Aging, Health, and Reproductive Options

As men age, the force of mortality shifts from extrinsic to intrinsic sources. Hormone levels also change with age, although there is considerable between- and within- population variation in the degree of age-related decreases in testosterone (Ellison et al. 2002; Harman et al. 2001). Other hormones, such as gonadotropins, tend to exhibit less population variation in association with age although few non-Western populations have been examined (Bribiescas 2005). While decreases in male fertility and reproductive hormones are likely influenced by decreased selection pressure, aging can also influence male reproductive strategies. While women undergo menopause around the age of 50, and men exhibit a “decline in fertility”, significant potential for reproduction remains until death in a broad range of populations (Tuljapurkar et al. 2007). The prospect of continued fitness even at later ages opens the door for selection for reproductive strategies that are conducive with the inevitable somatic and health changes that occur with aging and senescence (Bribiescas 2006a, b, 2010).

Unlike other great apes (Muller and Wrangham 2004; Emery Thompson et al.

2012), human males appear to have evolved the capacity to decouple physical vigor from reproductive fitness. For example, among Ache men, physical strength is greatest in the early twenties (Walker and Hill 2003). However hunting efficiency, a trait that has been associated with reproductive success (Kaplan and Hill 1985), is highest when men are in their forties (Walker et al. 2002). The implication is that compared to other great apes, human male reproductive strategies have the capacity for some adjustment to somatic aging, most likely through leveraging greater cognitive capacity, larger brains, and the evolution of extrasomatic assets such as tools and social complexity.

Nonetheless, men must adapt to the natural degenerative changes that occur with aging. Indeed, given the long lives of humans, the capacity for significant fertility at older ages, and the broad range of reproductive strategies, there should be selection for protective mechanisms that attenuate age-related sources of intrinsic mortality and morbidity. One primary source of intrinsic mortality that is theorized to be associated with aging is oxidative stress and damage. Toxic reactive oxygen species (ROS), such as superoxide molecules, are created during aerobic metabolism and can outpace the body’s ability to absorb or disarm them. There is evidence that excess ROS damage cellular components, including DNA, and this damage is implicated in many aging-related illnesses (Finkel and Holbrook 2000). Other downstream toxins such as hydrogen peroxide can induce lipid peroxidation and damage cellular components and also contribute to aging.

Given the shorter life spans of males in many species, Alonso-Alvarez theorized that testosterone-driven increases in metabolic rate during prenatal development may contribute to overall male fragility compared to females (Alonso-Alvarez et al.

2007). Data from zebra finches has provided some preliminary support for this theory (Tobler and Sandell 2009; Tobler et al. 2013), but results are mixed for men. Since men tend to exhibit shorter life spans compared to women, it might be predicted that men would present higher levels of oxidative stress compared to women, perhaps in response to higher metabolic rates. But this does not seem to be the case. In two large epidemiological studies in the USA and Japan, men were found to have lower levels of peroxidative stress as measured in venous blood and urine, respectively (Sakano et al. 2009; Block et al. 2002). Greater adiposity in women was initially believed to underlie this result; however, corrections for body mass index (BMI) did not alter the difference. Body fat was not measured directly.

A study of dose-dependent responses to testosterone administration after treatment with a GnRH agonist resulted in different levels of oxidative stress in older and younger men. Younger men showed a significant decrease in oxidative stress, while older men did not (Roberts et al. 2014). However, results from these studies merit caution since many potentially relevant factors were not considered. Investigations that attempt to test the existence of a trade-off between mating effort (higher testosterone) and oxidative stress often fail to account for important factors such as energetic status, key resource restriction, and appropriate assessments of reproductive effort (Metcalfe and Monaghan 2013).

Studies using measures of whole-body oxidative stress may not detect localized or cumulative tissue-specific effects implicated in aging-related disease and dysfunction. For example, testosterone promotes greater levels of DNA damage in prostate cancer cell lines in culture (Ide et al. 2012). More tissue-specific effects of

Clinical Dementia Rating Scale Sum of Boxes Scores

Fig. 6.5 Clinical Dementia Rating Scale Sum of Boxes Scores (CDRSUM), a measure of cognitive dysfunction, and the influence of oxidative stress and endogenous testosterone. In the high oxidative stress condition, testosterone significantly increased CDRSUM scores in Caucasian men, but significantly decreased CDRSUM scores in Mexican American men (Cunningham et al. 2014)

ROS, such as on aging-related changes in cognitive function, have also received attention. Cunningham and colleagues (Cunningham et al. 2014), for example, examined oxidative stress, testosterone levels, and level of cognitive dysfunction in normal, mildly cognitive impaired, and Alzheimer’s disease patients. Their result showed that white male Alzheimer’s disease patients with high testosterone and high oxidative stress (as measured by looking at levels of superoxide dismutase 1 and glutathione S-transferase alpha in venous blood) exhibited significantly higher levels of cognitive dysfunction (Fig. 6.5).

The role of oxidative stress and other forms of aging-related cellular damage is a ripe area of research for human evolutionary biologists and others interested in pleiotropic effects that may underlie men’s health challenges. New technologies and the deployment of these research methods to a broader range of human populations, cultures, and ecological settings are likely to yield promising and informative results.

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