in families through genetic transmission. As I noted in Chapter One, most people who use alcohol or other drugs don’t become addicted. If you’re speaking with a group of addiction treatment patients or people in recovery and ask them to raise their hand if they have a biological relative—mother, father, grandparent, uncle, aunt, brother, or sister who struggled with addiction, you’ll see most every hand go up.
NIDA-supported research has studied patterns of drug use in pairs of identical versus fraternal twins in order to clarify the roles and interrelationship of genetic and environmental risk factors in the development of drug use, abuse, and addiction. Researchers examined the patterns of marijuana and cocaine use by female twins and found that genetic factors play a major role in the progression from drug use to abuse and addiction. This research supported other studies that showed family and social environmental factors to be influential in determining whether an individual begins using drugs. The findings further indicated that the progression from the use to abuse or dependence was due largely to genetic factors.4, 5, 6
Although it’s not the case that someone has to have a family history of addiction in order to become addicted, the reality is that genetics play a significant role in the development of addiction.
What seems to be the science behind the statistics is that people inherit a biological vulnerability to addiction. It’s called biological vulnerability or susceptibility to addiction, so if your mom or dad or grandparent or aunt or uncle was addicted to alcohol, you’re more likely than someone without that family history to become addicted yourself. However, it doesn’t have to be to the same drug.
Addiction is a disease that encompasses many different substances. Addiction is about substance-generated neuroanatomical and neurochemical changes that have profound similarities across a wide range of substances. The genetic component seems to result in an increased susceptibility to those substance-generated neuroanatomical and neurochemical changes that take place in addiction.
Addiction also runs in families through other factors that are related to the environment in which someone grows up, such as social learning and observation. People who grow up in addicted families see how their parents or other relatives handle the stress of life by drinking and doing other drugs, and learn this as a primary coping strategy as well. Mommy gets depressed or anxious so she has a few drinks or smokes some pot to feel better. One’s community, neighborhood, and peer group are also powerful environmental influences. If substances are easily accessible and substance use is common where you grow up, you are much more likely to become addicted. If the group of friends you hang out with are all using regularly, you’re likely to use regularly as well. So the development of addiction is part genetic, part environmental, and part experiential/neurochemical.
The balance of this chapter will focus on the anatomical areas of the brain involved in the reward pathway; the neurotransmitter systems that activate the reward pathway; the receptors activated by psychoactive drugs; and the anatomical areas of the brain involved in withdrawal from psychoactive drugs. I’m going to dedicate this section of the book to the mice, rats, and monkeys for their contribution to our knowledge in this area of science!
Throughout the history of medicine, there have been various theories of addiction. Historically, addiction was thought to be a form of spiritual possession, and this provided the origin of referring to alcohol as “spirits.” Sometimes the behavior of addicted persons seems more animal than human. This is typified by the aggressive behavior and lack of attention to hygiene and other basic forms of self-care frequently associated with active addiction. At various times, addiction has been considered a moral failing, an indication of personal weakness, or a lack of willpower, especially in the Western hemisphere and the United States where historically we tend to demonize addicts. There are many people, even in the twenty-first century, who continue to hold this archaic view. The inability to handle stress except with the aid of alcohol or other drugs has become a popular explanation for addiction.
Fortunately, perspectives on addiction have become more enlightened, evolving into its current conception as a disease and chronic health condition. Interestingly, the disease model of addiction was actually endorsed by AA as early as the 1930s. In 1956, both the American Osteopathic Association and the American Medical Association released formal statements reporting the definition of alcoholism as a disease.
As I mentioned earlier, the current understanding of addiction is that there exists a reward pathway in the brain that is activated by pleasurable and survival activities such as eating food, imbibing water, and having sex, but is turned on to a much greater degree by mind- and mood-altering drugs. Other things that can stimulate this reward pathway include positive things like nurturing and caring for others, as well as less-healthy activities such as gambling, and thrill-based activities such as hang gliding and riding roller coasters. Ultimately, if we didn’t have this reward pathway we could neglect to eat and forget to reproduce, but the fact that these substances and activities give us pleasure causes us to repeat the behaviors associated with them.
It’s important to have at least a basic understanding of the different parts and processes of the brain that are involved with the reward pathway because they are fundamental to addiction. There are neuropeptides that activate the various chemical receptors and act on the reward pathway. Neurotransmitters are chemicals that relay, amplify, and modulate signals within the brain, transmitting information between neurons (nerve cells). Neurons consist of several parts, including dendrites, a cell body (called a soma), an axon, and terminal branches. Neurons are separated by gaps or spaces known as synapses. As the brain’s chemical messagers, neurotransmitters must find receptors on other neurons in order to transmit the messages they contain. Figure 1 shows the neurotransmitter dopamine waiting to be released from a terminal branch of one neuron into the synapse where it will cross over and attach to the receptors on the dendrites of another neuron.
FIGURE 1
www.nida.nih.gov Used courtesy of R.D. Schwartz-Bloom & G.G. de Nunez
It is helpful for addiction counselors to be familiar with the neurotransmitters affected by drugs. This information is also important in understanding how psychiatric medications are thought to work. There are many neurotransmitters in the brain, but we will focus on the ones that are involved with the reward pathway. Different drugs have differential effects on neurotransmitters. Marijuana and opiates/opioids can activate neurons because their chemical structure emulates that of a natural neurotransmitter. Cocaine and crystal meth, on the other hand, can cause the nerve cells to release much larger than normal amounts of natural neurotransmitters or prevent the usual reabsorption of these brain chemicals.
Serotonin is a neurotransmitter that affects mood, memory processing, and cognition. Psychiatric medications frequently “target” serotonin in order to modify the levels of this neurotransmitter in the brain. Selective Serotonin Reuptake Inhibitors (SSRIs) are a class of antidepressant medications that includes Prozac and Paxil. SSRIs are believed to modulate serotonin in the brain as their primary mechanism of action, and are often prescribed to treat depression and anxiety.
Dopamine is the primary neurotransmitter and the final activation chemical in the reward pathway. Dopamine is linked to motivation, pleasure, and motor functioning. Dopamine activates the dopamine receptors and is responsible for reinforcing behavior. Figure 2 shows dopamine exiting from a terminal branch of one neuron into the synapse where it crosses over and attaches to the receptors on the dendrites of another neuron.
FIGURE 2
