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Background: Depressive symptoms and stress are common in adults with intellectual disabilities. Our aim was to explore long-term biological stress levels, assessed by hair cortisol (HairF) and cortisone (HairE) concentrations, in adults with intellectual disabilities and depressive symptoms and to investigate the effects of bright light therapy (BLT) on hair glucocorticoids. Method: Scalp hair samples (n = 14) were retrospectively examined at baseline and post-BLT (10.000 and 300 lux). Liquid chromatography-tandem mass spectrometry was used to measure hair glucocorticoids. Results: A significant correlation was found between baseline HairF and depression scores (r = 0.605, p = 0.028). Post-intervention HairE levels were significantly increased ([95% CI: 11.2-17.4 pg/mg], p = 0.003), in particular after dim light (300 lux) ([95% CI: 10.0-18.3 pg/mg], p = 0.020). Conclusions: This study showed that retrospectively examining biological levels of stress in adults with intellectual disabilities seems a potentially promising and objective method to gain insight in the stress level of adults with intellectual disabilities.

ABSTRACT Background Methods Results Conclusion Obesity can result in persistent metabolic changes despite weight loss, which may affect liver health. We aimed to investigate associations between young adulthood obesity and metabolic dysfunction‐associated steatotic liver disease (MASLD), at‐risk steatohepatitis and increased liver stiffness measurement (LSM) in a general population setting.We studied NHANES 2017–2020 community‐dwelling participants aged > 40 years with BMI ≥ 18.5 and no heart failure. Weight at age 25 was obtained through questionnaires and compared to current weight. Assessment included controlled attenuation parameter (CAP) and LSM. Associations between obesity status change with MASLD or at‐risk metabolic dysfunction‐associated steatohepatitis (MASH) and increased LSM were investigated and adjusted for demographics and metabolic health.The cohort comprised 4,580 participants (57% stable non‐obesity, 33% gained obesity, 2% lost obesity and 8% stable obesity). Compared to stable no‐obesity, stable obesity was strongly associated with MASLD (odds ratio [OR]: 5.47, 95% confidence interval [95%CI]: 3.97–7.66) as was gained obesity (OR: 4.68, 95% CI: 3.93–5.59), whereas no increased risk was demonstrated for lost obesity (OR: 1.26, 95% CI: 0.76–2.10). Similar associations for stable obesity and gained obesity with at‐risk MASH and LSM ≥ 8 kPa were demonstrated. No residual risk was found for lost obesity (MASH–OR: 1.05 95% CI: 0.36–2.49; LSM ≥ 8 kPa–OR: 0.85, 95% CI: 0.29–1.97). Results were consistent in sensitivity analysis where obesity change was calculated over the past 10 years and weight change was stratified in normal weight/overweight/obesity.Young adulthood obesity is an important risk factor for MASLD, at‐risk MASH and increased LSM among the general population aged 40–80 years. Losing obesity resulted in normalisation of odds for MASLD, at‐risk MASH and increased LSM. These findings underline the importance of preventing and treating young adulthood obesity to maintain liver health. [ABSTRACT FROM AUTHOR]

Introduction: Corticosteroids are widely prescribed and their use has been linked to adverse cardiometabolic outcomes. A pivotal role in the action of corticosteroids is reserved for the glucocorticoid receptor (GR). Here, we assessed the relationship of glucocorticoid sensitivity-altering GR polymorphisms with anthropometrics and metabolic syndrome (MetS) in corticosteroid users. Methods: In this population-based cohort study (Lifelines), we genotyped 10,621 adult participants for GR hypersensitive (1/2 copies BclI and/or N363S) and GR resistant (1/2 copies ER22/23EK and/or 9β) variants. We assessed the relationship between functional GR polymorphisms with BMI, waist circumference (WC), and MetS in users of corticosteroids. Results: Overall corticosteroid use was associated with a significantly higher BMI and WC in GR wild-type (WT) users (BMI, +0.63 kg/m2 [0.09–1.16], p = 0.022; WC, +2.03 cm [0.61–3.44], p = 0.005) and GR hypersensitive (BMI, +0.66 kg/m2 [95% CI, 0.31–1.01]; WC, +2.06 cm [1.13–2.98], both p < 0.001) but not in GR resistant users. Significantly higher WC in GR resistant carriers was observed only for inhaled corticosteroid users. With respect to MetS, again only GR WT users (odds ratio [OR] 1.44 [1.07–1.94], p = 0.017) and GR hypersensitives (OR 1.23 [95% CI, 1.00–1.50], p = 0.046) were more likely to have MetS; even more pronounced in only inhaled corticosteroid users (GR WT users, OR 1.64 [1.06–2.55], p = 0.027; GR hypersensitive users, OR 1.43 [1.08–1.91], p = 0.013). Conclusions: Polymorphisms associated with increased GR sensitivity and WT GR are related to increased BMI, WC, and an increased MetS presence in corticosteroid users, especially of the inhaled types, when compared to nonusers. The adverse effects of corticosteroid use are less pronounced in users harboring GR resistant polymorphisms. [ABSTRACT FROM AUTHOR]

Purpose: Central serous chorioretinopathy (CSC), a distinct form of macular degeneration, has been associated with glucocorticoid use and possibly also with an increased endogenous activity of the hypothalamic‐pituitary‐adrenal (HPA) axis. To estimate long‐term glucocorticoid exposure, measurement of hair cortisol concentrations (HCC) has emerged. This cross‐sectional study aimed to investigate HCC, as a reflection of chronic endogenous steroid exposure, in a cohort of patients with chronic CSC (cCSC). Methods: Hair cortisol concentrations (HCC) were determined in 48 patients with cCSC and 230 population‐based controls (Lifelines cohort study), not using exogenous corticosteroids. Results: Increased HCC (defined as >10.49 pg/mg) were present in 2 (4%) patients with cCSC and 13 (6%) controls. Mean HCC values were not different between patients and controls, and no difference in HCC was found between patients with active cCSC disease and patients with inactive disease. No correlation between HCC and urinary free cortisol (UFC) levels in patients with cCSC was found. Conclusions: This study shows that HCC in patients with cCSC are not elevated compared to population‐based controls, and no association between HCC and cCSC severity was found. This finding questions the previous suggestion that cCSC is associated with increased HPA axis activity. In line, HCC do not seem useful in monitoring cCSC disease activity. [ABSTRACT FROM AUTHOR]

Posttraumatic stress disorder (PTSD) is associated with altered hypothalamic-pituitary-adrenal (HPA) axis function. Measurement of hair cortisol concentrations (HCC) allows retrospective assessment of HPA axis regulation over prolonged periods of time. Currently, research investigating HCC in PTSD remains sparse. Previous cross-sectional studies have included only civilian populations, although it is known that trauma type moderates associations between PTSD status and HPA axis function. We investigated differences in HCC between trauma-exposed female police officers with current PTSD (n = 13) and without current and lifetime PTSD (n = 15). To investigate whether HCC was associated with neural correlates of PTSD, we additionally performed exploratory correlational analyses between HCC and amygdala reactivity to negative affective stimuli. We observed significantly lower HCC in participants with PTSD than in participants without PTSD, d = 0.89. Additionally, within participants with PTSD, we observed positive correlations between HCC and right amygdala reactivity to negative affective (vs. happy/neutral) faces, r = .806 (n = 11) and left amygdala reactivity to negative affective (vs. neutral) pictures, r = .663 (n = 10). Additionally, left amygdala reactivity to negative faces was positively correlated with HCC in trauma-exposed controls, r = .582 (n = 13). This indicates that lower HCC is associated with diminished amygdala differentiation between negative affective and neutral stimuli. Thus, we observed lower HCC in trauma-exposed noncivilian women with PTSD compared to those without PTSD, which likely reflects prolonged HPA axis dysregulation. Additionally, HCC was associated with hallmark neurobiological correlates of PTSD, providing additional insights into pathophysiological processes in PTSD. [ABSTRACT FROM AUTHOR]