Education
Endocrine regulation of metabolism & appetite
Set-point, arcuate POMC/AgRP, leptin and ghrelin, PYY and GLP-1, satiety index, sleep, and appetite hacks.
1. Set-point and the hypothalamus
Weight feels like conscious math—but adipose tissue is defended as a survival organ via a metabolic set-point.
Arcuate nucleus architecture
- POMC/CART (anorexigenic): suppress appetite, raise expenditure—satiety vector.
- AgRP/NPY (orexigenic): acute hunger, lower metabolic rate—starvation vector.
Dropping below set-point triggers AgRP dominance—dieting becomes a biological fight.
2. Leptin and ghrelin
Leptin (satiety)
From adipocytes; scales with fat mass. Activates POMC, suppresses AgRP. On a diet leptin falls faster than fat—adaptive thermogenesis and hedonic food drive.
Ghrelin (hunger)
From the stomach; rises when empty, hits AgRP. Eating distends the stomach—ghrelin drops. Chronic deficit keeps baseline ghrelin elevated post-meal.
3. Postprandial signals: PYY and GLP-1
The gut signals during the meal:
- PYY: protein and fiber trigger delayed gastric emptying and hunger suppression—Henselmans' high-protein, high-vegetable dieting rationale.
- GLP-1: carbs and fats boost insulin and satiety termination—the pharmacologic template for modern obesity drugs.
4. Henselmans satiety heuristics
- Satiety index: low energy density, high volume—potatoes, lean fish, egg whites, cruciferous vegetables—less ghrelin, more PYY.
- Avoid fat + sugar combos that hijack dopamine and bypass leptin.
- Sleep: restriction cuts leptin ~15–20% and raises ghrelin ~25–30%—appetite control fails without sleep.