1,720,991 research outputs found
Fetal programming of autonomic and HPA function: do people who were small babies have enhanced stress responses?
No full textStudies in several species have demonstrated that an adverse early environment can influence the development of the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis. The autonomic nervous system and HPA axis are key components of the neuroendocrine response to stress and many of these animal models show altered biological responses to stress. Recent research now suggests that these processes operate in humans. An adverse early environment, as evidenced by reduced birth or infant weight, is associated with enhanced autonomic and HPA responses to experimental psychological stress. However, there appear to be marked sex differences in the mechanisms involved. Epidemiological studies demonstrate that physiological changes in these neuroendocrine systems may predispose to cardiovascular disease through their influence on risk factors such as plasma glucose and lipid concentrations and blood pressure. Thus the combination of enhanced stress susceptibility and the psychosocial stressors to which people are exposed may be an important component of the disease risk in human population
Transgenerational inheritance of stress pathology
No full textIt is becoming increasingly evident that maternal exposure to adversity during pregnancy leads to life-long effects in offspring. While there appears to be some commonality in the effects of maternal stress on endocrine and behavioral outcomes in the first generation offspring, it is clear that effects are highly dependent on species, sex and age, as well as on the time in pregnancy when stress is experienced. Recent studies have identified that the effects of maternal stress are not confined to the first generation and that they can extend over multiple generations. These effects are also evident in humans. While our understanding of the potential mechanisms by which transgenerational programming of the stress response occurs remain largely undetermined, recent studies have begun to identify potential mechanisms of transfer. These include modified maternal adaptations to pregnancy, altered maternal behavior and transgenerational epigenetic programming. Such transgenerational programming of stress responses and pathologies has important societal consequences as it could provide a biological explanation for the generational persistence of human behaviors in populations exposed to adversity.<br/
Seasonality of thyrotoxicosis
No full textStudy of a large and representative series of thyrotoxic patients showed a higher frequency of diagnosis in the spring and summer. The median interval between onset and diagnosis was 12 weeks, indicating a peak in onset of the disease from January to June. The seasonality of thyrotoxicosis may be related to seasonal variations in iodine intake.</p
Birth weight and perceived stress reactivity in older age
No full textStress reactivity is a disposition that underlies individual differences in stress responses, thereby affecting vulnerability for the development of disease. Besides genetic and early postnatal environmental factors, stress reactivity has been shown to be influenced by an adverse prenatal developmental environment, but it is unclear if such effects persist into older age. We tested associations between fetal growth and perceived stress reactivity in 421 participants from the Hertfordshire Cohort at age 66-75?years. Regression analysis showed a U-shaped association between birth weight and perceived stress reactivity with increased levels of stress reactivity at the lower and upper end of the birth weight distribution. These effects were stable after adjustment for markers of early adversity and recent adversity and chronic stress. Although the effects were small, they are consistent with findings from studies in younger cohorts, and demonstrate that such effects can persist into older age.<br/
Stress responsiveness in adult life: influence of mother's diet in late pregnancy
No full textCONTEXT: Men and women whose mothers ate an unbalanced high-protein, low-carbohydrate diet in late pregnancy have raised blood pressure. We recently showed that they also have raised fasting plasma cortisol concentrations. Because raised fasting cortisol concentrations probably reflect a greater response to the stress of fasting and venesection, we suspected that this diet may have led to increased stress responsiveness in the adult offspring. OBJECTIVE: The aim was to determine whether an unbalanced high-protein diet during pregnancy is associated with increased cortisol secretion in response to psychological stress in the offspring. DESIGN AND PARTICIPANTS: Salivary cortisol concentrations were measured during a modified Trier Social Stress Test in 70 men and women aged 36.3 yr whose mothers had taken part in a dietary intervention in which they were advised to eat 1 pound (0.45 kg) of red meat daily during pregnancy and to avoid carbohydrate-rich foods. RESULTS: The offspring of women who reported greater consumption of meat and fish in the second half of pregnancy had higher cortisol concentrations during the Trier Test. Compared with the offspring of mothers who had reported eating no more than 13 meat/fish portions per week, the average cortisol concentrations were raised by 22% (95% confidence interval, 13 to 71%) and 46% (5 to 103%) in the offspring of those eating 14-16 and at least 17 portions per week, respectively. CONCLUSIONS: These findings provide the first human evidence that an unbalanced high protein maternal diet during late pregnancy leads to increased cortisol secretion in response to psychological stress in the offsprin
Insulin resistance and cortisol metabolism. Reply to Kerstens MN, Dullaart RPF [letter]
Full text linkBirth weight, stress, and the metabolic syndrome in adult life
No full textThere is now widespread agreement that small size at birth is associated with an increased risk of the metabolic syndrome (glucose intolerance, high blood pressure, and dyslipidemia) and related pathologies, including cardiovascular disease in later life. Evidence is emerging that suggests that programming of hormonal systems in response to an adverse fetal environment may be one of the mechanisms underlying these long-term consequences of growth restriction in early life. In particular, alterations in neuroendocrine responses to stress may be important. Recent research suggests that increased adrenocortical and sympathoadrenal responses are associated with small size at birth. Epidemiological studies show that such physiological alterations in these neuroendocrine systems may have potent effects on risk of cardiovascular disease through their influence on risk factors, such as plasma glucose and lipid concentrations and blood pressur
Is there a gender difference in the associations of birthweight and adult hypothalamic-pituitary-adrenal axis activity?
No full textObjective: increased hypothalamic–pituitary–adrenal (HPA) axis activity in men of low birthweight may be an important link between early life and the adult metabolic syndrome. In animal models females are more sensitive than males to HPA axis programming, but whether gender influences susceptibility in humans is unknown. Design: birth cohort study. Methods: we studied 106 women aged 67–78 years, from Hertfordshire, UK, in whom birthweight was recorded. Negative feedback sensitivity was assessed by an overnight low-dose (0.25 mg) dexa-methasone suppression test, and adrenal sensitivity by a low-dose (1 µg) ACTH1 – 24 stimulation test. Cortisol and its metabolites were analysed in a 24 h urine collection. Data were compared with previously published identical measurements in 205 men aged 66–77 years from the same cohort. Results: in women, plasma cortisol levels after dexamethasone were lower (P < 0.0001) and peak cortisol following ACTH1 – 24 were higher (P < 0.0001) than in men, suggesting a more responsive HPA axis. As in men, women with lower birthweight had enhanced plasma cortisol responses to ACTH1 – 24 (P = 0.05 for trend) but no difference in plasma cortisol after dexamethasone or in urinary cortisol metabolite excretion. The strength of the association in women was not different from that in men; a 1 lb decrease in birthweight was associated with an incremental rise in cortisol of 12.6 nmol/l (95% confidence interval (CI) 1.4, 23.8) in men, P = 0.03, and 14.8 nmol/l (95% CI –0.4, 29.9) in women, P = 0.05 (P = 0.82 for birthweight x gender interaction). In a combined analysis of men and women adjusted for gender (n = 302), a 1 lb decrease in birthweight was associated with a 13.4 nmol/l (95% CI 4.5, 22.4) greater incremental rise in plasma cortisol, P = 0.003. Conclusions: associations between lower birthweight and increased HPA axis activity are similar in men and women, supporting the hypothesis that HPA axis activation is an important mechanism underlying programming of adult disease
Haploinsufficiency of the SERPINA6 gene is associated with severe muscle fatigue: a de novo mutation in corticosteroid-binding globulin deficiency
No full textCorticosteroid-binding globulin (SERPINA6) deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. Here, we present a patient with severe muscle fatigue, normal blood pressure, and abnormal high saliva cortisol levels following a standardized stress test. This patient was found heterozygous for a de novo 367 asparagine-encoding variant of the corticosteroid-binding globulin gene, previously described as "transcortin Lyon". Both parents were homozygous for the ("wildtype") 367 aspartate-encoding allele. To the best of our knowledge, this case represents the first de novo mutation reported for corticosteroid-binding globulin deficiency, implicating a pathogenic role of variants of SERPINA6 in some cases of muscle fatigue
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