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

A young adolescent girl (13.5 years old) with a compulsive eating disorder and gross obesity was treated with a combination of behavior therapy and fenfluramine (Ponderax). The behavior modification program used was adapted from Reiss's program, an approach that had proven effective in individuals with hyperphagia and overweight who had no additional emotional problems or brain damage. In our patient the problem was complicated by the presence of autism, with compulsive eating being particularly ingrained as a form of stereotyped behavior. We therefore decided to administer fenfluramine concurrently because it is known to have both an appetite-depressing effect and a positive effect on behavioral disturbances characteristic of autistic individuals. During inpatient treatment the girl lost weight and showed changes in behavior. The changed eating behavior was still being maintained many months after discharge and after fenfluramine had been discontinued. We assume that drug treatment provided an important kind of support for the behavioral treatment program. Further, we attribute the emotional stabilization in this autistic girl to fenfluramine. We now plan to extend this treatment approach to other subjects with similar problems.
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PMID:[Treatment of compulsive eating disorders in an autistic girl by combining behavior therapy and pharmacotherapy. Case report]. 376 95

Due to asymmetry of brain neurotransmitters and differential hemispheric information processing modes, it is suggested that the excessive use of one information processing mode could engender a state of brain reactivity whose neurochemical correlates would be either a rise in melatonin or beta-endorphin in systemic circulation. Since melatonin and beta-endorphin have opposite effects on lung-mediated regulation of prostaglandins, it is further suggested that the pulmonary inactivation of prostaglandin E1 would either be increased or inhibited. Low levels of PGE1 would engender high levels of PGE2 whose effects would explain the findings in schizophrenics of: 'reducing' pattern of visual evoked response, cerebral atrophy, and viral and autoimmune phenomena. The primacy of the disordered cognitive style in leading up to the immunological, biochemical and neuropathological processes is stressed. Implications of this model for understanding depression, anxiety and phobic disorders, autism, attention deficit disorder, obesity, alcoholism, smoking, drug addiction, sexual deviations, and certain psychosomatic and psychophysiological disorders are suggested.
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PMID:How information processing mode could affect prostaglandin E1 metabolism and lung inactivation: relevance of hemispheric specialization, neurotransmitter asymmetry and brain reactivity. 614 17

This study examined stress-support in 42 families of 3 to 18-year-old children with Prader-Willi syndrome. Parents were asked about themselves and their families, their child with Prader-Willi syndrome, family supports, and family stress. Compared to reported stress levels in families of children with mixed etiologies of retardation, parents of children with Prader-Willi syndrome showed higher levels of parent and family problems, and comparable levels of pessimism. Parents of children with Prader-Willi syndrome listed other family members and friends as their main supporters; often such supporters lived outside of the respondent's town or city. Although the child's age, IQ, and degree of obesity were not related to familial stress, families experienced greater stress when the child showed more behavior problems overall, more externalizing and internalizing problems, and more problems on five of the nine narrow-band domains of Achenbach's Child Behavior Checklist.
J Autism Dev Disord 1997 Feb
PMID:Families of children with Prader-Willi syndrome: stress-support and relations to child characteristics. 901 79

Child and adolescent therapy outcome research findings attest to the efficacy of a variety of treatments. This article illustrates promising treatments for selected internalizing (anxiety and depression), externalizing (oppositional, and antisocial behavior), and other (obesity and autism) conditions, and for other aims (preparation for medical and dental procedures). Studies in these areas illustrate worthwhile characteristics that can help inform the search for empirically supported treatments. These characteristics include randomized controlled trials, well-described and replicable treatments, tests with clinical samples, tests of clinical significance, broad-based outcome assessment including measures of real-world functioning, and others. Continued research progress will depend on greater attention to magnitude and maintenance of therapeutic change, long-term follow-up, moderators and mediators of change, and development and testing of treatment in conditions relevant to clinical practice.
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PMID:Identifying and developing empirically supported child and adolescent treatments. 948 60

Based on cases that had been excluded from a previous clinical study of Sotos syndrome, Cole and Hughes [1991: Am J Med Genet 41:115-124] reported a new syndrome associated with marked obesity, occasional delayed bone age, distinctive facial anomalies, mental retardation, and progressive postnatal macrocephaly in the context of autosomal dominant familial macrocephaly. Subsequently, Stevenson et al. [1997: Lancet 349:1744-1745] emphasized the association of progressive postnatal macrocephaly with autism, and they suggested that this might comprise a recognizable autism syndrome. We report two additional patients with Cole-Hughes syndrome and associated autistic characteristics with attention deficit hyperactivity disorder. These patients seem to manifest a distinctive behavioral phenotype associated with Cole-Hughes syndrome and they manifest a distinct subgroup of persons with autism that may ultimately shed light on the pathogenesis of this disorder.
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PMID:Cole-Hughes macrocephaly syndrome and associated autistic manifestations. 1098 71

The highly evolutionarily conserved serotonin transporter (SERT) regulates the entire serotoninergic system and its receptors via modulation of extracellular fluid serotonin concentrations. Differences in SERT expression and function produced by three SERT genes and their variants show associations with multiple human disorders. Screens of DNA from patients with autism, ADHD, bipolar disorder, and Tourette's syndrome have detected signals in the chromosome 17q region where SERT is located. Parallel investigations of SERT knockout mice have uncovered multiple phenotypes that identify SERT as a candidate gene for additional human disorders ranging from irritable bowel syndrome to obesity. Replicated studies have demonstrated that the SERT 5'-flanking region polymorphism SS genotype is associated with poorer therapeutic responses and more frequent serious side effects during treatment with antidepressant SERT antagonists, namely, the serotonin reuptake inhibitors (SRIs).
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PMID:Serotonin transporter: gene, genetic disorders, and pharmacogenetics. 1508 84

Comorbidity is the rule, not the exception, in bipolar disorder. The most common mental disorders that co-occur with bipolar disorder in community studies include anxiety, substance use, and conduct disorders. Disorders of eating, sexual behavior, attention-deficit/hyperactivity, and impulse control, as well as autism spectrum disorders and Tourette's disorder, co-occur with bipolar disorder in clinical samples. The most common general medical comorbidities are migraine, thyroid illness, obesity, type II diabetes, and cardiovascular disease. Bipolarity is a marker for comorbidity, and comorbid disorders, especially multiple conditions occurring when a patient is young, may be a marker for bipolarity. Relatively few controlled clinical studies have examined the treatment of bipolar disorder in the context of comorbid conditions (i.e., complicated or comorbid bipolar disorder). However, the first step in treating any type of complicated bipolar disorder--stabilizing a patient's mood--may be associated with improving the comorbid disorder. Standard mood stabilizers, atypical antipsychotics, and non-antimanic antiepileptic agents are emerging as potentially useful treatments for several of the disorders that frequently co-occur with bipolar disorder, and therefore may be useful treatments for comorbid bipolar disorder.
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PMID:Diagnosing and treating comorbid (complicated) bipolar disorder. 1555 95

Autism is a neurodevelopmental disorder that according to the Centers for Disease Control and Prevention (CDC) affects 1 in 150 children in the United States. Autism is characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recently emerging evidence suggests that mercury, especially from childhood vaccines, appears to be a factor in the development of the autistic disorders, and that autistic children have higher than normal body-burdens of mercury. In considering mercury toxicity, it has previously been shown that testosterone significantly potentates mercury toxicity, whereas estrogen is protective. Examination of autistic children has shown that the severity of autistic disorders correlates with the amount of testosterone present in the amniotic fluid, and an examination of a case-series of autistic children has shown that some have plasma testosterone levels that were significantly elevated in comparison neurotypical control children. A review of some of the current biomedical therapies for autistics, such as glutathione and cysteine, chelation, secretin, and growth hormone, suggests that they may in fact lower testosterone levels. We put forward the medical hypothesis that autistic disorders, in fact, represents a form of testosterone mercury toxicity, and based upon this observation, one can design novel treatments for autistics directed towards higher testosterone levels in autistic children. We suggest a series of experiments that need to be conducted in order to evaluate the exact mechanisms for mercury-testosterone toxicity, and various types of clinical manipulations that may be employed to control testosterone levels. It is hoped by devising therapies that address the steroid hormone pathways, in addition to the current treatments that successful lower heavy metal body-burdens of mercury, will work synergistically to improve clinical outcomes. In light of the fact that there are a number of other diseases that may have a chronic mercury toxicity component, such as Alzheimer's disease, heart disease, obesity, ALS, asthma, and other various forms of autoimmune disorders, it is imperative that further research should be conducted to understand mercury-testosterone toxicity.
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PMID:The potential importance of steroids in the treatment of autistic spectrum disorders and other disorders involving mercury toxicity. 1578 Apr 90

Obesity and attention-deficit hyperactivity disorder (ADHD) are both increasing in prevalence. Childhood exposure to television has shown linkage to both ADHD and obesity with the former ascribed to dysfunctional cognitive hyperstimulation and the latter to altered patterns of diet and exercise. Empirical evidence has contradicted prior presumptions that the hyperactivity of ADHD would decrease the risk of obesity. Instead, obesity and ADHD demonstrate significant comorbidity. We propose that obesity and ADHD represent different manifestations of the same underlying dysfunction, a phenomenon we term environmental oversampling syndrome. Oversupply of information in the form of nutritional content and sensory content may independently predispose to both obesity and ADHD. Moreover, the pathogenic mechanisms of these conditions may overlap such that nutritional excess contributes to ADHD and cognitive hyperstimulation contributes to obesity. The overlapping effects of medications provide further evidence towards the existence of shared etiologic pathways. Metabolism and cognition may represent parallel systems of intelligence, and oversampling of content may constitute the source of parallel dysfunctions. The emerging association between psychiatric and metabolic disorders suggests a fundamental biologic link between these two systems. In addition, the immune system may represent yet another form of intelligence. The designation of syndrome X subsumes seemingly unrelated metabolic and inflammatory entities. Environmental oversampling syndrome may represent an even more inclusive concept that encompasses various metabolic, inflammatory, and behavioral conditions. Apparently disparate conditions such as insulin resistance, diabetes, hypertension, syndrome X, obesity, ADHD, depression, psychosis, sleep apnea, inflammation, autism, and schizophrenia may operate through common pathways, and treatments used exclusively for one of these conditions may prove beneficial for the others.
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PMID:Obesity and ADHD may represent different manifestations of a common environmental oversampling syndrome: a model for revealing mechanistic overlap among cognitive, metabolic, and inflammatory disorders. 1590 45

Imprinted genes are epigenetically modified genes whose expression is determined according to their parent of origin. They are involved in embryonic development, and imprinting dysregulation is linked to cancer, obesity, diabetes, and behavioral disorders such as autism and bipolar disease. Herein, we train a statistical model based on DNA sequence characteristics that not only identifies potentially imprinted genes, but also predicts the parental allele from which they are expressed. Of 23,788 annotated autosomal mouse genes, our model identifies 600 (2.5%) to be potentially imprinted, 64% of which are predicted to exhibit maternal expression. These predictions allowed for the identification of putative candidate genes for complex conditions where parent-of-origin effects are involved, including Alzheimer disease, autism, bipolar disorder, diabetes, male sexual orientation, obesity, and schizophrenia. We observe that the number, type, and relative orientation of repeated elements flanking a gene are particularly important in predicting whether a gene is imprinted.
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PMID:Genome-wide prediction of imprinted murine genes. 1593 Apr 97


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