A cross-sectional study on 220 men, aged 41-93 yr, was conducted to determine whether age-related changes in circulating pituitary and gonadal hormone levels are related to quantitatively assessed changes in sexuality over this age span. The conclusion of most previous studies, that total and free plasma testosterone (T) levels decline with advancing age as gonadotropins increase, was corroborated. These changes were found to roughly parallel a decline in sexual function affecting the level of sexual activity, libido, and potency measures. PRL and estradiol did not change with age, and the age-related decline in free T was greater than that in total T. Decreases in free T and increases in LH manifested significant, but small, correlations with sexual hypofunction. Behavioral variables were also clearly related to LH and to the ratio of free T to LH and estradiol. The data also suggested that aging and hormonal changes were more strongly related to sexual activity and nocturnal erections that to libido (enjoyment, drive, and thoughts). Partial correlation procedures demonstrated that diseases and drugs were not responsible for the hormone-behavior relationships. Declining androgen levels, reduced sexual activity, and decreased sexual interest thus appear to be related sequelae of the aging process in men. Hormonal factors do not completely account for age-related changes in sexuality, although the full explanation of these changes must include a consideration of hormonal factors.
Lesions of the suprachiasmatic nuclei (SCN) completely eliminated phasic LH release in ovariectomized rats as measured by the positive feedback response to estradiol benzoate (EB)/progesterone or the response to mating. Basal LH levels and the negative feedback response to EB were not affected. Lesions of the medial preoptic area (MPOA) or bed nucleus-dorsal MPOA also inhibited phasic LH release in ovariectomized rats as measured by positive feedback. However, the inhibition was not complete if there was no damage to the SCN, and the degree of inhibition was correlated with the size of the lesion. Basal LH levels and negative feedback were not significantly affected. It is suggested that both the SCN and MPOA are involved in phasic LH release, the former in its role as a neural regulator of circadian rhythms and the latter as part of a diffuse system possibly including estrogen-sensitive and/or LH-RH neurons. Sexual behavior (lordosis) in hormone-primed, ovariectomized rats was not significantly affected by lesions of any structure in the suprachiasmatic-preoptic region.
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