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THE general belief that the thyroid is related to reproductive function in the human female arose from the observations that the thyroid enlarges at puberty, at menstruation and during pregnancy (Gamier, 1921; Marine, 1935; Neumann, 1937; and others). This opinion was strengthened 1) by reports that sterility is frequently associated with a basal metabolic rate of –10 or lower (Litzenberg, 1926; Litzenberg and Carey, 1929), and 2) that pregnancy often occurs after treatment with thryoid preparations (Hertoghe, 1914; Veil, 1917; Huntington, 1929; Breckenridge, 1932; Mussey, 1938; King and Herring, 1939; Mason, 1939; Nicodemus and Ritmiller, 1945). Hypothyroidism has been incriminated as a causative factor in secondary amenorrhea and menorrhagia (Hertoghe, 1914; Garnier, 1921; Fluhmann and Murphy, 1941). These and other menstrual irregularities are often alleviated by thyroid therapy (Breckenridge, 1932; Mussey and Haines, 1934; Mason, 1939; Mussey, 1939; Foster and Foster, 1941; Lisser, 1942; Thompson, Thompson and Jeppson, 1947).
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Peterson et al. (1952) studied this question.
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