The Influence of Advertising on Tobacco Consumption: a reply to Boddewyn

This paper presents a rejoinder to Boddewyn's critique of our earlier work. We show that many of his concerns are unfounded or have been addressed in our subsequent work. Our original conclusion that cigarette advertising has a significant effect on aggregate consumption remains unchanged. We concede that the analysis could be improved by a fuller data set and appeal to the tobacco industry to open their data for independent analysis.     

The Influence of Advertising on Tobacco Consumption: a reply to Jackson & Ekelund

This paper re-examines the model for quarterly cigarette consumption presented earlier (Chetwynd et al., 1988) in the light of criticisms by Jackson & Ekelund of a number of possible deficiencies in the econometric procedures employed. A thorough interrogation of the model has been pursued using a comprehensive battery of econometric testing procedures which go beyond those suggested by Jackson & Ekelund. The model is found to perform well against all of these tests and the original conclusions drawn from the model are sustained, including the significant impact of advertising on aggregate cigarette consumption.     

The Influence of Advertising on Tobacco Consumption: some problems with Chetwynd et al.'s analysis

In a recent study of the relationship between cigarette advertising and the aggregate consumption of cigarettes in New Zealand between 1973 and 1985, Chetwynd et al. (1988) argue that quarterly data suggest that advertising affects overall consumption of cigarettes with an elasticity of +0.07. In addition, they argue that advertising has a ‘carry over’ effect of about four quarters on current consumption. These results are potentially important for two reasons. Although the evidence is mixed, the conventional view is that cigarette advertising affects brand choice among smokers but not aggregate demand for cigarettes. Chetwynd et al.'s results, (hereafter, Chetmynd) contradict this traditional view. Secondly, if advertising does increase the aggregate demand for cigarettes, then a public policy banning cigarette advertising might reduce aggregate demand for cigarettes. Unfortunately, the Chetwynd, study is sufficiently flawed with conceptual and econometric problems that their inference that advertising increases cigarette demand is questionable. Certainly cigarette advertising may increase or decrease cigarette consumption. The point we wish to make is that, any inference one way or the other based on the results of Chetwynd, cannot be viewed as well-grounded in either scientific methodology or statistical principles.     

The Effects of Tobacco Advertising on Children

The London Based Children's Research Unit (CRU) has investigated juvenile smoking initiation and advertising in 15 countries. Each country investigated differed with respect to tobacco advertising restrictions, ranging from Norway, which has had a long-term ban on all advertising of tobacco products, to Hong Kong and Japan, which had few advertising restrictions at the time of the research. Advertising was not found to significantly influence juvenile smoking initiation and it was also found to be a poor predictor of juvenile smoking prevalence. That is, countries with tobacco advertising did not have a higher level of juvenile smoking prevalence than countries without advertising.     

Will Restrictions on Alcohol Advertising Reduce Alcohol Consumption?

The effects of restrictions of alcohol advertisements in Manitoba, Canada and in the United States are examined using statistical data on alcohol consumption. The relationships between consumption and alcoholism rates for the U.S. and advertising regulations were very weak and not statistically significant. Subsequent to a restriction on beer advertising in Manitoba, beer consumption in that province rose at a similar rate as in a control province of Alberta. It is considered unlikely that restrictions on advertising will reduce consumption.     

The Relationship Between Genetic Influences on Alcohol Dependence and on Patterns of Alcohol Consumption

Background: Genetic factors impact substantially both on alcohol consumption (AC) and on the risk for alcohol dependence (AD). However, we know little about the degree to which measures of AC index the genetic risk for AD. Methods: We assessed a lifetime history of AD by DSM‐IV criteria and four measures of AC at the time of heaviest drinking (drink frequency, regular quantity, maximum quantity, and drunk frequency) in 5,073 adult twins from same‐sex pairs from the Virginia Twin Registry. Structural models were fitted using Mx. Results: We found evidence for different genetic structure in the sexes. In women, genetic risk for AD and for the four measures of AC was entirely shared. In men, the AC measures captured 85% of the genetic risk for AD. In women, the genetic relationship with AD was strongest for drunk frequency and in men for both drunk frequency and regular quantity. Conclusions: In a population‐based sample of twins, four relatively simple measures of AC obtained for the time of lifetime heaviest drinking were able to capture all (in women) or a very large proportion (in men) of the genetic risk for the complex multi‐dimensional construct of AD. If replicated, these results have practical implications for studies aiming to assess genetic risk for AD.     

Genetic and Environmental Influences on Ethanol Consumption: Perspectives From Preclinical Research

Background: Alcohol use disorders (abuse and dependence, AUD) are multifactorial phenomena, depending on the interplay of environmental and genetic variables. Method: This review describes current developments in animal research that may help (a) develop gene therapies for the treatment of alcoholism, (b) understand the permissive role of stress on ethanol intake, and (c) elucidate why exposure to ethanol early in life is associated with a greater risk of AUD. Results: The polymorphisms found in liver alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) affect the elimination of ethanol and the susceptibility to ethanol intake. A highly active ADH protects against alcoholism, an effect related to a presteady state burst in arterial acetaldehyde. Social stressors, such as repeated early maternal separation or social defeat, exert a permissive effect on ethanol intake, perhaps by altering the normal development of the hypothalamic‐pituitary‐adrenal axis. Ethanol exposure during gestation, infancy, or adolescence increases the likelihood of AUD later in life. Early perception of ethanol’s positive and negative (anti‐anxiety) reinforcing effects may play a role in this phenomenon. Conclusions: The review underscores the advantages of using preclinical animal models of AUD and highlights points of intersection between the topics to help design a more integrated approach for the study of alcohol‐related problems.     

Environmental Influences on Alcohol Consumption Practices of Alcoholic Beverage Servers

Public drinking establishments have long been associated with heavy drinking among both their patrons and servers. Whether these environments represent locations where heavy drinking is learned (learning hypothesis) or simply places where already-heavy drinkers gather in a supportive environment (selection hypothesis) remains an important question. A sample of licensed alcoholic beverage servers in the state of Indiana, USA, was surveyed to better understand the drinking behaviors of servers within the alcohol service industry. Responses (N=938) to a mailed questionnaire were analyzed to assess the relative influence of environmental and demographic factors on the drinking behavior of servers. Stepwise regression revealed “drinking on the job” as the most influential environmental factor on heavy drinking behaviors, followed by age and gender as influential demographic factors. Support was found for the selection hypothesis, but not for the learning hypothesis. Policy implications are discussed.