Aldosterone

Aldosterone is an adrenal steroid hormone whose chronic elevation Ray Peat treated as a primary driver of inflammation, fibrosis, and degenerative disease, referring to it increasingly as an endogenous toxin. 2 Its canonical role is to retain sodium, but Peat emphasized that it achieves this at the expense of the increased loss of potassium, magnesium, and probably calcium, a mineral disruption that directly causes heart rhythm problems by impairing the repolarization of cardiac muscle. 2 Secretion rises nocturnally, and this rise is exaggerated in depressed, stressed, and aging individuals, linking it to the worsening of inflammatory conditions like rheumatoid arthritis and asthma during the night. 2

The primary physiological trigger for aldosterone synthesis is a perceived deficit of sodium chloride or blood volume. Peat argued that low sodium intake, hypothyroidism (which causes sodium loss), low blood sugar, and protein deficiency all signal the kidneys to activate the renin-angiotensin system, increasing aldosterone to retain sodium. 3 This creates a pathological paradox where a sodium-restricted diet activates processes that cause cells to take up sodium inappropriately, leading to intracellular swelling and alkalinity. 10 Georgi Dinkov has noted that this mechanism makes mainstream guidelines for restricting dietary sodium in heart failure nonsensical, as the resulting spike in aldosterone is itself a primary contributor to heart failure. 5 Peat observed that pre-emptive salt loading over several days allows aldosterone to adjust downward, preventing the edema that a sudden dose of salt can cause. 9

Aldosterone’s pro-inflammatory effects are amplified by a network of other stress mediators. Serotonin, estrogen, and cortisol all increase its secretion, while aldosterone itself promotes the formation of angiotensin II, a potent inflammatory messenger. 2 It inhibits oxidative energy metabolism, increases insulin resistance, and stimulates the production of proinflammatory substances in fat cells. 2 Peat detailed that aldosterone activates the enzyme ornithine decarboxylase (ODC) to produce polyamines that promote cell division, and it raises intracellular pH, both factors that stimulate inappropriate cell proliferation and set the stage for fibrosis. 10 Parathyroid hormone (PTH), which rises on a calcium-deficient diet, further increases aldosterone, creating a link between low calcium intake and hypertension. 7

The suppression of aldosterone is a hallmark of a high-energy, anti-inflammatory state. Peat explained that the adrenal cortex produces aldosterone first in the shock phase, but as the organism survives with adequate sugar, it shifts toward producing glucocorticoids and finally the protective sex steroids. 6 Once in this healthy state, an abundance of progesterone and testosterone actively turns off aldosterone production. 6 Nutritional interventions that lower aldosterone include adequate sodium chloride, calcium, and vitamin D, as well as gelatin, which lacks tryptophan and thus limits the formation of serotonin, a major activator of aldosterone synthesis. 3 Sodium bicarbonate can also lower aldosterone by providing sodium and converting to carbon dioxide, which acidifies cells into a protected, oxidized state. 8 Danny Roddy has summarized that aldosterone, alongside adrenaline, cortisol, serotonin, estrogen, prolactin, and PTH, constitutes a core group of adaptive hormones that suppress the metabolic rate and undermine the goal of producing youthful energy. 3