Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0277787 (stigma)
 13,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost 19 million Americans require treatment for an "alcohol problem"; however, only 2.4 million have been diagnosed and just 139,000 receive medication to treat it. Chronic heavy drinking contributes to cardiovascular illnesses, liver disease, cancer, and psychiatric disorders. Imaging studies demonstrate structural changes in the human brain with prolonged exposure to alcohol. Alcoholism can thus be described as an acquired brain dysfunction with specific neurochemical and neuroanatomic pathways. There is a need to intervene early because the average age of alcohol experimentation is 11-13 years--delaying onset reduces the rate of alcoholism. A survey sponsored by the Community Anti-Drug Coalitions of America (CADCA) set out to measure the attitudes and misperceptions of 1000 adults from the general population plus 300 physicians and 503 individuals in recovery from alcohol use disorder (AUD) to better understand approaches toward alcohol treatment. In these surveys, 74% of the general public indicated that alcoholism affects their daily lives, with 41% reporting having to encourage a loved one to seek help for an alcohol problem. The vast majority (= 80%) indicated a stigma toward alcoholics. Denial or refusal to admit severity and fear of social embarrassment were the top 2 reasons for not seeking help. The majority of the general population believes that alcoholism is caused partly by moral weakness. The survey revealed that most Americans are open to medications to treat alcoholism if physician-recommended and if it could reduce alcohol cravings and maintain abstinence. In the past 55 years, only 3 medications (disulfiram, naltrexone, and acamprosate) have been US Food and Drug Administration (FDA)-approved for the treatment of AUD, each with unique mechanisms of action.
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PMID:Alcoholism and pathways to recovery: new survey results on views and treatment options. 1691 32

Kraepelin's dichotomy, manic-depressive insanity and dementia praecox, are contrasting and true endogenous disease entities which affect excitability, the fundamental property of the CNS. Kraepelin wanted to establish a valid classification and hit the extremes in brain structure and function at a time when we had no knowledge of brain dysfunction in "functional" psychoses. The aetiology is now known: the psychoses are part of human growth and maturation and might be classified according to their brain dysfunction, which is exactly what Kraepelin wanted. However, presumably to reduce the stigma attached to the word "psychosis", there is currently a strong initiative to eliminate the concept. But knowledge of what is happening in the brain in a psychosis might be more helpful in reducing stigma. It is suggested that psychosis is due to an affection of the supplementary motor area (SMA), located at the centre of the Medial Frontal Lobe network. The SMA is one of the rare universally connected areas of the brain, as should be the case for such a key structure that makes decisions as to the right moment for action. This important network, which partly has continuous neurogenesis, has sufficiently widespread connections. The SMA, a premotor area located on the medial side of the frontal lobes, is one of the last regions to reach a concurrence of synaptogenesis. An affection of the SMA, a deficient or abolished Delayed Response Task, seriously disturbs our relation and adaptation to the surroundings. We usually master the Delayed Response Task around the age of 7 months, a time at which the second CNS regressive event takes place, which proceeds from the posterior to the anterior of the brain. In very late maturation, a persistent affection of the SMA might occur. We experience a chronic psychosis: infantile autism (IA), a chronic inability to act consciously, which contrasts with the episodic SMA affection post-puberty, when excitation is reduced due to excessive pruning of excitatory synapses. Silent spots are the result of insufficient fill-in mechanisms following a breakdown of circuitry. They may affect the SMA in the case of very late puberty. An acute reduction in excitation and concomitantly a marked increase in silent spots might lead to an acute psychosis. A frontal preference is likely, given that a reduction might occur anywhere in the cortex, but particularly in the areas maturing latest. The varying localisations probably explain the difficulty in accepting schizophrenia as a disease entity. The multifactorial inheritance of the dichotomy implies that the genetics are not fate, a psychotic development might be prevented given enough epigenetic factors: brain food (omega 3). Might the present dietary adversity, with its lack of brain food, be responsible for a rising incidence in psychosis? A psychosis is an understandable and preventable dysfunction of the brain, and its mechanisms are known. Primarily a disorder of reduced excitation in an attenuated CNS, this explains why all the neuroleptics are convulsants, raising excitation, in contrast to all antidepressives, which are anti-epileptic.
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PMID:What is a psychosis and where is it located? 1851 23

Anorexia nervosa is a serious illness with major physical and psychological morbidity. It has largely been understood in terms of cultural and environmental explanations. However these are insufficient to explain the diverse clinical features of the illness, nor its rarity given the universality of sociocultural factors. Over the last 20 years, there has been a steady accumulation of neurobiological evidence requiring a re-formulation of current causal models. We now offer a new empirically-derived hypothesis implicating underlying rate-limiting dysfunction of insula cortex as a crucial risk factor for the development of anorexia nervosa. Supporting evidence for this hypothesis is drawn from anatomical and clinical research of insula cortex damage in humans and neuroscientific studies of relevant clinical features including taste, pain perception and reward processing. This hypothesis, if sustainable, would be the first fully to explain the disorder and predicts promising novel treatment possibilities including Cognitive Remediation and Motivation Enhancement Therapies. The knowledge that the challenging behaviours, so characteristic of AN, are the result of underlying cerebral dysfunction, rather than being purely volitional, could help to reduce the stigma patients experience and improve the therapeutic alliance in this poorly understood and difficult to treat disorder.
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PMID:Anorexia nervosa and the insula. 2184 16

Fragile X syndrome is considered the most common heritable form of X-linked intellectual disability (ID). The syndrome is caused by silencing of the fragile X mental retardation 1 gene (Xq27.3) due to hypermethylation. This mutation results in absence or deficit of its protein product, the fragile X mental retardation protein (FMRP) that affects synaptic plasticity in neurons, hence leads to brain dysfunction. The syndrome is widely distributed throughout the world. This study reported for the first time the frequency of the fragile X mental retardation 1 gene mutations in intellectually disabled children in Pakistan. We recruited 333 intellectually disabled children and 250 normal children with age ranging from 5 to 18 years for this study. Genomic DNA was extracted from peripheral blood and full mutations were identified by methylation sensitive PCR using primers corresponding to modified methylated and unmethylated DNA. Southern blot was used for confirmation of the results. The frequency of fragile X syndrome with full mutation was found as 4.8%. It was 6.5% in males as opposed to 0.9% in females; 29 CGG repeats were found as the most common allele; 31.5% in the intellectually disabled and 34% in control subjects. In Pakistan intellectual disability is considered as a social stigma for the individuals and their families. Due to lack of knowledge and cultural background people make such patients and families isolated. This study will increase public awareness about the intellectual disability and importance of prenatal screening and genetic counseling for vulnerable families.
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PMID:Frequency of FMR1 gene mutation and CGG repeat polymorphism in intellectually disabled children in Pakistan. 2447 67

The aim of this survey study was to examine the etiologies of attention-deficit/hyperactivity disorder (ADHD) attributed by caregivers of Taiwanese children with ADHD, particularly factors affecting such attribution. This study had 400 caregivers of children with ADHD as participants. We examined the caregiver-attributed etiologies of ADHD and factors affecting such attribution. Caregivers completed the self-report questionnaire to rate how likely they perceived various etiologies of ADHD to be; the Affiliate Stigma Scale for the level of affiliate stigma; and the short Chinese version of the Swanson, Nolan, and Pelham, Version IV Scale for child's ADHD and oppositional symptoms. Brain dysfunction (84.8%) was the most commonly attributed etiology, followed by failure of caregivers in disciplining the child (44.0%); a poor diet, such as a sugar-rich diet (40.8%); a poor living environment (38.8%); the child imitating their peers' improper behavior (37.3%); failure of school staff in disciplining the child (29.0%); the education system's overemphasis on academic performance (27.3%); and supernatural beings or divination-based reasons (3.8%). Caregivers' affiliate stigma was significantly associated with the attribution of several nonbiological etiologies other than brain dysfunction. Caregivers' education level and children's sex, hyperactivity/impulsivity, and oppositional symptoms were significantly associated with various caregiver-attributed etiologies. Therefore, to deliver more accurate knowledge about ADHD in educational programs, health professionals should consider those etiologies that are attributed by caregivers of children with ADHD.
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PMID:Caregiver-Attributed Etiologies of Children's Attention-Deficit/Hyperactivity Disorder: A Study in Taiwan. 3214 81