Historical Investigation
of PMS Etiology

Frank in 1931 initially found high serum estrogen and low estrogen metabolites in urine, or unopposed estrogen build up. Later studies (Greenhill, Bickers, Mukherjee) attributed PMS to water retention secondary to high estrogen and disrupted salt and fluid mechanisms, possibly adrenal. Sufferers of PMS were found to be B vitamin deficient in the 1940’s (Biskind), causing dysfunction of many biochemical pathways that B vitamins were cofactors in, including estrogen conjugation in the liver. Vitamin A (Simkins 1947) deficiency has been associated with decreased thyroid levels and increased estrogen levels.

PMS subjects demonstrate hyperinsulinism secondary to decreased adrenal function causing a reactive hypoglycemia (Morton 1952) with a flat GTT curve. Also noted was a melanocyte stimulating hormone increase which lowered dopamine, leading to depression, irritability and water retention.

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