“Curing” a High Metabolic Rate with Unsaturated Fats

Also see:
Fat Deficient Animals – Activity of Cytochrome Oxidase
Errors in Nutrition: Essential Fatty Acids
Thumbs Up: Fructose
Cardiolipin, Cytochrome Oxidase, Metabolism, & Aging
Medium Chain Fats from Saturated Fat – Weight Management Friendly
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
Protective “Essential Fatty Acid Deficiency”
Anti-Inflammatory Omega -9 Mead Acid (Eicosatrienoic acid)

Some of the discoveries listed in the studies below were made by the same researcher (George Burr) who discovered the “essential fatty acids.” With a different perspective, we can conclude that the “EFA” lower the metabolic rate of animals that are “deficient” in these fats.

The implications of this change in perspective is noteworthy. It points out the longevity depressing characteristics of “EFA” and also suggests their non essentiality since the “EFA” cured the skin disease of fat deficient rats only by lowering their metabolic rate and thus their exceedingly high nutritional requirements.

Through misinterpretation, we are poisoning ourselves with fats meant for lower temperatured organisms. Organisms with a high body temperature can consume saturated fats with no harmful side effects. The accumulation of unsaturated fats in the tissues of warm-blooded animals progressively lowers the metabolic rate, increases damage from the toxic form of oxidation (lipid peroxidation), damages the heart, lungs, and liver, promotes diabetes, cancer and immunosuppression, lowers our resistance to stress and shock, and harms development.

Also see this blog in relation to the “EFA’s” effect on cytochrome oxidase, a crucial respiratory enzyme.

Quotes by Ray Peat, PhD:
“The mitochondria are responsible for the efficient production of energy needed for the functioning of complex organisms, and especially for nerves. The enzyme in the mitochondria that reacts directly with oxygen, and that is often rate limiting, is cytochrome oxidase.”

“Burr didn’t understand that it was his rats’ high sugar diet, freed of the anti-oxidative unsaturated fatty acids, that caused their extremely high metabolic rate, but since that time many experiments have made it clear that it is specifically the fructose component of sucrose that is protective against the antimetabolic fats.

Although Brown, et al., weren’t focusing on the biological effects of sugar, their results are important in the history of sugar research because their work was done before the culture had been influenced by the development of the lipid theory of heart disease, and the later idea that fructose is responsible for increasing the blood lipids.”

“By l950, then, it was established that unsaturated fats suppress the metabolic rate, apparently creating hypothyroidism. Over the next few decades, the exact mechanisms of that metabolic damage were studied. Unsaturated fats damage the mitochondria, partly by suppressing the repiratory enzyme, and partly by causing generalized oxidative damage. The more unsaturated the oils are, the more specifically they suppress tissue response to thyroid hormone, and transport of the hormone on the thyroid transport protein.”

“The choice of foods which have less unsaturated fat tends to reinforce the achievements of evolution.”

“The fetus produces saturated fats such as palmitic acid, and the monounsaturated fat, oleic acid, which can be turned into the Mead acid, ETrA (5,8,11-eicosatrienoic acid), and its derivatives, which are antiinflammatory, and some of which act on the “bliss receptor,” or the cannibinoid receptor.

At birth, the baby’s mitochondria contain a phospholipid, cardiolipin, containing palmitic acid, but as the baby eats foods containing polyunsaturated fatty acids, the palmitic acid in cardiolipin is replaced by the unsaturated fats. As the cardiolipin becomes more unsaturated, it becomes less stable, and less able to support the activity of the crucial respiratory enzyme, cytochrome oxidase.”

“The respiratory activity of the mitochondria declines as the polyunsaturated oils replace palmitic acid, and this change corresponds to the life-long decline of the person’s metabolic rate.”

Exp Biol Med May 1934 vol. 31 no. 8 911-912
…The results show clearly that fat-deficient rats are very different from stock animals and that fat-deficient rats which have been cured with small doses of fats return to a much more nearly normal gas exchange. The most marked differences shown by the fat-deficient rats are higher basal rate, higher specific dynamic action of food, and higher respiratory quotients. These results are of especial interest since the runs were made over long periods of time under normal conditions. The respiratory quotients of the fat-deficient rats remain above unity for as long as 12 hours out of 24. They, therefore, synthesize every day large amounts of fat, but this synthetic fat does not prevent the fat deficiency.

Fat-deficient rats may synthesize much fat each day as indicated by high respiratory quotients. The fat synthesized from carbohydrate does not contain appreciable quantities of the essential fatty acids since these must be added to the diet to prevent decline and death. Although much smaller, the rats have a higher metabolic rate than their controls. Consequently, they have a much higher rate calculated as calories per square meter of surface. A normal diurnal activity is shown for all groups, which is independent of light and food.

J. Biol. Chem., vol. 91, pp. 525-539.
The metabolic rate and respiratory quotients of rats on a fat-deficient diet.
WESSON, L. G., AND G. O. BURR 1931
1. The metabolic rate and respiratory quotients following a
carbohydrate test meal have been determined in the case of rats
maintained for some time on a fat-deficient diet, and are compared
with those obtained on normal rats and under approximately the
same conditions.
2. The respiratory quotients in the 1st hours following the
carbohydrate feeding are in many cases well above unity, definitely
indicating the formation of fat from carbohydrate by these rats in
various stages of the fat-deficiency disease.

3. The fact that no relief is obtained from the symptoms of the
fat-deficiency disease by the fat thus formed from carbohydrate
indicates that the curative linolic and linolenic acids are not
formed by the rat from the carbohydrate or from the fat.

4. The basal and assimilatory metabolic rate in the case of rats
showing the early symptoms of the fat-deficiency disease was well
above the normal value, while the metabolic rate in the later
stages of the disease was normal or subnormal.

5. The possible relationship of thyroid activity to several phases
of the fat-deficiency disease is discussed.

Additional sources portraying the high metabolic rate of animals of “EFA” deficient animals:
Arch Int Physiol Biochim. 1990 Aug;98(4):193-9.
Non-shivering thermogenesis and brown adipose tissue activity in essential fatty acid deficient rats.
Goubern M, Yazbeck J, Senault C, Portet R.
The effects of essential fatty acid (EFA) deficiency on energetic metabolism and interscapular brown adipose tissue (BAT) activity were examined in the cold acclimated rat. Weanling male Long-Evans rats were fed on a low fat semipurified diet (control diet, 2% sunflower oil; EFA deficient diet, 2% hydrogenated coconut oil) for 9 weeks. They were exposed at 5 degrees C for the last 5 weeks. In EFA deficient rats, compared to controls, growth retardation reached 22% at sacrifice. Caloric intake being the same in the two groups, it follows that food efficiency was decreased by 40%. Resting metabolism in relation to body surface area was 25% increased. Calorigenic effect of norepinephrine (NE) in vivo (test of non-shivering thermogenesis) underwent a marked decrease of 34%. BAT weight was 21% decreased but total and mitochondrial protein content showed no variation. A 26% increase in purine nucleotide binding per BAT (taken as an index of thermogenic activity) was observed, suggesting that the enhancement in resting metabolism observed was mainly due to increased BAT thermogenesis. However, BAT mitochondria respiratory studies which are more direct functional tests showed a marked impairment of maximal O2 consumption of about 30% with palmitoyl-carnitine or acetyl-carnitine (both in presence of malate) or with alpha-glycerophosphate as substrate. It is likely that this impaired maximal BAT oxidative capacity may explain the impaired NE calorigenic effect in vivo. A possible increase in mitochondrial basal permeability is also discussed.

J Nutr. 1988 May;118(5):627-32.
Effect of dietary linoleic acid and essential fatty acid deficiency on resting metabolism, nonshivering thermogenesis and brown adipose tissue in the rat.
Rafael J, Patzelt J, Elmadfa I.
Rats were fed a diet either deficient (0.05%) in essential fatty acids (EFA), or providing 4% (control) and 10% (surplus) of the total energy intake in the form of linoleic acid. All diets were isoenergetic and provided 13.9% of the energy as fat. The rats were kept at 29 or 5 degrees C. Growth and food intake of rats fed linoleic acid surplus at either temperature for 10 wk were not different from that of controls; basal metabolism, norepinephrine-induced nonshivering thermogenesis (NST) and thermogenic variables in the brown adipose tissue (amount of mitochondria and mitochondrial uncoupling protein) also were not different. The effects of EFA deficiency were drastically enhanced in the cold: After 10 wk of consuming a diet low in EFA at 5 degrees C, the body weight of rats was 75% of that of controls (87% at 29 degrees C); the food intake was 135% of controls at 5 degrees C (120% at 29 degrees C). The resting respiration in deficient rats was 125% of controls at 5 degrees C (110% at 29 degrees C); body temperatures as low as 35.1 degrees C were measured in deficient rats after 3 wk at 5 degrees C; the cold tolerance of the rats was significantly diminished (30% died within 3 wk at 5 degrees C), thus emphasizing the essential role of dietary EFA during cold stress. Norepinephrine-induced NST and the thermogenic parameters in brown fat were not influenced by EFA deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Comp Biochem Physiol A Comp Physiol. 1989;94(2):273-6.
The effects of essential fatty acid deficiency on brown adipose tissue activity in rats maintained at thermal neutrality.
Yazbeck J, Goubern M, Senault C, Chapey MF, Portet R.
1. The consequences of essential fatty acid (EFA) deficiency on the resting metabolism, food efficiency and brown adipose tissue (BAT) thermogenic activity were examined in rats maintained at thermal neutrality (28 C). 2. Weanling male Long-Evans rats were fed a hypolipidic semi-purified diet (control diet: 2% sunflower oil; EFA-deficient diet: 2% hydrogenated coconut oil) for 9 weeks. 3. They were kept at 28 C for the last 5 weeks. Compared to controls, in EFA-deficient rats the growth shortfall reached 21% at killing. 4. As food intake was the same in EFA-deficient and control rats, food efficiency was thus decreased by 40%. 5. Resting metabolism expressed per surface unit was 15% increased. 6. Non-renal water loss was increased by 88%. 7. BAT weight was 28% decreased but total and mitochondrial proteins were not modified. 8. Heat production capacity, tested by GDP binding per BAT was 69% increased in BAT of deficient rats. 9. The stimulation of BAT was established by two other tests: GDP inhibition of mitochondrial O2 consumption and swelling of mitochondria. 10. It is suggested that the observed enhancement of resting metabolism in EFA-deficient rats is, in part, due to an activation of heat production in BAT.

J Nutr. 1984 Feb;114(2):255-62.
The effect of essential fatty acid deficiency on basal respiration and function of liver mitochondria in rats.
Rafael J, Patzelt J, Schäfer H, Elmadfa I.
Rats were fed a diet poor (0.05%) in essential fatty acids (EFA) with hydrogenated coconut oil as fat component, or a control diet containing 4% of the total energy intake in the form of linoleic acid. Effects of dietary EFA deficiency were investigated during a period of 2-30 weeks. Growth retardation becomes significant after 4 weeks of deficiency and attains about 25% when the deficiency is maintained for longer than 12 weeks. Respiration, body weight and age of EFA-deficient rats and controls are in a nonlinear relationship. Basal respiration in relation to the body weight is significantly increased by EFA deficiency; it is unchanged when related to total animals under the employed experimental conditions. Oxidative phosphorylation in isolated liver mitochondria is unaffected by EFA deficiency, i.e., the increased metabolic rate of EFA-deficient rats, related to the body weight, cannot be explained from impaired functional integrity of the inner mitochondrial membrane. Respiratory chain enzyme activities in mitochondria from heart and skeletal muscle and specific amounts of mitochondria in these tissues are unchanged by EFA deficiency.

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