Smoking and drinking are behaviors that often appear inexorably linked. Although the behaviors are voluntary decisions, new research suggests a biological basis may account for the observation that smokers drink more than nonsmokers. Moreover, the additional alcohol consumption may contribute to the development of chronic alcohol-related diseases.
In a mammalian study, researchers from Texas A&M found that nicotine can reduce blood alcohol concentrations (BACs). In turn, more alcohol consumption is required to achieve the “buzz” that drinker’s desire.
“Since the desired effect of alcohol is significantly diminished by nicotine – particularly among heavy or binge drinkers such as college students – this may encourage drinkers to drink more to achieve the pleasurable or expected effect,” said Wei-Jung A. Chen, associate professor of neuroscience and experimental therapeutics at The Texas A&M Health Science Center College of Medicine. “In other words, cigarette smoking appears to promote the consumption of alcohol.”
Study results are published in the August issue of Alcoholism: Clinical & Experimental Research.
The concept of “cross tolerance” – where a decrease in the reward of one drug appears to facilitate the increased use of another other drug in order to achieve the desired effects – has been around since at least the 1950s. Yet only two studies have examined the pharmacokinetic interactions between alcohol and nicotine, noted co-author Scott Parnell, postdoctoral research fellow at the University of North Carolina. “Other than these two studies, little is known about the interaction of effects of nicotine on alcohol metabolism, and especially how nicotine lowers BACs.”
For this study, researchers administered a range of individual nicotine doses (0, 0.25, 0.5, 1, 2, 4 and 6 mg/kg body weight) along with an alcohol dose (4 g/kg body weight) via intragastric intubation (into the stomach) or intraperitoneal injection (into the abdominal cavity) to adult female rats. BAC levels were then measured at various time points.
There were two key findings, said Chen. “One is that the presence of nicotine will significantly reduce peak BAC, and such a pharmacokinetic interaction between alcohol and nicotine may be related to the nicotine dose,” he said.
There are numerous detrimental consequences to this finding, said Susan Maier, health scientist administrator at the National Institutes of Health.
“In the human condition, persons desiring to drink ‘to effect’ will need to drink more alcohol while smoking in order to reach this effect, and this will lead to an increased amount and lingering presence of toxic byproducts of alcohol metabolism, such as acetaldehyde,” she said. “This would be particularly harmful for adolescents and young adult drinkers, since these populations are amenable to this type of drinking pattern, and may develop chronic alcohol-related diseases earlier in life because of it.
Furthermore,” she added, “cross tolerance can lead to a permanent alteration of the physiology of metabolism to the extent that beneficial drugs used to treat an illness may have reduced efficacy in some individuals who use both alcohol and nicotine.”
“The second key finding is that the capability of nicotine to decrease BAC can only be observed if alcohol is given through the oral route of administration,” said Chen, suggesting that this decrease may be related to gastric function.
“Nicotine appears to delay the emptying of the stomach contents, including alcohol, into the intestines, a major site for absorption. A portion of the alcohol molecules are then subject to metabolism within the stomach, leaving less alcohol passing from the stomach to the intestinal tracts for absorption, thus decreasing alcohol concentration measured downstream in the blood.”
“These findings are important in that they highlight the effects of polydrug interactions, which has implications for other drugs, not necessarily illicit drugs, that may be co-used with alcohol, such as aspirin,” said Maier. “These results suggest, but do not directly test the hypothesis, that other drugs that modify specific stomach functions – such as the active ingredients of Pepcid®, Zantac®, Tagamet® – may also alter alcohol metabolism when consumed simultaneously.”
These concerns will be, in fact, a focus of Chen’s future research: understanding the interactive effects of abuse substances, particularly on the brain’s development.
“Individuals who abuse alcohol are likely to use other drugs,” said Chen, “and the significance of this study is to re-affirm that when examining the effects of alcohol on any given organ tissue system, the potential interactive effects of alcohol with other drugs needs to be considered.
For example, the co-use of alcohol and cocaine will result in the formation of cocaethylene, which is highly toxic and has led to a higher mortality rate in animal studies. In sum, the current findings should be a warning to the general public regarding the danger of abusing multiple drugs, since the pharmacokinetic interactions among these substances are often unpredictable and injurious.”
Source: Texas A&M Health Science Center