Review Article: Why do women live longer than men?

Sex, Gender, and Longevity
In the modern scientific community, there are clear distinctions that can be made between the ideas of sex and gender. The sex of an organism is the biological label, attached to it as a result of standard characteristics[1], both morphological and genetic, although mainly genetic. The male is the sex that produces the smaller, usually fairly motile, gametes, and the female is the sex that produces the larger, immotile gametes. In humans, the sex is determined by a specific pair of chromosomes called the sex chromosomes. Males are designated XY, which are associated with a male identity and masculine behaviour, while the female sex has the XX chromosomes. The distinction between sex and gender comes from the importance of distinguishing between inherent biological differences present from conception, and the range of mental and behavioral characteristics pertaining to, and differentiating between, masculinity and femininity (Nobelius, 2004). In summary, sex is purely physical and biological. Whereas gender is a word that should be used to describe a social construct created as a result of culture and interactions with other humans. Theoretically, gender should have no relationship to sex. However, in practice, they most likely influence each other, especially in the highly influential gender roles that modern western society has created for us. While gender will realistically have an effect on lifespan, which I will cover in a later section, the effect will be as a result of a variable rather than a biological constant like sex. The rate of ageing, or senescence, is essentially the rate at which damage to our genes accumulates and results in functional failure, or death. This is different to lifespan, and also displays different trends, yet overall women age less quickly and at different points (Clutton-Brock & Isvaran, 2007). Characteristically, it is the female sex in humans that lives longer, by an average of 5 years worldwide, according to the United Nations World Population Prospects 2012 Revision. Life expectancy will vary massively depending on socioeconomic background and geography, but in general it is clearly seen that women have the advantage in lifespan. According to Eurostat, the death rates for men (2010) were higher than for women for all of the main causes of death, except breast cancer. The instances for ischaemic heart diseases (relating to a restriction in blood supply to tissues) were about twice as high in men (105.7 deaths per 100,000 inhabitants), while this ratio “rose to four to five times higher for drug dependence and alcohol abuse, and three to four times higher for suicide, AIDS and cancer of the larynx, trachea, bronchus, and lung.” I will be discussing possible explanations behind these varied causes of death in the later sections of my essay. This sex-based mortality bias is true for most animals, although with some exceptions, as I will come on to explain.
For this section, and further ones, I will be excluding the intersexes from my writing. I am not denying their existence on any account; I am instead avoiding confusion with references to genetic abnormalities and their potential effects on longevity throughout the article.[1]
Sexual Selection
In this section, I will be looking at origins for differences in ageing and length of lifespan in terms of sexual conflict, which appears to be the traditional theory based on the scientific literature. Classical models interpret ageing as a cost of reproduction, but evolutionary theory so far has not solidified this conceptual link. Evidence suggests that it is male reproductive strategies that are associated with higher mortality risks and weaker selection for longer lifespans compared to females. Modern hominids, as we understand them, would most likely not have taken part in sexual selection to such a damaging intensity as other animals, and this process certainly does not occur today. At points in our evolutionary history, however, we will have utilised damaging and risky mating strategies, which will have shaped our lifespan and ageing rate. This is down to a few key features of sex; in terms of energy usages and resources males tend to contribute less to each offspring than mothers do. This means that other resources that the males have can also be used to compete for sexual selection, resulting in higher variance in male fitness[1] than female fitness. Males can increase their chances of mating by sacrificing longevity through the pursuance of high-risk high-return strategies over a short time period, whereas females are generally expected to pursue low-risk moderate-return strategies over a long time period on account of the fact that female fitness is limited by the investment of time and resources inherent in offspring production (Frayer & Wolpoff, 1985). This prediction, however, fails to account entirely for species with secondarily convergent sexual strategies, such as monogamous or sex role-reversed animals, or species with male sexual traits that are dependent on age, where the male reproductive rate often increases with age. Sexual dimorphism[2] in life span therefore seems to be a result of a complex arrangement of mating system factors rather than just one – yet all of these traits will have stemmed originally from anisogamy [3].
The strategies that males utilize for reproduction generally involve high rates of somatic[4] damage, which is particularly the case in polygynous[5] species. One example of this is when males engage in combat with each other to ‘win’ the female, often resulting in cumulative damage – this idea is especially true in insects because they are unable to repair damage to their exoskeleton. On the other hand, females do not engage in combat. So the result of this somatic damage building up in males might be to shorten their lifespans compared to females. This could also drive the evolution of more rapid ageing. It should be noted, however, that even though males contribute less to each offspring the net cost of reproduction must be equal for males and females – as in most species each individual has a mother and a father. A factor that often coincides with combat is male-specific hormone secretion. Hormones induce expressions of sexual traits that enhance somatic damage and increase mortality risks, probably weakening selection on longer lifespans and somatic maintenance. Generally testosterone is present in higher concentrations in males than in females, and influences sexual traits such as territoriality and courtship, both of which are high-risk factors in terms of potential somatic damage. It has also been found that, in addition to these traits that are damaging to longevity, testosterone has negative physiological effects on the body (Alonso-Alvarez, et al., 2007). Reduced immunocompetence, increased susceptibility to oxidative stress, and increased metabolic rate[6] are all known costs associated with testosterone secretion. Males therefore appear to favor enhanced sexual performance over longevity, whereas it is beneficial for females to invest more in immunity and longevity. If it happens that male produces low testosterone counts, he may need to consult a doctor for the right ed treatment or testosterone therapy.
It is not always the case that males trade longevity for enhanced sexual traits, as is seen from some empirical studies, and mortality rates are not always male-biased. There are cases where males can be selected for longer lifespan; it has been observed that in species where the male invests more in the offspring, and the female competes more for mating, the male is selected for a female-type strategy for ageing and somatic maintenance. This selection for longer lifespan is therefore dependent on a role-reversal of the sexes, and is not the status quo in nature. One example of this case would be the African Penguin. The male has an average lifespan in the wild of 17 years, whereas the female has an average lifespan of 15 years (Sea Research Foundation, 2008) – although this will have factors attached to it that may distort the figures in some way, such as predation. It is also true that sexual competition encourages strong male condition and selects for genes with positive effects on longevity. In certain cases where the mating success of males increases with age, possibly as a result of increased size or social status, selection for enhanced somatic maintenance will occur and males will live longer. It is a general principle, however, that (at least from comparing vertebrates) the mortality rate in males varies with sexual size dimorphism – the greater the differences, the wider the divide in lifespans – and usually it is the male that suffers a reduction in lifespan. The disposable soma model predicts exactly this outcome. The allocation of resources to sexual traits prevents as much investment in somatic maintenance, therefore shortening lifespan. It has also been shown that increased sexual activity in a species that only contributes gametes to the progeny (e.g. the male fruit fly) leads to a reduced lifespan (Partridge & Farquhar, 1981), yet it appears that after further investigation the effect seems to be short-lived, and the males live just as long as the others, leading questions to be asked about the way the evolution of ageing is tested (Partridge & Andrews, 1985). Such studies do not distinguish, however, between the increased allocation of resources to sexual functions and the increased amount of somatic damage that occurs as a result of extra intra-sexual conflict. These mechanisms of changing lifespan are being understood more clearly now, yet the link, if any, between lifespan and ageing rate remains unknown. In some taxa, there is sexual dimorphism in the rate of ageing, yet the initial mortality rates also vary, and the reasons behind it are not fully understood. In humans, it appears that the onset of ageing in females is earlier than in males, even though the mortality rates are biased in the opposite direction. It is incredibly difficult to carry out controlled experiments with humans, however, because of the plasticity of ageing and how it changes in response to environmental influences such as diet, temperature, population density, and even stimuli such as food odours (Libert, et al., 2007). What is relatively clear, however, is the strong link between intensity of sexual selection and mortality and selection on lifespan (Bonduriansky, et al., 2008).
[1] Fitness in the biological sense – the ability of an organism to mate and pass on its genetic information to as many offspring as possible – as opposed to the current usage related to physical health.
[2] Sexual dimorphism: the differences in size or appearance between the sexes in addition to genitalia.
[3] Anisogamy: sexual reproduction by the combination of different gametes.
[4] Somatic: any other cell that is not a gamete.
[5] Polygynous sexual behaviour is the system in which a single male mates with multiple females, but each female mates with only one male.
[6] Metabolic rate is not in itself a factor that negatively affects lifespan, but will do when combined with increased free radical production that is not prevented or protected against.
Psychological and Social Factors
Ultimately the way that males and females act in response to their environment and to each other will have a large impact on their future offspring and their chances of survival until reproductive age. Humans are a special case, as far as we can tell, in terms of our brain developments and psychological and social constructs. We have shaped our environment to the best of our abilities, and that seems to be a key difference between our species and any other. How exactly the sexes have become to appear so differently in both a physical sense and psychological sense depends on a great deal of factors and while it cannot be explained entirely by biology or psychology, there have been multiple attempts to reconcile the two. Most theorists that have looked for origins for the sex differences of human behaviour have settled on one of two explanations; essentialist perspectives emphasise the inherent psychological dispositions that have evolved from biological differences between men and women, while social constructionist perspectives emphasise the variation in behaviour between the sexes across societies and their roles in specific contexts. It has evolved more recently, however, that essentialist views came to be seen as biased, as they portray a somewhat patriarchal view of the theory. Social constructivist views seem to be somewhat more liberal, and notably have been taken up by equal rights activists to help explain the differences between sex and gender.
Evolutionary psychologists, the main advocates of essentialism, reason that psychological differences occur between the sexes as a result of the asymmetry in their parental investment. Since women inherently invest more in each offspring they reasoned that women became choosier about a mate, while men had to compete for sexual access to women, leading to aggressive traits, competition, and risk-taking. The main rationale therefore is that genders, and the behaviours associated with it, are a relatively pre-determined condition arising from sexual selection. While it may vary between individuals the emphasis is very much on the behaviours originating from the two sexes. Constructionist attitudes are more recent and took root throughout the social sciences. Psychological constructionists “consider the gender system in a society a product of relations between people and the language that they use to describe their world.” In the Western world we experience a social dichotomy, in other words a polarisation of genders, traditionally masculine males and feminine females, as a result of the social inequalities inherent in the language and ways we interact with other people, which has been around for a long time relative to modern society. These polarised genders are maintained through the language we use and the media that we are exposed to from a very young age. It is easier to see what we might be like if we look at other cultures that are isolated from the modern world, such as tribes without contact or outside influence. Traditional paternity, for example, is associated with one biological father, a genitor, and one social father, a pater, in all of Western culture, and has been throughout history. In many Native South American tribes, and other indigenous people around the globe, paternity is believed to be a shared effort (Beckerman & Valentine, 2002), and there are usually multiple men that take on the role of primary and secondary fathers. Interestingly enough in a study of 227 children, when comparing those that had just a primary father as opposed to a secondary father as well, the percentage that lived past the age of 10 was higher with the children with two fathers compared to just one by 15%. As a social mechanism, the evolutionary benefits incurred include extra resources for the offspring, extra protection, and so on. In addition to this example, when considering the assumption that men are universally the provider of resources, empirical evidence from cross-cultural analyses demonstrates that the contribution from each sex varies with the food acquisition strategies of a society, such that in many societies women are the primary resource gatherers as opposed to men.
What does this implicate for lifespan? Depending on whether the gender differences are as polarised and as inherent as it is reasoned by essentialists or whether they are as salient and fluid as social constructionists will have an impact on the way we view male behaviour, and mortality and its underlying causes. It has been posed that as a result of sexual selection pressures there is not only physical dimorphism between the sexes, but also psychological differences. There has been research into this assumption, however, by comparative studies carried out on primates. There is evidence to show consistency with the idea that “human psychological sex differences do not necessarily covary with physical ones or reflect the same causal antecedents.” For example, it is clearly shown in one study that humans have the lowest body size dimorphism in relation to the other 86 species of primates, as well as minimal canine dimorphism, yet both of these traits are strongly related to the magnitude of sexual selection. Therefore, “in relation to other primates, humans’ physical dimorphism is small in magnitude, and such levels have unclear implications for male aggressiveness and mating patterns.” In addition to this there is evidence that the weight of men is “at least partly a function of variation in female body size” (Plavcan & Schaik, 1997) By comparing the ratio of fossil sizes from Australopithecus females to Homos it can be seen that the mean body weight was 1.53 times greater in the Homos, whereas mean male body weight was only 1.21 times as great[1]. Theories behind this are evolutionary pressures towards larger female size and lesser dimorphism, potentially caused by the sexes’ convergence in their resource use or the increase in available food resources from the invention of cooking. Also relevant to increasing female size and other physical changes in human evolution is the elevated pressure to carry a foetus with a larger head and accommodate the longer gestation periods associated with it. It is therefore apparent that human size dimorphism is likely to have arisen from many selection pressures on females as well as any pressures on males. This evidence reduces the significance of sexual selection on the way men and women behave in modern society, but does not eliminate it. A theory called the biosocial theory, developed by Wood and Eagly, attempts to integrate evolutionary psychology with social constructionist views (Wood, et al., 2002). The reconciling attitude is that while men and women are different in their physiology, which has arisen from a variety of selection pressures, and this enables certain roles to be performed more efficiently by each sex, it is the men that perform the activities that yield status and power – an advantage in a society like our own with a gender hierarchy. Thus, patriarchy is “not a uniform feature of human societies but instead emerges to the extent that, for example, women’s reproductive activities conflict with the behaviours that yield status in society.” The variability that we then observe across societies, in addition to these slight differences, is a result of extensive socialisation that orientates boys and girls to function differently, that is, to occupy different social roles within society. Critically, this suggests that the behaviours we record and the mortality rates associated with them are somewhat superficial and variable. While the characteristically male roles can have detrimental effects on male lifespan, such as relatively dangerous or strenuous roles in nonindustrial societies (e.g. hunting, metalworking, lumbering, etc.), it is incredibly dependent on the types of resources available to the society. The fact that men have higher mortality rates due to extrinsic factors is therefore a product of the social framework that is in place, and thus, on the whole, not a result of sexual selection. This is not to say that sexual selection is not an important factor in determining human lifespan; instead the likelihood is that sexual selection acts with a combination of factors to reduce male lifespan in comparison to female lifespan, and mortality statistics associated with masculine-type gender (such as male-only combatants in war, gun-related deaths, alcohol and drug abuse, high suicide rates, etc.) are mostly unrelated to sexual selection and are not products of an underlying cause. The most likely explanation, therefore, will be based in genetics.
[1] Note: males are still larger than females on average by body weight, but what the fossil evidence is showing is the comparative rate of change amongst the same sex over time in relation to an extinct family of hominids.
Selfish Mitochondria
One way to answer the question would be to consider why humans die in the first place and then perhaps to work backwards. Currently there is not a united scientific consensus as to why we age; instead there are many possible theories. In addition to this, the environmental and genetic factors that vary between populations and individuals can only confuse matters more, and make it harder to discern cause from correlation. Despite the disparity across the board, it is recognised that our lifespans and the diseases we acquire during that time are heavily influenced by our metabolic rates. For example, men suffer ischaemic heart diseases at twice the rate that women do, and also have higher blood pressure in general, caused by fatty atheroma building up in the blood vessels. Cardiovascular diseases are known to have a strong degree of correlation with metabolic syndrome, which is an affliction of the metabolic process, and therefore a fault with the mitochondria (U. & Ghosh, 2013). Mitochondria are also involved in obesity and hypertension, which seems logical since so many metabolic pathways converge there. From this perspective, mitochondria seem like an interesting place to look for the differences in lifespan.
Mitochondria are the organelles in every single one of our cells that carry out aerobic respiration, among various other metabolic functions. This process breaks down glucose, stripping it of some protons and electrons, and sends them through various complexes (known as the respiratory chain). The end result is the production of ATP, the so-named universal energy currency. In Power, Sex, Suicide, Lane makes the conclusion that as a result of damage done to the mitochondrial DNA – by the free radicals produced in the respiratory chain – the mitochondria begin to fail at performing their job efficiently, that is, producing ATP. The “continuous oxidative damage to mtDNA is responsible for an age-related decline in oxidative phosphorylation capacity” (Mitochondrial Disorders, Anon., online). The only way to remedy the situation is to create more mitochondrial clones. The only way to do it, however, is to use the DNA from another mitochondrion. If this is damaged as well then the number of faulty mitochondria builds up in the cell until a critical point is reached, after which they promote apoptosis, cell death. The loss of cells from tissues combined with the inability of the body to replace them creates a net loss of cell mass, and the body starts to waste away. Cells that don’t get replaced often, indeed sometimes never get replaced, such as some types of heart tissue or brain cells, eventually just die. This places stress on the entire body, particularly the heart, and invites plenty of other diseases and afflictions that wouldn’t normally be a problem to deal with, which is eventually the cause of death in most cases. This is the free radical ageing theory.
There is also lot of conclusive evidence supporting the disposable soma theory, and the link between investment in protection at the molecular level against oxidative damage and longer lifespans has been strongly supported. There is current controversy over how important the metabolic rate is in determining lifespan, and while some studies support the idea of a reduced food intake being responsible for lengthening lifespan, in my opinion there is not enough consideration given to the comparison between metabolic rates and free radical leakage. As Nick Lane writes in his book, while some mammals have a high metabolic rate and a short lifespan, such as rats, others have very high metabolic rates yet have lifespans far longer than predicted. For example, birds require a fast metabolism to keep up with such an energy-intensive exercise as flight, yet have unexpectedly long lifespans. The solution lies in the level of protection that has been invested in, common in fact to most of our avian friends. Birds have high-levels of anti-oxidising enzymes, and have developed efficient ways of dealing with the high levels of oxygen radicals produced from the electron transport chain. “A direct relation between species longevity and rate of mitochondrial ROS (reactive oxygen species) production in captive mammals has also been found, as has a similar relationship between mammals and similar-sized but much longer-lived birds” (Kirkwood & Austad, 2000).
It seems to be the case then that mitochondria are, along with a complex system of environmental and genetic reasons, a main reason for the cessation of the human life, indeed all true eukaryotic life as well[1]. In that case it seems only right to consider possible mitochondrial origins for the divide in lifespan. In the majority of cases it is only the female gametes that pass on mitochondrial DNA, and the ovum works incredibly hard – and with ruthless efficiency – to eliminate the male mitochondria. This avoids competition, which is unhealthy for the cell and the body as a whole, and means only one set of DNA for the mitochondria is passed on – the mother’s. In a bacterial sense, where mitochondria are known to have originated from, speed of replication is very competitive, and this influences many things such as gene retention – if the genes aren’t absolutely necessary for vital processes then they are shed quickly. On the other hand if there is a trait that gives one particular bacterium an advantage over any others, then this trait will be amplified hugely and exploited to the full. Putting this idea in terms of mitochondria, who only get passed on in the female gametes, brings the possibility of selective pressures being put on mitochondria to be maternal in heritage. There are clear “indications that mitochondria attempt to distort the sex balance by harming males” (Lane, 2005).
Examples of this can be seen in a few species. In angiosperms, the most diverse group of land plants, the male mitochondria resist their eradication. These flowers are hermaphrodite, and the mitochondria try to avoid being trapped in the male sex organs – a dead end for them, as they are not passed on in the pollen. To avoid ending up in pollen the mitochondria actually sterilise the male sex organs, resulting in the change of sex of the plant to female. The process is called male cytoplasmic sterility. Since this process upsets the balance of sexes in the species, “various nuclear genes that counteract the selfish mitochondrial actions have been selected over evolution, restoring full fertility” (Lane, 2005). Over time it can be seen that multiple conversions have been enacted and suppressed through observing genetic remnants. Clearly there is an evolutionary battle being waged here, between the host organism and the mitochondria, which have effectively invaded, and still retain some of their own ‘agenda’ as can be seen here. There is a more extreme example of this. The organism Wolbachia has a particularly striking course of action in arthropods; in crustaceans Wolbachia converts males to females, and when this cannot be accomplished the males are simply killed. What has to be kept in mind is that the overall aim, if that word can be used, of this particular organism is to pass its DNA onto the next generation, and the only way to do that is in the female gametes. The act of conversion or eradication improves the chances of Wolbachia being transmitted, as it distorts the sex ratio. There are also many other examples of symbiotic organisms that are transmitted matrilineally.
This brings me onto the main point of this section – whether mitochondria are strongly influential on the divide in lifespan between males and females. There are many organisms that currently exploit the mitochondrial factor to pass on their genes, and this has stemmed from the original problem of uniparental inheritance. Clearly, while mitochondria ‘want’ to pass on their genes, they can only do so in the female gametes. This creates a selection pressure to be female, and so this selfish mitochondrial theory predicts that the origins of differences in lifespan and ageing between the sexes stems from the mitochondria actively trying to be female and avoid being male, much like the Wolbachia mentioned above . On the other hand, a species can’t thrive if the sex balance is distorted too much, or if the males don’t survive for very long, so there is a large counter-selective pressure against this behaviour. Mitochondria that don’t respire efficiently are selected against, yet there remains an interest as to whether remnants of this behaviour still remain. Certainly there are aspects to the male-female dimorphism of mitochondrial effects that have been observed; whether these irregularities are directly linked to the mitochondrial theory is as of yet unproved. Mutations in the mitochondria are associated with a wide range of degenerative conditions, such as Leber’s hereditary optic neuropathy, various muscle and heart conditions, poor aerobic performance, Parkinson’s, Alzheimer’s, reduced sperm motility, male infertility – the list goes on. Not only are there specific diseases associated with the male sex and mitochondria, but there are also imbalances in the effects of some genetic variations. For example, “an inherited mitochondrial mutation was associated with early-onset Pearson marrow-pancreas syndrome in a male but only late-onset progressive eye disease in the mother” (Frank, 1996). Another case would be where “a mother and her two sons shared a tendency for spontaneous, somatic deletions in mitochondrial DNA. The mother was asymptomatic but the two sons were severely affected by anaemia and mitochondrial myopathy” (Frank, 1996). There are also faults in sperm motility and male fertility in general that are widely observed across human populations, and also other species. Disease is observed only after normal mitochondria functioning drops below ten or twenty percent, yet such traits are strange considering the powerful selection that exists against alleles with deleterious effects on fertility. The important thing to note here is that these conditions can occur as a direct result of specific mitochondrial mutations that strongly affect sperm vigour, but only have weak effects on female fitness. The possibility of selective pressures being applied in the female but not the male remains strong, but it is very difficult finding conclusive evidence to support or reject the evolutionary theory of the selfish mitochondria being a direct cause of these types of disease, and harder still to find evidence to link it to the gaps in lifespan between the sexes.
There have been experiments looking at the role of mitochondria and mitochondrial metabolism in determining the processes that influence ageing, albeit so far mainly in Drosophila. It is in fact the case that in this species females tend to have shorter lifespan, higher levels of hydrogen peroxide (an ROS), and lower levels of catalase (the enzyme that breaks the molecule down). On the other hand mammalian females have comparatively longer lifespans, lower levels of ROS production, and higher levels of protection against them (Ku, et al., 1993). There is still debate about how much oxidative damage to the mtDNA affects lifespan and ageing, but it is recognised that the process is important if not crucial in signalling cell death and that in general the sex that lives longer has more protection against the damage. Contrary to the predicted result from the mitochondrial theory of ageing, that increased proton leak results in decreased free radical production and therefore longer lifespan, it has been found that in the shorter-lived sex the rate of proton leakage was greater, by about 25% in Drosophila (Ballard, et al., 2007). It could be noted, however, that the increased rate of proton leakage might have been selected for as a defence mechanism against mtDNA damage because of an inherent mitochondrial bias, but that is just speculation. A greater coupling efficiency was also observed in the shorter lived sex, which is again contrary to predictions. The data collected so far does support the mitochondrial free radical theory of ageing, but shows no obvious implications for the origins of sex-specific differences in lifespan. It is, however, being investigated under the pretence of sexual conflict and selection, so perhaps this will be illuminated further in the future.
[1] Since it is a characteristic of eukaryotic life to have mitochondria – and not, for example bacteria, being prokaryotic – it seems only reasonable then to apply the statement to all of the members, not just humans.
It is clear that the sex that invests heavily in sexual competition will experience the greatest decline in longevity, unless the survival into old age results in the expression of important sexual traits that improve chances of reproduction. It can also be stated that involvement in more intense sexual selection and conflict will lead to more rapid ageing in one, or both sexes. Artificial selection and experimental evolution has been a major part of this research, yet it has mainly been conducted with ‘model’ species such as Drosophila melanogaster, and so a broader review of taxa would only contribute in a positive way to these theories, and provide more evidence for these generalisations, as would more comparative techniques. In addition to refinement of experimental technique, as ageing and lifespan are very plastic, further theory needs to be developed since the relationship between ageing rate and life expectancy remains poorly understood, due to the highly sheltered environments observed in laboratories compared to nature. Overall, however, in terms of the ageing process, the variations in lifespans are relatively easy to show in experiments. The difficulty arises with predicting the rate of ageing based on evolutionary theory, possibly as a result of theoretical difficulties inherent in characterising ageing rate. It is likely, however, that sexual selection accounts for less of a difference between the sexes in terms of lifespan and ageing, and should be considered as a part of the whole answer rather than the traditionally main theory.
Psychological and social factors determine how we act as part of a society, and can potentially have a great effect on our lifespans, considering the substantial plasticity of ageing. The formation of anti-adaptive behaviour as the result of allocation in gender in the Western world certainly leads to higher mortality rates among men, with examples being higher alcohol abuse (leading to liver diseases), drug abuse, various cancers of the airways from smoking, some types of heart disease from excess consumption of food, and elevated suicide rates. This type of behaviour, however, is not universal by any means, and understanding the evolutionary basis for why many cultures are so different to ours has allowed us to focus on the real underlying causes.
Potentially, looking for a genetic basis for this division in lifespans is certainly a promising pathway and with the current advancements in molecular biology, investigating this should become progressively easier to test these hypotheses. Mitochondria also should remain a strong candidate to investigate, especially considering how complicated they are. The \’selfish mitochondrial theory\’, should be considered more seriously across the field. Unfortunately, it is difficult to test such a theory as it depends largely on instruments precise enough to detect minute differences in mitochondrial function between men and women, as well as the reliability of original theory.
In summary, the question should not be answered with a single favored hypothesis, no matter how much it is pushed for. In the complex history of the human species there have been many pressures that have mounded and formed us. Therefore, the answer to this question deserves to be comprised of the above topics covered, and potentially more. The answer also requires collaborations from all across the field of science.
Personally, I think that mitochondria should be investigated further because they potentially hold the key to the human lifespan.
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