA, which is the most immunosuppressive of the fats, strongly inhibits proteolysis in some cells. The natural killer (NK) cells and phagocytic cells are two types of cell that are suppressed by PUFA, and they are involved in many kinds of physiological events, not just the killing of tumor cells and virus infected cells.

The immunosuppressive effects of PUFA are very general. Many metabolites that are known to have harmful effects on the immune system are increased by the PUFA (histamine [Masini, et al., 1990], serotonin, lactate, nitric oxide [Omura, et al., 2001]).
These substances are also involved in tumor development.
Besides inhibiting enzymes and being converted into prostaglandins, the polyunsaturated fatty acids have direct effects, as signals (or interference with signals) on many tissues. The belief that the PUFA are essential nutrients has influenced the way cellular excitability thresholds are being interpreted. Anxiety and panic may be interpreted as alertness, calmness may be interpreted as stupidity. Specifically, long-term potentiation (LTP) may contribute to seizures, senility, and excitotoxicity, as well as to learning, but many titles and conclusions equate increased LTP with "improved LTP," implying that it has biological value to the animal.

The ability of nerve cells to become quiescent after excitation is essential to learning and perception. This ability is lost with aging, as the functional balance in the brain shifts away from GABA-ergic to glutamatergic nerves. The polyunsaturated fatty acids promote the excitatory nervous state. The combination of respiratory inhibition with excitation can produce excitotoxic cell death. If the doctrine of "essentiality of PUFA" hadn't been so influential, different interpretations of excitatory thresholds, energy metabolism, and even cell structure would have been allowed to develop more fully.

The concentration of polyunsaturated fats in the brain has led many people to say that the "nutritionally essential fatty acids," especially the omega -3 fatty acids, are essential for brain development (for the formation of nerve cell membranes), and for the formation of synapses, and that increasing the amount of those fats in the diet would be desirable. The types of argument they use simply ignore the real evidence: Cells can multiply indefinitely in culture dishes without the essential fatty acids, insects can multiply for generations on diets without the unsaturated fats, forming normal synapses and brains, and mammals fed diets with extremely small amounts of the unsaturated fats grow with perfectly normal--possibly superior--brains.

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Cet article est étayé par plusieurs sources scientifiques. J'en posterais quelques unes ci-après.

En résumé, les AGPI inhibent le métabolisme, favorisent le cancer, l’athérosclérose, Alzheimer, le diabète, contribuent à la cirrhose du foie, vous rendent stupide et généralement vous tuent lentement, (si vous n'y prenez pas garde, mais vous allez avoir une potion magique, ndlr) 

PUFA (omega 3 and 6) inhibit pyruvate dehydrogenase, a key enzyme that links glycolysis into the Kreb’s (TCA) cycle (Da Silva et al. 1993). Inhibition of pyruvate dehydrogenase is known to contribute to the Warburg effect, the aerobic glycolysis characteristic of cancer (McFate et al. 2008).

PUFA breakdown products (acrolein, malondialdehyde, hydroxynonenal, crotonaldehyde) inhibit mitochondrial respiration (Humphries et al. 1998, Picklo and Montine 2001).

PUFA (including fish oil) promote cancer (Griffini et al. 1998), high DHA is associated with prostate cancer (Brasky et al. 2011).

Linoleic acid (omega 6) is required for carcinogenesis in some animal models (Ip et al. 1985).

PUFA suppress metabolism, this can be seen most obviously in the elevated metabolisms of lab animals fed an “essential” fatty acid deficient diet, (Burr and Beber 1934), “essential” fatty acid deficiency is associated with increased activity of cytochrome oxidase a fundamental mitochondrial respiratory enzyme (Kunkel and Williams 1951).

Animals fed “essential” fatty acid sufficient diets gain more weight than deficient animals (Rafael et al. 1988).

PUFA inhibit thyroid hormone activity (Clarke and Hembree 1990).

PUFA, LA (w6), ALA (w3), AA (w6), DHA (w3) all cause brain swelling, oleic acid (MUFA) and palmitic acid (SFA) do not (Chan and Fishman, 1980).

PUFA cause nervous system damage and impair learning, (Harman et al. 1976).

Neuroprostanes breakdown products of DHA are implicated in Alzheimer’s, they are found in cerebrospinal fluid of Alzheimer’s patients at higher levels than age-matched controls (Roberts et al. 1998).

PUFA, both omega 3 and 6 are involved in atherosclerosis, a study examining fatty acid composition of aortic plaques found a positive association between omega 3 and 6 fatty acids of plaques with adipose tissue content, no association was found for saturated fatty acids (Felton et al. 1994).

PUFA, both omega 3 and 6 impair lung function (Wolfe et al. 2002).

PUFA interfere with insulin sensitivity and increase diabetes risk, a study looking at safflower and fish oil found that both increased fasting blood glucose, the fish oil group had higher blood glucose (Borkman et al. 1989).

PUFA promote liver cirrhosis, saturated fats and cholesterol are protective against liver cirrhosis (Nanji and French 1986). In another study fish oil promoted cirrhosis and saturated fat was found to reverse cirrhosis, whilst ethanol administration was ongoing!! So if you’re going out drinking make sure to eat lots of butter and coconut oil (Nanji et al. 2001).

Omega 3 fats lower endurance in rats (Ayre and Hulbert 1997).

Fish oil lowered mitochondrial activity and increased oxidative stress in… Atlantic salmon, wow fish oil sucks even for fish (Kjaer et al. 2008).

Omega 3 and 6, especially 3 impair wound healing (Cardosso et al. 2004).

There’s good evidence that PUFA especially the longer chain highly unsaturated AA and DHA accumulate with aging (Tamburini et al. 2004, Nourooz-Zadeh and Pereira 1999).

PUFA shorten lifespan, a number of animal studies show that the degree of unsaturation of tissue fatty acids corresponds inversely with maximum lifespan, i.e. eating lots of “essential” fatty acids will shorten your life (Bajra 2004). Naked mole-rats display unusual longevity for a rodent of their size they live around 28 years similarly sized mice live only 3-4 years. Mole-rats have low DHA (2-6%) in comparison to mice (27-57%), this low DHA means they are less susceptible to peroxidative damage (Mitchell et al. 2007).

In a study in Italy a high PUFA to saturated fat ratio was found to increase all-cause mortality (Solfrizzi et al. 2005).