As noted, the initial three parts of the chapter (Sections 3.2 to 3.4) focussed upon themes related to gender, age and ageing from the social sciences that have influenced archaeological practice in relation to identity studies. The chapter now pivots towards an engagement with a range of theoretical and biological fields that are also engaged with the broad subject of human ageing. The initial section of this group (Section 3.5) discusses some of the major developments, with a specific focus on childhood and senescence, towards evolutionary aspects of ageing. This then followed, at Section 3.6,
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with a discussion on human ageing and bioarchaeological approaches to age estimations in relation to subadults and the elderly.
The human ageing process is complex with a range of conflicting theories vying towards the explanation of post-maturational decline and senescence (Crews, 1993, Crews, 2003). Growth and developmental changes in the early phases (i.e. embryonic, pre-natal, post-natal etc.) of life are well understood (see Section 3.6). Further, evolutionary studies of primates have found that the phases of childhood and adolescence are significant to humans with childhood being identified as a unique period of development across the lifespan (Key, 2000, Halcrow and Tayles, 2008a). Bogin notes that childhood includes the infant period from 3 to 7 years followed by the juvenile, pubescent and adolescent phases (Bogin, 1996, Bogin, 1999, Bogin, 2001). From an evolutionary perspective, childhood follows the weaning period and ceases when the brain has stopped growing (at 7 years) (Bogin, 1997, Bogin, 1999). It is characterised as the key period of cognitive development, although the child still requires assistance for security and sustenance (Bogin, 1996, Bogin, 1997). In addition, Bogin argues that additional advantages to the presence of a human childhood period relate to developmental plasticity; the ‘cost’
benefits of slow growth and body size for limited resources in competition with adults; the social benefits of a slow childhood coupled with cognitive development enabling care-giving flexibility by a social group or by the individual as they mature; that care-giving
is stimulated, neurologically, by the child’s appearance and; as an adaptive period for
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Notwithstanding, studies related to the processes involved in extreme ageing, longevity, and senescence remain elusive and contested (Crews, 2003, Goldsmith, 2006). Modern demographic profiles indicate increased longevity with the elderly continuing to be associated with physiological and functional decline, trauma, infection and malnutrition (Finch, 2007) more or less mediated by sex, ethnicity, and socio-economic status (Crews, 1993, Finch, 2007). Studies focussed on understanding the human ageing process (including longevity and senescence) are dominated by a broad range of theories categorised as programmed or damage-based theories (Schulz-Aellen, 1997, Holliday, 2007, Sigelman and Rider, 2009, Cefalu, 2011). Senescence relates to biological change where the individual, through the process of ageing, is less able to maintain homeostasis and physiological functionality due to internal and external factors (Crews, 2003). Early theorists of human senescence argued for the key role of genetic
programming where, once the periods of growth and reproductive fitness has elapsed, the survivability of the organism is increasingly diminished (Licastro et al., 2005, Austad and Kirkwood, 2008). A good example of this is the effect of immunosenescence in relation to age-related diseases where there is a trade-off of immunity benefits of resistance to disease between the early and later (post-reproductive) stages of life (Licastro et al., 2005).
The ‘Hayflick Limit’, which relates to the accumulation of mutated genes, or antagonistic pleiotropy, is a dominant theory regarding human ageing. Hayflick, through in vitro
culturing of human embryonic fibroblasts, found that cells doubled a maximum of fifty times for infants but that cellular doubling decreased significantly in the very old
(Hayflick, 1980, Sigelman and Rider, 2009). Further research found that the cessation of growth in human fibroblasts is primarily caused by the shortening, or loss, of telomeric
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DNA at each chromosomal mitosis event (Klapper et al., 2001, Zhang et al., 2016). Telomeres occupy the tips of each eukaryotic chromosome and are shortened following a
cell’s division (Sigelman and Rider, 2009, Zhang et al., 2016). This process is thought to be highly deterministic in biological ageing. Studies found that with each cell division its chromosome replicates but that its telomere does not as, with each chromosomal replication, the telomere is split between the new and old chromosome (Sigelman and Rider, 2009). It is hypothesised that continuous shortening of telomeres (absence of telomerase activity), which increases as humans age (decreased doubling), ultimately brings about cellular death and through it senescence (Klapper et al., 2001, Crews, 2003, Miller, 2009, Cefalu, 2011). Apoptosis (programmed cell death) occurs to provide increased survivability (i.e. cellular homeostasis, removal of mutated and/or cancerous cells, T cells etc.) following the death of defective cells (Crews, 2003, Gupta et al., 2005, Cefalu, 2011). Supporters of ageing as a consequence of an accumulation of mutated genes argue that an adaptation to an organism’s fitness in early life are offset, at a biochemical and physiological level, in the latter aspects of the lifespan where maintenance and repair of a system are negatively impacted (Bellamy, 1995, Crews, 2003). Antagonistic pleiotropy, introduced by Williams in the 1950s and underpinned by natural selection, suggests that genetic mutations in the organism may be positive in the earlier phases of the life cycle (survivability) with respect to reproductive fitness but that these mutations are offset in the latter phases of the life cycle (Ikels and Beall, 2001, Aviv et al., 2003, Goldsmith, 2006, Finch, 2007, Austad and Kirkwood, 2008). Similarly, the Disposable Soma Theory sees deleterious ageing occur in the latter parts of the lifespan from an accumulation of randomly damaged cellular and molecular sources to offset benefits to the maintenance of the organism during its growth and reproductive phases (Goldsmith, 2006, Austad and Kirkwood, 2008). The basis of natural selection
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suggests an organism’s fitness decreases with increasing age (Borkan et al., 1982, Schulz-Aellen, 1997, Goldsmith, 2006, Austad and Kirkwood, 2008).
Other theoretical approaches to ageing include physiological factors such as immunology, neuroendocrinology, metabolic changes, oxidative stress and insulin signalling (Schulz-Aellen, 1997, Mattson, 2009, Cefalu, 2011). The autoimmune theory proposes that, as ageing occurs, the body produces autoantibodies, primarily affecting T- cell functionality that heightens risk of disease (mainly autoimmune diseases such as rheumatoid arthritis or lupus) and infection (Burns and Goodwin, 2003, Gupta et al., 2005, Vasto et al., 2006, Bürkle et al., 2007, Finch, 2007, Weinberger et al., 2009, Cefalu, 2011). This is referred to as immunosenescence. Social factors, such as nutritional or socio-economic status will influence the efficacy of an older individual’s
immune system (Mayer, 1994, Lesourd et al., 1998, Lesourd et al., 2002). Further study of the immune system suggests that an over-production of pre-inflammatory genotypes may be both beneficial, in youth, and detrimental, in advancing years (Licastro et al., 2005, Bürkle et al., 2007, Campisi et al., 2009). Oxidative Stress Theory, which may influence the shortening of telomeres, has two aspects, with the first arguing that free radicals bring about an accumulation of damage to the mitochondrial DNA with the second aspect considering the effect of oxidative stress on chromosomes (Klapper et al., 2001, Aviv et al., 2003, Cefalu, 2011, Zhang et al., 2016).
The extended post-reproductive lifespan of females, within the theoretical framework of the Grandmother Hypothesis, suggests that care-giving investments bestowed upon grandchildren (descendants) is advantageous to their offspring and ultimately to the older female following the cessation of her reproductive phase, although this position
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has its detractors (Peccei, 2001, Crews, 2003, Harper, 2005, Hrdy, 2005, Melby and Lampl, 2011). Studies have noted physiological benefits to infants from the presence of grandmothers, as allomothers, in this context (Hrdy, 2005, Austad and Kirkwood, 2008). Grandmotherhood is seen as an adaptive process benefitting longevity with menopause, some argue, seen as a secondary effect of this adaptation (Peccei, 2001). Menopause, associated with heightened risk in a range of clinical conditions (e.g. hormonal level variation, bone loss, breast cancer, cardiovascular diseases etc.), marks the end of the menstrual and reproductive phase with cessation normally occurring by the fifth decade of life (Crews, 1990, Plato et al., 1994, Finch, 2007, Austad and Kirkwood, 2008, Fretts et al., 2008, Sowers, 2009, Curtis and Nawrocki, 2010, Homeier, 2014). The
menopausal process, brought about by changes to a female’s hypothalamic, pituitary and ovarian systems, can take several years (i.e. on average up to 5.5 years) to occur and includes pre- and peri- menopausal (i.e. climacteric period 10+ years following cessation of menstruation) phases. Due to its link with oestrogen and cognitive function, menopause is associated with variable thermal regulation and cognitive issues (i.e. mood, memory etc.) (Llewellynn-Jones et al., 1999, Brinton et al., 2009, Rubinow et al., 2009, Sowers, 2009, Melby and Lampl, 2011). Menopause is believed to have evolved in response to the altricial nature of human offspring and increased periods of infant dependency for security and nourishment and is virtually unique to the human species (Peccei, 2001, Austad and Kirkwood, 2008). Antagonistic pleiotropy has been put
forward as an explanation for human menopause where, in the individual’s youth,
hormonal stability is critical for reproductive fitness but that this is offset in the latter
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