Reducing the amount of orexin in the body might be very well the way it’s modulated physiologically. Plenty of animals hibernate in the winter when they sleep more and eat less.
Ok now I think you just didn’t get what I mean by that. I mean how a bacterium will make lactase when there’s lactose, but won’t make lactose when there isn’t lactose. That’s a physiological adaptation as opposed to a genetic adaptation. It’s of course mediated by genetically programmed mechanisms, but the variation is mediated by physiological changes, not by naturally selected changes in a gene pool. I’m asking why orexin wouldn’t be physiologically adaptive to the amount of food that’s generally around.
I mean how a bacterium will make lactase when there’s lactose, but won’t make lactose when there isn’t lactose.
It’s quite easy to have a receptor protein that binds to lactose and then leads to a protein being expressed that turns lactose into lactase.
“amount of available food in the environment” is not as simple to measure inside of a cell and as a result, the regulation is much more complex.
I’m asking why orexin wouldn’t be physiologically adaptive to the amount of food that’s generally around.
That assumes that orexin is independent of food that’s around, which clearly isn’t true. Fasting increases orexin levels, it’s just that chronic food restriction that doesn’t change it.
Hm. So orexin is increased initially during a fast, and also when eating high-caloric food? That’s weird. Do people who eat high-caloric food need less sleep?
Reducing the amount of orexin in the body might be very well the way it’s modulated physiologically. Plenty of animals hibernate in the winter when they sleep more and eat less.
But then why don’t modern well-fed humans sleep much less without detriment? (Or do they?)
Because evolution didn’t had the time to select for the mutations that would result in that outcome.
Ok now I think you just didn’t get what I mean by that. I mean how a bacterium will make lactase when there’s lactose, but won’t make lactose when there isn’t lactose. That’s a physiological adaptation as opposed to a genetic adaptation. It’s of course mediated by genetically programmed mechanisms, but the variation is mediated by physiological changes, not by naturally selected changes in a gene pool. I’m asking why orexin wouldn’t be physiologically adaptive to the amount of food that’s generally around.
It’s quite easy to have a receptor protein that binds to lactose and then leads to a protein being expressed that turns lactose into lactase.
“amount of available food in the environment” is not as simple to measure inside of a cell and as a result, the regulation is much more complex.
That assumes that orexin is independent of food that’s around, which clearly isn’t true. Fasting increases orexin levels, it’s just that chronic food restriction that doesn’t change it.
Hm. So orexin is increased initially during a fast, and also when eating high-caloric food? That’s weird. Do people who eat high-caloric food need less sleep?
Where did you get the claim about eating high caloric food?
“Here, we review a fat-burning mechanism that is turned on by the brain hormone orexin during high-caloric food consumption.”
Maybe they’re not saying that the diet upregulates orexin?
We’re talking about a physiological adaptive mechanism.