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Genetic load and biological changes to extant humans

Saniotis, Arthur; Henneberg, Maciej; Mohammadi, Kazhaleh (2021). Genetic load and biological changes to extant humans. Journal of Biosocial Science, 53(4):639-642.

Abstract

Extant humans are currently increasing their genetic load, which is informing present and future human microevolution. This has been a gradual process that has been rising over the last centuries as a consequence of improved sanitation, nutritional improvements, advancements in microbiology and medical interventions, which have relaxed natural selection. Moreover, a reduction in infant and child mortality and changing societal attitudes towards fertility have led to a decrease in total fertility rates (TFRs) since the 19<jats:sup>th</jats:sup> century. Generally speaking, decreases in differential fertility and mortality have meant that there is less opportunity for natural selection to eliminate deleterious mutations from the human gene pool. It has been argued that the average human may carry ~250–300 mutations that are mostly deleterious, as well as several hundred less-deleterious variants. These deleterious alleles in extant humans mean that our fitness is being constrained. While such alleles are viewed as reducing human fitness, they may also have had an adaptive function in the past, such as assisting in genetic complexity, sexual recombination and diploidy. Saying this, our current knowledge on these fitness compromising alleles is still lacking.

Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Evolutionary Medicine
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Social Sciences & Humanities > General Social Sciences
Health Sciences > Public Health, Environmental and Occupational Health
Uncontrolled Keywords:Public Health, Environmental and Occupational Health, General Social Sciences
Language:English
Date:1 July 2021
Deposited On:20 Oct 2020 15:43
Last Modified:08 Mar 2025 04:33
Publisher:Cambridge University Press
ISSN:0021-9320
OA Status:Closed
Publisher DOI:https://doi.org/10.1017/s0021932020000413
PubMed ID:32778193
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