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Psychiatria Danubina 2021The aim of the paper was to describe the multidimensional character of alcoholism and its effects on oral health, with a review of the relation between the traumatogenic... (Review)
Review
The aim of the paper was to describe the multidimensional character of alcoholism and its effects on oral health, with a review of the relation between the traumatogenic factor of temporomandibular disorders (TMDs) and bruxism development. The difference between moderate drinking and the development of alcohol addiction which leads to alcoholism-related medical, social, legal and economic issues is not always clear. Alcoholism is often hidden within the private and wider social framework of a patient. Oral diseases are easy to notice in recorded alcoholics as well as in, for example, smokers. TMDs consist of a disorder of masticatory muscles and/or a disorder of temporomandibular joint (TMJ). Since the traumatogenic factor of individuals under the influence of alcohol is clearly evident, it can potentially become an initializing factor of TMJ disorder's clinical signs and symptoms development. A modern approach to the etiopathogenesis is to include the multifactorial model, that is, combinations of potential factors with various individual importances. In everyday dental practice, co-morbidities of oral diseases and alcoholism are expected more often, as well as oral diseases with their etiopathogenesis partially related to alcohol use.
Topics: Alcoholism; Bruxism; Humans; Temporomandibular Joint; Temporomandibular Joint Disorders
PubMed: 34718294
DOI: No ID Found -
Alcoholism, Clinical and Experimental... May 2017Advanced alcoholic liver disease (ALD) represents a substantial public health burden, threatening the lives of more than ten million people in the United States.... (Review)
Review
Advanced alcoholic liver disease (ALD) represents a substantial public health burden, threatening the lives of more than ten million people in the United States. Although the direct harmful effects of alcohol in the liver are nearly universally recognized, emerging evidence suggests alcohol also adversely affects other organs such as the intestine, skeletal muscle, adipose tissue, and likely many other tissues. In fact, the extrahepatic effects of alcohol clearly converge to impact the morbidity and mortality associated with chronic alcohol abuse. In the intestine alcohol consumption can profoundly impact both gut barrier function as well as reorganizing intestinal microbial communities. In the skeletal muscle, chronic alcohol consumption promotes sarcopenia by altering protein homeostasis or proteostasis. In parallel, alcohol can impact the normal endocrine and metabolic function of adipose tissue. Collectively, chronic alcohol abuse sustains an interorgan cross talk that provides the multiple hits necessary for progression to end stage liver disease. Here we briefly highlight several recent examples of interorgan cross talk underlying the morbidity and mortality associated with alcohol abuse, and discuss how these recent advances have the potential to impact therapeutic strategies for those suffering with ALD.
Topics: Adipose Tissue; Alcoholism; Animals; Humans; Intestinal Diseases; Liver Diseases, Alcoholic; Muscle, Skeletal
PubMed: 28295407
DOI: 10.1111/acer.13370 -
Journal of Alzheimer's Disease : JAD 2022The association between lifetime alcohol abuse and a higher risk to develop dementia is well known. However, it is unknown whether older adults who begin abusing alcohol...
BACKGROUND
The association between lifetime alcohol abuse and a higher risk to develop dementia is well known. However, it is unknown whether older adults who begin abusing alcohol late in life have an underlying neurodegenerative disease.
OBJECTIVE
Identify the frequency of lifelong alcohol abuse (L-AA), late-onset alcohol abuse (LO-AA), and alcohol abuse as a first symptom of dementia (AA-FS) in patients with neurodegenerative diseases.
METHODS
Cross-sectional retrospective study of patients evaluated at an academic referral center with a clinical diagnosis of behavioral variant frontotemporal dementia (bvFTD), Alzheimer-type dementia (AD), and semantic variant primary progressive aphasia (svPPA) (n = 1,518). The presence of alcohol abuse was screened with the National Alzheimer's Coordinating Center questionnaire. L-AA was defined as onset < 40 years, LO-AA as onset ≥40 years, and AA-FS was defined when the abuse started within the first three years from symptom onset.
RESULTS
The frequency of LO-AA was 2.2% (n = 33/1,518). LO-AA was significantly more frequent in patients with bvFTD than AD (7.5%, n = 13/173 versus 1.3%, n = 16/1,254, CI:1.0;11.4%), but not svPPA (4.4%, n = 4/91, CI: -4.4;10.7%). Similarly, AA-FS was more frequent in bvFTD patients than AD (5.7%, n = 10/173 versus 0.7%, n = 9/1,254, CI:0.5%;9.5%), but not svPPA (2.2%, n = 2/91, CI:-2.4;9.1%).
CONCLUSION
LO-AA can be a presenting symptom of dementia, especially bvFTD. Alcohol abuse onset later in life should prompt a clinical investigation into the possibility of an underlying neurodegenerative process because delay in diagnosis and treatment may increase patient and caregiver burden. The results need to be interpreted with caution due to the limitations of the study.
Topics: Aged; Alcoholism; Alzheimer Disease; Cross-Sectional Studies; Frontotemporal Dementia; Humans; Neurodegenerative Diseases; Neuropsychological Tests; Retrospective Studies
PubMed: 35180118
DOI: 10.3233/JAD-215369 -
Alcohol Research : Current Reviews 2022This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as... (Review)
Review
This article is part of a Festschrift commemorating the 50th anniversary of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Established in 1970, first as part of the National Institute of Mental Health and later as an independent institute of the National Institutes of Health, NIAAA today is the world's largest funding agency for alcohol research. In addition to its own intramural research program, NIAAA supports the entire spectrum of innovative basic, translational, and clinical research to advance the diagnosis, prevention, and treatment of alcohol use disorder and alcohol-related problems. To celebrate the anniversary, NIAAA hosted a 2-day symposium, "Alcohol Across the Lifespan: 50 Years of Evidence-Based Diagnosis, Prevention, and Treatment Research," devoted to key topics within the field of alcohol research. This article is based on Dr. Sinha's presentation at the event. NIAAA Director George F. Koob, Ph.D., serves as editor of the Festschrift.
Topics: United States; Humans; Alcoholism; Neurobiology; National Institute on Alcohol Abuse and Alcoholism (U.S.); Alcohol Drinking; Alcohol-Related Disorders
PubMed: 36338609
DOI: 10.35946/arcr.v42.1.12 -
Pancreatology : Official Journal of the... Jul 2015The majority of those who drink excessive amounts of alcohol do not develop pancreatic disease. One overarching hypothesis is that alcohol abuse requires additional risk... (Review)
Review
The majority of those who drink excessive amounts of alcohol do not develop pancreatic disease. One overarching hypothesis is that alcohol abuse requires additional risk factors, either environmental or genetic, for disease to occur. However, another reason be a result of alcohol-induced activation of adaptive systems that protect the pancreas from the toxic effects of alcohol. We show that mechanisms within the unfolded protein response (UPR) of the endoplasmic reticulum (ER) that can lead to protection of the pancreas from pancreatic diseases with alcohol abuse. The remarkable ability of the pancreas to adapt its machinery to alcohol abuse using UPR systems and continue functioning is the likely reason that pancreatitis from alcohol abuse does not occur in the majority of heavy drinkers. These findings indicate that methods to enhance the protective responses of the UPR can provide opportunities for prevention and treatment of pancreatic diseases.
Topics: Alcoholism; Animals; Endoplasmic Reticulum Stress; Humans; Pancreas; Pancreatitis, Alcoholic; Unfolded Protein Response
PubMed: 25736240
DOI: 10.1016/j.pan.2015.01.011 -
The American Journal of Drug and... Mar 2017Concurrent use of tobacco and alcohol or psychostimulants represents a major public health concern, with use of one substance influencing consumption of the other.... (Review)
Review
Concurrent use of tobacco and alcohol or psychostimulants represents a major public health concern, with use of one substance influencing consumption of the other. Co-abuse of these drugs leads to substantial negative health outcomes, reduced cessation, and high economic costs, but the underlying mechanisms are poorly understood. Epidemiological data suggest that tobacco use during adolescence plays a particularly significant role. Adolescence is a sensitive period of development marked by major neurobiological maturation of brain regions critical for reward processing, learning and memory, and executive function. Nicotine exposure during this time produces a unique and long-lasting vulnerability to subsequent substance use, likely via actions at cholinergic, dopaminergic, and serotonergic systems. In this review, we discuss recent clinical and preclinical data examining the genetic factors and mechanisms underlying co-use of nicotine and alcohol or cocaine and amphetamines. We evaluate the critical role of nicotinic acetylcholine receptors throughout, and emphasize the dearth of preclinical studies assessing concurrent drug exposure. We stress important age and sex differences in drug responses, and highlight a brief, low-dose nicotine exposure paradigm that may better model early use of tobacco products. The escalating use of e-cigarettes among youth necessitates a closer look at the consequences of early adolescent nicotine exposure on subsequent alcohol and drug abuse.
Topics: Adolescent; Adolescent Behavior; Alcoholism; Animals; Brain; Humans; Substance-Related Disorders; Tobacco Use Disorder
PubMed: 27532746
DOI: 10.1080/00952990.2016.1209512 -
Neurotherapeutics : the Journal of the... Jan 2020The receptor tyrosine kinases (RTKs) are a large family of proteins that transduce extracellular signals to the inside of the cell to ultimately affect important... (Review)
Review
The receptor tyrosine kinases (RTKs) are a large family of proteins that transduce extracellular signals to the inside of the cell to ultimately affect important cellular functions such as cell proliferation, survival, apoptosis, differentiation, and migration. They are expressed in the nervous system and can regulate behavior through modulation of neuronal and glial function. As a result, RTKs are implicated in neurodegenerative and psychiatric disorders such as depression and addiction. Evidence has emerged that 5 RTKs (tropomyosin-related kinase B (TrkB), RET proto-oncogene (RET), anaplastic lymphoma kinase (ALK), fibroblast growth factor receptor (FGFR), and epidermal growth factor receptor (EGFR)) modulate alcohol drinking and other behaviors related to alcohol addiction. RTKs are considered highly "druggable" targets and small-molecule inhibitors of RTKs have been developed for the treatment of various conditions, particularly cancer. These kinases are therefore attractive targets for the development of new pharmacotherapies to treat alcohol use disorder (AUD). This review will examine the preclinical evidence describing TrkB, RET, ALK, FGFR, and EGFR modulation of alcohol drinking and other behaviors relevant to alcohol abuse.
Topics: Alcohol Drinking; Alcoholism; Animals; Brain; ErbB Receptors; Ethanol; Humans; Proto-Oncogene Mas; Receptor Protein-Tyrosine Kinases; Signal Transduction
PubMed: 31617071
DOI: 10.1007/s13311-019-00795-4 -
Learning & Memory (Cold Spring Harbor,... Sep 2018Alcohol use disorders include drinking problems that span a range from binge drinking to alcohol abuse and dependence. Plastic changes in synaptic efficacy, such as... (Review)
Review
Alcohol use disorders include drinking problems that span a range from binge drinking to alcohol abuse and dependence. Plastic changes in synaptic efficacy, such as long-term depression and long-term potentiation are widely recognized as mechanisms involved in learning and memory, responses to drugs of abuse, and addiction. In this review, we focus on the effects of chronic ethanol (EtOH) exposure on the induction of synaptic plasticity in different brain regions. We also review findings indicating that synaptic plasticity occurs in vivo during EtOH exposure, with a focus on ex vivo electrophysiological indices of plasticity. Evidence for effects of EtOH-induced or altered synaptic plasticity on learning and memory and EtOH-related behaviors is also reviewed. As this review indicates, there is much work needed to provide more information about the molecular, cellular, circuit, and behavioral consequences of EtOH interactions with synaptic plasticity mechanisms.
Topics: Alcoholism; Animals; Humans; Learning; Neuronal Plasticity
PubMed: 30115764
DOI: 10.1101/lm.046722.117 -
The American Journal of Medicine Feb 2017Alcohol is a leading cause of liver disease worldwide. Although alcohol abstinence is the crucial therapeutic goal for patients with alcoholic liver disease, these... (Review)
Review
Alcohol is a leading cause of liver disease worldwide. Although alcohol abstinence is the crucial therapeutic goal for patients with alcoholic liver disease, these patients have less access to psychosocial, behavioral, and/or pharmacologic treatments for alcohol use disorder. Psychosocial and behavioral therapies include 12-step facilitation, brief interventions, cognitive behavioral therapy, and motivational enhancement therapy. In addition to medications approved by the US Food and Drug Administration for alcohol use disorder (disulfiram, naltrexone, and acamprosate), recent efforts to identify potential new treatments have yielded promising candidate pharmacotherapies. Finally, more efforts are needed to integrate treatments across disciplines toward patient-centered approaches in the management of patients with alcohol use disorder and alcoholic liver disease.
Topics: Alcoholism; Behavior Therapy; Disease Progression; Humans; Liver Diseases, Alcoholic
PubMed: 27984008
DOI: 10.1016/j.amjmed.2016.10.004 -
Alcoholism, Clinical and Experimental... Apr 2021Recent studies in alcohol use disorders (AUDs) have demonstrated some connections between carnitine metabolism and the pathophysiology of the disease. In this scoping... (Review)
Review
Recent studies in alcohol use disorders (AUDs) have demonstrated some connections between carnitine metabolism and the pathophysiology of the disease. In this scoping review, we aimed to collate and examine existing research available on carnitine metabolism and AUDs and develop hypotheses surrounding the role carnitine may play in AUD. A scoping review method was used to search electronic databases in September 2019. The database search terms used included "alcohol, alcoholism, alcohol abuse, alcohol consumption, alcohol drinking patterns, alcohol-induced disorders, alcoholic intoxication, alcohol-related disorders, binge drinking, Wernicke encephalopathy, acylcarnitine, acetyl-l-carnitine, acetylcarnitine, carnitine and palmitoylcarnitine." The inclusion criteria included English language, human-based, AUD diagnosis and measured blood or tissue carnitine or used carnitine as a treatment. Of 586 studies that were identified and screened, 65 underwent abstract review, and 41 were fully reviewed. Eighteen studies were ultimately included for analysis. Data were summarized in an electronic data extraction form. We found that there is limited literature available. Alcohol use appears to impact carnitine metabolism, most clearly in the setting of alcoholic cirrhosis. Six studies found carnitine to be increased in AUD, of which 5 were conducted in patients with alcoholic cirrhosis. Only 3 placebo-controlled trials were identified and provide some support for the use of carnitine in AUD to decrease cravings, anhedonia, and withdrawal and improve cognition. The increase in plasma carnitine in alcoholic cirrhosis may be related to disordered fatty acid metabolism and oxidative stress that occurs in AUD. The multiple possible therapeutic effects carnitine could have on ethanol metabolism and the early evidence available for carnitine supplementation as a treatment for AUD provide a foundation for future randomized control trials of carnitine for treating AUD.
Topics: Alcoholism; Carnitine; Dietary Supplements; Humans
PubMed: 33576525
DOI: 10.1111/acer.14568