Introduction to the information for preventing and managing psychological and/or developmental disorders, such as autism, depression, and obsessive compulsive disorder.
Curing insomnia in people with depression could double their chance of a full recovery. The findings are based on a study of 66 patients after four sessions over eight weeks of cognitive behavior therapy for insomnia, or CBT-I for short. The therapist teaches people to establish a regular wake-up time and stick to it; get out of bed during waking periods; avoid eating, reading, watching TV or similar activities in bed; and eliminate daytime napping.
Benefit of alpha tocopherol (Vitamin E) in mild to moderate Alzheimer disease (AD) by slowing functional decline: A double-blind, placebo-controlled, parallel-group, randomized clinical trial involving 613 patients with mild to moderate AD suggests 2000 IU/d of alpha tocopherol compared with placebo resulted in slower functional decline.
Studies suggest a causal relationship between depression and cardiovascular events. A prospective cohort study (Whitehall II study in 10,036 civil servants in England, mean age at start 44.4 years, total follow up 24 years) provided evidence of a dose–response effect of depressive symptoms on risk of coronary heart disease. In contrast, prospective associations of depressive symptoms with stroke appeared to arise wholly or partly through reverse causation.
Another randomized controlled trial in 235 primary care patients 60 years or older with major depression or dysthymia (Improving Mood-Promoting Access to Collaborative Treatment, IMPACT) in the US revealed that collaborative depression care delivered before cardiovascular disease (CVD) onset halved the excess risk of the hard CVD events among older, depressed patients, but not in those patients with baseline CVD.
Autism incidence linked to environmental factors. The spatial incidence patterns of autism spectrum disorders (ASD) and intellectual disability (ID) in nearly one third of the US population showed that adjusted for gender, ethnic, socioeconomic, and geopolitical factors, the ASD incidence was strongly linked to population-normalized rates of congenital malformations of the reproductive system, a surrogate for environmental exposure of parents to unmeasured developmental risk factors, including toxins. Such congenital malformations were barely significant for ID. Furthermore, the state-mandated rigor of diagnosis of ASD for consideration in the special education system was predictive of a considerable decrease in ASD and ID incidence. The quest for the etiology of neurodevelopmental disorders should include environmental, demographic and socioeconomic factors, and governmental policies.
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