Adrenaline

Adrenaline is a catecholamine released from the adrenal glands whose chronic elevation Ray Peat treated as a central feature of the hypothyroid state. 2 Peat observed that hypothyroid individuals can exhibit 30 to 40 times the normal daily output of adrenaline, a compensatory mechanism to mobilize glucose when thyroid-mediated oxidative metabolism is deficient. 4 This surge is the body's first response to insufficient glucose, triggering the release of stored liver glycogen; only when glycogen is exhausted does the organism resort to the more destructive cortisol-driven breakdown of tissue protein. 6 Peat argued that a surge of adrenaline serves as a practical warning to either improve efficient sugar metabolism or increase dietary carbohydrate intake. 6

The mechanistic consequences of adrenaline excess are profoundly disruptive to mitochondrial respiration. Adrenaline is lipolytic, liberating free fatty acids from storage. 3 When these liberated fats are polyunsaturated fatty acids (PUFAs), they directly inhibit the production and transport of thyroid hormone, interfere with mitochondrial respiratory functions, and block ATP production. 2 Peat detailed a cascade in which unsaturated fatty acids suppress mitochondrial respiration, stimulate serotonin secretion, and promote vascular leakage and edema. 9 Furthermore, adrenaline decreases the conversion of T4 to the active T3 hormone while increasing the formation of the antagonistic reverse T3. 3 On a cellular level, high concentrations of adrenaline decrease the efficiency of phosphorylation, an effect that can be fatal in the stressed heart when combined with adrenaline’s acceleration of clotting and constriction of blood vessels. 5

Clinically, Peat linked nocturnal adrenaline peaks to the sleep disturbances of hypothyroidism. Because blood sugar falls at night and hypothyroid people store very little glycogen, adrenaline typically peaks around 1 or 2 A.M., causing a pounding heart and insomnia that is often relieved by eating. 7 Peat recommended practical interventions to lower adrenaline, noting that salt is very effective at reducing it, and that consuming fat alongside carbohydrate at bedtime slows sugar absorption and helps sustain blood glucose through the night. 2 He also cautioned that introducing thyroid supplements to a person with a hyperadrenergic state must be done gradually over months, because even a small amount of T3 will acutely increase sensitivity to the existing excess adrenaline, causing overexcitation. 4 Danny Roddy has extended this framework by noting that environmental stressors, such as proximity to cell phone towers, have been documented to increase adrenaline release in populations. 10

Within the broader stress system, adrenaline operates as the first tier of a hierarchy. Peat distinguished the adaptive short-term mobilization of glycogen by adrenaline from the catabolic long-term action of cortisol, which breaks down muscle tissue for gluconeogenesis. 2 Roddy summarized this by categorizing adrenaline among the adaptive stress hormones that are protective in the short term but destructive when chronically elevated. 11 Peat also contrasted the mitochondrial effects of adrenaline with those of the parasympathetic system: while acetylcholine increases the efficiency of energy conservation and carbon dioxide production, adrenaline increases the rate of oxygen consumption via succinate oxidation, a pattern consistent with F.Z. Meerson’s conception of the parasympathetic system as a “stress limiting” mechanism. 5