Are Better Workers Also Better Humans? On Pharmacological Cognitive Enhancement in the Workplace and Conflicting Societal Domains

The article investigates the sociocultural implications of the changing modern workplace and of pharmacological cognitive enhancement (PCE) as a potential adaptive tool from the viewpoint of social niche construction. We will attempt to elucidate some of the sociocultural and technological trends that drive and influence the characteristics of this specific niche, and especially to identify the kind of capabilities and adaptations that are being promoted, and to ascertain the capabilities and potentialities that might become diminished as a result. In this context, we will examine what PCE is, and how and why it might be desirable as a tool for adaptation within the workplace. As human beings are, or at least should be allowed to be, more than merely productive, able-bodied and able-minded workers, we will further examine how adaptation to the workplace niche could result in problems in other domains of modern societal life that require the same or other cognitive capabilities. In this context we will also focus on the concept of responsibility and how it pertains to PCE and the modern workplace niche. This will shed some light on the kind of trends related to workplace niche construction, PCE and capability promotion that we can expect in the future, and on the contexts in which this might be either beneficial or detrimental to the individual as a well-rounded human being, and to other members of society

Prenatal Hyperandrogenization Induces Metabolic and Endocrine Alterations Which Depend on the Levels of Testosterone Exposure

Prenatal hyperandrogenism is able to induce polycystic ovary syndrome (PCOS) in rats. The aim of the present study was to establish if the levels of prenatal testosterone may determine the extent of metabolic and endocrine alterations during the adult life. Pregnant Sprague Dawley rats were prenatally injected with either 2 or 5 mg free testosterone (groups T2 and T5 respectively) from day 16 to day 19 day of gestation. Female offspring from T2 and T5 displayed different phenotype of PCOS during adult life. Offspring from T2 showed hyperandrogenism, ovarian cysts and ovulatory cycles whereas those from T5 displayed hyperandrogenism, ovarian cysts and anovulatory cycles. Both group showed increased circulating glucose levels after the intraperitoneal glucose tolerance test (IPGTT; an evaluation of insulin resistance). IPGTT was higher in T5 rats and directly correlated with body weight at prepubertal age. However, the decrease in the body weight at prepubertal age was compensated during adult life. Although both groups showed enhanced ovarian steroidogenesis, it appears that the molecular mechanisms involved were different. The higher dose of testosterone enhanced the expression of both the protein that regulates cholesterol availability (the steroidogenic acute regulatory protein (StAR)) and the protein expression of the transcriptional factor: peroxisome proliferator-activated receptor gamma (PPAR gamma). Prenatal hyperandrogenization induced an anti-oxidant response that prevented a possible pro-oxidant status. The higher dose of testosterone induced a pro-inflammatory state in ovarian tissue mediated by increased levels of prostaglandin E (PG) and the protein expression of cyclooxygenase 2 (COX2, the limiting enzyme of PGs synthesis). In summary, our data show that the levels of testosterone prenatally injected modulate the uterine environment and that this, in turn, would be responsible for the endocrine and metabolic abnormalities and the phenotype of PCOS during the adult life

Oxidative stress in pregnancies complicated by diabetes

The placenta is essential for normal foetal metabolism and growth. However, maternal diabetes is an unfavourable environment for embryonic and fetoplacental development, which may disrupt normal foetal programming, leading later to metabolic disease. Additionally, an adverse in utero environment may lead to foetal congenital anomalies. Existing diabetes before pregnancy (pregestational type 1 and or type 2 diabetes mellitus) may have negative effects on the embryonic development, while gestational diabetes mellitus (GDM) that occurs during late stages of pregnancy may affect the growth and maturation of the foetus. Many of the damaging effects of diabetes in pregnancy have been attributed to oxidative stress. Reactive oxygen and nitrogen species are by-products of a number of important biological pathways of pregnancy, including embryo development, implantation, angiogenesis, placental development and function. In healthy pregnancies, these reactive oxygen and nitrogen species can be controlled to ensure no damage ensues. However, in pregnancies complicated by diabetes, their excessive production and/or a reduction in antioxidant defence mechanisms results in a number of damaging outcomes. Animal models of diabetes in pregnancy have provided supportive evidence of reactive oxygen and nitrogen species generation and their damaging effects, which are dependent on the developmental stage. In this chapter, we will review the available data on oxidative stress in human diabetic pregnancies as well as in animal models of diabetes in pregnancy during early gestation, fetoplacental development and the perinatal period, as well as on its postnatal consequences. Human and animal data supportive of antioxidant treatments will be also discussed