Growth Hormone

Growth hormone (GH) is a pituitary stress hormone whose chronic elevation Ray Peat treated as a primary driver of degenerative aging and metabolic disease. 2 Peat argued that GH is not simply a beneficial anabolic agent but a stress-responsive hormone that rises during hypoglycemia, heat, and shock, sometimes to levels ten or twenty times normal. 2 He identified it as the closest known substance to W.D. Denckla's hypothetical "death hormone," noting that animals genetically lacking GH or surgically deprived of pituitary function live roughly twice as long as normal controls, provided they receive thyroid support. 3

The hormone's core pathological mechanism, in Peat's view, is its diabetogenic action—mobilizing free fatty acids from storage in a manner similar to adrenalin. 2 This flood of lipids, particularly unsaturated fats, blocks the oxidation of glucose and creates a generalized antithyroid effect that suppresses respiratory metabolism. 2 Peat emphasized that GH consistently increases the proportion of unsaturated fatty acids in the blood, which promotes oxidative damage and interferes with cellular energy production. 2 This shift toward fatty acid oxidation underlies GH's well-established ability to antagonize insulin and progressively worsen insulin resistance with age. 2

Peat documented that GH's degenerative influence extends directly to tissue structure, particularly through vascular leakiness and kidney pathology. 3 He noted that GH, working as a system with estrogen and nitric oxide, increases the permeability of blood vessels, causing leakage of albumin into the urine and thickening of the capillary basement membrane—hallmarks of diabetic kidney disease. 3 The hormone also causes overt edema by disrupting water and mineral regulation, a function Peat traced back to its ancient evolutionary role in osmoregulation in fish. 2 He cited evidence that GH blocks gonadotropin-stimulated progesterone production, further compromising the protective hormones that maintain vascular integrity and oppose estrogen. 1

In clinical contexts, Peat warned that exogenous GH administration mimics the accelerated degeneration seen in acromegaly, where patients suffer from extremely high rates of atherosclerosis and kidney failure. 2 He directly advised that lowering GH is one of the great advantages of dietary carbohydrate, since sugar and starch suppress the hypoglycemia-driven GH surge. 9 Georgi Dinkov has reinforced this position, characterizing GH as part of an ancient stress cascade alongside serotonin and prolactin that should not be upregulated, and noting that a single glucagon stimulation test is insufficient to diagnose deficiency given how sensitively GH responds to sleep deprivation and fasting state. 2 Peat did acknowledge that vitamin D sufficiency around 50 ng/ml can alleviate a genuine GH deficiency, but the overarching framework treats chronic GH elevation as a pro-aging, pro-diabetic force best kept low through stable blood sugar and thyroid-supported metabolism. 2