Endogenous opioids and hot flushes still hypothetical

Both withdrawal and activation of endogenous opioids have been suggested as mechanisms of menopausal hot flushes. Casper and Yen1 proposed that hot flushes are hypothalamic thermoregulatory events originating from increased brain norepinephrine activity due to decreased activity of hypothalamic opioids, which in turn is caused by oestrogen withdrawal. Consistent with this hypothesis, Elizabeth Nedstrand and colleagues recently proposed that acupuncture reduces the frequency of hot flushes by increasing hypothalamic beta-endorphin activity. However, opioid activation has also been suspected because people receiving chlorpropamide flush after drinking alcohol. Research has linked raised norepinephrine and opioids as well as oestrogen withdrawal to hot flushes, but current evidence is insufficient to ascertain the role of opioid withdrawal, because of an absence of studies with appropriate design.