Miscarriage and Preeclampsia

Preeclampsia is fundamentally a disorder of malnutrition, not a genetic inevitability, and its progression reflects a cascade of physiological stress that can culminate in eclampsia (convulsions) and fetal damage. 3 Ray Peat argued that the medical dogma of genetic determinism, which blamed "bad genes" for eclampsia and poverty, served to obscure the central role of protein deficiency and salt restriction in causing the condition. 2 The work of Tom Brewer was pivotal in demonstrating that ensuring pregnant women consumed adequate protein (at least 80 grams daily), salted their food to taste, and drank plenty of milk could essentially prevent preeclampsia, directly contradicting the then-standard practice of prescribing low-salt diets and diuretics. 3

The mechanistic chain of causality begins with a diet deficient in protein, which impairs liver function. 2 This impairment reduces the liver's capacity to store glycogen, inactivate estrogen, and produce albumin. 2 Concurrently, high estrogen actively destroys the liver's ability to produce albumin, while low thyroid function causes sodium to be lost. 3 The resulting loss of sodium albuminate leads to tissue edema, but critically, the blood volume is decreased, a state of hypovolemia and hemoconcentration that impairs circulation and paradoxically increases blood pressure. 2 This hypovolemic state is exacerbated by the nighttime rise in stress hormones like adrenalin and cortisol, which makes blood more viscous and prone to clotting. 1 The unstable blood sugar and rising cortisol further increase the likelihood of premature labor, while the combination of high estrogen, hypoglycemia, and viscous, clot-prone blood can trigger the seizures characteristic of eclampsia. 4

Peat identified thyroid as the "essential fertility hormone" because it suppresses excessive estrogen and supports the production of protective hormones like progesterone and pregnenolone. 3 A low thyroid state, indicated by a TSH level above 2.5 during pregnancy, contributes directly to the pathology by preventing cells from retaining magnesium, a mineral traditionally used intravenously to stop eclamptic convulsions. 2 Peat noted that administering triiodothyronine (T3) promotes cellular absorption of magnesium, and that without adequate thyroid function, supplemented magnesium is simply excreted in the urine. 2 Progesterone itself is a crucial protective factor; researchers found that a single injection could sometimes eliminate signs of toxemia, and Katherina Dalton's work showed that progesterone treatment throughout pregnancy resulted in remarkably healthy offspring with high IQs, in stark contrast to the average IQ of 85 for babies delivered after a toxemic pregnancy. 6 This protective effect is partly mediated through glucose and oxygen availability to the fetal brain, countering estrogen's demonstrated effect of reducing cerebral cortex size. 6

The clinical picture is one of systemic energy failure and circulatory collapse. The failing physiology shifts from efficient glucose oxidation to the inefficient use of free unsaturated fatty acids, a state mirrored in heart failure and shock. 1 Aspirin has been shown to protect against intrauterine growth retardation, likely by counteracting excesses of unsaturated fatty acids and estrogen, though its use near childbirth is risky due to its anticoagulant effects. 1 The most effective interventions are nutritional: consuming high-quality protein from sources like milk, eggs, and potatoes to restore serum albumin and osmotic pressure, and liberal salt intake to restore blood volume and proper oxygenation of the fetus. 2 Peat emphasized that simply eating extra protein quickly restores blood albumin, and that hypertonic solutions of glucose and sodium, along with magnesium and T3, would be ideal to address the shock-like state by restoring blood volume and reducing the wasteful conversion of glucose to lactic acid. 1