Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Never Start, or Quit as Early as Possible: Because genetics is only a tendency, the highest-impact action stays in your hands: not starting, or stopping if you already smoke. Quitting at any age brings real health benefits, and the earlier you quit, the more risk you reverse - over years, the excess risk of heart disease and lung cancer falls substantially toward that of people who never smoked. If you have never smoked, a higher genetic score is a reason to keep it that way. World Health Organization
Combine Support With Your Own Plan: Quitting works better with structured support than on willpower alone. Counseling, motivational interviewing and telephone quitlines each help, and combining them beats any single approach. Planning a quit date and identifying your triggers in advance are the parts you can start on today. US Preventive Services Task Force
Use a Free Quitline or Quit-Smoking Service: Free, evidence-based support is widely available. In the United States, calling 1-800-QUIT-NOW connects you to a trained coach, and smokefree.gov offers a build-your-own quit plan, a free app, and a text-message program. Pairing this kind of structured support with medication is one of the most reliable ways to quit for good. Smokefree.gov (National Cancer Institute)
Modify Your Environment and Address Triggers: Remove smoking cues - discard cigarettes, lighters, and ashtrays - and steer clear of settings where you used to smoke. Identify and plan ahead for high-risk situations such as stress, alcohol, and social gatherings, since these are common relapse triggers. Smoking rates are also higher among people with depression, anxiety, or ADHD, so treating a co-occurring mental health condition alongside cessation tends to improve outcomes. CDC, How to Quit Smoking
How much of this is genetic?
Genetics explains 50% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Maes et al. 2004, Psychol Med
Background and further reading
Smoking behavior covers several distinct things: how likely someone is to ever start smoking, how much they smoke, how dependent on nicotine they become, and how hard it is to quit. What your genetics capture here is a tendency, not a verdict - whether you smoke at all is a choice shaped heavily by your environment. The stakes are high because tobacco use remains the leading preventable cause of death. Smoking causes more than 480,000 deaths each year in the United States alone [1], and tobacco kills over 8 million people worldwide annually [2]. Inherited differences influence how rewarding nicotine feels, how quickly the body clears it, and how difficult cessation becomes - but none of that fixes whether a person smokes.
Genetic Basis: Twin studies estimate that genetics accounts for roughly 40-60% of the variation in smoking behavior, with the figure tending to be lower for whether someone starts and higher for nicotine dependence once they do [3]. The strongest single signal sits in the CHRNA5-CHRNA3-CHRNB4 gene cluster on chromosome 15, which encodes nicotinic acetylcholine receptor subunits - the direct molecular targets of nicotine. A common variant there, rs16969968 in CHRNA5, is robustly associated with smoking more cigarettes per day, greater nicotine dependence, and higher lung cancer risk [5]. Separately, the CYP2A6 gene encodes the main enzyme that breaks down nicotine; variation in it makes people faster or slower metabolizers, which shapes how much they smoke and how they respond to cessation medication [6]. The largest GWAS to date, from the GSCAN consortium, has scaled up enormously: an initial study of up to 1.2 million people identified 566 variants across 406 loci [4], and a later multi-ancestry analysis of up to 3.4 million people mapped thousands of associated variants, implicating nicotinic, dopaminergic, and glutamatergic signalling [7]. Each common variant contributes only a tiny effect.
Environmental Factors: Environment is decisive for whether smoking starts in the first place: peer smoking, parental modelling, advertising, socioeconomic deprivation, and cultural norms all strongly predict uptake, and most people who smoke begin in adolescence [1]. Stress and adverse childhood experiences raise both initiation and dependence risk. On the other side, tobacco control policies - taxation, advertising bans, and smoke-free laws - have driven large declines in smoking [2]. Gene and environment interact: an inherited vulnerability to nicotine dependence is far more likely to express itself when there is easy access and social permission to smoke. This is why a higher genetic tendency is not destiny - the single most protective step, never starting or quitting, stays firmly within a person's control.
The published research behind your score, and the variants it draws on.
42 published scores from 6 studies
The smoking behavior score combines 42 polygenic scores drawn from 6 published studies.
Centers for Disease Control and Prevention. Cigarette Smoking. CDC, Smoking and Tobacco Use (2024)
World Health Organization. Tobacco. WHO Fact Sheets (2023)
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
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