Menopause and Andropause

Menopause is a discrete event defined retrospectively: the final menstrual period, confirmed after twelve consecutive months without bleeding. Its cause is exhaustion of the ovarian follicle pool, so inhibin B and estradiol fall, negative feedback on the pituitary is lost and FSH rises sharply into a hypergonadotropic state. Andropause is structurally different: Leydig output declines slowly across decades while LH rises only modestly, a mixed primary and secondary picture rather than clean gonadal failure.

The median age at menopause is around 51 in Western populations, and the STRAW+10 system stages the transition by cycle variability rather than by hormone levels. Male testosterone falls roughly one percent a year from midlife, but the European Male Ageing Study found only about two percent of men aged 40 to 79 met a syndromic definition combining three sexual symptoms with both a low total and a low free testosterone. Menopause happens to every woman who lives long enough; late-onset hypogonadism does not.

That difference decides how each is diagnosed. Menopause needs no blood test in a woman over 45 with typical symptoms, and an FSH adds little because it swings wildly through perimenopause. Male hypogonadism does need biochemistry, repeated on two morning samples, because its symptoms - fatigue, low mood, reduced libido - are shared with obesity, sleep apnoea, depression and opioid use, each of which lowers testosterone.

The clinical error is importing the menopause framing into male ageing: if the decline were universal and hormonal, replacement would look like restoring a deficiency, and marketing leans hard on that symmetry. The reverse error also happens, with perimenopause dismissed because one FSH came back normal. It often does, since the transition is defined by erratic hormones rather than by a persistently low estradiol.