Moderate Consumption Levels Research Articles

Moderation in Australia-policy and achievements.

Alcohol has been consumed in Australia since European settlement in 1788. In 1998, approximately 60% of Australians consumed an alcoholic beverage at least once per week. The effects of alcohol on the human body are dose dependent, where the harmful effects of alcohol are generally observed only when alcohol consumption exceeds moderate consumption levels of 30 to 40 g of alcohol per day. The discovery that a J-shaped curve described the relationship between level of alcohol consumption and risk of cardiovascular disease was, however, only made in 1990-cardiovascular disease is the leading cause of death in the western world. Thus prior to 1990, Australian public health policy focused primarily on the harmful effects of alcohol consumption and the health benefits of a moderate level of alcohol consumption have only recently been recognized in public policy. This paper chronicles changes in Australian Federal government policy on alcohol since the initial draft National health policy on alcohol in Australia was presented to the Ministerial Council on Drug Strategy in 1987 to the National Drug Strategic plan for action 2001 to 2003-2004 which was launched in July last year.

Liver function test abnormalities in users of aqueous kava extracts.

Hepatic toxicity from manufactured herbal remedies that contain kava lactones has been reported in Europe, North America, and Australia. There is no evidence for serious liver damage in kava-using populations in Pacific Island societies or in Indigenous Australians who have used aqueous kava extracts. This article presents evidence that liver function changes in users of aqueous kava extracts appear to be reversible. Data from one Arnhem Land community [Northern Territory (NT), Australia] with 340 indigenous people older than 15 years of age in 2000 are used. This study was a cross-sectional study with 98 participants, 36 of whom had never used kava. Among 62 kava users, 23 had discontinued kava at least 1 year before the study. Continuing users had not used kava for 1 to 2 months (n = 10) or 1 to 2 weeks previously (n = 15). Some (n = 14) had used kava within the previous 24 hr. Liver function tests were compared across these groups, taking into account differences due to age, sex, alcohol, and other substance use. The average quantity of kava powder consumed was 118 g/week, and median duration of use was 12 years (range, 1-18 years). Kava usage levels were less than one-half of those found in previous studies. More recent kava use was independently associated with higher levels of liver enzymes gamma-glutamyl transferase (GGT) (p < 0.001) and alkaline phosphatase (ALP) (p < 0.001), but not with alanine aminotransferase or bilirubin, which were not elevated. In those who were not heavy alcohol users, only those who used kava within the previous 24 hr showed GGT levels higher than nonusers (p < 0.001), whereas higher ALP levels occurred only in those who last used kava 1 to 2 weeks (p = 0.015) and 24 hr previously (p = 0.005). Liver function changes in users of aqueous kava extracts at these moderate levels of consumption appear to be reversible and begin to return to baseline after 1 to 2 weeks abstinence from kava. No evidence for irreversible liver damage has been found.

Whose drinking does the liberalization of alcohol policy increase? Change in alcohol consumption by the initial level in the Finnish panel survey in 1968 and 1969

To study how the annual volume of alcohol consumed changed among population groups in different categories of initial consumption in a situation where per capita consumption strongly increased due to a new alcohol law. A post-hoc quasi-experiment with a two-wave panel study. The regression to the mean effect was accounted for by using reference data from two auxiliary panel studies. Finland in 1968 and 1969, when per capita consumption increased by 46% in a year. Reference data come from Norway in 1975 and 1976, and the United States in 1993 and 1994. General population sample of 1720 (1292 men) aged 15-69 (response rate 91.4%). REFERENCE DATA: General population surveys in a Norwegian town (n=254) and in the United States (n=658). Annual volume of alcohol consumed. In Finland, the greatest change in observed consumption levels occurred among those with moderate consumption levels, but the same phenomenon was observed in the reference data. A comparison between the Finnish and the reference data indicated that in Finland consumption increased at all levels, and the higher the initial consumption level, the greater the increase. A best estimate for the differential impact of future increases in alcohol consumption is that moderate and particularly heavy drinkers will be affected to a greater extent than will light drinkers or abstainers.

Stable acetaldehyde--protein adducts as biomarkers of alcohol exposure.

The consumption of alcoholic beverages has been associated with increased risks of a number of chronic disorders including cancers. It is still not clear whether ethyl alcohol or other components such as metabolites are directly involved in the carcinogenic process or whether the effects are due to the modulation of metabolism of other carcinogens. At present, there is no good biomarker of alcohol intake, particularly at low or moderate levels of consumption. A number of studies have shown the ability of the major metabolite acetaldehyde to react with proteins in vitro to give stable and unstable adducts. The interaction of acetaldehyde with model peptides, which correspond to N-terminal globin sequences, was studied. The major stable adduct was identified by mass spectrometry and NMR as a diastereoisomeric mixture of imidazolidinones. This is believed to be formed by reaction and cyclization of the initial Schiff base adduct with the N-terminal valine. Incubation of human globin with acetaldehyde (0-2 mM) yielded products which were identified as the N-terminal adducts by electrospray ionization mass spectrometry (ESI-MS) of proteolytic digests. The specificity and sensitivity of the analysis was improved by the use of on-line HPLC-ESI-MS. Tryptic digests of the modified globin which contained both the N-terminal acetaldehyde adducts of alpha-globin (heptapeptide) and beta-globin (octapeptide) were resolved. These results suggest that analysis of stable imidazolidinone adducts is a promising approach to estimation of alcohol exposure.

Risk of Breast Cancer in Relation to Lifetime Alcohol Consumption

Although an association between alcohol consumption and risk of breast cancer has been observed in many studies, questions of major importance remain, including the nature of the dose-response relationship and the effects of drinking at various periods in life. Our goal was to address the issues listed above with a large case-control study. We conducted a population-based case-control study in Maine, Massachusetts (excluding the four counties that include metropolitan Boston), New Hampshire, and Wisconsin. Case patients were eligible if their diagnosis of invasive breast cancer was first reported to one of the four statewide cancer registries during the period of 1988 through 1991. During the accrual period, 11,879 potentially eligible case patients and 16,217 control subjects were identified. After excluding ineligible women from the study, telephone interviews were obtained from 6888 case patients and 9424 control subjects. Complete data for recent alcohol consumption, and thus final eligibility for study participation, were determined for 6662 case patients and 9163 control subjects. The average age at time of interview was 58.7 years. The questions on alcohol use addressed average consumption during five periods of the subjects' lives: ages 16-19, 20-29, 30-39, 40-59, and 60-74 years. Similar responses from 211 control subjects upon reinterview 6-12 months later were taken to be indicative of the reliability of the questionnaire used in this study. Lifetime average alcohol consumption (measured as the average grams per day consumed from age 16 to the recent past) and recent alcohol consumption (average grams per day consumed in the previous age interval) were associated with risk of developing breast cancer. The multivariate relative risk of breast cancer, in those who drink compared with abstainers, associated with average lifetime consumption of 12-18 g/day of alcohol (about one drink) was 1.39 (95% confidence interval [CI] = 1.16-1.67), of 19-32 g/day (about two drinks) was 1.69 (95% CI = 1.36-2.10), of 33-45 g/day (about three drinks) was 2.30 (95% CI = 1.51-3.51), and of greater than or equal to 46 g/day (four or more drinks) was 1.75 (95% CI = 1.16-2.64) (P for trend < .0001). The multivariate relative risk per 13 g/day (about one drink) of alcohol consumed before 30 years of age was 1.09 (95% CI = 0.95-1.24), whereas the relative risk associated with recent consumption of 13 g/day was 1.21 (95% CI = 1.09-1.34). In these data, alcohol consumption was clearly related to breast cancer risk. Risk appeared to increase even at moderate levels of consumption. For women of all ages combined, consumption before 30 years of age was not an important determinant of risk.

The roles of alcohol in the epidemiology of cardiovascular diseases.

Alcohol, both alone and in concert with deficiencies or excesses of other substances, can produce cardiomyopathy. In addition, alcohol can directly affect the cardiac conduction system and produce arrhythmias. Alcohol also affects known risk factors for stroke and coronary heart disease (CHD). Alcohol increases blood pressure, which may lead to hypertension and thus increase the risk of stroke. HDL cholesterol, which is inversely related to CHD risk, increases with alcohol, and LDL cholesterol, which is positively related to CHD risk, may decrease with alcohol, a potentially dually protective effect. However, both case-control and population based studies indicate only moderate levels of consumption, defined as two drinks per day or less, may be of benefit. Preliminary data from the Lipid Research Clinics Follow-up Study suggest that the beneficial effect of moderate amounts of alcohol may be mediated in part by increased HDL cholesterol and in part by another factor, possibly reduced coagulation. Clinical and laboratory data, in addition to epidemiologic data, suggest alcohol intake above two drinks per day leads to excess cardiovascular disease (CVD), probably reflecting hypercoagulability as well as hypertension at higher levels of intake. Because alcohol can lead to excess morbidity and mortality from CVD as well as several other diseases and conditions, public health policy should continue to discourage the drinking of alcohol, especially non-moderate consumption.

Relevance of brain dysfunction to treatment objectives: should alcohol-related cognitive deficits influence the way we think about treatment.

Abstract Chronic heavy consumption of alcohol is associated with cognitive deficits, such as impaired ability to abstract, to solve problems and to learn new information. Since much treatment for alcoholism involves the learning of coping strategies of various levels of complexity, an assessment of the cognitive abilities of the clients would appear to be required both for differential assignment to treatment and for the prediction of duration of treatment. This argument is based upon the assumption that learning-in-treatment is an important determinant of outcome, and that alcohol-related cognitive deficits account for a significant proportion of the variance in learning ability. There is very little literature, of even a descriptive nature, on the relationship of neuropsychological status to treatment outcome, although research interest has accelerated in the last two years. Formidable methodological problems are inherent in such research. Problems in designing a study of the possible relationship of cognitive deficit to treatment outcome are discussed. An alternative procedure would be to continue descriptive studies, and to assess the impact of objective feedback about physiological and functional consequences of chronic drinking on subsequent decisions to drink. This approach is proposed. In a treatment study of problem drinkers recovery of function resulted from abstinence or very low levels of consumption, but moderate levels of consumption prevented this process. These data should inform the setting of target levels for consumption in the initial stages in programs teaching non-problematic drinking.