Anna Crown

Why is the management of glucocorticoid deficiency still controversial: a review of the literature

All endocrinologists would like to make glucocorticoid replacement therapy for their hypoadrenal patients as physiological as possible. Many would like the reassurance of a method of monitoring such treatment to confirm that they are achieving this aim. Advances in our knowledge of the normal physiology are relevant to our attempts to do this. The cortisol production rate in normal subjects is lower than was previously believed. The normal pattern of glucocorticoid secretion includes both a diurnal rhythm and a pulsatile ultradian rhythm. Glucocorticoid access to nuclear receptors is ‘gated’ by the 11‐β‐hydroxysteroid dehydrogenase enzymes, which interconvert active cortisol and inactive cortisone. Such complexities make the target of physiological glucocorticoid replacement therapy hard to achieve. The available evidence suggests that conventional treatment of hypoadrenal patients may result in adverse effects on some surrogate markers of disease risk, such as a lower bone mineral density than age‐sex matched controls, and increases in postprandial glucose and insulin concentrations. Although the quality of life of hypoadrenal patients may be impaired, there is no evidence of an improvement on higher doses of steroids, although quality of life is better if the hydrocortisone dose is split up, with the highest dose taken in the morning. Thus the evidence suggests that most patients may safely be treated with a low dose of glucocorticoid (e.g. 15 mg hydrocortisone daily) in two or three divided doses, with education about the appropriate action to take in the event of intercurrent illnesses.

Endocrine intervention for transsexuals.

Gender identity disorder, gender dysphoria, transgenderism and transsexualism are terms used to describe an individual’s wish to live and be accepted as a member of the opposite sex. The condition manifests as discomfort with one’s phenotypic sex and a wish to have treatment to make one’s body correspond to that of the preferred sex. In transsexualism, genotype and somatic differentiation do not conform to brain programming as male or female. The persistent cross-gender identification that results transcends a desire for any cultural advantages of being the other sex. Transsexualism is distinct from sexual orientation, and transsexuals, like nontranssexuals, may be heterosexual, homosexual, bisexual or asexual (Schilder et al ., 2001). All strata of society are affected by gender dysphoria (Hoenig & Kenna, 1974) and the similar prevalence of 1 in 13–15 000 males and 1 in 30–35 000 females across Western (van Kesteren et al ., 1996a) and Eastern Europe, Singapore and the Indian subcontinent suggests that the influence of culture on the underlying condition is relatively small (van Kesteren, 2002). In Southeast Asia amongst the Hindu and Buddhist population, transsexual individuals often evoke relatively little concern on the part of those affected and their families as the condition is attributed to residues of a previous life as a member of the opposite sex (Stevenson, 1977). In other societies, the challenges that people with gender dysphoria face may transcend those faced by lesbian, gay and bisexual individuals, and they may be at greater risk of harassment and violence which in turn leads to an increased incidence of depression, substance abuse (Seal et al ., 2001) and suicide (Lee, 2000; Lombardi et al ., 2001; Schilder et al ., 2001; Cochran et al ., 2002). These risks are further compounded by marginalization from society (Landen & Innala, 2000) and inconsistent legislation with, variously, lack of precedents for changing the sex of birth certification, confused marital rights, criminalization of genital contact between people of the same sex and exclusion of sex reassignment surgery from health service funding and health insurance (Gordon, 1991). In this review, we discuss predisposing factors to transsexualism, and the diagnosis, assessment and hormone treatment of transsexual patients. We also discuss the risks and organ-specific effects of crosssex hormone treatment. We will briefly summarize the current legal position of transsexuals in the UK and recommendations for the culturally competent delivery of transgender health care.

The four-dimensional stress test: Psychological, sympathetic–adrenal–medullary, parasympathetic and hypothalamic–pituitary–adrenal responses following inhalation of 35% CO2

BACKGROUND Hypercapnia is a threat to homeostasis and results in neuroendocrine, autonomic and anxiogenic responses. The inhalation of carbon dioxide (CO2) may, therefore, provide a good paradigm for exploring the pathways by which stress can lead to increased susceptibility to ill-health through physiological and psychological stress reactivity. The current study was designed, therefore, to assess the psychological and physiological responses to the inhalation of CO2. METHODS Healthy participants (N = 24) inhaled a single vital capacity breath of a mixture of CO2 (35%) and oxygen (65%). Blood pressure and heart rate were recorded for 5 min before and after the test and blood and saliva samples were taken immediately before and 2, 10, 20 and 30 min post-inhalation for the measurement of noradrenaline, salivary and serum cortisol and salivary alpha amylase. In addition, psychosomatic symptoms were recorded immediately before and after the test. The same protocol was repeated 4-6 weeks later at the same time of day. RESULTS A single inhalation of CO2 increased blood pressure, noradrenaline, salivary alpha amylase and psychosomatic symptoms, but decreased heart rate at both testing sessions. Analyses of salivary cortisol data revealed that 70% of the sample could be reliably classified as either responders (i.e. demonstrated a post-CO2 cortisol increase) or non-responders (i.e. responded with a decrease or no change in cortisol following CO2) at both test sessions. Responders also perceived the test to be more aversive than non-responders. CONCLUSIONS Inhalation of 35% CO2 reliably stimulated the key mechanisms involved in the human stress response. The inter-individual differences in the reactivity of the hypothalamic-pituitary-adrenal axis were also related to differences in the perception of the test.

An exploration into physiological and self-report measures of stress in pre-registration doctors at the beginning and end of a clinical rotation

The first year practising medicine, pre-registration, is considered to be a stressful time for junior doctors. The aims of this study were to explore how levels of psychological distress were affected by changes in the working environment and to examine these effects across subjective (i.e. self-report) and objective (i.e. stress hormone cortisol) indices of psychological distress. A cohort of 36 pre-registration house officers (males = 15) completed a battery of psychosocial measures and collected salivary samples for the measurement of diurnal cortisol at the beginning and end of a 3–4-month clinical rotation with the assumption that the end of a rotation would be less stressful than the beginning. Results from the self-report measures remained constant over the two-time points suggesting no perceived change in emotional well-being on a subjective level. However, there is some evidence of neuro-endocrine changes across the two time points suggestive of hypothalamic–pituitary–adrenal axis dysregulation. In particular, there was a significant difference between the cortisol awakening rise with the greatest rise seen at the beginning of a rotation. In addition, the daily cortisol decline (diurnal slope) was also significantly less at this test time. These findings have implications for the discord apparent between self-report and physiological measures of psychological stress.

Maternal Mood and Neuroendocrine Programming: Effects of Time of Exposure and Sex

Adverse exposures that influence growth in prenatal and early postnatal periods are considered to influence vulnerability to chronic diseases via their effects on the neuroendocrine system. In humans, the assessment of the underlying mechanisms has been restricted. The present study aimed to investigate the effects of adverse early‐life exposures, specifically maternal mood, on hypothlamic‐pituitary‐adrenal (HPA) axis, sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) responses to an acute physiological stressor. In addition, we conducted a preliminary examination into whether these effects varied by time of exposure and sex. One hundred and thity‐nine individuals (mean age 15.12 years) were recruited from the ALSPAC (Avon Longitudinal Study of Parents and Children) birth cohort. Participants underwent the CO2 stress test and indices of the PNS, SNS and HPA axis were measured. Pre‐existing data on demographic and psychosocial factors of the mothers during pregnancy (18 and 32 weeks) and postnatally (8 weeks and 8 months) were extracted, as were participants’ clinical and demographic data at birth. Increases in both pre‐ and postnatal anxiety and depression were associated with greater SNS reactivity to the stressor and slower recovery, as well as blunted HPA axis responses. Programming effects on the SNS appeared to be restricted to male offspring only. No consistent relationships were evident for any of the measures of pre‐stress function. We have found preliminary evidence that both pre‐ and postnatal maternal anxiety and depression have sustained programming effects on the SNS and HPA axis. Effects on the SNS were restricted to male offspring.

Relationship of early childhood illness with adult cortisol in the Barry Caerphilly Growth (BCG) cohort

BACKGROUND The developmental origins hypothesis suggests that pre- and postnatal exposures may influence vulnerability to later disease. The hypothalamic-pituitary-adrenal (HPA) axis is one pathway by which this may occur. Analyses were conducted in the Barry Caerphilly Growth (BCG) cohort to explore whether the postnatal exposure of childhood infections was related to HPA axis activity in adulthood. METHODS Detailed data on type and frequency of illnesses were collected in the first 5 years of life. At the recent follow-up of this cohort (N=566; mean age of participants=25 years) three salivary cortisol samples were taken: two fasting samples in the morning (within 30 min of arrival at the study site and after venesection and cognitive test procedures) and one evening sample (2200 h). These data were transformed to provide AUCi and AUCg (indices reflecting axis reactivity and total hormonal output, respectively). FINDINGS Negative associations were evident between number of upper respiratory illnesses and adult cortisol (as captured by the second morning sample, evening sample and AUCg). These relationships remained after controlling for other potential prenatal, postnatal and adult determinants. These associations were not observed for gastrointestinal illnesses suggesting that confounding by socioeconomic factors is unlikely to be the explanation. CONCLUSIONS Childhood respiratory illnesses were associated with reduced HPA axis activity in adulthood. Further follow-ups will determine whether this pattern of activity influences vulnerability to diseases associated with HPA regulation.

Growth Hormone in Adults: Physiological and Clinical Aspects

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