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glucose transport, hot flashes, menopause



  1. Dormire, Sharon L.
  2. Reame, Nancy King


Objective: Although a majority of women (80%) at menopause experience hot flashes, the symptoms' physiological trigger has yet to be identified. To determine the relationship between glucose availability and hot flashes in menopausal women, hot flash frequency was compared between intervals while the subjects were fasting and/or infusing in a sample of menopausal women (38-55 years of age).


Design: An experimental study was conducted in 10 postmenopausal women taking hormone therapy (HT) between the ages of 38 and 55. Following a clinic visit to screen for general health and absence of diabetes, HT participants were asked to stop the medication for 7 to 10 days and to maintain a diary of hot flash frequency. When hot flashes were experienced at least four times per day in a consecutive 3-day period, participants were admitted to the General Clinical Research Center for a 30-hour experimental protocol, including frequent blood sampling and two experimental periods of intravenous infusion of glucose or normal saline. Blood glucose levels were manipulated to provide conditions of postprandial versus fasting states.


Results: There was a significant reduction in the incidence of hot flashes during the experimental elevation of glucose concentrations (130 to 140 mg/dl) compared to the fasting state (<110 mg/dl) (t = -2.4, df = 9, p = .04).


Conclusions: Conditions of fasting may stimulate the trigger mechanism for menopausal hot flashes.


The hot flash is the most frequently reported symptom of menopause. It is generally associated with declining estrogen levels related to depletion of ovarian follicles in the aging ovary, although a direct cause and effect relationship between estrogen level and hot flashes has not been demonstrated (Sterns & Hayes, 2002). Furthermore, in most studies absolute concentrations of estrogen neither predict nor correlate with hot flash severity (Freedman, 2002;Hutton, Jacobs, Murray, & James, 1978). While various hypotheses have been proposed, the mechanism is unknown by which estrogen decline at menopause causes activation of sympathetic heat dissipation.


A majority of women (75-80%) undergoing the natural course of menopause and an even greater number of oophorectomized women (95-100%) experience hot flashes associated with the decline in ovarian steroids (Bachmann, 1999). Currently in the United States, there are 20,047,000 women of menopausal age (45-54), of which an estimated 15,035,250 experience hot flashes (United States Census Bureau, 1999). Approximately 3 million of those women seek medical assistance for symptom relief. The current optimal treatment for hot flashes is use of hormone replacement therapy (HT). However, recent findings regarding potential risks in use of HT reported in the Heart and Estrogen Replacement Study II (Grady et al., 2002) and the Women's Health Initiative (Writing group for the Women's Health Initiative Investigators, 2002) create complex decision-making dilemmas for women suffering from hot flashes. Research focused on uncovering the hot flash mechanism has the potential to redirect treatment strategies.


An emerging model based on rat studies suggests that menopausal hot flashes result from transient inadequacies in central nervous system glucose transport (Shi & Simpkins, 1997). The decline in glucose delivery to the brain is a secondary result of diminished estrogen-stimulation of glucose transporter production. With fewer glucose transporter molecules available to maintain adequate glucose transport, the brain receives less glucose. This is further compounded under physiological conditions such as fasting, in which less glucose is available for transport. The end result is a transient alteration in available glucose to brain neurons (Shi & Simpkins, 1997). In this paradigm, the hot flash is viewed as a counter-regulatory attempt to increase blood flow and subsequent delivery of glucose to the brain.


The purpose of this study was to examine the research question:Is there a significant difference in the incidence of menopausal hot flashes between conditions of fasting and experimentally sustained (130 to 140 mg/dl) blood glucose concentrations?