Cigarette smoking is the leading cause of preventable deaths in all the developed countries. Despite increased federal and state initiatives (as well as those of numerous non-governmental organizations) to combat this affliction in the United States, the response to the anti-smoking campaign has been mixed at best. Though there has been a decrease in male smoking as a whole, however, this victory is weakened by the increase in smoking among females. The campaigns have also spurred a change in the habit’s demographic, as current smoking in the United States is positively associated with younger age, lower income, reduced educational achievement, and disadvantaged neighborhood environment (Krogh 115). But puzzling statistics point out that factors beyond demographics contribute to the problem. Throughout the scientific community, conclusive links between depression and cigarette smoking have been found regardless of demographic. And although it has been proven that cigarettes are comparable in addictivity to Heroin (Seppa), scientists were baffled to find that only one third of all beginning smokers become regular users (Pomerleau). Increasingly scientists are seeking out (and finding) cohesive genetic links to aspects of tobacco use. Scientists have thus far identified a gene in part responsible for cigarette addiction as well as a certain genotype that significantly increases the probability of commencing tobacco use. The implications of these findings are immense. By developing an understanding of the complexities of the habit, anti-smoking campaigns of the future will be able to far more effectively combat the killer and save millions of lives.
Long before smoking began to be thought of as a societal affliction, scientists began to see evidence of an inherited predisposition to smoke. As early as 1962, scientists stumbled upon the possibility of heritability in conjunction with smoking by examining the habits of several sets of identical twins (Krogh 116). The 1962 study set a new precedent, suggesting for the first time smoking was not entirely a question of nurture rather than nature, and its results have been replicated numerous times. Twin studies have continued in the present day to provide a conclusive and stunning link between tobacco use and genetics. In a study of 778 reared-apart twins, the correlation in smoking habits between identical (monozygotic) twins was found to be significantly more similar than that of fraternal (dizygotic) twins (Kendler, Thornton, Pederson). These results support the possibility of genetic influences on both the predilections to begin smoking and to continue, which accurately foreshadowed the roles of the two exact genes isolated thus far which definitively play a hand in the smoking habit. Other twin studies have made even more exact correlations, finding that genetics can play a hand in age of onset of smoking and number of cigarettes smoked per day (Heath, Martin) as well as persistence of smoking and intensity of smoking—with significant genetic variation evident for both light and heavy smoking though not for moderate smoking (Heath, Martin). Perhaps these more specific results will lead to more genes being isolated. Twin studies, along with studies among adopted children’s habits in relations to their adoptive parents provided the necessary incentive for scientists to take a closer look (Krogh 120).
It is not surprising that the gene responsible for nicotine metabolization plays a role in determining a person’s level of addictivity. This gene, referred to by scientists as CYP2A6, works to eliminate nicotine from a person’s system. Its level of effectiveness at this task is determined by the inheritance pattern of the gene within an individual. If the individual has either homozygous recessive or heterozygous alleles, the nicotine is metabolized very little if at all because less or no proteins are being synthesized to perform that task. However, if the person has a homozygous dominant inheritance pattern, then the nicotine they introduce into their system is metabolized normally, meaning the person might crave more. The lucky twenty percent of the population with a recessive or homozygous genotype maintain more than normal amounts of nicotine in their system and don’t need to replenish it, leaving them with little or no craving for a cigarette, which would tip the balance of nicotine even further out of line. Even if a person with an abnormal genotype does begin smoking, studies have shown far less trouble quitting (De Sousa). Another benefit of this gene defect is less efficient conversion of procarcinogens into carcinogens, which drastically reduces the probability of the development of smoking-related cancers. Though this genetic link provides a conclusive reason for why some members of society are impervious to the addictive qualities, it is a different genotype that explains the psychological link to increased dependence.
. Most smokers smoke cigarettes to maintain nicotine levels in the brain, primarily to avoid the negative effects of nicotine withdrawal, but some also smoke to adjust their mood. Dopamine, a chemical enzyme utilized in brain activity, serves as a neurotransmitter, transporting and receiving messages between nerve cells, under normal circumstances. However, some substances (such as cigarettes and alcohol) change the function of dopamine into a mood or pleasure enhancer by increasing the amount of it flowing in the brain. Recent studies have isolated a specific dopamine transmitter genotype, SLC6A3-9, which causes a dopamine deficiency that creates the psychological need to smoke. The gene that SLC6A3-9 is a genotype of is responsible for the number of dopamine receptors a person has, meaning the impact of the dopamine “reward” is determined by the person’s genotype. Either A1A2 or B1B2 inheritance patterns of SLC6A3-9 have less receptors than normal, which means the natural “feel-good” effect of dopamine is lacking. People with this genotype are therefore naturally predisposed to depression. The effects of dopamine on people of this genotype are more pronounced, in that nicotine creates their “reward” by signaling the SLC6A3 gene to synthesize more receptors and dopamine is released increasingly in parallel as soon as it can be compensated for. Smokers with this genotype begin to rely on nicotine to feel “normal” as their receptors numb from over stimulation and the creation of more is a psychological necessity (Seppa). Further psychological connections with the SLC6A3-9 genotype also have been found to increase the probability that a person will start smoking.
Genes have been known to influence an estimated 50% of the personality, and the effects of the SLCA3-9 genotype on the personality are significant. Those with the aforementioned A1A2 or B1B2 allele inheritance patterns have a significantly higher curiosity to seek novelty (data supporting this, table 3) (Hamer). Though less statistically clear, it has been found that some manifest other related characteristics such as reward dependence and persistence, which are instrumental in the effectiveness in cessation programs. Regular smokers exhibit higher and lower levels of stress and arousal, respectively, than nonsmokers, as well as higher impulsivity. The curiosity for novelty is arguably a manifestation of an individual’s lack of dopamine according the findings of Dr. Hamer; in fact it is merely the brain signaling for more dopamine to be introduced into the system. Attention Deficit Disorder and severe depression can in some ways be accounted for as more serious manifestations of this lacking. These effects are widespread, in fact, Nicotine dependence is the single most common psychiatric diagnosis in the United States. It is interesting to note the increasingly established ties between race and smoking prevalence that are in fact tied to the SLC6A3-9 genotype. African-Americans and Native Americans have been shown to have a higher probability of inheriting this genotype, explaining some of the demographics mentioned earlier (Lerman, et all). New research results such as these have shown scientists that smoking is a far more complex human behavior than how society has come to view it. However, in understanding the deep psychological, genetic, and demographic roots to the problem the future of fighting it becomes brighter.
If new scientific knowledge is taken into account, a reformatted anti-smoking movement could potentially save millions more lives by shifting advertising foci and creating better cessation programs. Research has shown it is one in three adolescents (average age in America to begin smoking is 17) are predisposed to find nicotine pleasurable and it is they who will grow into lifetime smokers. The key to solving this problem is preventing these genetically inclined one in three from ever sampling their first cigarette. One scientist theorizes that if those at risk are identified at an early age and educated, smoking in the United States would decrease drastically (Pomerleau). To help those already addicted, the structure of cessation programs need reorganization based on the new genetic information available. Though nearly all smokers have made serious attempts to quit, only 20% of the population has been able to effectively do so (Jegalian). Many of the smokers who have found it difficult or impossible to quit may have the A1A2 or B1B2 genotype that leads to the deep psychological dependence that many don’t know they have. If this theory holds true, scientists will be able to restructure the psychoeducation and pharmalogical aspects of the programs to better suit this genetic predilection (Hamer). Simply being able to run a quick screening of smokers seeking help for their genotype could help many undiagnosed depressives get more efficient help. Smoking is undeniably a multifaceted issue that cannot be ignored, and fortunately more and more society is recognizing this.
Today, efforts to stem the tide of cigarette smoking have been largely unsuccessful. Even within North America, where governments have taken the lead in providing funding as well as effective legislation to educate the public, 30% of the adult population smokes (Jegalian). But the fight against smoking is on the cusp of great changes for the better. In the United States especially, society has given a huge amount of publicity to the issue. The media has stepped up in unexpected ways, with movies like The Insider providing highly visible support. Politicians, beginning in 1962 with then-Surgeon General Luther L. Terry, have stepped up and taken a stand on the issue. And in light of new research on the dangers of secondhand smoke and a growing death toll, very few people are still willing to argue that smoking is a private issue. However, there remains to be any acknowledgement on the movement’s part of the genetic or even the deeper psychological issues that are now fairly undeniably associated with smoking. There is a strong sense that smoking is a matter of choice, and that those who have significant troubles quitting or don’t even want to try are weak willed. This Darwinist viewpoint coupled with semi-ignorance is what perpetuates the tobacco industry, takes large sums of money away from other worthy causes, and most importantly claims millions of lives a year. In order for the world to stop unnecessary deaths related to smoking, there must be increased research and more action taken with the information now available.
References
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Jegalian, Karin. “Smoking out the cause of addiction: Genetic coding may affect how
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