Explain the Epidemiology of Alcoholism Essay
According to Alcohol Concern Organisation (2015) more than 9 million people in England consume alcoholic beverages more than the recommended daily limits. In relation to this, the National Health Service (2015) actually recommends no more than 3 to 4 units of alcohol a day for men and 2 to 3 units a day for women. The large number of people consuming alcohol more than the recommended limits, highlights the reality that alcoholism is a major health concern in the UK which can lead to a multitude of serious health problems.
Moss (2013) states that alcoholism and chronic use of alcohol are linked to various medical, psychiatric, social and family problems. To add to this, the Health and Social Care Information Centre (2014) reported that between 2012 and 2013, a total of 1,008,850 admissions related to alcohol consumption where an alcohol-related disease, injury or condition was the primary cause for hospital admission or a secondary diagnosis. This shows the detrimental impact of alcoholism on the health and overall wellbeing of millions of people in the UK. It is therefore vital to examine the aetiology of alcoholism in order to understand why so many people end up consuming excessive alcohol. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) (n.d.) supports this by stating that learning the natural history of a disorder will provide information essential for assessment and intervention and for the development of effective preventive measures. This essay will also look into the different public health policies that address the problem of alcoholism in the UK. A brief description of what alcoholism is will first be provided. Explain the Epidemiology of Alcoholism Essay.
It is safe to declare that alcoholism is a lay term that simply means excessive intake of alcohol. It can be divided into two forms namely; alcohol misuse or abuse and alcohol dependence. Alcohol misuse simply means excessive intake of alcohol more than the recommended limits (National Health Service Choices 2013). A good example of this is binge drinking. Alcohol dependence is worse because according to the National Institute for Health and Care Excellence (2011, n.p.) it “indicates craving, tolerance, a preoccupation with alcohol and continued drinking regardless of harmful consequences” (e.g. liver disease). Under the Diagnostic Statistical Manual of Mental Disorders (DSM)- 5, these two have been joined as one disorder called alcohol use disorder or AUD with mild, moderate and severe sub-classifications (NIAAA 2015).
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Alcoholism is a complex disorder with several factors leading to its development (NIAAA 2005). Genetics and other biological aspects can be considered as one factor involved in the development of alcohol abuse and dependence (NIAAA 2005). Other factors include cognitive, behavioural, temperament, psychological and sociocultural (NIAAA 2005). According to Goodwin (1985) as far as the era of Aristotle and the Bible, alcoholism was believed to run in the families and thus could be inherited. To some extent, there is some basis that supports this ancient belief because in reality, alcoholic parents have about four to five times higher probability of having alcoholic children (Goodwin 1985).Explain the Epidemiology of Alcoholism Essay. Today, this belief seems to lack substantially clear and direct research-based evidence. On the other hand, studies also do not deny the role of genetics in alcoholism. With this view, it is therefore safe to argue that genetics is considered still as an important aetiologic factor in alcoholism. The current consensus simply indicates that there is more to a simple gene or two that triggers the predisposition of an individual to become an alcoholic. Scutti (2014) reports that although scientists have known for some time that genetics take an active role in alcoholism, they also propose that an individual’s inclination to be dependent on alcohol is more complicated than the simple presence or absence of any one gene. The National Institute on Alcohol Abuse and Alcoholism (2008) states that there is no one single gene that fully controls a person’s predisposition to alcoholism rather multiple genes play different roles in a person’s susceptibility in becoming an alcoholic. The NIAAA (2005) further claims that the evidence for a genetic factor in alcoholism lies mainly with studies that involve extended pedigree, those that involve identical and fraternal twins and those that include adopted individuals raised apart from their alcoholic parents. For pedigree studies, it is believed that the risk of suffering from alcoholism is increased four to seven fold among first-degree relatives of an alcoholic (Cotton 1979; Merikangas 1990 cited in NIAAA, 2005.). First degree relatives naturally refer to parent-child relationships; hence, a child is therefore four to seven times at higher risk of becoming an alcoholic, if one or both of their parents are alcoholics. Moss (2013) supports this by stating that children whose parents are alcoholic are at higher risk of becoming alcoholics themselves when compared to children whose parents are non-alcoholics. A study conducted by McGue, Pickens and Svikis (1992 cited in NIAAA 2005) revealed that identical twins generally have a higher concordance rate of alcoholism compared to fraternal twins or non-twin siblings. This basically means that a person who has an alcoholic identical twin, will have a higher risk of becoming an alcoholic himself when compared to if his alcoholic twin is merely a fraternal twin or a non-twin sibling. This study further proves the role of genetics in alcoholism because identical twins are genetically the same; hence, if one is alcoholic, the other must therefore also carry the alcoholic gene. The genetic factor in alcoholism is further bolstered by studies conducted by Cloninger, Bohman and Sigvardsson 1981 cited in NIAAA 2005 and Cadoret, Cain and Grove (1980 cited in NIAAA 2005) involving adopted children wherein the aim was to separate the genetic factor from the environmental factor of alcoholism. In these studies, children of alcoholic parents were adopted and raised away from their alcoholic parents but despite this, some of these children still develop alcoholism as adults at a higher rate than those adopted children who did not have an alcoholic biological parent (Cloninger et al., 1981 cited in NIAAA 2005 and Cadoret et al., 1980 cited in NIAAA 2005). One interesting fact about aetiologic genetic factor is that although there are genes that indeed increase the risk of alcoholism, there are also genes that protect an individual from becoming an alcoholic (NIAAA 2008). For example, some people of Asian ancestry carry a gene that modifies their rate of alcohol metabolism which causes them to manifest symptoms such as flushing, nausea and tachycardia and these generally lead them to avoid alcohol; thus, it can be said that this gene actually helps protect those who possess it from becoming alcoholic (NIAAA 2008). Explain the Epidemiology of Alcoholism Essay.
Another clearly identifiable factor is environment, which involves the way an individual is raised and his or her exposure to different kinds of activities and opportunities. The National Institute on Alcohol Abuse and Alcoholism (2005) relates that the genetic factor and the environmental factor have a close relationship in triggering alcoholism in an individual. This can be explained by the simple fact that even if an individual is genetically predisposed to becoming an alcoholic, if he is not exposed to a particular kind of environment which triggers activities that lead to alcohol intake, the likelihood of his becoming an alcoholic will be remote. There are certain aspects within the environment that makes it an important aetiologic factor. According to Alcohol Policy MD (2005) these aspects include acceptance by society, availability and public policies and enforcement. Acceptance in this case refers to the idea that drinking alcoholic drinks even those that should be deemed excessive is somewhat encouraged through mass media, peer attitudes and behaviours, role models, and the overall view of society. Television series, films and music videos glorify drinking sprees and even drunken behaviour (Alcohol Policy MD 2005). TV and film actors and sports figures, peers and local role models also encourage a positive attitude towards alcohol consumption which overshadows the reality of what alcohol drinking can lead to (Alcohol Policy MD 2005). In relation to this, a review of different studies conducted by Grube (2004) revealed that mass media in the form of television shows for instance has an immense influence on the youth (age 11 to 18) when it comes to alcohol consumption. In films, portrayals regarding the negative impact of alcohol drinking are rare and often highlight the idea that alcohol drinking has no negative impact on a person’s overall wellbeing (Grube 2004).Explain the Epidemiology of Alcoholism Essay. In support of these findings, a systematic review of longitudinal studies conducted by Anderson et al. (2009) revealed that the constant alcohol advertising in mass media can lead adolescents to start drinking or to increase their consumption for those who are already into it. Availability of alcoholic drinks is another important environmental aetiologic factor of alcoholism simply because of the reality that no matter how predisposed an individual is to become an alcoholic, the risk for alcoholism will still be low if alcoholic drinks are not available. On the other hand, if alcoholic beverages are readily available as often are today, then the risk for alcoholism is increased not only for those who are genetically predisposed to alcoholism but even for those who do not carry the “alcoholic genes”. The more licensed liquor stores in an area, the more likely people are to drink (Alcohol Policy MD 2005). The cheaper its price, the more affordable it is for people to buy and consume it in excess (Alcohol Policy MD 2005). Another crucial environmental aetiologic factor is the presence or absence of policies that regulate alcohol consumption and its strict or lax enforcement. It includes restricting alcohol consumption in specified areas, enacting stricter statutes concerning drunk driving and providing for penalties for those who sell to, buy for or serve to underage individuals (Alcohol Policy MD 2005). It is worthy to point out that in the UK, the drinking age is 18 and a person can be stopped, fined or even arrested by police if he or she is below this age and is seen drinking alcohol in public (Government UK 2015a). It is also against the law for someone to sell alcohol to an individual below 18; however, an individual age 16 or 17 when accompanied by an adult can actually drink but not buy alcohol in a pub or drink beer, wine or cider with a meal (Government UK 2015a). Explain the Epidemiology of Alcoholism Essay.
One public health policy that can help address the problem on alcoholism is the mandatory code of practice for alcohol retailers which banned irresponsible alcohol promotions and competitions, and obliged retailers to provide free drinking water, compelled them to offer smaller measures and required them to have proof of age protocol. It can be argued that this policy addresses the problem of alcoholism by restricting the acceptance, availability and advertising of alcohol (Royal College of Nursing 2012). Another is the Police Reform and Social Responsibility Act 2011 which is a statute that enables local authorities to take a tougher stance on establishments which break licensing rules about alcohol sale (Royal Collage of Nursing 2012). There is also the policy paper on harmful drinking which provides different strategies in addressing the problem of alcoholism. One such strategy is the advancement of the Change4Life campaign which promotes healthy lifestyle and therefore emphasises the recommended daily limit of alcohol intake for men and women (Government UK 2015b). Another strategy within this policy is the alcohol risk assessment as part of the NHS health check for adults ages 40 to 75 (Government UK 2015b). This policy aims to prevent rather than cure alcoholism which seems to be logical for after all, an ounce of prevention is better than a pound of cure.
Alcoholism which includes both alcohol misuse and alcohol dependence is a serious health problem which affects millions in the UK. Its aetiology is actually a combination of different factors. One vital factor is genetics wherein it can be argued that some people are predisposed to becoming an alcoholic. For example, an individual is at higher risk of becoming an alcoholic if he or she has a parent who is also alcoholic. When coupled with environmental factors, the risk of suffering from alcoholism becomes even greater. Environment refers to the acceptability and availability of alcohol and the presence or absence of policies that regulate alcohol sale and consumption. Vital health policies such as Harmful Drinking Policy Paper advocated by the government, are important preventive measures in reducing the incidence and prevalence of alcoholism in the UK. Explain the Epidemiology of Alcoholism Essay.
Alcohol Concern Organisation (2015). Statistics on alcohol. [online]. Available from: https://www.alcoholconcern.org.uk/help-and-advice/statistics-on-alcohol/ [Accessed on 28 September 2015]. Alcohol Policy MD (2005). The effects of environmental factors on alcohol use and abuse. [online]. Available from: https://www.alcoholpolicymd.com/alcohol_and_health/study_env.htm[Accessed on 28 September 2015]. Anderson, P., de Brujin, A., Angus, K., Gordon, R. and Hastings, G. (2009). Impact of alcohol advertising and media exposure on adolescent alcohol use: A systematic review of longitudinal studies. Alcohol and Alcoholism. 44(3):229-243. Goodwin, D. (1985). Alcoholism and genetics: The sins of the fathers. JAMA Psychiatry. 42(2):171-174. Government UK (2015a). Alcohol and young people. [online]. Available from: https://www.gov.uk/alcohol-young-people-law [Accessed on 28 September 2015]. Government UK (2015b). policy paper 2010 to 2015 government policy: Harmful drinking. [online]. Available from: https://www.gov.uk/government/publications/2010-to-2015-government-policy-harmful-drinking/2010-to-2015-government-policy-harmful-drinking [Accessed on 28 September 2015]. Grube, J. (2004). Alcohol in the media: Drinking portrayals, alcohol advertising, and alcohol consumption among youth. [online]. Available from:https://www.ncbi.nlm.nih.gov/books/NBK37586/ [Accessed on 28 September 2015]. Health and Social Care Information Centre (2014). Statistics on alcohol England, 2014. [online]. Available from: Explain the Epidemiology of Alcoholism Essay.https://www.hscic.gov.uk/catalogue/PUB14184/alc-eng-2014-rep.pdf [Accessed on 28 September 2015]. Moss, H.B. (2013). The impact of alcohol on society: A brief overview. Social Work in Public Health. 28(3-4):175-177. National Health Service (2015). Alcohol units. [online]. Available from: https://www.nhs.uk/Livewell/alcohol/Pages/alcohol-units.aspx [Accessed on 28 September 2015]. National Health Services Choices (2013). Alcohol misuse. [online]. Available from: https://www.nhs.uk/conditions/alcohol-misuse/pages/introduction.aspx [Accessed on 28 September 2015]. National Institute on Alcohol Abuse and Alcoholism (2015). Alcohol use disorder: A comparison between DSM-IV and DSM-5. [online]. Available from: https://pubs.niaaa.nih.gov/publications/dsmfactsheet/dsmfact.pdf [Accessed on 28 September 2015]. National Institute on Alcohol Abuse and Alcoholism (2008). Genetics of alcohol use disorder. [online]. Available from: https://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-use-disorders/genetics-alcohol-use-disorders [Accessed on 28 September 2015]. National Institute on Alcohol Abuse and Alcoholism (2005). Module 2: Etiology and natural history of alcoholism. [online].Explain the Epidemiology of Alcoholism Essay. Available from: https://pubs.niaaa.nih.gov/publications/Social/Module2Etiology&NaturalHistory/Module2.html [Accessed on 28 September 2015]. National Institute for Health and Care Excellence (2011). Alcohol-use disorders: Diagnosis, assessment and management of harmful drinking and alcohol dependence. [online]. Available from: https://www.nice.org.uk/guidance/CG115/chapter/Introduction [Accessed on 28 September 2015]. Royal College of Nursing (2012). Alcohol: policies to reduce alcohol-related harm in England. [online]. Available from: https://www.rcn.org.uk/__data/assets/pdf_file/0005/438368/05.12_Alcohol_Short_Briefing_Feb2012.pdf [Accessed on 28 September 2015. Scutti, S. (2014). Is alcoholism genetic? Scientists discover link to a network of genes in the brain. [online]. Available from: https://www.medicaldaily.com/alcoholism-genetic-scientists-discover-link-network-genes-brain-312668 [Accessed on 28 September 2015].
This paper presents examples to illustrate the utility and limitations in the use of epidemiology in alcohol research and discusses some promising new directions.
Review of literature, concentrating on epidemiological alcohol research with relevance to public health.
Epidemiology offers tools for assessment of causes and effects of alcohol consumption as well as the effects of efforts to prevent alcohol consumption and its consequences. Epidemiological studies have made significant contributions to alcohol research with respect to public health and public policy.Explain the Epidemiology of Alcoholism Essay. Fixed-effects modelling, difference-in-differences estimation and integrated qualitative and epidemiological methods are promising but underused methods in epidemiological studies. Many epidemiological studies have limited transferability of knowledge to other cultures and jurisdictions.
This paper illustrates the use of epidemiology in alcohol research by presenting some examples of its utility and limitations and discussing some promising new directions. The focus is on a few selected topics within alcohol research and some key achievements in the building of knowledge to understand drinking behaviour and related problems more clearly and effective ways to prevent these problems. Examples have been chosen for their relevance to public health and public policy, but the choice is obviously also influenced by the authors’ own research interests over the years. Unfortunately, it is impossible to pay fair tribute to the many significant contributions that can be found in this huge literature.
There is no single or standard definition of epidemiology; the definition assumed for this paper is: ‘Epidemiology is the study of the distribution and determinants of health-related states or events in specified populations, and the application of this study to the control of health problems’ 1. This definition has the advantage of acknowledging that a public health perspective is central to epidemiological studies.Explain the Epidemiology of Alcoholism Essay. This is also the case in alcohol research, as illustrated by the following reasons given by Edwards 2 for including epidemiological research in the addiction sciences: to illuminate public understanding, to assist in assessment of health service need, to explain the genesis of cases, to explain the relationship between substance use and substance use problems, to assess the efficacy of preventive strategies and to project the future.
Within this framework, this paper limits its focus to studies of association, concentrating on assessing causes and effects of alcohol use as well as the effects of efforts to prevent alcohol use and its consequences. This paper regards epidemiology as a toolbox for the assessment of associations and interpretation of causation. While the latter is generally far from trivial, Bradford Hill’s classic considerations are useful in attempting to distinguish causal from non-causal associations 3.
The first example is the single distribution theory (often referred to as the total consumption model). A basic empirical regularity underlying this theory is the stability of the distribution of alcohol consumption which, in turn, predicts a close relationship between the population mean consumption and the prevalence of heavy drinkers 4. In his seminal work, Skog 4 provided further empirical support for the single distribution theory and a theoretical foundation for how the regularity in the distribution of alcohol consumption can be explained. The empirical distribution of alcohol consumption in various populations has provided important insights contradictory to several popular beliefs: there is no clear demarcation between heavy drinkers (or alcoholics) and other drinkers; thus, alcohol-related problems exist in various degrees of severity throughout the entire population.Explain the Epidemiology of Alcoholism Essay. Further, all categories, from light to heavy drinkers, tend to ‘move in concert’ when total consumption changes 5. This suggests that the prevalence of heavy drinking is best understood in the context of a population’s characteristics 6. However, changes in drinking behaviour are not necessarily collective across population groups, as determinants of drinking may change differently for different population groups 7.
One implication of the total consumption model is that the prevalence of alcohol-related problems follows changes in population drinking; when total consumption increases, the prevalence of problems is also expected to increase, and vice versa. This is, however, not always the case. For instance, in Iceland and Norway total consumption of alcohol has increased substantially since the early 1990s, yet indicators of alcohol-related harm do not display similar trends 8. In more recent years arguments have been forwarded for examining both the theoretical foundation and empirical implications of the total consumption model 9,10.
A central task in epidemiology is to analyse and quantify the association between putative risk factors and various outcomes. A major threat to validity in such analyses is the possible presence of confounders; that is, factors that are not considered and that are related to the risk factor as well as the outcome at issue. While association between alcohol consumption and harm is assessed mainly by individual-level data, aggregate time–series data sometimes provide a feasible alternative. The highly relevant policy question of how various harm rates respond to changes in population drinking is especially hard to address on the basis of individual-level findings. One reason for this is the complexity of aggregating risk curves, as in the case of J-shaped risk functions. Another is that some forms of alcohol-related harm, such as violence, are inflicted on people other than the drinker himself. A further merit of aggregation that is not always recognized is that the problem of confounding due to self-selection does not operate at this level 11. The following two examples will illustrate this and also address the relevance of aggregate analyses to address public health issues. Explain the Epidemiology of Alcoholism Essay.
Numerous cohort studies have reported a U-shaped or J-shaped risk curve for the association between alcohol consumption and cardiovascular disease (CVD), suggesting that moderate drinkers have a lower risk of CVD compared to abstainers and heavy drinkers 12,13. Whether this reflects a preventive effect of moderate consumption is debatable 14, and it has been argued that selection to abstention may well inflate the risk difference between abstainers and moderate drinkers 15. However, there seems to be a compelling argument for causation 16, yet the implications for public health strategies remain uncertain. Skog 15 argued that what is optimum for an individual is typically too much for a population. Thus, changes that benefit some individuals could have the opposite impact on the population as a whole. Indeed, studies of population drinking and CVD often indicate that an overall increase in consumption does not have a beneficial effect on CVD mortality 17, but rather the opposite 18,19,20; yet this is not entirely consistent 21.
A strong association between alcohol consumption and violence is generally found in individual-level studies 22, which could suggest that violence would be effectively prevented by reducing drinking. However, inferring causality from these observations is problematic for several reasons: the many potential confounding factors are not controlled for easily, and alcohol’s role in violence seems complex and dependent upon interactions between alcohol consumption of aggressor and victim and environmental and individual factors 23,24. These problems may be overcome by applying time–series analyses of how changes in alcohol consumption at the population level impact on violence in a society. Quite a few such studies have been conducted since Lenke’s early work 25, and beyond substantiating the association between population drinking and violence rates, many of these studies have also suggested that this association is contingent upon characteristics of the drinking culture, i.e. the association tends to be stronger in populations where intoxication is a prominent feature of the drinking pattern 22,25,26.
The most commonly reported measure of association between a risk factor and the outcome at issue is the relative risk (or the odds ratio). However, from a public health perspective it is interesting to take the risk assessment one step further by factoring in the extent of exposure; that is, by estimating the population-attributable fraction (PAF). This measure expresses the proportion of the problem load for which the risk factor accounts 27,28. Obviously, the higher the PAF of a risk factor, the larger the potential to curb a problem by reducing exposure to the risk factor in question. Explain the Epidemiology of Alcoholism Essay.
This analytical strategy was applied to estimate the relative importance of alcohol consumption for the disease burden in a global perspective. The estimates suggest that alcohol use is the third leading risk factor for loss of healthy life years [disability-adjusted life years (DALYs)] in the world, and that alcohol accounts for a larger disease burden (DALYs) than tobacco and illicit drug use in most parts of the world 29. This illustrates the significant potential for curbing the global disease burden by reducing alcohol consumption 30,31. Furthermore, with respect to policy initiatives and calls for action in international bodies and in national and local authorities, this suggests that the weaker emphasis on alcohol, compared to tobacco and illicit drugs, may well be reconsidered and altered.
Studies of the prevention paradox constitute another example of the importance of assessing alcohol consumption’s relative contribution to a problem. A common way of thinking about prevention is that prevention efforts should be targeted towards those most at risk (high-risk strategies; 32). However, for many types of acute alcohol-related harms (e.g. violence and accidents), only a minor fraction of all harm incidents can be attributed to the relatively few high-risk individuals. It is the large majority of drinkers who individually are at less risk but who in sum account for most of the harm incidents 33,34,35. For these types of harm a population strategy is likely to be more efficacious than a high-risk strategy 32,36.
An important, yet often tricky, task is the evaluation of prevention efforts at the community level. How do we know that a change in consumption or harms can be attributed to the intervention and not some other factor or random variation? One way of minimizing the risk of confounding is to use data provided by natural experiments with marked changes.Explain the Epidemiology of Alcoholism Essay. These occur, for instance, when consumption shifts as a result of a significant policy change, and as the cause of the shift is known it is less likely that an observed impact on a harm indicator would be due to some third factor. In this research tradition it is well documented that significant changes in the availability of alcohol tend to impact upon population drinking (for reviews, see 36,37). One interesting example is the sharp increase in Danish spirits taxes in 1917 leading to a drop in per capita consumption by about 80% over 2 years. Analysing data from this period, Skog 38produced a very strong case for an effect of population drinking on suicide mortality. The experiences from the anti-alcohol campaign in the Soviet Union from 1985 to 1987 is another noteworthy example. The campaign led to a 25% reduction of estimated consumption and along with this a marked reduction in mortality, particularly from alcohol-attributable causes 39,40. A more recent natural experiment is provided by the cut in alcohol taxes and large decrease in alcohol prices and the ensuing 10% increase in total consumption that occurred in Finland in 2004. This was accompanied by an increase in alcohol-related mortality, but also a decrease in CVD mortality among older people 21,41. Interestingly, mortality increased most strongly in the less privileged groups, but very little among the great majority of gainfully employed people 21,41.
Compared to a simple pre- and post-intervention comparison, the research design is much strengthened if the shift occurs in a geographically confined area, making it possible to use other areas as controls, thereby reducing the risk of confounding. Alcohol policy interventions have been evaluated by such quasi-experimental designs. For instance, Holder and co-workers examined the effects of community-based environmental interventions in three communities and matched controls and found that the interventions led to a reduction in alcohol-related injuries 42. Other examples comprise evaluations of community-based interventions in Finland 43 and Norway 44, and an evaluation of restricting pub closing times in an Australian city 45. It should, however, be noted that the effect estimate in such studies may be inflated by selection to intervention. Explain the Epidemiology of Alcoholism Essay.
The ideal study design for assessment of community intervention effects would therefore be a type of randomized controlled trial. However, this type of study design is usually not applicable for interventions at the community level, yet a few interesting exceptions may be noted. A change from over-the-counter to self-service sales of alcoholic beverages in monopoly outlets occurred during the 1990s in Sweden and some years later in Norway. In both cases the state-owned monopolies implemented the change as a controlled experiment with assigned intervention and control areas. The change was evaluated with respect to impact on total alcohol sales by Skog 46 and Horverak 47, who applied identical methods and found similar and substantial effects on alcohol sales. Also, the introduction of Saturday opening of alcohol monopoly outlets in Sweden and Saturday closing of alcohol monopoly outlets in Norway were subject to controlled experiments and evaluated by Norström & Skog 48 and Nordlund 49 who, in both cases, found a fairly modest change in alcohol sales in response to the changed availability.
While epidemiologists very often pay due caution to inferences of causality, some topics are debated strongly with respect to whether—or to what extent—it may be reasonable to infer causality from observed associations and what the implications are for prevention. One of these topics pertains to the association between age at onset of drinking and the risk of alcohol use disorders (AUD) later in life. Numerous studies have shown consistently that those who have their first drink earlier than their peers are at higher risk of AUD as adults 50,51.Explain the Epidemiology of Alcoholism Essay. On these grounds, many authors have recommended that to prevent cases of AUD, efforts should be taken to delay onset of drinking 52,53. However, for several reasons such inference of causation seems dubious. The probable mechanisms for causation are not clear (lack of biological plausibility); many studies are based on cross-sectional data (lack of temporal order), and the observed association could be explained by selection to early onset of drinking and failure to control for significant confounders (e.g. behavioural undercontrol) 54 and retrospective bias in report of age at first drink 55.
In the previous sections we have discussed several methods that may be adequate for assessment of causal associations, and we will discuss here some research designs that have proved useful in this context but that are underused in alcohol epidemiology.
Assessing the risk of alcohol intake for various outcomes is often based on longitudinal data where drinking is measured at baseline and the outcome at a later point in time. The issue of confounding factors is alleviated in the traditional manner by including them as control variables, some of which may be omitted, while others cannot be observed. An alternative way of using panel data is offered by fixed-effects (FE) modelling (also referred to as the first difference method). Put simply, this method implies that the analyst explores to what degree a change in the exposure is accompanied by a change in the outcome. The method thus offers a safeguard against confounding due to omitted variables that are stable across time. Although FE modelling is a standard approach in econometrics 56, it is little used in alcohol epidemiology. One exception is the topic concerning the association between drinking and violence which may, in part, be produced spuriously by some third stable factor, e.g. weak self-control 57. All the four studies 58,59,60,61 that have submitted this association to the stricter test for causality provided by FE modelling obtained statistically significant FE estimates. Three of these studies 58,59,61 compared these estimates with those from cross-sectional ones and reported that the former were much weaker, suggesting that cross-sectional estimates are highly confounded. Explain the Epidemiology of Alcoholism Essay.
Another underused approach in alcohol epidemiology is the difference-in-differences estimation (DiD) 62,63,64. Nilsson 65 applied this technique to assess the long-term effects of increased availability of alcohol to young people, including women who have newly conceived, during an 8-month period in western Sweden in the late 1960s. The results provide compelling evidence of worsened labour market outcomes (relative to controls) at age 30 years for those potentially exposed in utero due to this quasi-experiment. Generally, DiD has proved to have surprisingly high power to detect effects even of quite weak exposures 66.
Even though the analytical strategies that have been discussed above have their merits, it is clear that they also have their limitations: FE modelling does not remedy time-varying confounders and cannot assess the direction of causality; outcomes from quasi-experiments can be flawed due to unobserved differences between the experiment and the control areas; estimates from time–series analysis may be plagued by omitted variable bias. A prudent strategy is thus to weigh together the evidence from various analytical strategies, rather than to rely on one kind of data only. The rationale of such triangulation is that an association that is supported by various kinds of data, analysed by different methods, is less likely to be impaired by one common source of bias.
Epidemiology is traditionally a single approach in empirical studies; however, in recent years there has been an increasing interest in mixed methods. In particular, the integration of qualitative methods and epidemiological methods in evaluation of complex interventions seems important with respect to explaining the outcome of the effect evaluation 67,68.
Epidemiological studies have no doubt contributed significant knowledge and insight with respect to the health consequences of alcohol consumption and the effects of many types of interventions. Over the past couple of decades data sources have expanded and the use of statistical methods and tools have advanced. However, in many respects our knowledge is still limited and sparse. Much of the focus has been on somatic consequences, whereas social harms and harms inflicted on others have gained less attention 69,70. Moreover, the bulk of studies stem from high-income countries where alcohol consumption is widespread and integrated, and societal structures allow for alcohol controls 36. It seems clear that there is limited transferability of knowledge from these societies to other cultures and jurisdictions, and therefore a need for a broader basis of knowledge 31,71. The request for more research may thus be well justified. The challenge lies in directing future research onto these tracks.
Sources of funding for work with this paper are the Norwegian Institute for Alcohol and Drug Research and the Swedish Institute for Social Research. We are most grateful for the valuable comments and suggestions from Ellen J. Amundsen, Pia Rosenquist and two anonymous reviewers on earlier versions of this manuscript. Explain the Epidemiology of Alcoholism Essay.