estrogen replacement therapy (ERT), tends to ameliorate dysfunction in carbohydrate metabolism (see reviews by Sharp and Diamond, 1993; Gaspard et al., 1995; FaustiniFustini et al., 1999; Meinhardt and Mullis, 2002; Rochira et al., 2002; Murata et al., 2002). Estrogen also has demonstrable cardiovascular protective effects, such as associated reductions in lipid levels and suppression of the vascular response to chronic inflammatory stress (Gaspard et al., 1995; Farhat et al., 1996; Nathan and Chaudhuri, 1997; Mendelsohn and Karas, 2001; Mendelsohn, 2002; Baker et al., 2003). It should be noted, however, that there is still considerable controversy surrounding estrogen’s role in cardiovascular protection (Barrett-Connor and Grady, 1998; Mendelsohn and Karas, 2001; Mikkola and Clarkson, 2002; Pradhan and Sumpio, 2004). Taken all together, the two main features of Finch’s neuroendocrine cascade hypothesis seem to be upheld. The pathologies of senescence, such as those associated with the metabolic syndrome, do in fact involve neuroendocrine cascades. Further, these neuroendocrine cascades are late-life occurrences of homeostatic mechanisms that operate in coordinated fashion during developmentally critical periods in ontogeny well before the onset of senescence. Evolutionary Ramifications: Relation to the Evolution of Senescence
As indicated in the background chapter on senescence and the IGF-I axis, the evolution of senescence can be explained by the disposable soma (DS) theory. However, the DS theory—in its present formulation at least—can say nothing about the statistical genetic expectations regarding senescence. On the other hand, there are two other theories of the evolution of senescence that are formulated in terms of population genetics and that make statistical genetic predictions (these should be viewed as being
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