Top priorities for alcohol regulators in the United States: protecting public health or the alcohol industry?

Aims This paper describes alcohol industry involvement in the 2010 annual conference proceedings of the National Conference of State Liquor Administrators (NCSLA) in the United States. Design The author attended the conference, observed conference attendees and panelists and identified key themes in the panel sessions. Setting The NCSLA Annual Meeting took place 20–24 June 2010 in New Orleans, Louisiana. Participants NCSLA meeting attendees and panelists were professionals from state alcohol control systems; federal government agencies; and companies representing the alcohol industry. Measurements The total number of conference attendees and participants were counted as well as the number of attendees and participants from regulator, industry and public health sectors. Findings More than two‐thirds (72.2%) of the 187 conference attendees were from alcohol producers, importers, wholesalers, retailers or their attorneys. Nearly two‐thirds (65.0%) of the 40 panelists were from the alcohol industry. The author of this paper was the only attendee, and the only panelist, representing public health policy. Conclusions The National Conference of State Liquor Administrators in the United States is dominated by the private, global companies that produce, import, distribute and sell alcohol, highlighting a lack of public health considerations within the Association's liquor control agenda.     

Is alcohol anti-inflammatory in the context of coronary heart disease?

Although the cardioprotective effect of alcohol has been primarily explained by its effect on blood lipids and platelets, could an anti-inflammatory mechanism be involved?     

Are the effects of gamma-hydroxybutyrate (GHB) treatment partly physiological in alcohol dependence?

It has been hypothesized that the therapeutic effects of Gamma-hydroxybutyrate (GHB) in alcohol dependence could be related to ethanol-mimicking action of the drug and that GHB could reduce alcohol craving, intake and withdrawal by acting as a "substitute" of the alcohol in the central nervous system. Nevertheless, alcohol being the strongest trigger of craving and intake, it is difficult to ascribe reduction of craving and intake to ethanol-mimicking activity of GHB. I have recently proposed that alcohol/substance dependence could result from a GHB-deficiency-related dysphoric syndrome in which alcohol/substances would be sought to "substitute" for insufficient GHB effect. GHB is the sole identified naturally occurring gamma-aminobutyric acid B (GABA (B)) receptor agonist. Here, I propose that exogenous GHB might in fact "substitute" for deficient endogeneous GHB and represent true substitutive treatment for GHB-deficiency. And that baclofen and GHB could both compensate for deficient effect of the physiological GABA (B) receptor agonist(s).     

Measuring alcohol consumption—should the ‘graduated frequency’ approach become the norm in survey research?

AIMS: To analyse whether recommendations for the graduated frequency (GF) approach to measure alcohol consumption are justified in a multi-cultural comparative study. DESIGN: Representative surveys, conducted between 1995 and 2003, of 10 countries participating in the GENACIS project (Gender, Alcohol and Culture: an International Study). MEASUREMENTS: Usual quantity, usual frequency and mean consumption per day measured with three instruments: GF, generic quantity-frequency (QF) and beverage-specific quantity-frequency (QFBS). FINDINGS: The GF did not consistently yield higher volumes and quantities across all countries compared with the generic QF, while the QFBS resulted in higher quantities and higher volumes compared with the GF (in all but one country) and the QF. Frequencies were mostly higher on the GF compared with the QF and QFBS but there was also evidence of over-reporting of frequencies with the GF. Results for the GF suggested that it was implemented improperly in at least three of the 10 countries. CONCLUSION: The GF does not appear to be appropriate for cross-cultural research. It results in over-reporting of frequencies and appears to be too complex to be administered correctly in many countries. The best measure for these purposes appeared to be the QFBS particularly because it captures more effectively the variability of different alcoholic beverages with different ethanol contents and consumption with different vessel sizes.     

Alcoholic liver injury： Pathological features and models—Role of alcohol in the regulation of iron metabolism

Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate alcohol consumption has been shown to increase the prevalence of iron overload. Moreover, increased hepatic iron content is associated with greater mortality from alcoholic cirrhosis, suggesting a pathogenic role for iron in alcoholic liver disease. Alcohol increases the severity of disease in patients with genetic hemochromatosis, an iron overload disorder common in the Caucasian population. Both iron and alcohol individually cause oxidative stress and lipid peroxidation, which culminates in liver injury. Despite these observations, the underlying mechanisms of iron accumulation and the source of the excess iron observed in alcoholic liver disease remain unclear. Over the last decade, several novel iron-regulatory proteins have been identified and these have greatly enhanced our understanding of iron metabolism. For example, hepcidin, a circulatory antimicrobial peptide synthesized by the hepatocytes of the liver is now known to play a central role in the regulation of iron homeostasis. This review attempts to describe the interaction of alcohol and iron-regulatory molecules. Understanding these molecular mechanisms is of considerable clinical importance because both alcoholic liver disease and genetic hemochromatosis are common diseases, in which alcohol and iron appear to act synergistically to cause liver injury.     

Morbidity and mortality in liver diseases in Sweden 1969–2001 in relation to alcohol consumption

Objective. In Sweden, there is stable or slightly increased total alcohol consumption but a decrease in mortality in liver disease. The aim of the study was to determine the temporal relation between alcohol-related liver disease morbidity and mortality and type of alcohol beverage consumption. Material and methods. Data on patients with liver disease from the Swedish Hospital Discharge Register and from the Causes of Death Register between 1969 and 2001were analysed. Data on the registered sales of the different beverages were taken from the Swedish State Monopoly. Results. Liver disease mortality increased from 1969 to 1976, coinciding with the increase in sales of spirits. Both mortality and spirits sales decreased thereafter, whereas there was no decrease in beer or wine sales. Hospitalization rates were reduced after 1987. Depending on age and gender, there was a 30–80% 5-year mortality rate following discharge. Among men, but not among women, differences in the alcohol and non-alcohol-related liver diagnoses in the Hospital Discharge Register and in the Cause of Death Register were sometimes recorded in the same patient. Conclusions. There was a reduction in hospitalization rates and mortality in liver diseases, and the reduction in mortality in liver diseases in Sweden from 1969 to 2001 seems to be associated with sales of spirits. Patients hospitalized for liver disease have a poor prognosis. There were difficulties in differentiating between alcohol and non-alcohol liver diseases.     

Dynamic changes in the expression of matrix metalloproteinases and their inhibitors,TIMPs,during hepatic fibrosis induced by alcohol in rats

AIM:To determine the dynamic changes in the expressionof matrix metalloproteinases (MMPs) and the endogenoustissue inhibitors of MMPs inhibitors (TIMPs) during hepaticfibrosis induced by alcohol.METHODS:Male Sprague-Dawley rats were randomly dividedinto normal,4 d,2 wk,4 wk,g wk and 11 wk groups,and themodel rats were fed with a mixture of alcohol by gastricinfusion at the designed time,respectively,then decollatedand their livers were harvested for the examination of MMP-2,MMP-3,MMP-9,MMP-13,TIMP-1 and TIMP-2 by immunoh-istochemistry,zymograghy and Western blotting,respectively.RESULTS:Normal rats had moderate expression of MMP-2,which was decreased in the model rats except in the 11 wkgroup,where MMP-2 expression slightly increased.MMP-3had the similar changing pattern to MMP-2 despite weakerexpression.MMP-9 expression decreased in the 4 d and 2 wkgroups,rose in the 4 wk group,decreased again in the 9 wkgroup and returned to normal levels in the 11 wk group.MMP-13 expression decreased in the 4 d and 2 wk groups,and returned to normal levels in the 4 wk,9 wk and 11 wkgroups.TIMP-1 expression decreased in the 4 d and 2 wkgroups,but sharply increased in the 4 wk group and sustainedat a high level even after modeling was stopped for 2 wk.Innormal rats TIMP-2 expression was strong.However,itdecreased as soon as modeling began,and then graduallyrose,but remained to a level lower than that in normal ratseven after modeling was stopped for 2 wk.CONCLUSION:MMP-2 may not always expresses at a highlevel during hepatic fibrosis.MMP-13 and MMP-3 areacutely affected by TIMP-1.In this model TIMP-1 is the mostpowerful factor imposed on capillarization and peri-sinusoidalfibrosis.TIMP-2 is the most effective regulator on the metabolismof type Ⅳ collagen located in the basement of sinus.     

Is alcohol ablation of the septum associated with recurrent tachyarrhythmias?

QUESTIONS UNDER STUDY: Alcohol ablation (AA) of the septum has been introduced as new therapy in hypertrophic cardiomyopathy (HCM). It was feared that iatrogenic myocardial infarction due to AA may induce re-entry tachyarrhythmias and increase sudden cardiac death. METHODS AND RESULTS: Twenty-four patients (mean age 52 years) underwent successful AA. Clinical follow-up (FU) ranged from 0.3 to 0.7 years (mean 2.8). One patient died (suicide) 4 years after AA. Left ventricular (LV) outflow gradient (peak-to-peak) decreased (median) after AA from 43 (IQR 25 to 4) mmHg to 1 (IQR 0 to 12) mmHg (rest) (p <0.001) and from 130 (IQR 75 to 165) mmHg to 13 (IQR 0 to 31) mmHg (postextrasystolic) (p <0.001). Transient AV block occurred in 22% (5/24) necessitating temporary pacing. A permanent pacemaker was implanted in 4% (1/24). NYHA-class was 2.5 (IQR 2.0 to 3.0) before and 1.5 (IQR 1.3 to 2.0) (p <0.001) after AA. During FU, 2 pacemakers were implanted due to bradycardia (no AV block). A right bundle branch block was found in 13% (2/24) before and 46 % (11/24) after AA (p = 0.003). Non-sustained ventricular tachycardia (NSVT) was observed in 13% (2/16) before and 22% (5/23) (p = 0.46) after AA. Two patients required ICD implantation. CONCLUSIONS: Long-term FU is excellent in HCM after AA. The pressure gradient drops below 25 mm Hg in 95% (23/24) of all patients. Transient AV block occurs in 22% (5/24), but permanent pacemaker implantation is rarely needed (13%, 2/24). Severe NSVT occurs in 13% (2/16) before and 22% (5/23) after AA but ICD implantation is only occasionally required.