Physiology of hot flashes

Authors
Citation
Rr. Freedman, Physiology of hot flashes, AM J HUM B, 13(4), 2001, pp. 453-464
Citations number
65
Categorie Soggetti
Sociology & Antropology","Medical Research General Topics
Journal title
AMERICAN JOURNAL OF HUMAN BIOLOGY
ISSN journal
10420533 → ACNP
Volume
13
Issue
4
Year of publication
2001
Pages
453 - 464
Database
ISI
SICI code
1042-0533(200107/08)13:4<453:POHF>2.0.ZU;2-H
Abstract
Hot flashes are the most common symptom of the climacteric, although preval ence estimates are lower in some rural and non-Western areas. The symptoms are characteristic of a heat-dissipation response and consist of sweating o n the face, neck, and chest, as well as peripheral vasodilation. Although h ot flashes clearly accompany the estrogen withdrawal at menopause, estrogen alone is not responsible since levels do not differ between symptomatic an d asymptomatic women. ne Until recently it was thought that hot flashes wer e triggered by a sudden, downward resetting of the hypothalamic setpoint, s ince there was no evidence of increased core body temperature. Evidence obt ained using a rapidly responding ingested telemetry pill indicates that the thermoneutral zone, within which sweating, peripheral vasodilation, and sh ivering do not occur, is virtually nonexistent in symptomatic women but nor mal (about 0.4 degreesC) in asymptomatic women. The results suggest that sm all temperature elevations preceding hot flashes acting within a reduced th ermoneutral zone constitute the triggering mechanism. Central sympathetic a ctivation is also elevated in symptomatic women which, in animal studies, r educes the thermoneutral zone. Clonidine reduces central sympathetic activa tion, widens the thermoneutral zone, and ameliorates hot flashes. Estrogen virtually eliminates hot flashes but its mechanism of action is not known. (C) 2001 Wiley-Liss, Inc.