Objective: The objective of this study was to assess the global burden of disease for developmental and intellectual disabilities caused by iodine deficiency from 1990 to 2019.
Methods: Using data from the global burden of disease (GBD) 2019, we conducted a cross-country inequity analysis to examine the worldwide burden of developmental and intellectual disabilities caused by the issue of iodine deficiency from 1990 to 2019. Absolute and relative inequality were assessed by the slope index of inequality and the concentration index, respectively. After summarising the latest evidence, we also projected the age-standardized prevalence and years lived with disability (YLD) rates up to 2030 using the BAPC and INLA packages in R statistical software.
Results: In 2019, the global age-standardized prevalence and YLD rates for developmental and intellectual disabilities due to iodine deficiency were 22.54 per 100,000 population (95% UI 14.47 to 29.23) and 4.12 per 100,000 population (95% UI 2.25 to 6.4), respectively. From 1990 to 2019, the age-standardized prevalence and YLD rates of developmental and intellectual disabilities due to iodine deficiency decreased significantly. Geographic distribution showed that areas with lower socio-demographic indices (SDI) were the most affected. The correlation between higher SDI and lower prevalence highlights the role of economic and social factors in the prevalence of the disease. Cross-national inequity analysis shows that disparities persist despite improvements in health inequalities. In addition, projections suggest that the disease burden may decline until 2030.
Conclusion: This research underscores the necessity for targeted interventions, such as enhancing iodine supplementation and nutritional education, especially in areas with lower SDI. We aim to provide a foundation for policymakers further to research effective preventative and potential alternative treatment strategies.
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http://dx.doi.org/10.3389/fnut.2024.1366525 | DOI Listing |
PeerJ
January 2025
Genomic Mechanisms of Ontogenesis, Institute of Cytology and Genetics, Novosibirsk, Novosibirsk, Russia.
Copy number variations of the human gene, resulting from megabase-scale microdeletions or microduplications in the 3p26.3 region, are frequently implicated in neurodevelopmental disorders such as intellectual disability and developmental delay. However, duplication of the full-length human gene presents with variable penetrance, resulting in phenotypes that range from neurodevelopmental disorders to no visible pathologies, even within the same family.
View Article and Find Full Text PDFFront Psychiatry
January 2025
Laboratoire Lorrain de Psychologie et Neurosciences de la Dynamique des Comportements, Université de Lorraine, Nancy, Lorraine, France.
Background: This study examined the profiles of adaptive behavior development in adults with autism spectrum disorder (ASD) and severe intellectual disability (ID), and the relationships between the levels of the different domains and subdomains of adaptive development and the intensity of autistic symptomatology.
Participants: This study involved 71 adults (44 men and 27 women with average ages of 39 years 7 months and 36 years 2 months, respectively) living in medico-social institutions and having a level of adaptive development corresponding to age below 3 years 4 months and a level of cognitive development corresponding to ages between 12 and 24 months.
Methods: ASD was diagnosed using Pervasive Development Disorder-Mental Retardation Scale (PDD-MRS) and Childhood Autistic Rating Scale (CARS), ID and its severity were determined based on the Diagnostic Statistical Manual-5 (DSM-5) criteria, and the very low cognitive developmental level was assessed using the Socio-emotional Cognitive Evaluation Battery (Adrien, Pearson-ECPA, 2007), adapted for adults (SCEB-A).
Proc Natl Acad Sci U S A
January 2025
Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, Department of Neuroscience, School of Life Sciences, Southern University of Science and Technology, Shenzhen 518055, China.
Ankyrin Repeat Domain-containing Protein 11 () is a causative gene for KBG syndrome, a significant risk factor for Cornelia de Lange syndrome (CdLS), and a highly confident autism spectrum disorder gene. Mutations of lead to developmental abnormalities in multiple organs/tissues including the brain, craniofacial and skeletal bones, and tooth structures with unknown mechanism(s). Here, we find that ANKRD11, via a short peptide fragment in its N-terminal region, binds to the cohesin complex with a high affinity, implicating why mutation can cause CdLS.
View Article and Find Full Text PDFInt Med Case Rep J
January 2025
Vincent van Gogh Centre of Excellence for Neuropsychiatry, Venray, The Netherlands.
Introduction: Levocarnitine is essential for brain functioning and fatty acid metabolism and stems largely from dietary sources. The Epsilon-Trimethyllysine Hydroxylase () gene encodes the enzyme N-Trimethyllysine hydroxylase (TMLH) which catalyses the first step in the biosynthesis of carnitine. Lack of TMLH enzyme activity is associated with developmental delay and autistic behaviours described as X-linked recessive autism, type 6 (OMIM#300872).
View Article and Find Full Text PDFJ Appl Res Intellect Disabil
January 2025
Department of Psychiatry, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire; Department of Pediatrics, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire; The Dartmouth Institute for Health Policy and Clinical Practice, Hanover, New Hampshire, Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire, USA.
Background: Little research has been conducted solely exploring gender diversity in people with intellectual disabilities. This review explores the literature, discusses the prevalence, and identifies clinical best practices for people at the intersection of gender diversity and intellectual disability.
Method: A scoping review was conducted utilising PRISMA methodology of the following databases: PubMed, CINAHL Complete (EBSCO), Cochrane Library (Wiley), Dissertations & Theses Global (ProQuest), PsycInfo (EBSCO), Scopus and Web of Science.
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