Puberty and Resonance : A Hypothesis

A new mechanism for puberty is proposed . Puberty appears to result from the interaction of two physiologic oscillators within the hypothalamus : the arcuate nucleus, which produces the gonadotropin-releasing hormone, and the suprachiasmatic nucleus, which is a master oscillator that regulates many circadian rhythms . Puberty results when the frequency of the arcuate nucleus has slowed sufficiently to resonate with a harmonic of the suprachiasmatic nucleus rhythm . The onset of puberty is earlier in blind girls and rats reared in darkness because they have circadian rhythms which are more rapid than usual . Therefore, the frequency of the arcuate nucleus does not have to slow as much to resonate with the same harmonic of the suprachiasmatic nucleus rhythm, and puberty can occur at an earlier age. The proposed mechanism also accounts for the occurrence of luteinizing hormone pulses only during sleep in early puberty, and for the elevation of gonadotropins at birth. 39 autumn of 1909 (2, 3). In 1936 Hohlweg found that estradiol treatment was more effective suppressing castration hypertrophy in prepubertal rats than in adult rats (4) . Hohlweg's observation provided the rationale for the view, later put forward by Ramirez and McCann (5), that puberty is caused by a sudden decrease in sensitivity of the hypothalamic-pituitary unit to sex hormone feedback. The immature gonads were known to produce small amounts of sex steroids, even in very young animals . These hormones were believed to inhibit the hypothalamic-pituitary production of the gonadotropins, follicle stimulating hormone (FSH), and luteinizing hormone (LH). It was hypothesized that around the time of puberty, the hypothalamic-pituitary axis lost its sensitivity to such small amounts of sex steroids, a sudden outpouring of gonadotropins occurred, and puberty was the result. In other words, the "gonadostat" had been reset and would only respond to the feedback effect of much higher levels of sex hormones . In the past few years, assay techniques that make possible the continuous measurement of gonadotropin levels have cast doubt on the gonadostat hypothesis . These measurements reveal that LH, for example, is elevated not only at puberty but also at birth in both rats and humans (Fig. 1). In humans, LH falls between the ages of two and four, then rises again at puberty . This fluctuation, which corresponds with the period of