No abstract

Exogenous testosterone increases the audience effect in healthy males: evidence for the social status hypothesis.

No abstract

Environmental and social stresses have deleterious effects on reproductive function in vertebrates. Global climate change, human disturbance and endocrine disruption from pollutants are increasingly likely to pose additional stresses that could have a major impact on human society. Nonetheless, some populations of vertebrates (from ®sh to mammals) are able to temporarily resist environmental and social stresses, and breed successfully. A classical trade-off of reproductive success for potential survival is involved. We de®ne ®ve examples. The stress-response plays a key role in allowing an organism to survive the acute challenge to homeostasis that constitutes the typical stressor. Energy is mobilized from storage sites and diverted to exercising muscle, cardiovascular tone is enhanced, long-term and costly anabolism is suppressed until a more auspicious time, and cognition is sharpened. However, following the pioneering work of Hans Selye in the 1930s, it is clear that an excess of stress can have pathogenic effects on metabolism, vascular function, growth, tissue repair, immune defences, and even the health of some neurones.Among the most consistently adverse consequences of prolonged stress is disruption of reproductive physiology and behaviour (Figs 1 and 2). Whether one is a clinician trying to understand a patient's loss of libido, a wildlife biologist grappling with how habitat degradation translates into decreased fertility of wild populations, or a conservationist faced with an endangered species refusing to mate in a zoo enclosure, stress must be considered in the equation. As a result of considerable research, a great deal is known about the neuroendocrine bases by which the stress-response can impair reproduction (Figs 1 and 2).In this review, we consider the general mechanisms by which such suppression occurs. More importantly, we provide examples where this yoking of stress and reproductive impairment does not occur. Such exceptions to the broad physiological effects of stress are not restricted to the reproductive axis. As an interesting recent precedent, socially subordinate mice subject to numerous bite wounds during ®ghting become resistant to the immunosuppressive effects of stress and glucocorticosteroids. The authors

No abstract

Why do we get the stress-related diseases we do? Why do some people have flare ups of autoimmune disease, whereas others suffer from melancholic depression during a stressful period in their life? In the present review possible explanations will be given by using different levels of analysis. First, we explain in evolutionary terms why different organisms adopt different behavioral strategies to cope with stress. It has become clear that natural selection maintains a balance of different traits preserving genes for high aggression (Hawks) and low aggression (Doves) within a population. The existence of these personality types (Hawks-Doves) is widespread in the animal kingdom, not only between males and females but also within the same gender across species. Second, proximate (causal) explanations are given for the different stress responses and how they work. Hawks and Doves differ in underlying physiology and these differences are associated with their respective behavioral strategies; for example, bold Hawks preferentially adopt the fight-flight response when establishing a new territory or defending an existing territory, while cautious Doves show the freeze-hide response to adapt to threats in their environment. Thus, adaptive processes that actively maintain stability through change (allostasis) depend on the personality type and the associated stress responses. Third, we describe how the expression of the various stress responses can result in specific benefits to the organism. Fourth, we discuss how the benefits of allostasis and the costs of adaptation (allostatic load) lead to different trade-offs in health and disease, thereby reinforcing a Darwinian concept of stress. Collectively, this provides some explanation of why individuals may differ in their vulnerability to different stress-related diseases and how this relates to the range of personality types, especially aggressive Hawks and non-aggressive Doves in a population. A conceptual framework is presented showing that Hawks, due to inefficient management of mediators of allostasis, are more likely to be violent, to develop impulse control disorders, hypertension, cardiac arrhythmias, sudden death, atypical depression, chronic fatigue states and inflammation. In contrast, Doves, due to the greater release of mediators of allostasis (surplus), are more susceptible to anxiety disorders, metabolic syndromes, melancholic depression, psychotic states and infection.

No abstract

Three strikingly different alternative male mating morphs (aggressive “Independents”, semi-cooperative “Satellites” and female mimic “Faeders”) coexist as a balanced polymorphism in the ruff, Philomachus pugnax, a lek-breeding wading bird1,2,3. Major differences in body size, ornamentation, and aggressive and mating behaviour are inherited as an autosomal polymorphism4,5. We show that development into Satellites and Faeders is determined by a supergene6,7,8 consisting of divergent alternative, dominant, non-recombining haplotypes of an inversion on chromosome 11, which contains 125 predicted genes. Independents are homozygous for the ancestral sequence. One breakpoint of the inversion disrupts the essential Centromere protein N (CENP-N) gene, and pedigree analysis confirms lethality of inversion homozygotes. We describe novel behavioural, testes size, and steroid metabolic differences among morphs, and identify polymorphic genes within the inversion that are likely to contribute to the differences among morphs in reproductive traits.