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To the Editor: Dr Zandi and colleagues¹ found that postmenopausal estrogen replacement therapy (ERT) reduced the risk of Alzheimer disease (AD), but only among long-term users of ERT. It is possible, however, that some of this trend may be mediated by indirect effects of estrogen. In particular, serum concentrations of gonadotropins, luteinizing hormone, and follicle-stimulating hormone are sensitive to changes in estrogen, since gonadotropins are the primary regulator of estrogen production. In postmenopausal women, the loss of estrogen results in a significant increase in circulating gonadotropin concentrations.² Conversely, when women take ERT, gonadotropin concentrations are suppressed due to the inhibitory feedback of estrogen on the hypothalamic-pituitary-gonadal axis.³ Thus, the effects of ERT may be related to hormones other than estrogen.

In their accompanying Editorial, Drs Resnick and Henderson⁴ suggest the idea of a "critical period" for the timing of ERT. Such a temporal effect might be better explained by changes . . . [Full Text of this Article]

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