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Adrenal in the adult male
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
What is, then, the physiological role of the ‘adrenal androgens’? Adrenal androgen and cortisol synthesis are both regulated by ACTH. In contrast with cortisol levels, which are constant throughout life, adrenal androgen levels are very low in childhood, rise during adrenarche to very high levels with maximum values at about 25 years and after that decline continuously to a low plateau value at about 60 years of age (adrenopause). Cortisol and adrenal androgens are synthesized from their common precursor 17α-hydroxy-5-pregnenolone (17OH5P). DHEA and 17OHP represent the first steps after 17OH5P, leading to adrenal androgens and to cortisol respectively (Figure 5). The ∂DHEA values following acute ACTH stimulation show the same age-related change as basal DHEA/DHEAS values, but the ∂17OHP values change in the opposite direction, with minimum values at about 25 years of age (Figure 6). Cortisol levels increase and adrenal androgens decrease in stressful situations such as trauma, chronic disease and malnutrition10.
Vasomotor symptoms and neurovegetative comorbidities on the menopause: insights from an Italian quantitative research
Published in Gynecological Endocrinology, 2019
Alessandra Graziottin, Vivek Banerji, Genevieve Hall
Although the VMS appearance coincides with estrogen decrease and withdrawal, this is not the only etiological cause of the condition since estrogen levels do not differ between symptomatic and asymptomatic women [10]. Genetic variability in brain (and other tissues) sensitivity to sexual hormones’ loss could contribute to the VMS variability. Moreover, the degree of decline of ovarian (menopause) and residual adrenal (adrenopause) production of sexual hormones could further contribute to the variability of VMS. New data suggest that changes in the intestinal microbiota and gut–brain axis may further modulate the individual well-being and potentially contribute to brain vulnerability (both as Central Nervous System, CNS, and Enteric Nervous System, ENS, or ‘gut–brain’) during and after the menopause [11]. On the other hand, modifications in the neurotransmitters levels (mainly serotonin and noradrenalin) and the dysregulation of systemic arterial tree may also have an important implication in VMS emergence during the menopause [12].
Involvement of serum dehydroepiandrosterone sulfate in erythropoietic activity
Published in The Aging Male, 2020
Ko Harada, Yoshihisa Hanayama, Mikako Obika, Koichi Itoshima, Ken Okada, Fumio Otsuka
Dehydroepiandrosterone (DHEA) is a steroid hormone produced in the adrenal cortex. It is synthesized from pregnenolone and further metabolized to androstenedione, testosterone, and estrogen. DHEA and its sulfated ester (DHEAS) are the most abundant circulating steroids in humans. DHEAS is converted to DHEA in a linear manner. Because its serum concentration is 300–500 times higher than that of DHEA, DHEAS serves as a circulating reservoir for DHEA [1]. DHEAS secretion increases during adrenarche, peaks between the ages of 15–25 years, and decreases steadily with age thereafter [2,3]. This age-related decline in DHEAS secretion is termed adrenopause [4] and is presumably the result of the normal aging processes [5].
Clinical relevance of insulin-like growth factor-1 to cardiovascular risk markers
Published in The Aging Male, 2020
Ko Harada, Yoshihisa Hanayama, Mikako Obika, Koichi Itoshima, Ken Okada, Fumio Otsuka
During the physiological process of aging, four hormone systems demonstrate declines in circulating hormone concentrations, namely, dehydroepiandrosterone and its sulfate in “adrenopause”, estrogen in “menopause”, testosterone in “andropause”, and the GH/IGF-1 axis in “somatopause” [2–4]. Among them, serum IGF-1 levels peak in the second decade of life, but subsequently decline rapidly until the sixth decade, when they plateau [5]. Owing to this pattern, IGF-1 is believed to contribute to the age-related loss of vitality, vigor, muscle mass, physical function, and activities of daily living, and to frailty and deterioration of mental function [6].