Why Men Matter: Mating Patterns Drive Evolution of Human Lifespan

Evolutionary theory predicts that senescence, a decline in survival rates with age, is the consequence of stronger selection on alleles that affect fertility or mortality earlier rather than later in life. Hamilton quantified this argument by showing that a rare mutation reducing survival is opposed by a selective force that declines with age over reproductive life. He used a female-only demographic model, predicting that female menopause at age ca. 50 yrs should be followed by a sharp increase in mortality, a “wall of death.” Human lives obviously do not display such a wall. Explanations of the evolution of lifespan beyond the age of female menopause have proven difficult to describe as explicit genetic models. Here we argue that the inclusion of males and mating patterns extends Hamilton's theory and predicts the pattern of human senescence. We analyze a general two-sex model to show that selection favors survival for as long as men reproduce. Male fertility can only result from matings with fertile females, and we present a range of data showing that males much older than 50 yrs have substantial realized fertility through matings with younger females, a pattern that was likely typical among early humans. Thus old-age male fertility provides a selective force against autosomal deleterious mutations at ages far past female menopause with no sharp upper age limit, eliminating the wall of death. Our findings illustrate the evolutionary importance of males and mating preferences, and show that one-sex demographic models are insufficient to describe the forces that shape human senescence

Relationship of human macrophage agglutination factor to other fibronectins.

Human macrophage agglutination factor (MAggF) is a lymphokine with a number of biochemical and immunochemical similarities to the fibronectins (FN). The present study was undertaken to define this relationship more exactly. Peripheral blood mononuclear cells (PBMC) and cloned human CD4+T-cell lines synthesized both MAggF and immunoreactive FN de novo following antigen or mitogen activation. MAggF produced under those conditions co-purified with an immunoreactive FN on gelatin-affinity and gel-filtration chromatography. This FN had a consistently slightly smaller relative molecular mass than plasma FN on both immunoblotting and gel filtration. Purified human MAggF was extremely active: it agglutinated human monocytes at fM concentrations and was up to 2,000,000 times more active in agglutinating mononuclear phagocytes than other purified FN. The action of MAggF on monocytes was dependent on at least two antigenically distinct cell-surface FN receptors. We suggest that the extreme activity of MAggF is a result of co-operative interactions between FN domains on the MAggF molecules and multiple distinct classes of FN receptors on responding cells

A Life History Perspective on Skin Cancer and the Evolution of Skin Pigmentation

The ancestral state of human skin pigmentation evolved in response to high ultraviolet radiation (UVR) stress. Some argue that pigmentation evolved to limit folate photolysis, therein limiting neural tube defects. Pigmentation also protects against sunburn which decreases the efficiency of sweating and potentiates skin infection. Pigmentation increases the efficacy of skin as a barrier to infection. Skin cancer has been rejected or minimized as a selective pressure because it is believed to have little or no effect on mortality during reproductive years. This argument ignores evidence of human longevity as a derived life history trait and the adaptive value of investment in offspring and kin, particularly during the post-reproductive lifespan. Opponents argue that lifespan in prehistoric hunter-gatherers was too short to be relevant to the evolution of skin pigmentation. This argument is flawed in that it relies on estimates of longevity at birth rather than adolescence. When appropriate estimates are used, it is clear that human longevity has a deep evolutionary history. We use a life history perspective to demonstrate the value of skin pigmentation as an adaptation to skin cancer with the following points: UVR exposure increases dysregulation of gene expression in skin cells leading to immortal cell lines; cutaneous malignant melanoma (CMM) affects individuals throughout reproductive years; and lifespan was longer than has previously been acknowledged, providing the opportunity for kin selection. This hypothesis is not at odds with the folate or barrier hypotheses. We stress that the evolution of skin pigmentation is complex and is an ongoing process