Explicating hypergonadotropism in postmenopausal women: a statistical model

Neurohormone secretion is viewed here as a variable (unknown) admixture of basal and pulsatile release mechanisms, convolved with individually fitted biexponential elimination kinetics. This construct allows maximum-likelihood estimates of both (regulated and constitutive) components of hormone secretion. Thereby we infer that a prolonged slow-component half-life of gonadotropin removal and amplified pulsatile (and total) daily luteinizing hormone (LII) secretion rates jointly explicate the postmenopausal elevation in serum LH concentrations without a necessary rise in basal LII secretion rates. This biomathematical formulation should be useful in exploring other neuroregulatory mechanisms that underlie single or dual alterations in the basal versus pulsatile modes of hormone secretion.