PubMed · 9603302
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R Knibbe. 1998. Measuring drinking context.. https://doi.org/10.1097/00000374-199802001-00003
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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.
BACKGROUND: Prostate cancer has become the most common cancer among men in the United States, but little is known about factors associated with prostate cancer incidence. METHODS: A meta-analysis of studies published prior to July 1998 was conducted to pool relative risk (RR) estimates from the existing literature on the association between prostate cancer and alcohol consumption, in an attempt to determine whether there is an association, and if so, what its magnitude is. RESULTS: The overall pooled RR estimate was 1. 05 for both fixed and random effects models, based on six cohort studies and 27 case-control studies. The RR estimate varied little by study design. Among types of consumption, the highest risk was found for beer (RR = 1.27), but this was based on only eight studies that reported type of alcohol consumed. A linear dose-response was fit to the 15 studies reporting amount of alcohol consumed, finding a RR of 1.05 (95% confidence interval (CI), 0.91-1.20) for each additional drink of alcohol per day or a RR of 1.21 for 4 drinks per day. When the average drinks per day consumed in the 15 studies were used to estimate the overall risk for all 33 studies, a RR of 1.02 was found for each additional drink of alcohol per day. CONCLUSIONS: Overall, no association between prostate cancer and alcohol consumption was seen. While some categories of consumption showed an increased risk, the studies reporting such categories appeared to be biased towards reporting a positive association among the categories.
OBJECTIVE: To summarise quantitatively the association between moderate alcohol intake and biological markers of risk of coronary heart disease and to predict how these changes would lower the risk. DESIGN: Meta-analysis of all experimental studies that assessed the effects of moderate alcohol intake on concentrations of high density lipoprotein cholesterol, apolipoprotein A I, fibrinogen, triglycerides, and other biological markers previously found to be associated with risk of coronary heart disease. PARTICIPANTS: Men and women free of previous chronic disease and who were not dependent on alcohol. Studies were included in which biomarkers were assessed before and after participants consumed up to 100 g of alcohol a day. INTERVENTIONS: Alcohol as ethanol, beer, wine, or spirits. MAIN OUTCOME MEASURES: Changes in concentrations of high density lipoprotein cholesterol, apolipoprotein A I, Lp(a) lipoprotein, triglycerides, tissue type plasminogen activator activity, tissue type plasminogen activator antigen, insulin, and glucose after consuming an experimental dose of alcohol for 1 to 9 weeks; a shorter period was accepted for studies of change in concentrations of fibrinogen, factor VII, von Willebrand factor, tissue type plasminogen activator activity, and tissue type plasminogen activator antigen. RESULTS: 61 data records were abstracted from 42 eligible studies with information on change in biological markers of risk of coronary heart disease. An experimental dose of 30 g of ethanol a day increased concentrations of high density lipoprotein cholesterol by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A I by 8.82 mg/dl (7.79 to 9.86), and triglyceride by 5.69 mg/dl (2.49 to 8.89). Several haemostatic factors related to a thrombolytic profile were modestly affected by alcohol. On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease. CONCLUSIONS: Alcohol intake is causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors.