Journal ArticleDOI
Quantifying the risk for alcohol-use and alcohol-attributable health disorders: present findings and future research needs.
TLDR
Extant databases should allow scientists and clinicians jointly to develop the framework for quantifying the drinking patterns that increase the risk of alcohol‐induced organ pathologies, to develop clinical practice guidelines, such as those used to diagnose other common complex diseases (e.g. diabetes and hypertension).Abstract:
The aim of the present review was to: (i) highlight epidemiological and other studies that have generated important data on the harmful patterns of drinking that increase the risk for chronic diseases, including alcohol dependence, and on the mechanisms by which alcohol produces and, in some instances, may protect against damage; and (ii) discuss a conceptual basis for quantifying risk criteria for alcohol-induced chronic disease based on the quantity, frequency, and pattern of drinking. The relationship between heavy drinking and risk for adverse health conditions such as alcoholic liver disease (ALD), dementia, and alcohol dependence is well known. However, not everyone who drinks chronically develops ALD or dementia, and the major risk factors for disease development and the mechanisms by which this occurs have remained unclear. Large-scale, general population-based studies have provided the evidence by which quantifying the frequency of a pattern of high-risk drinking can be related directly to risk and the severity of alcohol dependence. Cellular and molecular biology studies have identified the major pathways of alcohol metabolism and how genetics and the environment can interact in some individuals to further increase the risk of organ damage. Extant databases should allow scientists and clinicians jointly to develop the framework for quantifying the drinking patterns that increase the risk of alcohol-induced organ pathologies, to develop clinical practice guidelines, such as those used to diagnose other common complex diseases (e.g. diabetes and hypertension), and to propose future studies for refining such guidelines. Attention must be paid to comorbid conditions such as hepatitis B and C infections, HIV, obesity, and environmental exposures other than alcohol. Developing trait and state biomarkers is critical to the process of discovery and to fulfilling the promise of personalized medicine.read more
Citations
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Journal ArticleDOI
Mouse model of chronic and binge ethanol feeding (the NIAAA model)
TL;DR: This protocol for chronic-plus-single-binge ethanol feeding synergistically induces liver injury, inflammation and fatty liver, which mimics acute-on-chronic alcoholic liver injury in patients and will be very useful for the study of alcoholic liver disease (ALD) and of other organs damaged by alcohol consumption.
Journal ArticleDOI
Induction of innate immune genes in brain create the neurobiology of addiction.
TL;DR: The hypothesis that innate immune gene induction underlies addiction and affective disorders creates new targets for therapy.
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Chronic plus binge ethanol feeding synergistically induces neutrophil infiltration and liver injury in mice: a critical role for E-selectin.
TL;DR: It is shown that chronic plus binge ethanol feeding synergistically up‐regulated the hepatic expression of interleukin‐1β and tumor necrosis factor alpha and induced neutrophil accumulation in the liver, compared with chronic or binge feeding alone.
Journal ArticleDOI
Medications development to treat alcohol dependence: a vision for the next decade
Raye Z. Litten,Mark Egli,Markus Heilig,Changhai Cui,Joanne B. Fertig,Megan L. Ryan,Daniel E. Falk,Howard B. Moss,Robert J. Huebner,Antonio Noronha +9 more
TL;DR: Successful implementation of seven key objectives will result in the development of more efficacious and safe medications, provide a greater selection of therapy options and ultimately lessen the impact of this devastating disorder.
Journal ArticleDOI
Genetic Factors That Affect Risk of Alcoholic and Nonalcoholic Fatty Liver Disease
TL;DR: The functions of proteins encoded by risk variants of genes including patatin-like phospholipase domain-containing 3 and transmembrane 6 superfamily member 2, as well as epigenetic factors that contribute to the pathogenesis of alcoholic liver disease and nonalcoholic fatty liver disease are discussed.
References
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