Abstract
Hot flashes are the most prevalent symptom of menopause. Although the etiology of hot flashes has yet to be determined, it is increasingly apparent that the physiology of the underlying vasomotor instability is multifactorial. Estrogen and androgen receptors are present in the areas of the central nervous system relevant to hot flashes. Androgens are central to the synthesis of estrogen and to the bioavailability of free estrogen in peripheral tissues. In addition, androgens have direct central nervous system effects that modulate other endocrine factors associated with hot flashes. The pharmacodynamic differences of testosterone and methyltestosterone are briefly reviewed in the context of choice for individualized clinical use.
MeSH terms
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Algorithms
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Androgens* / deficiency
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Androgens* / physiology
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Androgens* / therapeutic use
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Biological Availability
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / physiology
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Body Temperature Regulation
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Central Nervous System / drug effects
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Central Nervous System / physiology
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Clinical Trials as Topic
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Decision Trees
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Estrogen Replacement Therapy / methods
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Evidence-Based Medicine
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Female
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Hormone Replacement Therapy / methods
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Hot Flashes / drug therapy*
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Hot Flashes / etiology
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Hot Flashes / metabolism
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Hot Flashes / physiopathology
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Humans
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Menopause* / drug effects
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Menopause* / physiology
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Methyltestosterone / pharmacology
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Methyltestosterone / therapeutic use
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Patient Selection
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Premenopause / drug effects
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Premenopause / physiology
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Receptors, Androgen / drug effects
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Receptors, Androgen / physiology
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Receptors, Estrogen / drug effects
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Receptors, Estrogen / physiology
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Testosterone / pharmacology
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Testosterone / therapeutic use
Substances
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Androgens
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Receptors, Androgen
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Receptors, Estrogen
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Testosterone
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Methyltestosterone