Hanley Brask (pairtwig89)

Weight-related health conditions and depression peak during adolescence and show relations with brain structure. Understanding how these conditions relate to each other prior to adolescence may guide research on the co-development of unhealthy weight conditions (both underweight and overweight) and depression, with a potential brain-based link. This study examines the cross-sectional relations between body mass index (BMI), depressive symptoms, and brain volume (total and regional) to determine whether BMI has a linear or quadratic relation with depressive symptoms and brain volume and how depressive symptoms and brain volume are related. Cross-sectional study using structural magnetic resonance imaging, height and weight to calculate BMI z-scores, and Child Behavior Checklist withdrawn depression scores. Data were from the Adolescent Brain Cognitive Development Study, collected at 21 sites across the United States from 11,875 9- and 10-year-old children recruited as a national sample. Mixed models were u improve our understanding of brain structural differences in depression. These findings also emphasize the importance of including the full spectrum of BMI from underweight to overweight and testing for nonlinear effects in models.Most people experience grief after a loss, about 10% develop complicated grief, often accompanied by sleep complaints. Yet, the role of objectively estimated poor sleep remains unclear. Therefore, we assessed the cross-sectional and longitudinal association of actigraphy-estimated sleep with grief. We included 1,776 participants (mean age 61.8 ± 8.9 years, 55% women) of a prospective population-based cohort. Of 1,471 participants (83%) repeated measures of grief were available (median follow-up 6 years, inter quartile range 5.6-6.3). At baseline, sleep was objectively estimated using actigraphy (mean duration 6.0 ± 0.8days). At baseline and follow-up, participants were asked about significant losses and completed the Dutch Inventory of Complicated Grief (17 items, cut-off ≥22). At baseline 1,521 (86%) participants experienced no grief, 44 (2%) acute grief ( less then 6 months, any grief score), 158 (9%) non-complicated grief (≥6 months, grief score less then 22), and 53 (3%) complicated grief (≥6 months, grief score≥22). In those indicating any grief (n = 255), low sleep efficiency (B = -0.16, 95%CI = -0.30;-0.02), long sleep onset latency (B = 0.07, 95%CI = 0.01; 0.14), and long wake after sleep onset (B = 0.06, 95%CI = 0.01; 0.10) were cross-sectionally associated with more grief symptoms. Over time, those with a short total sleep time (OR = 0.59, 95%CI = 0.39; 0.91), low sleep efficiency (OR = 0.95, 95%CI = 0.91; 0.99), long sleep onset latency (OR = 1.02, 95%CI = 1.00; 1.04), and long wake after sleep onset (OR = 1.02, 95%CI = 1.00; 1.03) at baseline more often experienced complicated grief than non-complicated grief at follow-up. This study suggests that objectively estimated poor sleep is associated with grief over time. Poor sleep might not only accompany grief, but also be a risk factor for developing complicated grief after a loss.The socio-economic implications of COVID-19 are devastating. Considerable morbidity is attributed to 'long-COVID' - an increasingly recognized complication of infection. Its diverse symptoms are reminiscent of vitamin B12 deficiency, a condition in which methylation status is compromised. We suggest why SARS-CoV-2 infection likely leads to increased methyl-group requirements and other disturbances of one-carbon metabolism. We propose these might explain the varied symptoms of long-COVID. Our suggested mechanismmight also apply to similar conditions such as myalgic encephalomyelitis/chronic fatigue syndrome. The hypothesis is evaluable by detailed determination of vitamin B12and folate status, including serum formate as well as homocysteine and methylmalonic acid, and correlation with viral and host RNA methylation and symptomatology. If confirmed, me