Now, if we look at the research, it’s certainly possible to say that there is a genetic component to addiction—that is to say, in general, certain variations in certain genes can increase the risk of developing certain addictions. (A story on the subject in the journal Nature reports that, “Joni Rutter, director of the Division of Basic Neuroscience and Behavioral Research at the US National Institute on Drug Abuse in Bethesda, Maryland, says that regardless of the drug involved, “about 50% of the risk is genetic, within a range of about 40–60%.”) But it is also absolutely true that genetics are only a part of the picture, and that you may very well have inherited genes that increase your risk of addiction to alcohol or cocaine (for instance) and yet still go through life without ever becoming an addict. In order to understand how genetics can affect risk, let’s take one example from recent research into a gene that regulates a neurotransmitter called anandamide.
Anandamide is a peculiar molecule; it is structurally very closely related to the same molecules found in marijuana that produce pleasure: the cannabinoids.
In a lengthy and fascinating story on this subject for the New York Times, Dr. Richard Friedman, a professor of clinical psychiatry at Weill Cornell Medical College, wryly notes:
“By now you must be wondering why on earth we have cannabinoid receptors in our heads in the first place. In fact, they are among the most numerous receptors in our brains. And while we’re on the subject, we also have opioid receptors and nicotine receptors that are lock and key with opiates and nicotine. The body makes its own endogenous “keys” for all these receptors. As for the benzodiazepine receptor, the brain manufactures the calming neurotransmitter GABA, which binds very close to the benzodiazepine site, the place where anti-anxiety drugs like Valium and Klonopin bind. Well, if you believe in intelligent design (count me out), you would have to credit the creator with a really wicked sense of humor to have hard-wired our brains for such varied temptations, to say nothing of the fact that, neurobiologically speaking, some of us are barely tempted at all. It’s all very unfair.”
In other words, we react to drugs the way we do because we already make substances in our brains that are chemically like those drugs!
The final pathway for every single substance that causes addiction, whether it’s alcohol, cocaine, marijuana, or what have you, is the dopamine system. As we’ve already seen, a dopamine release in the brain causes sensations of pleasure in itself, and also sets up a “reward circuit”—having experienced pleasurable associations with a particular substance, we feel compelled to “reward” ourselves by seeking it again. And if you happen to be more likely to release a lot of dopamine when a certain drug molecule is present—well, you’re more likely to become addicted.
In the same story, Friedman tells the tale of a gene for another substance: FAAH (which stands, if you’re interested, for fatty acid amide hydrolase.) FAAH is a protein, and like every protein in the body, the instructions on how to make it, and how much to make it, and when, are all “written down” in genetic code on a specific gene. The specific kind of protein FAAH is, is an enzyme—a kind of chemical screwdriver that can take other proteins apart, changing or deactivating them. The job of FAAH in the brain is to deactivate anandamide.
Anandamide is specifically responsible for regulating anxiety, and as it produces calmness and relaxation when released (it’s often called the “bliss” molecule) if you make less of it, you are probably going to be more prone to anxiety; in fact, many people who use marijuana do so exactly because the cannabinoids in pot (specifically, tetrahydrocannabinol) helps them cope with anxious feelings. Interestingly enough, however, there is a variation in the FAAH gene, which some people have, that weakens it—people with this variation make less FAAH, and since FAAH’s job is breaking down anandamide, that means if you have the variant, you have less FAAH and more anandamide. As it turns out, people with this variation are not only generally less prone to anxiety; they also actually have an aversion to marijuana.
Friedman writes:
“People with the variant FAAH gene are less anxious and are thus less inclined to like marijuana. They actually experience a decrease in happiness when smoking marijuana, compared with those with the normal FAAH gene, who find it pleasurable. If you naturally have more of the real thing you understandably have little use for marijuana.”
Remember how addiction works: you take in a substance, which boosts levels of dopamine in the brain’s pleasure centers. Those pleasure centers then communicate with centers in the brain involved in memory and planning: you remember having a good time, and you start planning to have a good time again. But in this case, a variation in a gene makes it likely that instead of having a good time when you smoke pot, you’ll actually become unhappy, dislike it and actively avoid it in the future. It works the other way, as well. In a review of the research into the connection between dopamine and cocaine addiction, published in 2004, a team of researchers at Columbia University discussed the connection between the gene that partly determines, in simple terms, how sensitive key parts of your brain are to dopamine. If there’s a variation in that gene that reduces sensitivity (in technical terms, by reducing the number of dopamine receptors) then there is a significantly higher risk of cocaine addiction (think of it this way: if you are less sensitive to dopamine, you need more dopamine to get the same bang for the buck.)
The question we all find ourselves asking after digging around in the latest research is, of course, does that mean if I got the short end of the stick genetically, that I’m doomed to be an addict? The answer is: absolutely not. Genetics can increase risk, sure, but that’s just one very small, and maybe not even the most, important part of the picture. Environment, upbringing and exposure to stress are just a few of the factors that can absolutely trump genetics in making it more or less likely you’ll develop an addiction. In the same Nature journal article mentioned earlier, author Maia Szalavitz discusses the role played by stress in what is known as epigenetics. “Epi” means above, or outside—as in “epidermis” the outermost layer of skin—and epigenetics is the science of understanding what increases or decreases the activities of certain genes. It is epigenetic mechanisms that in part, control whether or not certain risk factors can become real rather than theoretical problems.
Szalavitz writes: “Another factor that affects both epigenetics and addiction risk is childhood trauma. Severe stress in early life is known to dramatically increase the risk of addiction, and the risk increases with greater trauma exposure. For example, a recent study of the entire Swedish population showed that people who as children either lost their parents, experienced a parent’s diagnosis of cancer or witnessed domestic violence had twice the risk of a substance-use disorder later in life compared with those who did not have such stressful experiences…
“Indeed, some risk genes, such as those linked to the serotonin transporter, may not cause any problems unless there is a stressful early environment. Both chronic stress and addiction can induce some of the same epigenetic changes in stress systems and in those involved with pleasure, which may partly explain why addiction and trauma are so tightly linked.”
And the list of examples in which environment may be more important than genetics goes on and on; it’s well known, for instance, that if you put primates in stressful situations, they’re more apt to become cocaine addicts regardless of genetic risk factors under study.
It’s tempting to say, “Well, okay, if I have a gene variation that puts me at risk, it may not make it certain that I will become an addict, but it still means I have to beat the odds.” But again, it’s not that simple. You might have to struggle to beat the odds if you had a stressful or traumatic childhood—but if you didn’t, you might not at all; in fact, you can go through life without that particular “at risk” gene ever causing you trouble at all. We all want easy, broad answers, but the more research is done, the more clear it is that the real science of addiction suggests that addiction is the end result not of a single problem, but of many, many factors working together. And most importantly, science increasingly suggests that in medicine, as well as public policy, one-size-fits-all approaches are doomed to fail many, and that we need to pay attention to what the latest research is telling us if we want to craft treatment solutions with the best chance of working.
Regina Walker is a regular contributor to The Fix. She last wrote about the role of DBT in the treatment of addiction as well as the ACE test to predict future addiction.
Original Article from TheFix.com
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