Kairyū

Trovare un partner a 20 anni o a 30 cambia in modo abissale. A 30 anni è tosta. Le persone a 30 anni hanno paura dei sentimenti, dei legami, di provare emozioni, hanno brutti vissuti o hanno già investito tempo e bontà per la persona sbagliata.

Carbs show us who has type 2 diabetes. But they don’t cause it. If they did, people who consume a diet with a higher % of carbs would be at increased risk. They’re not. Hypothesis discarded.

It’s so weird to see “expert” academic cardiologists have zero idea that insulin resistance can CAUSE elevated ApoB IR is not a mere bystander that makes things worse (although it does) It actually —> ⬆️ApoB like this: 1. Fat cells become insulin-resistant → excess free fatty acids flood the liver Normally insulin tells fat tissue to stop releasing stored fats. In IR, that “stop” signal fails, so free fatty acids pour into the bloodstream and get delivered straight to the liver. This gives the liver way too much raw fat to work with. 2. The liver gets overloaded with fat and keeps making more (even though insulin signaling is broken) High insulin levels (hyperinsulinemia) still turn on the liver’s “fat factory” genes (via SREBP-1c). The liver starts cranking out its own triglycerides through de-novo lipogenesis. So now you have extra fat coming in from the bloodstream PLUS extra fat made inside the liver. 3. Insulin can no longer break down ApoB inside the liver cells Normally insulin helps destroy extra ApoB protein before it can be packaged into lipoproteins. In hepatic IR, this cleanup step fails, so more ApoB survives and is available to build new particles. 4. The liver ramps up MTP (microsomal triglyceride transfer protein) → it packages fat + ApoB into VLDL super-efficiently Insulin normally keeps MTP turned down. In IR, MTP stays high, so the liver rapidly coats all that extra ApoB with triglycerides and cholesterol and spits out huge numbers of VLDL particles (the triglyceride-rich precursors to LDL). 5. In the bloodstream, VLDL turns into LDL – often the small, dense, more dangerous kind These VLDL particles lose triglyceride and become LDL. High triglycerides also let CETP swap fats around, and hepatic lipase then shrinks the LDL particles. Result: you get more LDL particles overall (higher ApoB) that are smaller and denser – the exact pattern seen in metabolic syndrome. So even if you pray to the alter of ApoB, then you should be just as aggressive about IR as well. And. If you can’t articulate these pathways with humility, you don’t really understand the full picture and should probably stop lecturing everyone else from your high horse

Do you believe that Jesus Christ was wrapped in the burial shroud that we now call the “Shroud of Turin”? I do!