We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Sex differences in lifespan have been labelled as one of the most robust features in biology. In human populations, women live consistently longer than men, a pattern that encompasses most mammalian species. However, when expanding both the taxonomic scope beyond mammals and the range of mortality metrics the female survival advantage over males is no longer the rule. Moreover, current evidence suggests that sex differences in actuarial ageing parameters (i.e. age at the onset of ageing and rate of ageing) are far from consistent across the tree of life. This chapter first reviews current knowledge of sex differences in mortality patterns across animals and appraises how these diverse patterns can be explained by the current evolutionary framework. It then emphasizes the relevance of going beyond the differences in mortality patterns by exploring how natural and sexual selection have shaped age- and sex-specific changes in reproductive performance and body mass across the tree of life, and by identifying some possible biological pathways modulating ageing in a sex-specific way. Finally, it highlights how evolutionary theories can be relevant to understand the widespread differences in causes of death between sexes, offering a complementary approach to gain a comprehensive understanding of the evolution of sex differences in health and ageing, with likely biomedical implications.
The dream of eternal youth and immortality has always fascinated human societies. Even today, this quest is the source of major financial investments, particularly for the development of anti-ageing drugs. To unravel the mysteries of longevity, scientists have long been observing and quantifying the lifespan of animals. These decades of extensive comparative biology research have documented the extreme diversity of lifespan on Earth and identified key ecological and life history factors driving this diversity and, more recently, molecular pathways that might modulate it. However, the maximum lifespan of a species is far from being an accurate representation of a species’ ageing trajectory, both biologically and demographically. For a given species, the changes in mortality risk over the life course can be complex, and the ageing process is much more accurately described by ageing parameters, such as the age of onset of actuarial senescence and the rate of actuarial senescence. This chapter argues that current research in the comparative biology of ageing should now focus on the diversity of actuarial senescence patterns documented across the tree of life, as well as the species-specific causes of death, to identify key genetic and physiological determinants associated with delayed actuarial senescence or low actuarial senescence rate. Just a few years ago, such research projects would have seemed unrealistic, but the recent development of omics tools, coupled with the increased availability of demographic data for a wide range of species with contrasting life histories, lifestyles and habitats make such exciting comparative analyses now achievable and full of promise.
This opening chapter provides an overview of the future societal and subsequenl scientific challenges associated with population ageing. More specifically, it emphasizes how the field of biodemography constitutes a relevant framework for future research programmes aiming to address questions of paramount importance regarding both the causes (e.g. evolutionary, mechanistics) and consequences (demographic, medical) of the ageing process. Finally, this chapter details the book contents.
Why and how we age are probably two of science's oldest questions, echoing personal beliefs and concerns about our own finitude. From the earliest musings of ancient philosophers to recent pharmacological trials aimed at slowing ageing and prolonging longevity, these questions have fascinated scientists across time and fields of research. Taking advantage of the natural diversity of ageing trajectories, within and across species, this interdisciplinary volume provides a comprehensive view of the recent advances in ageing and longevity through a biodemographic approach. It includes the key facts, theories, ongoing fields of investigation, big questions, and new avenues for research in ageing and longevity, as well as considerations on how extending longevity integrates into the social and environmental challenges that our society faces. This is a useful resource for students and researchers curious to unravel the mysteries of longevity and ageing, from their origins to their consequences, across species, space and time.
Neuroimaging studies of vulnerability to Alcohol Use Disorder (AUD) have identified structural and functional variations which might reflect inheritable features in alcohol-naïve relatives of AUD individuals (FH+) compared to controls having no such family history (FH-). However, prior research did not simultaneously account for childhood maltreatment, any clinically significant disorder and maternal AUD. Therefore, we mainly aimed to investigate the brain structure and reward-related neural activations (fMRI), using whole-brain analysis in FH+ young adults with no prevalent confounders.
Methods:
46 FH+ and 45 FH- male and female participants had no severe childhood maltreatment exposure, neither any psychiatric disorder or AUD, nor a prenatal exposure to maternal AUD. We used a 3 T MRI coupled with a whole brain voxel-based method to compare between groups the grey matter volumes and activations in response to big versus small wins during a Monetary Incentive Delay task. The Childhood Trauma Questionnaire score was used as confounding variable in the analyses to account for the remaining variance between groups.
Results:
Compared to FH- controls, FH+ participants had smaller grey matter volumes in the frontal and cingulate regions as well as in the bilateral nucleus accumbens and right insula. The FH+ participants’ fMRI datasets denoted a blunted activation in the middle cingulum with respect to FH- controls’ during the processing of reward magnitude, and a greater activation in the anterior cingulum in response to anticipation of a small win.
Conclusions:
Family history of alcohol use disorder is linked to structural and functional variations including brain regions involved in reward processes.