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Master Metabolism
@lowmegatron

Seed oils ruin thyroid function! 🟥 Reducing thyroid hormone binding 🟥 Reducing thyroid hormoneconversion 🟥 Reducing nuclear receptor binding 🟥 Probable cause of hashimoto’s disease The thyroid gland produces several thyroid hormones. T3, is the active thyroid hormone. T4 is a precursor, one enzymatic step away from T3. The thyroid hormone (T3) aims to reach the cell’s nucleus and activate the nuclear receptor. Many things can go wrong along the way, and seed oils are a huge problem in this regard. T3 and Metabolic Health T3 helps regulate the speed at which your body’s cells work. When T3 levels are high, cells work faster. This means they use more energy and your resting metabolic rate increases. T3 enters the cell nucleus (the control center) and binds to specific receptors. This triggers the expression of genes that control the production of proteins involved in energy production and use. T3 stimulates the production of proteins within the mitochondria. These mitochondria produce ATP - energy currency. T3 increases the rate at which cells use oxygen and nutrients to produce energy. When T3 levels are high, your body is more efficient at converting food into usable energy rather than storing it as fat. Heat is generated as a byproduct of increased metabolism and energy production. This is why people with high levels of T3 (reaching the nucleus) feel warmer and have a higher body temperature. Hypothyroid people are usually cold all the time. Your body needs energy to maintain vital functions like breathing, circulating blood, and repairing cells. T3 influences the resting metabolic rate by keeping these processes running efficiently. Anything that interferes with T3 can lead to issues including fatigue, weight gain, depression, hormonal imbalances, sexual dysfunction, mental health problems, and serious heart conditions. The full list is endless. T3's final destination is the nuclear receptor of the cell, where it enters cells and binds to thyroid hormone receptors (TRs). This binding can either up-regulate or down-regulate the transcription of target genes, leading to changes in protein synthesis. These proteins regulate metabolism, cardiovascular function, lipid metabolism, protein synthesis, mitochondrial function, neurological function, and reproduction. These hormones ride binding proteins along the way. T4 may or may not be converted to T3, which must bind with the nuclear receptor. Anything that interferes with the flow of T3/T4 from the gland to T3, activating the nuclear receptor, can cause problems to any system in the body. Seed oils interfere with this flow in numerous ways. Thyroid Hormone Transport Thyroid hormones are transported around the body by binding proteins in blood serum. It’s been noted that these proteins drop or unbind thyroid hormones during illness. During stress (including illness), free fatty acids (FFAs) are released, including linoleic acids from seed oils. Because of this, researchers were curious whether FFAs could affect thyroid hormone binding to transport proteins, so they conducted experiments on healthy individuals’ blood serum. The blood serum was mixed with different FFAs, and the researchers looked at their effects on thyroid hormone binding to transport proteins. Arachidonic acid and linoleic acid had the most potent anti-thyroid effect. Another study showed similar effects; linoleic and arachidonic acids prevented binding, as did oleic acid, but saturated fatty acids did not. Linoleic acid is the major fatty acid in seed oils like soybean oil. We consume multiple times more linoleic acid than our grandparents did. Arachidonic acid comes from animal foods, and we can make it from linoleic acid. These two are the major omega-6 fatty acids. Linoleic acid also tends to increase arachidonic acid as a free fatty acid, inhibiting thyroid binding and lowering thyroid function. <a target="_blank" href="https://twitter.com/1529466607319142402/status/1865826137085005974" color="blue">x.com/15294666073191…</a>

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Master Metabolism
@lowmegatron

Seed Oils and Extrathyroidal Conversion of Thyroid Hormones Extrathyroidal conversion is the conversion of T4 to T3 outside the thyroid gland. It’s a critical process, as most of your T3 is not released by the thyroid gland but must be converted from T4 elsewhere in the body. T3 is the active hormone. Researchers discovered that the same fatty acids that interfere with thyroid hormone transport also inhibit the liver’s ability to convert T4 to T3. The liver is a major producer of T3 by converting T4 to T3. Linoleic and arachidonic acids decrease thyroid hormone conversion in the liver, reducing the amount of T3 available. That same study showed that phospholipase A2 (PLA2) also decreases thyroid hormone conversion in the rodent liver. PLA2 is an enzyme that releases fatty acids like linoleic and arachidonic acids from membrane phospholipids, increasing the amount of FFAs. When researchers examined the relationship between free fatty acids and T3 in the blood of people with various illnesses, they found that those with higher FFAs had lower levels of T3. That same study also showed elevated FFAs were associated with thyroid hormone binding inhibition. The Final Step The final leg of the thyroid hormone’s journey is the binding of T3 to the nuclear receptor in the cell's nucleus. For T3 to exert most of its benefits, it must bind to the nuclear receptor. Cell researchers investigated the effect of different fatty acids on T3 nuclear binding. Linoleic, arachidonic, linolenic, and oleic acids inhibited T3 nuclear binding. (Linoleic and linolenic acids are two fatty acids found in seed oils.) Palmitoleic acid, a monounsaturated fatty acid, caused the greatest nuclear receptor binding inhibition. Linoleic acid was a very close second place. Oleic, arachidonic, and linolenic acids also inhibited thyroid hormone binding to the nuclear receptor. Saturated fatty acids exhibited little to no inhibition of nuclear receptor binding. PLA2, an enzyme that releases free fatty acids, also decreases T3 binding to the nuclear receptor, probably because it increases FFAs. These are some of the more direct ways seed oils interfere with thyroid function. Other mechanisms are just as important but not as direct.

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Master Metabolism
@lowmegatron

Seed oils are implicated in Hashimoto’s thyroiditis and other “autoimmune” diseases. <a target="_blank" href="https://twitter.com/1744031563187150848/status/1848696740360188076" color="blue">x.com/17440315631871…</a>

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Master Metabolism
@lowmegatron

Sources Rafael J, Patzelt J, Schäfer H, Elmadfa I. The effect of essential fatty acid deficiency on basal respiration and function of liver mitochondria in rats. J Nutr. 1984 Feb;114(2):255-62. doi: 10.1093/jn/114.2.255. PMID: 6693988. Diniz YS, Cicogna AC, Padovani CR, Santana LS, Faine LA, Novelli EL. Diets rich in saturated and polyunsaturated fatty acids: metabolic shifting and cardiac health. Nutrition. 2004 Feb;20(2):230-4. doi: 10.1016/j.nut.2003.10.012. PMID: 14962692. Brown, W. R., Hansen, A. E., Burr, G. O., & McQuarrie, I. (1938). Effects of Prolonged Use of Extremely Low-Fat Diet on an Adult Human Subject. The Journal of Nutrition, 16(6), 511-524. Elsevier. Total daily energy expenditure has declined over the past three decades due to declining basal expenditure, not reduced activity expenditure. Nat Metab. 2023 Apr;5(4):579-588. doi: 10.1038/s42255-023-00782-2. Epub 2023 Apr 26. PMID: 37100994; PMCID: PMC10445668. Bregengård C, Kirkegaard C, Faber J, Poulsen S, Siersbaek-Nielsen K, Friis T. The influence of free fatty acids on the free fraction of thyroid hormones in serum as estimated by ultrafiltration. Acta Endocrinol (Copenh). 1987 Sep;116(1):102-7. doi: 10.1530/acta.0.1160102. PMID: 3661050. Tabachnick M, Korcek L. Effect of long-chain fatty acids on the binding of thyroxine and triiodothyronine to human thyroxine-binding globulin. Biochim Biophys Acta. 1986 Apr 11;881(2):292-6. doi: 10.1016/0304-4165(86)90016-4. PMID: 2869786. Chopra IJ, Huang TS, Beredo A, Solomon DH, Chua Teco GN, Mead JF. Evidence for an inhibitor of extrathyroidal conversion of thyroxine to 3,5,3'-triiodothyronine in sera of patients with nonthyroidal illnesses. J Clin Endocrinol Metab. 1985 Apr;60(4):666-72. doi: 10.1210/jcem-60-4-666. PMID: 2857729. Suzuki Y, Nanno M, Gemma R, Yoshimi T. Plasma free fatty acids, inhibitor of extrathyroidal conversion of T4 to T3 and thyroid hormone binding inhibitor in patients with various nonthyroidal illnesses. Endocrinol Jpn. 1992 Oct;39(5):445-53. doi: 10.1507/endocrj1954.39.445. PMID: 1478185. Wiersinga WM, Chopra IJ, Teco GN. Inhibition of nuclear T3 binding by fatty acids. Metabolism. 1988 Oct;37(10):996-1002. doi: 10.1016/0026-0495(88)90159-x. PMID: 3173114. Reed EB, Tarver H. The influence of diet on the lipogenic response to thyroxine in rat liver. Life Sci. 1975 Dec 15;17(12):1785-97. doi: 10.1016/0024-3205(75)90461-0. PMID: 3705.