Genetic variations account for a substantial portion of differences in smoking behaviours, ranging from 40% to 75%.
A recent study conducted at the University of Colorado Boulder delved into the intricate relationship between genetics and smoking behaviours, shedding light on how genetic variations influence nicotine addiction. Published in Drug and Alcohol Dependence, the research explored the impact of a well-known smoking-related genetic variant, SNP   rs16969968, dubbed “Mr. Big,” and its interaction with other genetic differences on smoking habits.

Lead study author Pamela Romero Villela, a PhD student in the Department of Psychology and Neuroscience, explained the significance of comprehending genetic factors in smoking. Genetic variations account for a substantial portion of differences in smoking behaviours, ranging from 40% to 75%. Understanding these genes and their interactions can help in developing personalized strategies for smoking cessation.

“Mr. Big” or the single nucleotide polymorphism (SNP) rs16969968, is located in the CHRNA5F gene, which affects nicotine’s binding to brain receptors. Individuals with the AA version of the SNP are less sensitive to nicotine and therefore tend to smoke more.

However, the study uncovered additional complexities. Analysing genetic data from 165,000 smokers of various descents, the researchers identified genes and variants outside the CHRNA5F region that interact with Mr. Big, influencing smoking habits differently.

Specifically, individuals carrying the risk-boosting version of Mr. Big along with another genetic variant, rs73586411, smoked significantly less than expected. This discovery suggests the existence of another variant that mitigates the effect of SNP rs16969968.

Including a polygenic risk score in smoking cessation programs

To this effect, the study proposed the development and inclusion of a “polygenic risk score” in smoking cessation programs. These would consider gene variants and interactions for personalized smoking cessation recommendations. In fact, preliminary studies indicate that individuals with high-risk genotypes in the CHRNA5 region, may benefit more from medications targeting nicotinic receptors.

Marissa Ehringer, a professor of Integrative Physiology and study co-author, stressed the importance of understanding genetic interactions for personalized medicine. By deciphering the genetic complexities of nicotine addiction, researchers could develop tailored strategies to aid smoking cessation, ultimately improving public health outcomes in the face of smoking-related deaths and nicotine addiction challenges.

Women have a harder time quitting

Meanwhile, a recently published study from the University of Kentucky, delved into why women may face greater challenges when trying to quit smoking, pointing to the role of oestrogen in nicotine addiction. Led by Sally Pauss, researchers found that women become dependent on nicotine faster than men and encounter more difficulty in quitting.

The study explored the connection between oestrogen and nicotine addiction, focusing on the role of olfactomedin, a protein in the brain’s reward system. Nicotine was found to suppress olfactomedin production, while oestrogen enhances it. This interaction between nicotine, oestrogen, and olfactomedin is believed to explain why women have a harder time giving up nicotine.

Study author Sally Pauss, under the guidance of Associate Professor Terry D Hinds Jr, highlighted the potential of their research to address the gender disparity in nicotine addiction treatment. Pauss emphasized the significance of their work in improving the lives of women battling substance use. By confirming oestrogen’s role in driving nicotine seeking and consumption through olfactomedins, drugs targeting these pathways could be developed to facilitate smoking cessation for women.

Teens of smoking parents are more likely to take up smoking

On the other hand, the study, “The associations of parental smoking, quitting and habitus with teenager e-cigarette, smoking, alcohol and other drug use in GUI Cohort ’98,” examined the association between parental smoking and quitting, with smoking and other substance use among teenagers.

The study sample consisted of 6,039 participants aged 9, 13, and 17/18 years old. The compiled results indicated that parental smoking was significantly associated with increased risk of teenage use. While smoking cessation by the primary caregiver was linked to lower risks of teenager smoking, e-cigarette use, and other drug use.

Non-surprisingly, primary caregiver smoking behaviour has stronger associations than that secondary caregivers, and exposure to smoking at age 13 has a greater impact than at age 9. The study implies that habits and lifestyle factors play a role, with wealth being protective against teenage smoking. The findings suggest that prevention interventions should target both caregivers and their children to address the complex interplay between parental smoking and teenager substance use.

In conclusion emerging research is showing that addiction is a complex issue, and therefore requires targeted and tailored treatment programmes. The factors mentioned in these studies are indicative of why prohibition is an outdated strategy that in actual fact has never worked.

New Research May Have Cracked The Code of Nicotine Addiction in Teens

 

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