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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The obesity epidemic has focused attention on obesity's health consequences beyond cardio-vascular disease and diabetes. To evaluate the potential consequences of obesity for Attention Deficit-Hyperactivity Disorder (ADHD), we surveyed the literature. Current findings link both obesity and ADHD to the dopamine system and implicate dopamine genes in body weight, eating, and ADHD. Detailed consideration suggests that dopaminergic changes in the prefrontal cortex among individuals with the ADHD subtype Attention Deficit Disorder (ADD) may increase their risk for obesity. Thus, individuals and populations with a high prevalence of hyperdopaminergic genes may experience higher rates of obesity in the presence of abundant food. From an evolutionary perspective, alterations in the dopamine system appear to effect a wide range of behavioral phenotypes. We suggest that recent evolutionary changes in the dopamine receptor genes selected to increase cognitive and behavioral flexibility may now be associated with attention problems and increased food consumption in an obesogenic environment.
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PMID:Obesity, attention deficit-hyperactivity disorder and the dopaminergic reward system. 1760 Sep 16

Recent studies suggest a possible comorbidity between Attention-Deficit/Hyperactivity Disorder (ADHD) and obesity. To gain insight into this potential association, we performed a systematic review of the literature excluding case reports, non-empirical studies, and studies not using ADHD diagnostic criteria. Empirically based evidence suggests that obese patients referred to obesity clinics may present with higher than expected prevalence of ADHD. Moreover, all reviewed studies indicate that subjects with ADHD are heavier than expected. However, data on the prevalence of obesity in subjects with ADHD are still limited. As for the mechanisms underlying the potential association between ADHD and obesity, ADHD might lead to obesity via abnormal eating behaviors, impulsivity associated with binge eating might contribute to ADHD in obese patients, or, alternatively, both obesity and ADHD might be the expression of common underlying neurobiological dysfunctions, at least in a subset of subjects. In patients with obesity and ADHD, both conditions might benefit from common therapeutic strategies. Further empirically based studies are needed to understand the potential comorbidity between obesity and ADHD, as well as the possible mechanisms underlying this association. This might allow a more appropriate clinical management and, ultimately, a better quality of life for patients with both obesity and ADHD.
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PMID:Attention-deficit/hyperactivity disorder (ADHD) and obesity: a systematic review of the literature. 1856 58

Recent research suggests that racial residential segregation may be detrimental to health. This study investigates the influence of neighborhood racial isolation on obesity and considers the role of neighborhood disorder as a mediator in this relationship. For the city of Philadelphia, we find that residence in a neighborhood with high black racial isolation is associated with a higher body mass index and higher odds of obesity among women, but not men, highlighting important sex differences in the influence of neighborhood structure on health. Furthermore, the influence of high racial isolation on women's weight status is mediated, in part, by the physically disordered nature of such neighborhoods. Disorder of a more social nature (as measured by incident crime) is not associated with weight status.
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PMID:Neighborhood Racial Isolation, Disorder and Obesity. 2017 75

11 beta-hydroxysteroid dehydrogenase (HSDs) enzymes regulate the activity of glucocorticoids in target organs. HSD1, one of the two existing isoforms, locates mainly in CNS, liver and adipose tissue. HSD1 is involved in the pathogenesis of diseases such as obesity, insulin resistance, arterial hypertension and the Metabolic Syndrome. The stress produced by HCl overload triggers metabolic acidosis and increases liver HSD1 activity associated with increased phosphoenolpyruvate carboxykinase, a regulatory enzyme of gluconeogenesis that is activated by glucocorticoids, with increased glycaemia and glycogen breakdown. The aim of this study was to analyze whether the metabolic modifications triggered by HCl stress are due to increased liver HSD1 activity. Glycyrrhetinic acid, a potent HDS inhibitor, was administered subcutaneously (20 mg/ml) to stressed and unstressed four months old maleSprague Dawley rats to investigate changes in liver HSD1, phosphoenolpyruvate carboxykinase (PECPK) and glycogen phosphorylase activities and plasma glucose levels. It was observed that all these parameters increased in stressed animals, but that treatment with glycyrrhetinic acid significantly reduced their levels. In conclusion, our results demonstrate the involvement of HSD1 in stress induced carbohydrate disturbances and could contribute to the impact of HSD1 inhibitors on carbohydrate metabolism and its relevance in the study of Metabolic Syndrome Disorder and non insulin-dependent diabetes mellitus.
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PMID:Hepatic 11 beta-hydroxysteroid dehydrogenase 1 involvement in alterations of glucose metabolism produced by acidotic stress in rat. 2035 45

Although a higher prevalence of overweight/obesity was reported in clinical samples of patients with Attention-Deficit/Hyperactivity Disorder (ADHD), an association between overweight and ADHD has yet not been established in the general population in childhood. As both disorders are common and significantly affect psychosocial functioning, we investigated the prevalence of ADHD in overweight/obese youth and vice versa. In a cross-sectional nationally representative and community based survey 2,863 parents and their children aged 11-17 years rated symptoms on the Diagnostic and Statistical Manual of Mental Disorders-based German ADHD Rating scale. Weight and height were assessed by professionals. Body mass index was categorized according to national age and sex specific reference values. Overall, 4.2% of the respondents met criteria for ADHD. The prevalence of ADHD was significantly higher for overweight/obese (7%) than for normal weight (3.5%) and underweight (4.9%) children. In a logistic regression analysis controlling for age, gender, and socio-economic status, overweight/obese children were twice as likely to have an ADHD diagnosis (OR = 2.0). Vice versa, adjusting for all covariates, children with ADHD had an OR of 1.9 for overweight/obesity status. For all weight-status groups, children with ADHD more frequently reported eating problems as compared to their non-clinical counterparts. Overweight/obese respondents with ADHD displayed the highest level of health services utilization. A clinician should be aware of the significant risk for a child with ADHD to become overweight and for an overweight child to have ADHD. Longitudinal studies are needed to better understand the mechanisms underlying the association between ADHD and overweight/obesity.
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PMID:Examining the relationship between attention-deficit/hyperactivity disorder and overweight in children and adolescents. 2212 Jul 61

Chromosome 15q24 microdeletion syndrome is a recently described rare microdeletion syndrome that has been reported in 19 individuals. It is characterized by growth retardation, intellectual disability, and distinct facial features including long face with high anterior hairline, hypertelorism, epicanthal folds, downslanting palpebral fissures, sparse and broad medial eyebrows, broad and/or depressed nasal bridge, small mouth, long smooth philtrum, and full lower lip. Other common findings include skeletal and digital abnormalities, genital abnormalities in males, hypotonia, behavior problems, recurrent infections, and eye problems. Other less frequent findings include hearing loss, growth hormone deficiency, hernias, and obesity. Congenital malformations, while rare, can be severe and include structural brain anomalies, cardiovascular malformations, congenital diaphragmatic hernia, intestinal atresia, imperforate anus, and myelomeningocele. Karyotypes are typically normal, and the deletions were detected in these individuals by array comparative genomic hybridization (aCGH). The deletions range in size from 1.7-6.1 Mb and usually result from nonallelic homologous recombination (NAHR) between paralogous low-copy repeats (LCRs). The majority of 15q24 deletions have breakpoints that localize to one of five LCR clusters labeled LCR15q24A, -B, -C, -D, and -E. The smallest region of overlap (SRO) spans a 1.2 Mb region between LCR15q24B to LCR15q24C. There are several candidate genes within the SRO, including CYP11A1, SEMA7A, CPLX3, ARID3B, STRA6, SIN3A and CSK, that may predispose to many of the clinical features observed in individuals with 15q24 deletion syndrome. The deletion occurred as a de novo event in all of the individuals when parents were available for testing. Parental aCGH and/or FISH studies are recommended to provide accurate genetic counseling and guidance regarding prognosis, recurrence risk, and reproductive options. Management involves a multi-disciplinary approach to care with the primary care physician and clinical geneticist playing a crucial role in providing appropriate screening, surveillance, and care for individuals with this syndrome. At the time of diagnosis, individuals should receive baseline echocardiograms, audiologic, ophthalmologic, and developmental assessments. Growth and feeding should be closely monitored. Other specialists that may be involved in the care of individuals with 15q24 deletion syndrome include immunology, endocrine, orthopedics, neurology, and urology. Chromosome 15q24 microdeletion syndrome should be differentiated from other genetic syndromes, particularly velo-cardio-facial syndrome (22q11.2 deletion syndrome), Prader-Willi syndrome, and Noonan syndrome. These conditions share some phenotypic similarity to 15q24 deletion syndrome yet have characteristic features specific to each of them that allows the clinician to distinguish between them. Molecular genetic testing and/or aCGH will be able to diagnose these conditions in the majority of individuals. DISEASE NAME AND SYNONYMS: Chromosome 15q24 deletion syndrome. 15q24 deletion syndrome. 15q24 microdeletion syndrome.
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PMID:Chromosome 15q24 microdeletion syndrome. 2221 33

After a general introduction into genetic risk factors for child psychiatric disorders, four specific child psychiatric disorders with a strong genetic component, namely, Autism Spectrum Disorders, Attention Deficit / Hyperactivity Disorder, Nocturnal Enuresis, and obesity, are discussed in detail. Recent evidence of linkage, candidate gene, and genome-wide association studies are presented. This chapter ends with a prospectus on further research needs.
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PMID:Behavioural genetics of childhood disorders. 2238 29

Recent studies suggest a possible correlation between Attention Deficit/Hyperactivity Disorder (ADHD) and obesity. In order to explore the topic a systematic review of the literature was performed excluding case reports, non-empirical studies, and studies not using the ADHD diagnostic criteria. Recent studies suggests that obese patients referred to obesity clinics may present themselves with a higher that predicted prevalence od ADHD. Moreover, all studies indicate that subjects with ADHD have higher body weight than expected. However, data on the prevalence of obesity in subjects with ADHD are still limited. Hypotheses about mechanisms underlying the potential correlation between ADHD and obesity suggests that ADHD may contribute to obesity by impulsive eating or disorganised eating habits, impulsivity associated with binge eating might contribute to ADHD symptoms in obese patients, or alternatively ADHD and obesity might be an expression of a common biological dysfunction such as deficit in the reward system. Prospective research, which ic still limited may lead to a better understanding of the correlation between ADHD and obesity as well as the possible mechanisms underlying this comorbidity, contributing to better therapy and thereby improve the quality of life in patient with ADHD and obesity.
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PMID:[Correlations between attention deficit hyperactivity disorder and obesity - a systematic review of the literature]. 2388 47

Birthweight is a marker for suboptimal fetal growth and development in utero. Offspring can be born large for gestational age (LGA), which is linked to maternal obesity or excessive gestational weight gain, as well as small for gestational age (SGA), arising from nutrient or calorie deficiency, placental dysfunction, or other maternal conditions (hypertension, infection). In humans, LGA and SGA babies are at an increased risk for certain neurodevelopmental disorders, including Attention Deficit/Hyperactivity Disorder, schizophrenia, and social and mood disorders. Using mouse models of LGA (maternal high fat (HF) diet) and SGA (maternal low protein (LP) diet) offspring, our lab has previously shown that these offspring display alterations in the expression of mesocorticolimbic genes that regulate dopamine and opioid function, thus indicating that these brain regions and neurotransmitter systems are vulnerable to gestational insults. Interestingly, these two maternal diets affected dopamine and opioid systems in somewhat opposing directions (e.g., LP offspring are generally hyperdopaminergic with reduced opioid expression, and the reverse is found for the HF offspring). These data largely involved evaluation at the transcriptional level, so the present experiment was designed to extend these analyses through an assessment of receptor binding. In this study, control, SGA and LGA offspring were generated from dams fed control, low protein or high fat diet, respectively, throughout pregnancy and lactation. At weaning, mice were placed on the control diet and sacrificed at 12 weeks of age. In vitro autoradiography was used to measure mu-opioid receptor (MOR), dopamine type 1 receptor (D1R), and dopamine transporter (DAT) binding level in mesolimbic brain regions. Results showed that the LP offspring (males and females) had significantly higher MOR and D1R binding than the control animals in the regions associated with reward. In HF offspring there were no differences in MOR binding, and limited increases in D1R binding, seen only in females in the nucleus accumbens core and the dorsomedial caudate/putamen. DAT binding revealed no differences in either models. In conclusion, LP but not HF offspring show significantly elevated MOR and D1R binding in the brain thus affecting DA and opioid signaling. These findings advance the current understanding of how suboptimal gestational diets can adversely impact neurodevelopment and increase the risk for disorders such as ADHD, obesity and addiction.
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PMID:Suboptimal maternal diets alter mu opioid receptor and dopamine type 1 receptor binding but exert no effect on dopamine transporters in the offspring brain. 2766 82

Autism Spectrum Disorder affects up to 2.5% of children and is associated with harmful health outcomes (e.g. obesity). Low levels of physical activity and high levels of sedentary behaviors may contribute to harmful health outcomes. To systematically review the prevalence and correlates of physical activity and sedentary behaviors in children with Autism Spectrum Disorder, electronic databases (PsycINFO, SPORTDiscus, EMBASE, Medline) were searched from inception to November 2015. The review was registered with PROSPERO (CRD42014013849). Peer-reviewed, English language studies were included. Two reviewers screened potentially relevant articles. Outcomes of interest were physical activity and sedentary behaviour levels and their potential correlates. Data were collected and analysed in 2015. Of 35 included studies, 15 reported physical activity prevalence, 10 reported physical activity correlates, 18 reported sedentary behavior prevalence, and 10 reported sedentary behavior correlates. Estimates of children's physical activity (34-166 mins/day, average 86 mins/day) and sedentary behavior (126-558 mins/day in screen time, average 271 mins/day; 428-750 mins/day in total sedentary behavior, average 479 mins/day) varied across studies. Age was consistently inversely associated, and sex inconsistently associated with physical activity. Age and sex were inconsistently associated with sedentary behavior. Sample sizes were small. All but one of the studies were classified as having high risk of bias. Few correlates have been reported in sufficient studies to provide overall estimates of associations. Potential correlates in the physical environment remain largely unexamined. This review highlights varying levels of physical activity and sedentary behavior in children with Autism Spectrum Disorder. Research is needed to consistently identify the correlates of these behaviors. There is a critical need for interventions to support healthy levels of these behaviors.
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PMID:Physical activity, sedentary behavior and their correlates in children with Autism Spectrum Disorder: A systematic review. 2824 24


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