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‘Female sexual dysfunction’ (FSD) is an umbrella term comprising a range of common disorders, including hypoactive sexual desire, reduced subjective and/or physical genital arousal (poor sensation, vasocongestion, lubrication), sexual pain and inability to achieve orgasm/satisfaction, which are multidimensional by nature and often coexisting. Psychological and contextual factors have a significant influence on organic components of sexual response and behavior and a tailored medical approach to sexual symptoms is inevitably limited. testosterone.

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Psychopathic individuals are notorious for their controlled goal-directed aggressive behavior. Yet, during social challenges, they often show uncontrolled emotional behavior. Healthy individuals can control their social emotional behavior through anterior prefrontal cortex (aPFC) downregulation of neural activity in the amygdala, with testosterone modulating aPFC-amygdala coupling. This study tests whether individual differences in this neuroendocrine system relate to the paradoxical lack of emotional control observed in human psychopathic offenders. Emotional control was operationalized with an fMRI-adapted approach-avoidance task requiring rule-driven control over rapid emotional responses. Fifteen psychopathic offenders and 19 matched healthy control subjects made approaching and avoiding movements in response to emotional faces. Control of social emotional behavior was required during affect-incongruent trials, when participants had to override affect-congruent, automatic action tendencies and select the opposite response. Psychopathic offenders showed less control-related aPFC activity and aPFC-amygdala coupling during trials requiring control of emotional actions, when compared with healthy control subjects. This pattern was particularly pronounced in psychopathic individuals with high endogenous testosterone levels. These findings suggest that reduced prefrontal coordination underlies reduced behavioral control in psychopathic offenders during emotionally provoking situations. Even though the modest sample size warrants replication, the modulatory role of endogenous testosterone on the aPFC-amygdala circuit suggests a neurobiological substrate of individual differences that is relevant for the advancement of treatment and the reduction of recidivism. testosterone.

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Decreased FPA levels were associated with worse metabolic profile and sexual symptoms. In addition, FPA was positively associated with both total and calculated free testosterone. In the longitudinal study, unadjusted incidence of MACE was significantly associated with lower baseline FPA. When FPA was introduced in a multivariate model, along with D-PSV, after adjusting for age and Chronic Disease Score, lower FPA, but not D-PSV, was associated with incident MACE in lower–risk-i.e., younger (HR = 0.48 [0.23-0.99]), nonhypertensive (HR = 0.59 [0.38-0.92]), nonobese (HR = 0.68 [0.49-0.96]), or nondiabetic (HR = 0.67 [0.49-0.96] subjects; all P < 0.05–but not in higher-risk ones. FPA demonstrated a threshold effect in predicting MACE at a value <1.17 m/s(2) which showed a threefold increase in incidence of MACE in apparently lower-risk individuals. testosterone.

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The dietary protein allowance for older men to maintain lean body mass and muscle strength and to accrue optimal anabolic responses to promyogenic stimuli is poorly characterized. The OPTIMEN trial was designed to assess in older men with moderate physical dysfunction and insufficient habitual protein intake (<recommended dietary allowance, RDA, 0.8g·kg(-1)·d(-1)) the efficacy of consuming diets containing 163% RDA (1.3g·kg(-1)·d(-1)) for protein, compared to RDA, to increase lean mass, muscle performance, and physical function. A second aim was to determine whether increasing protein intake to 1.3 versus 0.8g·kg(-1)·d(-1) would augment anabolic responses to a promyogenic agent, testosterone. For this randomized, double-blind, placebo-controlled six-month intervention trial, 92 men, 65years or older, with Short Physical Performance Battery scores 3-10, and habitual protein intakes <RDA, were assigned to one of four groups: 100% RDA plus placebo intramuscular injections weekly; 100% RDA plus weekly intramuscular injections of 100mg testosterone enanthate; 163% RDA plus placebo injections; or 163% RDA plus testosterone injections. All participants received portion-controlled packaged meals and group-specific dietary supplements containing either mixtures of casein and whey or carbohydrate, with identical appearance. The primary outcome was change in lean body mass assessed using dual energy X-ray absorptiometry. Secondary outcomes included maximal voluntary strength and power in leg press and chest press exercises, 6-minute walking distance, stair climbing power, and self-reported physical function. Results of the OPTIMEN trial have important implications for dietary protein guidance and policy, and efficacy of promyogenic drugs. testosterone.

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Vascular cell-specific AR deletion had no effect on neointimal lesion formation, while low systemic androgen levels adversely affect neointimal lesion size. These findings suggest that the cardio-protective effects of androgens are mediated either by AR outside the vasculature or by AR-independent mechanisms. testosterone.

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We review the hypothesized and observed effects of two of the major forms of genomic conflicts, genomic imprinting and sexual antagonism, on human health. We focus on phenotypes mediated by peptide and steroid hormones (especially oxytocin and testosterone) because such hormones centrally mediate patterns of physical and behavioral resource allocation that underlie both forms of conflict. In early development, a suite of imprinted genes modulates the human oxytocinergic system as predicted from theory, with paternally inherited gene expression associated with higher oxytocin production, and increased solicitation to mothers by infants. This system is predicted to impact health through the incompatibility of paternal-gene and maternal-gene optima and increased vulnerability of imprinted gene systems to genetic and epigenetic changes. Early alterations to oxytocinergic systems have long-term negative impacts on human psychological health, especially through their effects on attachment and social behavior. In contrast to genomic imprinting, which generates maladaptation along an axis of mother-infant attachment, sexual antagonism is predicted from theory to generate maladaptation along an axis of sexual dimorphism, modulated by steroid and peptide hormones. We describe evidence of sexual antagonism from studies of humans and other animals, demonstrating that sexually antagonistic effects on sex-dimorphic phenotypes, including aspects of immunity, life history, psychology, and behavior, are commonly observed and lead to forms of maladaptation that are demonstrated, or expected, to impact human health. Recent epidemiological and psychiatric studies of schizophrenia in particular indicate that it is mediated, in part, by sexually antagonistic alleles. The primary implication of this review is that data collection focused on (i) effects of imprinted genes that modulate the oxytocin system, and (ii) effects of sexually antagonistic alleles on sex-dimorphic, disease-related phenotypes will lead to novel insights into both human health and the evolutionary dynamics of genomic conflicts. testosterone.

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