Kaye Middleton Fillmore

Moderate alcohol use and reduced mortality risk: Systematic error in prospective studies

The majority of prospective studies on alcohol use and mortality risk indicates that abstainers are at increased risk of mortality from both all causes and coronary heart disease (CHD). This meta-analysis of 54 published studies tested the extent to which a systematic misclassification error was committed by including as ‘abstainers’ many people who had reduced or stopped drinking, a phenomenon associated with ageing and ill health. The studies judged to be error free found no significant all-cause or cardiac protection, suggesting that the cardiac protection afforded by alcohol may have been over-estimated. Estimates of mortality from heavier drinking may also be higher than previously estimated.

Cirrhosis mortality and per capita consumption of distilled spirits, United States, 1949-94: trend analysis

Abstract Objective: To describe, evaluate, and suggest interpretations for an observed aggregate level relation between trends in mortality from cirrhosis and per capita consumption of distilled spirits in the United States. Design: Trend analysis using data on US cirrhosis mortality and per capita alcohol consumption. Results: There is a consistent long term trend relation between mortality from cirrhosis and per capita consumption of distilled spirits in the United States from 1949 to 1994. Two instances of comparatively sharp drops in the consumption of spirits earlier in the 1940s generated mixed results in predicting changes in cirrhosis mortality. Conclusions: An aggregate level relation between trends in long term cirrhosis mortality and the consumption of spirits falls considerably short of establishing a direct causal link between the two for individuals. Moreover, two sharp drops in the consumption of spirits generated only mixed results with respect to the short term trend in cirrhosis. Nevertheless, the observed relation between the consumption of spirits and cirrhosis mortality merits further investigation. Key messages US cirrhosis mortality peaked in 1973 but alcohol consumption did not peak until the early 1980s Both shifts in the distribution of US drinking patterns (which are not reflected in per capita consumption statistics) and the increase in the availability of treatment for alcoholism have been suggested as potential sources of the decline in cirrhosis The trend in the consumption of distilled spirits from 1949 to 1994 shows a close, aggregate level association with cirrhosis mortality This aggregate level relation suggests that research is needed into the link between the effects of specific alcoholic beverages and cirrhosis

Alcohol use and prostate cancer: A meta-analysis

Past reviews have concluded that there is no association between alcohol use and prostate cancer incidence. We performed a meta-analysis of existing epidemiological studies finding, in contrast, evidence to suggest that prostate incidence is positively linearly associated with heavier alcohol use. This finding was largely due to the contribution of population case-control studies and those measuring men recruited before age 60. No relationship between alcohol consumption and prostate cancer was found for cohort and hospital case-control studies. Analyses of design effects modestly suggests that population case-control studies were probably better suited to identify potential alcohol-prostate cancer relationships due to the close temporal proximity of the measurement of level of alcohol consumption to diagnosis. Future efforts should be made to exclude all ill subjects from control groups/baseline samples in addition to accounting for changes in consumption with advancing age and the onset of illness. The alcohol-prostate cancer association remained significant despite controlling for the degree to which studies endeavored to eliminate false negatives from their control groups.

How good is the science

Ronksley and colleagues asserted that the association between moderate alcohol consumption and reduced mortality risk was “beyond question.”1 We reviewed all 67 studies that generated the 84 articles in their meta-analysis. All but two had at least one of six serious methodological problems, and these two had mixed findings (figure⇓); see http://carbc.ca/Portals/0/News/FeatureSupplement201203.pdf for bibliography).

Light-to-moderate drinking and dementia risk: The former drinkers problem re-visited

A growing literature ostensibly supports the contention that light-to-moderate drinking offers a protective effect with respect to late-onset dementia. The former drinkers problem, however, may mitigate or even erase any observed protective relationship. Using three recent meta-analyses as windows on the alcohol and dementia literature [Anstey, K.J., Mack, H.A., & Cherbuin, N. (2009). Alcohol consumption as a risk factor for dementia and cognitive decline: Meta-analysis of prospective studies. American Journal of Geriatric Psychiatry, 17, 542–555; Peters, R., Peters, J., Warner, J., Beckett, N., & Bulpitt, C. (2008). Alcohol, dementia and cognitive decline in the elderly: A systematic review. Age Ageing, 37, 505–512; Neafsey, E.J., & Collins, M.A. (2011). Moderate alcohol consumption and cognitive risk. Neuropsychiatric Disease and Treatment, 7, 465–484], we offer a critical review and re-examination of 24 studies employing one or another strategy to control or evaluate the impact of the former drinkers problem on the alcohol and cognitive impairment relationship. Our review is organized around four strategies and problem areas found in these studies, namely: (1) analyses using light drinkers instead of abstainers as reference, (2) time dimension problems attaching to the nondrinker category in analyses, (3) analyses excluding former drinkers or drinkers who changed categories over a studys course, and (4) other approaches and associated problems. Our review suggests that the former drinkers problem has been only incompletely addressed in this still new literature on alcohols possible protective cognitive effects. As evidenced in the three meta-analyses employed in this review, only a fraction of alcohol and dementia studies addressed the former drinkers problem and, among those, still fewer addressed the problem adequately. Several reasons for this deficiency in the literature are discussed. We conclude that the impact of former drinkers on the alcohol and dementia relationship remains an open question.

MENTAL DISORDERS THE MISSING PIECE

Mental disorders remain one of the world’s major international public health problems, and mental disorders may also interact with the progress and development of many physical diseases [1]. Mental health status (MHS) plays a central role in influencing the behaviours of individuals, especially those related to physical health [1]. Given this, MHS has the potential to confound observational research studies which seek to understand associations between physical health problems and behaviour factors. Two such health problems are coronary heart disease (CHD) and ischaemic stroke [1,2]. Many cohort studies from the medical epidemiology literature have observed a ‘J-shaped’ association between alcohol consumption and risk of CHD and stroke for middle-aged and older people [3–5]. Nondrinkers appear to have a higher risk of CHD and stroke than regular moderate drinkers. The direct implication is that moderate drinking is cardioprotective, but the veracity of the J-shaped curve is being scrutinized increasingly [e.g. 4]. As well as research concerned with cardiovascular health, studies have emerged recently which show consistently that the prevalence of depression is significantly higher among non-drinkers compared to moderate drinkers [6–8]. It is arguable that adjustment for socioeconomic factors may mitigate some MHS effects; however, the large-scale cohort study by Skogen et al. [8] adjusted for confounders typically controlled for in alcohol–CHD studies and the effects of MHS on cardiovascular health remained. Three alternative hypotheses explicate the association observed between mental disorders and alcohol consumption, as follows. 1. Better MHS leads to drinking at moderate levels. 2. Moderate alcohol consumption leads to lower risk of mental disorders (i.e. depression). 3. There is no causal relation between MHS and alcohol consumption, and the association is due to unknown confounding factors. If hypothesis 3 is true, hypotheses 1 and 2 must be rejected and if hypotheses 1 and 2 are true, hypothesis 3 must be rejected. However, hypotheses 1 and 2 are not mutually exclusive. Bringing the observations from the mental health and cardiovascular literature together: if hypothesis 2 is true, then moderate regular alcohol consumption may protect against cardiovascular disease via its positive effect on MHS (i.e. lower risk of depression). Alternatively, the action of drinking and/or the constituents of the beverage (e.g. alcohol) may produce a desirable effect on MHS and thereby a protective effect on CHD. Conversely, if hypothesis 2 is not true, the apparent cardioprotective effect of moderate drinking may be due, in fact, to the better MHS of moderate drinkers. It is not currently possible to determine whether or not this might be the case, as MHS is rarely investigated using reliable psychiatric measurements by cohort studies [2,3,5,9]. It is not feasible to test hypothesis 2 with animal studies; however, it would be useful to test how MHS may change among moderate drinkers who stop drinking or switch to lower-strength alcoholic beverages in a randomized controlled trial. Attempts to test this outside a randomized setting would be prone to bias, as people who cease alcohol consumption often do so because of failing health and/or increasing age [4]. The adjusted likelihood of depression among abstainers compared to moderate drinkers was 38% higher [8]—about 10% higher than the comparative likelihood of CHD among abstainers (1.25) [3]. We argue that a concerted effort to adjust for MHS with reliable, comprehensive measures will bring the apparent association between moderate alcohol consumption and CHD substantially closer to 1. Until such efforts are made, apparent cardioprotective effects of moderate drinking from observational studies will be questionable. Changing MHS over the life-span and its association with drinking behaviours may be key to understanding the true nature of the apparent cardioprotective effects of moderate alcohol consumption on older populations.

Has alcohol been proven to be protective against coronary heart disease

Department of Social and Behavioral Sciences, University of California, San Francisco Box 0612, San Francisco, CA 94148-0612, USA, Alcohol Research Group, 6475 Christie Avenue, Suite 400, Emeryville, CA 94608, USA, Centre for Addictions Research of British Columbia, University of Victoria, PO Box 1700 STN CSC, Victoria, BC V8W 2Y2, Canada, National Drug Research Institute, Curtin University, GPO Box U1987, Perth WA 6845, Australia, and Department of Epidemology and Biostatistics, University of California, San Francisco Box 0840, San Francisco, CA, USA

Overlooking Terris: A Speculative Reconsideration of a Curious Spot-Blindness in the History of Alcohol-Control Science

The authors argue that the overlooking or forgetting of a beverage-specific element of Milton Terriss classic 1967 paper linking per capita alcohol consumption with cirrhosis mortality trends sheds new light on the subsequent paradigmatic history of alcohol epidemiology. The historical standing and subsequent citation of Terriss paper are re-examined, and Terriss reasons for not reminding the alcohol epidemiology literature of this aspect of his paper are explored. Aspects of presentation and content of the 1967 paper are also discussed with respect to the explanation of the subsequently lost beverage-specific element of Terriss article. The authors suggest that an evolutionary aspect of the relationship and competition between the modern alcoholism and alcohol controls paradigms in alcohol epidemiology may offer the key to accounting for this historical-forgetting puzzle.

RESPONSE TO DR KARI POIKOLAINEN: THE PERSISTENT, ALTERNATIVE ARGUMENT TO APPARENT CARDIOPROTECTIVE EFFECTS OF ALCOHOL

The old Christian proverb that we use in our title recognizes the constraints related to serving two masters. Because of its universality, it is possible to find versions of these wise words in many cultures. The letter submitted to Addiction by Andrade [1] is an example of the impossibility of receiving funding from the alcohol industry and at the same time attempting to do effective public health work (particularly in an unregulated market such as Brazil). The request by several health science journals in recent years to acknowledge conflict of interest is a practical illustration of this issue. When researchers receive funds from interest groups (alcohol, tobacco or pharmaceutical companies), the results produced by their investigations will be evaluated in this light. And, of course, there are important reasons for doing things this way. Let us quickly examine the instance brought up by Andrade [1] about CISA, a Brazilian NGO 90% financed by Ambev. Since the NGO was formed, it has participated in outside activities and on a number of occasions its members have been sources of information about alcohol in newspapers. CISA’s scientific committee is formed mainly by medical doctors and psychologists associated with known Brazilian Universities. One of the newspaper articles written by a CISA affiliate was published a few months ago on the same page as an interview with the new Brazilian health minister where he articulated his intention to restrict alcohol advertising in the country [2]. While the minister defended restrictions on advertising, something completely new in Brazil, the CISA piece undermined the importance of regulating alcohol advertising: “. . . To the power that advertising allegedly exerts ( . . . ), there is no scientific evidence that its restriction would reduce the harms associated with alcohol abuse”. The article went on to suggest that the government’s proposal was a marketing stunt, proposing vague long term measures to contain alcohol problems in the country. At the end of the article is the real catch: if the piece had been signed by an alcohol industry official, the readers would be able to interpret the affirmations taking this information in account. Instead, the CISA’s name (without mentioning Ambev’s support) and two medical universities names appear side by side. The fact that CISA’s executive president chooses the scientific team and the organizations’ activities does not guarantee CISA’s independence. In effect, the sole existence of such an organization (or others sponsored by the alcohol industry) suggests a community of interest between health professionals and interest groups that does not exist. In the particular case of CISA, its connections with WHO through its World Mental Health Survey Initiative should be cause for concern and definitely sends the wrong message to the public at large. At this point in time it is a known fact that the alcohol industry uses both subtle and direct ways to influence public health (for instance, in Brazil, supporting the political campaigns of a significant number of congressmen). The congressmen also argue that the money they receive from interest groups is not going to influence their work in favour of the country.

Critical Explanations—Biological, Psychological, and Social—of Drinking Patterns and Problems from the Alcohol-Related Longitudinal Literature

Generalization of scientific findings is contingent on replication of results. This is particularly critical for research concerning the correlates and prediction of human behavior where cultural and temporal factors may alter findings. Alcohol-related longitudinal research is rich and bountiful; it permits exploration of the degree to which replication of findings has taken place, particularly replication across differing cultural and temporal frames, and the development of research strategies that might provide tests of replication.