We sought to investigate the association between employment conditions and health among working age British adults with and without intellectual impairments. Using data from the 1970 British Cohort Study, we undertook a series of cross sectional analyses of the association between employment conditions and health (self-reported general health, mental health) among British adults with and without intellectual impairments at ages 30, 34 and 42. Our results indicated that: (1) British adults with intellectual impairments were more likely than their peers to be exposed to non-standard employment conditions and experience job insecurity; (2) in both groups exposure was typically associated with poorer health; (3) British adults with intellectual impairments in non-standard employment conditions were more likely than their peers to transition to economic inactivity; (4) among both groups, transitioning into employment was associated with positive health status and transitioning out of employment was associated with poorer health status. British adults with intellectual impairments are significantly more likely than their peers to be exposed to non-standard and more precarious working conditions. The association between employment conditions and health was similar for British adults with and without intellectual impairments. As such, the study found no evidence to suggest that research on causal pathways between employment and health derived from studies of the general population should not generalize to the population of people with intellectual impairments.
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http://dx.doi.org/10.1016/j.ssmph.2018.02.003 | DOI Listing |
Front Child Adolesc Psychiatry
February 2023
Operative Unit of Medical Genetics Bianchi - Melacrino- Morelli Hospital, Reggio Calabria, Italy.
Malan syndrome (MALNS) is an ultra-rare genetic disorder caused by heterozygous chromosomal microdeletions involving the 19p13.2 region or loss-of-function variants in the gene. It is characterized by specific phenotypical features, intellectual disability (ID), and limitations in adaptive functioning and behavioral problems.
View Article and Find Full Text PDFJ Intellect Dev Disabil
March 2024
Faculty of Medicine, Department of Psychology, University of Novi Sad, Novi Sad, Republic of Serbia.
Background: Multiple disabilities represent separate entities that cannot be reduced to the sum of disabilities or the main disability. This study compared the health-related quality of life (HRQoL) of children and adolescents with multiple disabilities and those with one developmental disability. We further assessed how comorbidities and guardianship type affected HRQoL.
View Article and Find Full Text PDFJ Intellect Dev Disabil
December 2023
Department of Kinesiology, Temple University, Philadelphia, PA, USA.
Background: Having an intellectual disability increases the likelihood for exhibiting impairments in vision, hearing, and balance. The intersection of these issues has yet to be described in a large cohort.
Methods: By hosting the largest public health database for individuals with intellectual disability, Special Olympics (SO) offers ∼120,000 assessments completed at competitions between 2007 and 2018.
Epilepsia
January 2025
Department of Epilepsy Genetics and Personalized Medicine, Danish Epilepsy Center, Dianalund, Denmark.
Objectives: Developmental and epileptic encephalopathies (DEEs) caused by pathogenic variants in SCN8A are associated with difficult-to-treat and early-onset seizures, developmental delay/intellectual disability, impaired quality of life, and increased risk of early mortality. High doses of sodium channel blockers are typically used to treat SCN8A-DEE caused by gain-of-function (GoF) variants. However, seizures are often drug resistant, and only a few patients achieve seizure freedom.
View Article and Find Full Text PDFActa Neurobiol Exp (Wars)
January 2025
Laboratory of Animal Models, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity.
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