PUFA Promote Stress Response; Saturated Fats Suppress Stress Response

Also see:
Sugar (Sucrose) Restrains the Stress Response
Saturated and Monousaturated Fatty Acids Selectively Retained by Fat Cells
Ray Peat, PhD on Low Blood Sugar & Stress Reaction
Low Blood Sugar Basics
Low Carb Diet – Death to Metabolism
Saturated and Monousaturated Fatty Acids Selectively Retained by Fat Cells
Anti-Inflammatory Omega -9 Mead Acid (Eicosatrienoic acid)
Protect the Mitochondria
Toxicity of Stored PUFA
Dietary PUFA Reflected in Human Subcutaneous Fat Tissue
Israeli Paradox: High Omega -6 Diet Promotes Disease
PUFA Accumulation & Aging
Unsaturated Fats and Longevity
Arachidonic Acid’s Role in Stress and Shock
“Curing” a High Metabolic Rate with Unsaturated Fats
Fat Deficient Animals – Activity of Cytochrome Oxidase
Benefits of Aspirin

Quotes by Ray Peat, PhD:
“Saturated fatty acids terminate the stress reactions, polyunsaturated fatty acids amplify them.”

“Free unsaturated fatty acids turn on the stress hormones, and cortisol blocks oxidation of sugar and turns it into fatty acids and triglycerides. Keeping cortisol and stress low is the main thing. Keeping a high ratio of calcium to phosphate helps to oppose the stress metabolism.”

“Unsaturated fatty acids, but not saturated fatty acids, are signals which activate cell systems.”

“In a young person, good food, sunlight, and a high altitude can often overcome severe and progressive inflammatory conditions. In an older person, whose tissues contain larger amounts of polyunsaturated fats and their breakdown products, it takes more environmental support to get out of the inflammatory pattern.”

“Heavy drinking inhibits cellular respiration and sets up an inflammatory process, involving iron, which will still be harmful, but less so than in the presence of PUFA. If absolutely none of the dietary PUFA were in the body, no one really knows what that metabolic stress would do, maybe nothing cumulative.”

“There is a growing recognition that a persistent increase of free fatty acids in the serum, which is seen in shock, heart failure, and aging, indicates a bad prognosis, but there is no generally recognized explanation for the fact that free fatty acids are harmful. I want to mention some evidence showing that it is the accumulation of polyunsaturated fats in the body that makes them harmful.”

“My argument here will be that some of our adaptive, protective regulatory processes are overridden by the excessive supply of unsaturated fats–supported by a few other toxins–in our diet, acting as a false-signal system, and that cholesterol, pregnenolone, and progesterone which are our main long-range defenses, are overcome by the effects of the unsaturated fats, and that the resulting cascade of ineffective and defective reactions (including various estrogen-stimulated processes) leads to lower and lower energy production, reduced function, and death. At certain times, especially childhood and old age, iron (which also has important regulatory roles) accumulates to the point that its signal functions may be inappropriate.”

“There are many energy-related vicious circles associated with aging, but the central one seems to be the fat-thyroid-estrogen-free-radical-calcium sequence, in which the ability to produce stabilizing substances including carbon dioxide and progesterone is progressively lost, increasing susceptibility to the unstable unsaturated fats.”

“The random production of free radicals, rather than acting only by way of genetic damage or protein cross-linking, is also able to act as a signalling process, that is, on a strictly physiological level. An excess of unsaturated fatty acids itself constitutes a massive distortion of the regulatory systems, but it also leads to distortions in the “eicosanoid” system and the increasingly uncontrolled production of free radicals, and to changes in energy, thyroid activity, and steroid balance. The aging body, rather than being like a car that needs more and more repairs until it collapses from simple wear, is more like a car traveling a road that becomes increasingly rough and muddy, until the road becomes an impassable swamp.”

“I’ve known people who were eating 2-3 pounds of meat a day and who were getting sicker and sicker as their free fatty acids and free amino acids increased. That started me reading more about the free state of fatty acids in the blood. Just about everything that goes wrong, involves free fatty acids increase. If they’re totally saturated fatty acids, such as from coconut oil and butter, those are less harmful, but they still tend to shift the mitochondrial cellular metabolism away from using glucose and fructose, and turning on various stress-related things (by lowering the carbon dioxide production, I think, is the main mechanism).”

“The equivalent of just about a teaspoonful of unsaturated fat per day is enough to show a threshold increase in the incidence of cancer. When we eat natural foods, were’re always getting some of the unsaturated fats. On a normal diet it’s hard to get down to that threshold of about 4g of fat per day. It’s hard even eating coconut oil and butter fat, and beef fat, and so on ( they only have about 2% of unsaturated fats). So, besides eating the most saturated type of fats, that’s one of the arguments for using carbohydrates as a major part of your energy supply. Because if we have some extra carbohydrates more than we need to burn at the moment, they’ll turn into saturated fats and extend the proportions. So that in effect you can lower the unsaturated proportion below the threshold of carcinogenic fats.”

“Our innate immune system is perfectly competent for handling our normal stress induced exposures to bacterial endotoxin, but as we accumulate the unstable fats, each exposure to endotoxin creates additional inflammatory stress by liberating stored fats.”

“When mitochondria are functioning fully, either glucose or saturated fats can safely provide energy. Some glucose or saturated fat can be converted to polyunsaturated fats, that can be used as regulators or signals, for example to activate the formation of stem cells. But those PUFA don’t create disruptive cascades of increasing excitation or inflammation or excessive growth, and, from the evidence of animals that are fed fat free diets, or diets lacking omega -3 and omega -6 fatty acids, they aren’t toxic to mitochondria.”

Comp Biochem Physiol A Mol Integr Physiol. 2004 Feb;137(2):357-64.
Saturated fatty acids suppress adrenocorticotropic hormone (ACTH) release from rat anterior pituitary cells in vitro.
Katoh K, Asari M, Ishiwata H, Sasaki Y, Obara Y.
We studied whether fatty acids modify adrenocorticotropic hormone (ACTH) release induced by stimulation with corticotropin-releasing hormone (CRH) from rat anterior pituitary cells. Stimulation with CRH (0.01-100 nmol/l) significantly and concentration-dependently increased ACTH release, which was synergistically enhanced by the simultaneous stimulation with 1 nmol/l arginine-vasopressin. Addition of saturated fatty acids (butyrate, caprylate, laurate, palmitate and stearate) in a medium at 1 mmol/l, despite effects on the basal release, significantly reduced the ACTH release induced by CRH (1 nmol/l) stimulation. Caprylate suppressed ACTH release in a concentration-dependent manner. However, unsaturated C18 and C20 fatty acids (oleate, linolate, linolenate and arachidonate) at 1 mmol/l significantly increased the basal release, but none of them suppressed CRH (1 nmol/l)-induced ACTH release. In the presence of caprylate (1 mmol/l), CRH (1 nmol/l)-stimulated increase in cellular calcium ion concentration was diminished. From these results we conclude that saturated fatty acids have a suppressing effect on CRH-induced ACTH increase in primary cultured rat anterior pituitary cells.

Am J Physiol Regul Integr Comp Physiol. 2003 Jun;284(6):R1631-5. Epub 2003 Apr 10.
An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.
Bruder ED1, Ball DL, Goodfriend TL, Raff H.
Oxidized derivatives of linoleic acid have the potential to alter steroidogenesis. One such derivative is 12,13-epoxy-9- keto-10-(trans)-octadecenoic acid (EKODE). To evaluate the effect of EKODE on corticosterone production, dispersed rat zona fasciculata/reticularis (subcapsular) cells were incubated for 2 h with EKODE alone or together with rat ACTH (0, 0.2, or 2.0 ng/ml). In the absence of ACTH, EKODE (26 microM) increased corticosterone production from 5.3 +/- 2.3 to 14.7 +/- 5.0 ng. 10(6) cells. h(-1). The stimulatory effect of ACTH was increased threefold in the presence of EKODE (26.0 microM). Cholesterol transport/P-450scc activity was assessed by measuring basal and cAMP-stimulated pregnenolone production in the presence of cyanoketone (1.1 microM). EKODE (13.1 and 26.0 microM) significantly increased basal and cAMP-stimulated (0.1 mM) pregnenolone production. In contrast, EKODE decreased the effect of 1.0 mM cAMP. EKODE had no effect on early or late-pathway activity in isolated mitochondria. We conclude that EKODE stimulates corticosterone biosynthesis and amplifies the effect of ACTH. Increased levels of fatty acid metabolites may be involved in the increased glucocorticoid production observed in obese humans.

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