Dr Sam Soete

@sam_soete·3 public posts on ADHXView on X
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Dear BigPharma, Sunscreen use ↑↑↑ SPF levels ↑↑↑ $$$ Sun protection industry ↑↑↑ Melanoma rates ↑↑↑ Please explain.

4mo ago· 1 savePreview
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Seems like there is a mistake in the label, but it is interesting all the people claiming "muhh low leucine =bad for muscle protein synthesis" when in fact the blend allows for a much more balanced amino acid profile for optimal health. The specific ratio that comes up in the literature is roughly 1:1 methionine to glycine. But essentially most people consume far too much methionine relative to glycine and would likely benefit from this blend. Methionine is abundant in muscle meat, eggs, and dairy. Glycine is abundant in connective tissue, skin, bones, and organs, which modern diets almost entirely exclude. Excess methionine without adequate glycine drives elevated homocysteine (methionine's primary metabolic byproduct, also used as a cardiovascular risk factor). It will also deplete glycine pools, since glycine is one of the substrates used to clear homocysteine via the transsulfuration pathway. Probably reduced glutathione synthesis (glycine + cysteine + glutamate) as well. Most people are short 5-10g of glycine per day just from eating muscle meat exclusively. So actually I kinda like @paulsaladinomd 's bar, doesn't replace normal meals but that was never the point and all the carnivores using this argument are just straw-manning.

4mo ago· 1 savePreview
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Iron is essential for complex IV in the electron transport chain. Iron-heme centres work together with copper centres to reduce oxygen to water and generate ATP. If there is insufficient bioavailable iron or copper, oxygen utilization and ATP production go down. But excess free iron is one of the most potent generators of hydroxyl radicals via Fenton chemistry. This stuff will wreck mitochondrial membranes and mtDNA = higher heteroplasmy rate. So you need iron for energy production, but too much unbound or poorly handled iron is a major problem. The body manages this through ferritin, transferrin, copper‑dependent ferroxidases like ceruloplasmin ( (which needs copper and B6) and hephaestin, and the hepcidin-ferroportin axis that regulates iron absorption and release. This is why iron is never just about iron; it is about the whole network of nutrients, hormones, and proteins that handle it. Low ferritin with high transferrin saturation tells a completely different story than low ferritin with low saturation, and low ceruloplasmin often points to a copper issue that secondarily disrupts iron metabolism rather than primary iron deficiency. Testing matters and its important to do complete iron panels (ferritin, serum iron, transferrin/TSAT, CRP, and sometimes ceruloplasmin and copper) to actually try to figure out what's going on.

4mo ago· 1 savePreview