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Cardiovascular disease shows a distinct difference in incidence rates between men and women, a fact that has been known for many years. While initial theories supported that this could be attributed to the protective effect of estrogens in women, attempts to correlate endogenous estrogen levels with cardiovascular risk factors and the progression of atherosclerosis-related indexes indicate otherwise. Similarly, endogenous androgen levels seem to correlate with opposite effects in males and females, whereas exogenous treatment with either androgens or estrogens fails to correspond to scientific expectations entirely. A brief discussion of the merits and pitfalls of placing either estrogens or androgens alone at the root of the problem shows that current understanding is inadequate concerning this major anthropological issue, as it refers to the primary global mortality and morbidity cause.

The aging process is a normal stage in development characterized by the gradual deterioration of all life functions. As far as reproduction is concerned, aging is characterized by a significant limitation of fertility in both sexes. This process is, at least partially, attributed to the action (or loss of action) of sex steroids, coinciding with low activity of the pituitary-gonad axis. From an anthropological point of view, the study of reproductive aging is a unique opportunity to investigate various environmental and endogenous factors influencing sexual behavior and, thus, playing a significant role in human biology. Various techniques are now widely available to allow the detailed examination of reproductive hazards using only minor samples of genetic material. These methods are highly sensitive and specific and allow the characterization of distortions at subcellular and even molecular level. This short review briefly summarizes the current understanding of reproductive aging, as well as its potential clinical and anthropological impact.

Cardiovascular disease incidence rates have long been known to significantly differ between the two sexes. Estrogens alone fail to explain this phenomenon, bringing an increasing amount of attention to the role of androgens. Contrary to what was initially hypothesized, androgens seem to have an overall cardioprotective effect, especially in men. Recent studies and published data continue to support this notion displaying a consistent inverse correlation with atherosclerosis progression and cardiovascular disease both in regressive and prospective study models. Clinical studies have also revealed what seems to be a differential androgenic effect on various cardiovascular risk factors between men and women. Further insight indicates that in order to avoid confusion it may be also preferable to separately examine the effects of endogenous androgen levels from exogenous testosterone administration, as well as discern the differential results of low to normal and supraphysiological administration doses. This review summarizes old and recent data according to the above distinctions, in an attempt to further our understanding of the role of androgens in cardiovascular disease.

Androgens and estrogens have been a central issue in the study of the endocrinology of reproduction for several decades, because of their significance for sexual differentiation. The initial perception of exclusive expression of sexspecific hormones has now been substituted by a more complex pattern of interactions, in which the relative concentrations of various hormones and receptors according to the specific tissue and developmental stage are believed to determine the final phenotype. In the case of the prostate, the role of androgens in prostatic development is crucial; however, estrogens also play a significant role in the delicate regulation of the phenomenon. In particular, aromatization and expression of estrogen receptor alpha are prerequisites for the induction of branching morphogenesis and the differentiation-functional specialization of the gland. Overexposure to external estrogens during the perinatal period disturbs the subsequent development of the organ in a non-reversible manner, via the imprinting phenomenon. The consequences of this may vary, depending on the lobe, the cellular population and the developmental stage of the prostate, and are related to the expression of genes that control cellular adhesion and differentiation. Under androgen depletion conditions, the expression of the estrogen receptor is necessary to sustain the gland, and this requires the combined substitution of both testosterone and estrogens. It is of note that imprinting and certain polymorphisms of the estrogen receptor can both affect the likelihood of development of benign prostatic hyperplasia or carcinoma. For these reasons, better understanding of the details of the regulatory role of estrogens and their receptors in prostate physiology and pathophysiology may, in the near future, provide the foundation for the development of novel therapeutic options (e.g. SERMS) [ABSTRACT FROM AUTHOR]