Excerpt from Eclampsia in the Real Organism: A Paradigm of General Distress Applicable in Infants, Adults, Etc. by Ray Peat PhD

In outline, we can visualize a chain of causality beginning with a diet deficient in protein, impairing liver function, producing inability to store glycogen, to inactivate estrogen and insulin, and to activate thyroid. Low protein and high estrogen cause increased tendency of the blood to clot. High estrogen destroys the liver’s ability to produce albumin (G. Belasco and G. Braverman, Control of Messenger RNA Stability, Academic Press, 1994). Low thyroid causes sodium to be lost. The loss of sodium albuminate causes tissue edema, while the blood volume is decreased. Decreased blood volume and hemoconcentration (red cells form a larger fraction of the blood) impair the circulation. Blood pressure increases. Blood sugar becomes unstable, cortisol rises, increasing the likelihood of premature labor. High estrogen, hypoglycemia, viscous blood, increased tendency of the blood to clot cause seizures. Women who die from eclampsia often have extensive intravascular clotting, and sometimes the brain and liver show evidence of earlier damage, probably from clots that have been cleared. (Sometimes prolonged clotting consumes fibrinogen, causing inability to clot, and a tendency to hemorrhage.) M. M. Singh, “Carbohydrate metabolism in pre-eclampsia,” Br. J. Obstet. Gynaecol. 83, 124-131. 1976. Sodium decrease, R. L. Searcy, Diagnostic Biochemistry, McGraw-Hill, 1969. Viscosity, L. C. Chesley, ‘Hypertensive Disorders in Pregnancy, Appleton-Century-Crofts, 1978. Clotting, T. Chatterjee, et al., “Studies on plasma fibrinogen level in preeclampsia and eclampsia, Experientia 34, 562-3, 1978; D. M. Haynes, “Medical Complications During Pregnancy, McGraw-Hill Co. Blakiston Div., 1969. Progesterone decrease, G. V. Smith, et al., “Estrogen and progestin metabolism in pregnant women, with especial reference to pre-eclamptic toxemia and the effect of hormone administration,” Am. J. Obstet. Gynecol. 39, 405, 1940; R. L. Searcy, Diagnostic Biochemistry, McGraw-Hill, 1969.

Katherina Dalton observed that her patients who suffered from PMS (and were benefitted by progesterone treatment) were likely to develop “toxemia” when they became pregnant, and to have problems at the time of menopause. In these women, it is common for “menstruation” to continue on the normal cycle during the first several months of pregnancy. This cyclic bleeding seems to represent times of an increased ratio of estrogen to progesterone, and during such periods of cyclic bleeding the risk of miscarriage is high. Researchers found that a single injection of progesterone could sometimes eliminate the signs of toxemia for the remainder of the pregnancy. Katherina Dalton, who continued to give her patients progesterone throughout pregnancy, later learned that the babies treated in this way were remarkably healthy and bright, while the average baby delivered after a “toxemic” pregnancy has an IQ of only 85.

Marian Diamond’s work with rats clearly showed that increased exposure to estrogen during pregnancy reduced the size of the cerebral cortex and the animals’ ability to learn, while progesterone increased the brain size and intelligence. Zamenhof’s studies suggested that these hormones probably have their effects largely through their actions on glucose, though they also affect the availability of oxygen in the same way, and have a variety of direct effects on brain cells that would operate toward the same end.

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