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The MacArthur studies provide evidence for age-specific sex differences in AL [8]. In assessing the 12-year mortality risk between the sexes, Gruenewald et al. [12] found that high-risk pathways of AL biomarker clustering for men included adrenalin, noradrenalin, interleukin-6, C-reactive protein, and fibrinogen, while, for women, the pathways included interleukin-6, C-reactive protein, glycosylated hemoglobin, and systolic blood pressure. Interestingly, elevated systolic blood pressure occurred in 100% of female high-risk pathways but only in 17% of male high-risk pathways principally dominated by elevated fibrinogen, noradrenalin, and adrenalin levels, otherwise completely absent for females. In an earlier analysis of the MacArthur cohort, however, cardiovascular biomarkers were more often dysregulated for males, while neuroendocrine biomarkers were more often dysregulated for females [13].

These findings from the same cohort measured at different time points reveal that AL pathways indeed differ between the sexes, although sex-specific biomarker clusters might only emerge with advanced age. Indeed, data from a 15-year follow-up study using the Coronary Artery Risk Development in Young Adults (CARDIA) study found little evidence for sex or ethnicity differences in 40-year-old participants. Nevertheless, it must be noted that aggregate meta-factors including heart rate variability, blood pressure, inflammatory, metabolic, catecholaminergic, and gluco-corticoid biomarkers captured 84% of the statistical variance, suggesting that AL biomarkers indeed form a constellation of shared interrelations consistent with theory [14]. However, subtle physiological dysregulations of intertwined systems may not be easily detected and they do not differ significantly between the sexes when assessing younger adults. Consequently, it will be important to determine meaningful subclinical ranges of biomarkers between the sexes and among ages.

Table 1. Summary of AL findings throughout the lifespan

The cumulative physiological toll of AL is consistently associated with increasing age in populations worldwide but is nevertheless even detectable in disadvantaged children and adolescents (table 1). From a developmental perspective, we observe that increased AL and senescence interact with a vast array of risk factors and protective factors that carry different health benefits or detriments that affect different age groups in particular. Specifically, such factors as social support, work/home balance, hostility, caregiving, and spirituality are gender typical and of clinical importance as they are steadily associated with increased AL.