Peter Attia· MD
i would expect uh an enormous increase in insulin to produce that a level that wouldn't be otherwise physiologically described
The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
i would expect uh an enormous increase in insulin to produce that a level that wouldn't be otherwise physiologically described
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so think about what happens now to these rats or people with tumors you have the surgery you hyper secrete insulin you wake up from the surgery without carbohydrate supplies and unable to oxidize dietary fat so that would explain the hunger it's as though you've created a starvation state in the animal instantaneously
well in my model is first thing that have first observable effect from the bmh lesion is hyperinsulinemia so you lesion the brain and the animal hyper secretes insulin in response to even thinking about food
so the insulin is signaling its fat tissue to take up fat and to store it for food it's in store it for fuel it's inhibiting the process of lipolysis it's also inhibiting the oxidation of fatty acids and muscle tissue through the malonyl-coa pathway