PubMed Health⌕ Search

PubMed · 10890808

Treating problem drinking.

Abstract

Recent data suggest that most people experiencing alcohol problems have problems of mild to moderate severity. Relative to alcoholics, these drinkers have a shorter problem-drinking history, greater social and economic stability, and greater personal resources. This article describes a cognitive-behavioral treatment approach designed specifically for problem drinkers with low levels of physical dependence on alcohol who choose to reduce their drinking. After describing various drinking-reduction techniques, the article reviews empirical evidence for drinking-reduction training. The increasing availability of drinking-reduction interventions holds considerable promise for reducing alcohol-related dysfunction among problem drinkers.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K S Walitzer, G J Connors. 1999. Treating problem drinking.. https://pubmed.ncbi.nlm.nih.gov/10890808/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

FGF21 suppresses alcohol consumption through an amygdalo-striatal circuit.

Excessive alcohol consumption is a major health and social issue in our society. Pharmacologic administration of the endocrine hormone fibroblast growth factor 21 (FGF21) suppresses alcohol consumption through actions in the brain in rodents, and genome-wide association studies have identified single nucleotide polymorphisms in genes involved with FGF21 signaling as being associated with increased alcohol consumption in humans. However, the neural circuit(s) through which FGF21 signals to suppress alcohol consumption are unknown, as are its effects on alcohol consumption in higher organisms. Here, we demonstrate that administration of an FGF21 analog to alcohol-preferring non-human primates reduces alcohol intake by 50%. Further, we reveal that FGF21 suppresses alcohol consumption through a projection-specific subpopulation of KLB-expressing neurons in the basolateral amygdala. Our results illustrate how FGF21 suppresses alcohol consumption through a specific population of neurons in the brain and demonstrate its therapeutic potential in non-human primate models of excessive alcohol consumption.

Alcohol Drinking↗

Studies on a model of long term alcohol drinking.

This study investigated the effects of a dihydropyridine calcium channel antagonist in a free drinking model previously reported to show increased and 'uncontrolled' drinking. The results showed, rather than the previously reported increase in consumption, a gradual decrease in alcohol intake over 9-18 months. When the alcohol was withdrawn from one group of rats after 55 weeks free choice, the animals showed no behavioural signs of physical withdrawal, but they did demonstrate the expected elevated ethanol intake on reintroduction to ethanol after 2 weeks abstinence. A second group of rats were given 62 weeks free choice access to ethanol in groups of four, then transferred to single housing and baseline drinking levels established. Intraperitoneal injections of nimodipine 5 mg/kg, 20 mg/kg or Tween vehicle were then given once daily. Nimodipine had no effect on ethanol intake of animals with continuous access to ethanol, or of those animals withdrawn from ethanol and then reintroduced after 2 weeks of abstinence. However the unexpectedly low alcohol intake may have prevented any effects of nimodipine being seen.

Alcohol Drinking↗

[Beer, wine, spirits and mortality. Results from a prospective population study].

INTRODUCTION: The aim of the present population-based cohort study was to examine the association between alcohol intake and mortality from all causes, coronary heart disease, and cancer. METHODS: A prospective population study with baseline assessment of beer, wine and spirit consumption, smoking habits, educational level, physical activity, and body mass index in a total of 257,859 person-years follow-up on mortality. RESULTS: A total of 4833 participants died, 1075 of these from coronary heart disease and 1552 of cancer. Compared with non-drinkers, light drinkers, who avoided wine, had a relative risk of death from all causes of 0.90 (0.82-0.99) and those who drank wine had a relative risk of 0.66 (0.55-0.77). Heavy drinkers, who avoided wine, were at higher risk of death from all causes than were heavy drinkers, who included wine in their alcohol consumption. Wine drinkers had a significantly lower mortality from both coronary heart disease and cancer than had non-wine drinkers (p = 0.007 and p = 0.004, respectively). CONCLUSION: A moderate consumption of wine may have a beneficial effect on all causes of mortality, which is additive to that of alcohol. This effect may be attributable to a reduction in death from both coronary heart disease and cancer.

Alcohol Drinking↗