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O brother, where art thou? Investment in siblings for inclusive fitness benefits, not father absence, predicts earlier age at menarche.

ABSTRACT: Numerous studies have indicated that father absence is associated with earlier age at menarche, with many evolutionary theories assuming that father absence is a causal factor that accelerates reproductive development. However, an alternative interpretation suggests that offspring may reproduce earlier in the presence of half- or step-siblings as the indirect fitness benefits to investing in them are lower, relative to delaying reproduction and investing in full siblings. From this perspective, father absence may perform no causal role in facilitating the onset of menarche. Using data from the Avon Longitudinal Study of Parents and Children, I find that individuals with only half- or step-siblings reach reproductive age earlier than those with only full siblings, with no independent effect of father absence. These results suggest that inclusive fitness benefits to investing in siblings, rather than father absence, may predict variation in age at menarche. These results provide a greater understanding of the adaptive mechanisms involved in reproductive decision-making, as well as potential implications for human life-history evolution and cooperative breeding more broadly.

SUBMITTER: Smith D

PROVIDER: S-EPMC5665773 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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O brother, where art thou? Investment in siblings for inclusive fitness benefits, not father absence, predicts earlier age at menarche.

Smith Daniel D

Biology letters 20171001 10

Numerous studies have indicated that father absence is associated with earlier age at menarche, with many evolutionary theories assuming that father absence is a causal factor that accelerates reproductive development. However, an alternative interpretation suggests that offspring may reproduce earlier in the presence of half- or step-siblings as the indirect fitness benefits to investing in them are lower, relative to delaying reproduction and investing in full siblings. From this perspective, ...[more]

PMID: 29046373

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Project description:Mild cognitive impairment (MCI) can be an early manifestation of Alzheimer's disease (AD) pathology, other pathologic entities [e.g., cerebrovascular disease, Lewy body disease, LATE (limbic-predominant age-related TDP-43 encephalopathy)], or mixed pathologies, with concomitant AD- and non-AD pathology being particularly common, albeit difficult to identify, in living MCI patients. The National Institute on Aging and Alzheimer's Association (NIA-AA) A/T/(N) [β-Amyloid/Tau/(Neurodegeneration)] AD research framework, which classifies research participants according to three binary biomarkers [β-amyloid (A+/A-), tau (T+/T-), and neurodegeneration (N+/N-)], provides an indirect means of identifying such cases. Individuals with A+T-(N+) MCI are thought to have both AD pathologic change, given the presence of β-amyloid, and non-AD pathophysiology, given neurodegeneration without tau, because in typical AD it is tau accumulation that is most tightly linked to neuronal injury and cognitive decline. Thus, in A+T-(N+) MCI (hereafter referred to as "mismatch MCI" for the tau-neurodegeneration mismatch), non-AD pathology is hypothesized to drive neurodegeneration and symptoms, because β-amyloid, in the absence of tau, likely reflects a preclinical stage of AD. We compared a group of individuals with mismatch MCI to groups with A+T+(N+) MCI (or "prodromal AD") and A-T-(N+) MCI (or "neurodegeneration-only MCI") on cross-sectional and longitudinal cognition and neuroimaging characteristics. β-amyloid and tau status were determined by CSF assays, while neurodegeneration status was based on hippocampal volume on MRI. Overall, mismatch MCI was less "AD-like" than prodromal AD and generally, with some exceptions, more closely resembled the neurodegeneration-only group. At baseline, mismatch MCI had less episodic memory loss compared to prodromal AD. Longitudinally, mismatch MCI declined more slowly than prodromal AD across all included cognitive domains, while mismatch MCI and neurodegeneration-only MCI declined at comparable rates. Prodromal AD had smaller baseline posterior hippocampal volume than mismatch MCI, and whole brain analyses demonstrated cortical thinning that was widespread in prodromal AD but largely restricted to the medial temporal lobes (MTLs) for the mismatch and neurodegeneration-only MCI groups. Longitudinally, mismatch MCI had slower rates of volume loss than prodromal AD throughout the MTLs. Differences in cross-sectional and longitudinal cognitive and neuroimaging measures between mismatch MCI and prodromal AD may reflect disparate underlying pathologic processes, with the mismatch group potentially being driven by non-AD pathologies on a background of largely preclinical AD. These findings suggest that β-amyloid status alone in MCI may not reveal the underlying driver of symptoms with important implications for enrollment in clinical trials and prognosis.

Dataset Information

O brother, where art thou? Investment in siblings for inclusive fitness benefits, not father absence, predicts earlier age at menarche.

Publications

O brother, where art thou? Investment in siblings for inclusive fitness benefits, not father absence, predicts earlier age at menarche.

Similar Datasets

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