Evolution of sexually dimorphic longevity in humans

Gems, David

doi:10.18632/aging.100640

Cited by 33 publications

(29 citation statements)

References 58 publications

(89 reference statements)

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“…Though whales and elephants may have a comparable post-reproductive lifespan to humans (Kuhle, 2007; Lahdenperä et al, 2014; Ward et al, 2009), they are not close relatives to our species, and extended longevity after reproductive senescence has not been observed in non-human primates (Gems, 2014; Sievert, 2014). Cooperative social dynamics and relatedness to other conspecifics within each species can also be a tool to understand longevity beyond reproductive senescence (Johnstone and Cant, 2010).…”

Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 78%

“…However, this seems unlikely considering that women tend to live longer than men and that the average lifespan is increasing, yet the age of menopause onset has remained relatively stable (Amundsen and Diers, 1973, 1970; Mennenga and Bimonte-Nelson, 2013; Regan and Partridge, 2013; Seifarth et al, 2012; Sherwin, 2003), indicating that the number of reproductive-age years is not proportionally increasing along with the rising average lifespan. Additionally, the rate at which chimpanzees (the closest living relatives to humans) and human females’ ovarian follicles deplete is remarkably similar, yet a chimpanzee's lifespan is much shorter than modern humans and they lack an extended post-menopausal life stage, indicating that humans’ unique capacity for longevity evolved long ago (Gems, 2014). Despite the fact that the average life expectancy started to increase in the twentieth century (Hawkes and Coxworth, 2013), anthropological evidence suggests that “menopause and post-reproductive life are not new phenomena” (Sievert, p. 1153, 2014) even in early civilizations and other hominid ancestors (Kuhle, 2007; Sievert, 2014).…”

Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 99%

“…The “Patriarch Hypothesis” postulates that older men continue to reproduce late in life with younger women, and this selection for older male fathers increases the probability for offspring to also have a long lifespan. According to this hypothesis, longevity in women is a byproduct of selective mating with older males (Gems, 2014; Kuhle, 2007). This theory also leads to evidence for antagonistic pleiotropy, or the effect that a particular genetic trait may have benefits early in life (e.g.…”

Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 99%

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Trajectories and phenotypes with estrogen exposures across the lifespan: What does Goldilocks have to do with it?

Koebele

Bimonte-Nelson

2015

Hormones and Behavior

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Estrogens impact the organization and activation of the mammalian brain in both sexes, with sex-specific critical windows. Throughout the female lifespan estrogens activate brain substrates previously organized by estrogens, and estrogens can induce non-transient brain and behavior changes into adulthood. Therefore, from early life through the transition to reproductive senescence and beyond, estrogens are potent modulators of the brain and behavior. Organizational, reorganizational, and activational hormone events likely impact the trajectory of brain profiles during aging. A “brain profile,” or quantitative brain measurement for research purposes, is typically a snapshot in time, but in life a brain profile is anything but static – it is in flux, variable, and dynamic. Akin to this, the only thing continuous and consistent about hormone exposures across a female's lifespan is that they are noncontinuous and inconsistent, building and rebuilding on past exposures to create a present brain and behavioral landscape. Thus, hormone variation is especially rich in females, and is likely the destiny for maximal responsiveness in the female brain. The magnitude and direction of estrogenic effects on the brain and its functions depend on a myriad of factors; a “Goldilocks” phenomenon exists for estrogens, whereby if the timing, dose, and regimen for an individual are just right, markedly efficacious effects present. Data indicate that exogenously-administered estrogens can bestow beneficial cognitive effects in some circumstances, especially when initiated in a window of opportunity such as the menopause transition. Could it be that the age-related reduction in efficacy of estrogens reflects the closure of a late-in-life critical window occurring around the menopause transition? Information from classic and contemporary works studying organizational/activational estrogen actions, in combination with acknowledging the tendency for maximal responsiveness to cyclicity, will elucidate ways to extend sensitivity and efficacy into post-menopause.

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Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 78%

Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 99%

Section: Menopause: Etiology Evolution and Estrogensmentioning

confidence: 99%

See 1 more Smart Citation

Trajectories and phenotypes with estrogen exposures across the lifespan: What does Goldilocks have to do with it?

Koebele

Bimonte-Nelson

2015

Hormones and Behavior

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“…In this relation, it should be mentioned that our finding on sex specificity of the association between genotypes and aging is related to the aging around the age of average life span with an upper limit of 90 years. We could speculate that limited success of multiple genome-wide association studies in finding new genes associated with aging might be due to the concentration of efforts on a different aging interval of over 90 years on one side, and no consideration of sexually dimorphic aspects of the aging process [25] on the other side.…”

Section: Discussionmentioning

confidence: 99%

A Common Copy Number Variation Polymorphism in the <b><i>CNTNAP2</i></b> Gene: Sexual Dimorphism in Association with Healthy Aging and Disease

Iakoubov¹,

Mossakowska²,

Szwed³

et al. 2014

Gerontology

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Background: New therapeutic targets are needed to fight aging-related diseases and increase life span. A new female-specific association with diseases and limited survival past 80 years was recently reported for a copy number variation (CNV) in the CNTNAP4 gene from the neurexin superfamily. Objective: We asked whether there are CNVs that are associated with aging phenotypes within other genes from the neurexin superfamily and whether this association is sex specific. Methods: Select CNV polymorphisms were genotyped with proprietary TaqMan qPCR assays. Results: A case/control study, in which a group of 81- to 90-year-old community-dwelling Caucasians with no chronic diseases (case) was compared to a similar control group of 65- to 75-year-olds, revealed a negative association with healthy aging for the ins allele of common esv11910 CNV in the CNTNAP2 gene (n = 388; OR = 0.29, 95% CI: 0.14-0.59, p = 0.0004 for males, and OR = 0.82, 95% CI: 0.42-1.57, p = 0.625 for females). This male-specific association was validated in a study of an independent group of 76- to 80-year-olds. To look for a corresponding positive association of the allele with aging-related diseases, two case subgroups of 81- to 90-year-olds, one composed of individuals with cognitive impairment and the other with various diseases not directly related to the nervous system, such as cardiovascular diseases, etc., were compared to a healthy control subgroup of the same age. A positive male-specific association was found for both cases (OR = 2.75, p = 0.008 for association with cognitive impairment, and OR = 3.18, p = 0.002 for other diseases combined). Conclusions: A new male-specific association with aging is reported for a CNV in the CNTNAP2 gene. The polymorphism might be useful for diagnosing individual genetic predispositions to healthy aging versus aging complicated by chronic diseases.

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“…For example, in flies, mice, and humans, females have a tendency to live longer than males (in human populations, the lifespan advantage of women over men can achieve up to 7–8 years; Blagosklonny, 2010; Eskes & Haanen, 2007; Gems, 2014; La Croix et al. , 1997; Lints, Bourgois, Delalieux, Stoll & Lints, 1983; Tower, 2006; Tower & Arbeitman, 2009; Vina, Borrás, Gambini, Sastre & Pallardó, 2005).…”

Section: Introductionmentioning

confidence: 99%

Sex-specific regulation of aging inCaenorhabditis elegans

et al. 2018

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SummaryA fascinating aspect of sexual dimorphism in various animal species is that the two sexes differ substantially in lifespan. In humans, for example, women's life expectancy exceeds that of men by 3–7 years. Whether this trait can be attributed to dissimilar lifestyles or genetic (regulatory) factors remains to be elucidated. Herein, we demonstrate that in the nematode Caenorhabditis elegans, the significantly longer lifespan of hermaphrodites—which are essentially females capable of sperm production—over males is established by TRA‐1, the terminal effector of the sex‐determination pathway. This transcription factor directly controls the expression of daf‐16/FOXO, which functions as a major target of insulin/IGF‐1 signaling (IIS) and key modulator of aging across diverse animal phyla. TRA‐1 extends hermaphrodite lifespan through promoting daf‐16 activity. Furthermore, TRA‐1 also influences reproductive growth in a DAF‐16‐dependent manner. Thus, the sex‐determination machinery is an important regulator of IIS in this organism. These findings provide a mechanistic insight into how longevity and development are specified unequally in the two genders. As TRA‐1 is orthologous to mammalian GLI (glioma‐associated) proteins, a similar sex‐specific mechanism may also operate in humans to determine lifespan.

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Evolution of sexually dimorphic longevity in humans

Cited by 33 publications

References 58 publications

Trajectories and phenotypes with estrogen exposures across the lifespan: What does Goldilocks have to do with it?

Trajectories and phenotypes with estrogen exposures across the lifespan: What does Goldilocks have to do with it?

A Common Copy Number Variation Polymorphism in the <b><i>CNTNAP2</i></b> Gene: Sexual Dimorphism in Association with Healthy Aging and Disease

Sex-specific regulation of aging inCaenorhabditis elegans

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