In two previous posts, I addressed issues in defining addiction, how the brain’s reward circuitry is involved, and suggested that addiction may be influenced by a highly maladaptive form of learning in unconscious parts of the brain that are highly resistant to conscious influences. In this post, I briefly address the role of genes and environment in addiction.
How do genes affect addiction?
While genes clearly contribute to addiction, they do not cause addiction! The way genes contribute is by providing a predisposition that may or may not be expressed depending upon environmental circumstances.
Addiction does sometimes runs in families and many human behavioral genetic studies have used family data to estimate the heritability of addiction to various drugs. While estimates vary, all find a heritability greater than zero with the average of all the studies being around 0.5. A heritability of 0.5 would mean that, on average, 50% of the differences seen among individuals are caused by underlying genetic differences and 50%, by underlying environmental differences. However, heritability is a population statistic that tells you nothing about specific individuals.
Clearly some individuals appear more predisposed than others and require less drug exposure, although we have little understanding of the genes that might be involved. There is some evidence that the sensitivity of the brain reward circuitry and functioning of the frontal lobe may be different in some predisposed individuals. In other cases, it may be as simple as the varying sensitivities of brain receptors to respond to the drug and/or of the body to degrade and remove the drug. However, single genes with large contributions to addiction liability have not been discovered. The genetics likely involve many genes interacting in complex ways that may be somewhat different from one person to the next.
At the same time, some genetic predispositions may be from genes promoting behaviors that, for whatever reason, simply increase the likelihood of using an addictive drug. Although using a drug doesn’t necessarily result in addiction, it does statistically increase the likelihood. In the following, I provide some examples.
A genetic predisposition to alcoholism might be whether you like the taste. For example, one genetic strain of mice (C57BL/6J) prefers water adulterated with alcohol while another (DBA/2J) avoids it altogether. Similar preferences in humans could promote alcohol use and, in some of those who abuse it, result in addiction. Addiction to other drugs might be affected by similar ‘likes”.
When I was approaching adulthood in North Texas, we thought it “manly” to be able to “hold your liquor” and admired peers who could drink a lot with minimal outward effects (not sure what this says about me). However, we now know that such individuals are significantly more likely to become alcoholics. Again, this trait doesn’t dictate that you will become an alcoholic, but it does increase the likelihood. This principle likely applies to other addictive drugs as well. People less responsive to an addictive drug’s incapacitating effects will likely consume more of it, and more regularly, thereby increasing the risk of addiction.
In addition, many psychiatric conditions are associated with increased addiction risk. The increased likelihood seen among untreated individuals with ADHD is thought to be related to their higher impulsiveness and lower self-control. In the case of individuals suffering from schizophrenia, bipolar disorder, anxiety, or depression, the effects of the addictive drug sometimes overlap those of the therapeutic drugs used to treat these disorders (there is no clear boundary between addictive and therapeutic drugs!). While the initial motivation may be self-medication for symptomatic relief, with abuse, addiction is a potential outcome.
Conversely, if you avoid a drug, addiction to it is impossible. In the earlier example, an innate dislike for the taste of alcohol should provide protection against alcoholism. Additionally, there are individuals possessing a defective enzyme that allows the toxic buildup of aldehyde after drinking alcohol. These individuals experience extremely unpleasant symptoms, almost never drink alcohol after their first experience, and are at virtually no risk for developing alcoholism. A defective enzyme for nicotine degradation similarly reduces the risk for becoming an addicted smoker. At the same time these protections would not affect risk for other drugs.
So, genes are clearly involved in addiction, but the paths by which they exert their effects are often indirect and variable from person to person.
How do environmental factors contribute?
Although the focus here has been on genetic factors, the environment is approximately equally important. As with genes, the environment’s contribution is complicated and may vary from addict to addict. Like genes, environmental factors that promote drug use, or even drug access, are associated with a higher risk. Peer pressure, low educational opportunities, scarce job opportunities, low recreational opportunities, and environments in which drug dealers are role models, are all associated with a higher risk. Additionally, stress is definitely a factor in precipitating drug use. While I have focused on biological factors in my blogs on addiction, any comprehensive understanding of addiction must take environmental factors into consideration as well.
To learn more.
Advocat, Comaty & Julien (2019). Chapter 4: Epidemiology and neurobiology of addiction. In Julien’s Primer of Drug Action. Thirteenth Edition. Worth Publishers. 267-295. (A good textbook that I last used in my teaching. Many references to primary literature at the end of this chapter)
Charles P. O’Brian. Drug use disorders and addiction. Chapter 24 in Goodman and Gilman’s The pharmacological basis of therapeutics. McGraw-Hill Publishers. (written for medical professionals so fairly technical)