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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of physical dependence, morning drinking and binge drinking was assessed in alcoholic men in relation to family history of problem drinking. The incidence of physical dependence, binge drinking and morning drinking was higher in men with a family history of problem drinking than in men without such a history. Physical dependence also developed earlier in family history positive subjects than in family history negative ones. The incidence of physical dependence was higher in subjects who reported binge drinking or morning drinking than in others. These results indicate that family history of problem drinking is associated with severe alcohol abuse resulting in early development of physical dependence.
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PMID:Relationship of family history of alcoholism to patterns of drinking and physical dependence in male alcoholics. 673 26

Research in the area of problem drinking has traditionally relied on quantitative methodologies which view the problem from the researcher's perspective. The purpose of this hermeneutic-phenomenological study was to describe and understand the problem drinker's lived experience of suffering using a philosophy and research approach which preserves the uniqueness of the experience from the sufferer's point of view. The method involved conducting in-depth interviews with a sample of six problem drinkers. Interviews were analysed using an interpretive process, which aimed at generating a deeper understanding of the topic by facilitating a fusion of the world views of both participant and researcher. A reflexive journal recorded the involvement of the self of the researcher throughout the research process. Suffering was viewed as a spiralling vicious circle of physical, psychological, social and spiritual distress. Symptoms of physical dependence, shame and guilt emerged strongly as being both sequelae of heavy drinking and cues to further drinking bouts. Evoking memories of previous suffering through telling one's story was found to be an empowering and motivating force. The results have relevance to specialist and generic workers, who are urged to pay greater attention to the social, psychological and spiritual care of problem drinkers.
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PMID:The problem drinker's lived experience of suffering: an exploration using hermeneutic phenomenology. 951 27

Ethanol (alcohol) withdrawal-induced convulsions are a key index of physical dependence on ethanol and a clinically important consequence of alcohol abuse in humans. In rodent models, severity of withdrawal is strongly influenced by genotype. For example, many studies have reported marked differences in withdrawal severity between the WSR (Withdrawal Seizure Resistant) and WSP (Withdrawal Seizure Prone) mouse strains selectively bred for over 25 generations to differ in chronic withdrawal severity. Therefore, we used an F(2) intercross between the inbred WSP and WSR strains for a genome-wide search for quantitative trait loci (QTLs), which are chromosomal sites containing genes influencing the magnitude of withdrawal. We also used the recently developed HW, RHW (high withdrawal) and LW, RLW (low withdrawal) lines selectively bred for the same trait and in the same manner as the WSP, WSR lines. QTL analysis was then used to dissect the continuous trait distribution of withdrawal severity into component loci, and to map them to broad chromosomal regions by using the Pseudomarker 0.9 and Map Manager QT29b programs. This genome-wide search identified five significant QTLs influencing chronic withdrawal severity on Chromosomes (Chrs) 1 (proximal), 4 (mid), 8 (mid), 11 (proximal), and 14 (mid), plus significant interactions (epistasis) between loci on Chr 11 with 13, 4 with 8, and 8 with 14.
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PMID:Chromosomal loci influencing chronic alcohol withdrawal severity. 1292 94

Although ethanol has been repeatedly demonstrated to inhibit the hypothalamo-pituitary-testes axis by multiple mechanisms, plasma testosterone levels can be normal in alcoholics who do not exhibit severely compromised liver function and even increased in some abstinent alcoholics, suggesting that adaptive changes to chronic alcohol abuse may alter these regulatory mechanisms. To address this variability, we have investigated the effects of chronic ethanol and withdrawal on rat testosterone regulation using a well-characterized liquid diet model that we have previously demonstrated to (1) provide daily oral ethanol consumption that produces behaviorally relevant plasma ethanol levels during the active (awake) stage of the photoperiod; (2) establish physical dependence on ethanol; and (3) produce not only hypothalamo-pituitary-adrenal axis, but also behavioral (anxiety-like behavior, response to novelty, sucrose preference) changes consistent with those of actively drinking and subsequently abstinent alcoholics. The results demonstrate that chronic daily episodes of ethanol consumption and withdrawal by male Sprague-Dawley rats decreased (p < 0.01) plasma testosterone levels late in the afternoon (by 70% relative to ad libitum-fed controls and 63% relative to pair-fed controls), but not in the morning. During gradual cessation of daily ethanol consumption, morning plasma testosterone levels increased, and this 90-115% (p < 0.05) increase was maintained for 3 d after complete cessation of ethanol consumption. Three weeks after cessation of ethanol consumption, plasma testosterone levels were again increased by approx 100% (p < 0.01). Plasma luteinizing hormone (LH) concentrations and anterior hypothalamus/preoptic area gonadotropin-releasing hormone (GnRH) mRNA levels were not altered at any of these time points. Thus, chronic daily ethanol consumption and daily withdrawal induced changes in circulating testosterone regulation that (a) were time of day dependent and (b) included adaptive changes persisting long after consumption of ethanol ceased. Accordingly, resolution of changes in testosterone regulation and their potential roles in alcohol abuse and relapse will require evaluating changes throughout the circadian cycle during, shortly after, and long after active alcohol abuse.
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PMID:Chronic daily ethanol and withdrawal: 4. Long-term changes in plasma testosterone regulation, but no effect on GnRH gene expression or plasma LH concentrations. 1466 18

Several evidences indicate altered regulation of brain serotonergic mechanisms in alcohol abuse; changes in 5-HT2A receptor density and functioning have been observed in several lines of alcohol-preferring rats. Using quantitative autoradiography, the present study investigated the influence of chronic intragastric ethanol treatment on forebrain 5-HT2A binding sites in rats. Administration for 7 days of high doses of ethanol, which induced physical dependence, lowered the levels of 5-HT2A binding sites in the cingulate cortex, the frontal cortex and in the agranular insular cortex. The effect was observed immediately after the last ethanol administration, was statistically significant 14 h later, when marked withdrawal signs were observed, and remained significant after 8 days of detoxification, when withdrawal signs were no longer evident. No significant differences were detected in the claustrum, parietal cortex, piriform cortex, caudate putamen, olfactory tubercle, nucleus accumbens, shell and core. Chronic treatment with 6 g/kg of ethanol, which did not induce dependence, did not modify 5-HT2A binding sites. These long-lasting changes in brain 5-HT2A binding sites observed in the present study might contribute to specific aspects of ethanol dependence, such as development of depression and alcohol craving.
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PMID:Autoradiographic analysis of 5-hydroxytryptamine 5-HT2A binding sites in the rat brain after chronic intragastric ethanol treatments. 1508 May 2

The analysis of 826 autopsies is presented. 654 persons in their life abused alcohol but refused treatment; they were considered as hard drinkers. 172 persons were repeatedly treated for alcoholism and were included into the group of alcoholics. The control group consisted of persons who had not abused alcohol. Morphological and morphometric methods were used. It is shown that chronic alcoholic intoxication involves all internal organs with the same trend in pathological processes in hard drinkers and alcoholics. There was progressing alteration of microcirculatory bed, fat degeneration of parenchymatous organs, atrophic and sclerotic processes, primarily in the liver, lungs, heart and brain. While in hard drinking pathological processes can be considered reversible and well compensated, in alcoholism the degree of organ damage makes these lesions irreversible. It is suggested that less severe organ damage in hard drinking is due to the effect of ethanol while grave atrophic and sclerotic processes as well as psychic dependence on alcohol are due to acetaldehyde. The key point in alcohol abuse is hard drinking (or preclinical stage of alcoholism) as there is neither psychic no physical dependence on alcohol and organ alterations are reversible under adequate treatment. The treatment should be performed first of all of the liver to enhance its basal metabolism.
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PMID:[Pathologic anatomy of hard drinking and alcoholism]. 1544 79

Alcohol dependence is characterized by tolerance, physical dependence, and craving. The neuroadaptations underlying these effects of chronic alcohol abuse are likely due to altered gene expression. Previous gene expression studies using human post-mortem brain demonstrated that several gene families were altered by alcohol abuse. However, most of these changes in gene expression were small. It is not clear if gene expression profiles have sufficient power to discriminate control from alcoholic individuals and how consistent gene expression changes are when a relatively large sample size is examined. In the present study, microarray analysis (approximately 47,000 elements) was performed on the superior frontal cortex of 27 individual human cases (14 well characterized alcoholics and 13 matched controls). A partial least squares statistical procedure was applied to identify genes with altered expression levels in alcoholics. We found that genes involved in myelination, ubiquitination, apoptosis, cell adhesion, neurogenesis, and neural disease showed altered expression levels. Importantly, genes involved in neurodegenerative diseases such as Alzheimer's disease were significantly altered suggesting a link between alcoholism and other neurodegenerative conditions. A total of 27 genes identified in this study were previously shown to be changed by alcohol abuse in previous studies of human post-mortem brain. These results revealed a consistent re-programming of gene expression in alcohol abusers that reliably discriminates alcoholic from non-alcoholic individuals.
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PMID:Patterns of gene expression in the frontal cortex discriminate alcoholic from nonalcoholic individuals. 1629 26

Binge Drinking (BD) is often considered to be recurrent alcohol abuse amongst adolescents and young adults. However, the close link between adolescence and impulsivity has led many authors to define BD as intoxication-seeking behaviour. Medications may sometimes be justified because of the major short-term and long-term risks that underlie the most severe BD-related behaviours. The most common consequences in the long run are the occurrence of alcohol dependence, psycho- and neurodevelopmental disruptions and alcohol liver disease. To understand the specificities of BD among other forms of alcohol addiction, this article is based on a two-headed conception of alcohol dependence: on one hand, psychological dependence, which refers to the behavioural habituation of alcohol intake, clinically results in craving and is neurobiologically supported by the reward system, particularly the dopaminergic mesolimbic pathway (MLP); on the other hand, physical dependence, which refers to the pharmacological tolerance induced by chronic alcohol intake, results in Alcohol Withdrawal Syndrome (AWS) and is neurobiologically supported by the imbalance between GABA and Glutamate-NMDA neurotransmission. Medications for psychological dependence include anticraving drugs, which all act by regulating MLP. Medications for physical dependence on alcohol include GABA-A and perhaps GABA-B agonists and some NMDA antagonists. In practice, many alcohol-dependence treatments seem to have a dual action. This article proposes an attempt to classify current and forthcoming medications for alcohol addiction based on this two-headed approach to treating alcohol dependence. Drawing from this classification, specific therapeutic schemes for treating BD are proposed, with currently approved alcohol medications and possible future treatments. These schemes are justified by recent literature on the subject and propose to prioritize pure anticraving medications, taking into account the clinical specificities of BD. Furthermore, these schemes also mention harm-reductive neuroprotective and hepatoprotective strategies, which could be included in the arsenal of possible medications for BD in the near future.
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PMID:Pharmaceutical approaches of binge drinking. 2152 62

A report by the Centers for Disease Control and Prevention noted that excessive alcohol consumption is responsible for more than 4,600 deaths in underage youth annually. Alcohol abuse is common among college-age youth and may progress to alcohol dependence, which includes tolerance, craving, physical dependence, and loss of control. Although treatment for alcohol dependence is effective, like all other chronic disorders, relapse is common. The purpose of this article is to examine the issues surrounding alcohol abuse and dependence as well as maintaining sobriety in light of the high-risk college student drinking environment.
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PMID:Treatment of alcohol-dependent college students. 2299 38

It has long been known that people with alcohol use disorder (AUD) not only may develop physical dependence but also may experience devastating long-term health problems. The most common and identifiable alcohol-associated health problems include liver cirrhosis, pancreatitis, cardiomyopathies, neuropathies, and dementia. However, the lung also is adversely affected by alcohol abuse, a fact often overlooked by clinicians and the public. Individuals with AUD are more likely to develop pneumonia, tuberculosis (TB), respiratory syncytial virus (RSV) infection, and acute respiratory distress syndrome (ARDS). Increased susceptibility to these and other pulmonary infections is caused by impaired immune responses in people with AUD. The key immune cells involved in combating pulmonary conditions such as pneumonia, TB, RSV infection, and ARDS are neutrophils, lymphocytes, alveolar macrophages, and the cells responsible for innate immune responses. Researchers are only now beginning to understand how alcohol affects these cells and how these effects contribute to the pathophysiology of pulmonary diseases in people with AUD.
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PMID:Alcohol's Effects on Lung Health and Immunity. 2669 45


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