Читать книгу The Therapist's Guide to Addiction Medicine - Barry Solof - Страница 12
ОглавлениеThe Brain Anatomy and Chemistry of Addiction
It takes two elemental factors to produce an addicted individual. First, it takes a substance or behavior that stimulates the reward center of the brain. The reward center is located in an area called the limbic system, in the midbrain. The midbrain lies below the prefrontal cortex, under the “thinking” brain that thinks consciously and makes decisions. Stimulating the brain reward center requires an action (for example, eating or sex) or the ingestion of a substance via smoking, swallowing, snorting, or injecting that is experienced as “rewarding,” or in other words, pleasurable.
Broccoli and aspirin don’t stimulate the reward center of the brain, but alcohol, marijuana, Xanax, Valium, heroin, opioid pain medications, cocaine, and crystal meth do. Food, chocolate, and sex all stimulate that part of your brain, but certain drugs actually “hijack” the reward center by causing the brain to release excessive amount of chemicals (called neurotransmitters), resulting in a much higher level of pleasure than the normal everyday things that people generally get pleasure from.
The second elemental factor is that with enough time and experience using mind- and mood-altering substances, the brain chemistry of the now-addicted person is so out of balance that he or she can no longer derive pleasure from normally pleasurable activities. The addict has stimulated his or her brain so much with extraordinarily chemically rewarding substances that life’s normal, everyday pleasures are no longer rewarding. Drugs end up displacing the normally pleasurable activities of eating, drinking, and having sex. Drugs distort the functioning of the brain’s reward center to the point that addicted persons believe they have to take them in order to survive. Only abstinence over time in recovery can return them to what is called allostasis, or a steady state in the brain. Allostasis refers to the ongoing adaptive efforts of the body to maintain stability (homeostasis) in response to stressors.
It takes both of those components to turn a nonaddicted person (a cucumber, to use our analogy from the first chapter) into someone who is addicted (a pickle), plus several other factors we don’t fully understand. We know that addiction is partly genetic. Research generally seems to indicate that addiction has about a 65 percent genetic component and a 35 percent environmental and interactional component. Thirty-five years of experience in addiction treatment leads me to believe that the genetic influence is greater than that, but these are the figures most often cited.
Alcohol and other drugs hijack the reward center of the brain. Mind- and mood-altering substances do this by releasing a hell of a lot more of the neurotransmitter dopamine than chocolate or sex. But by itself, that process is not necessarily enough to produce the disease of addiction. If it were, every single person who uses substantial quantities of these substances would become addicted, but that is clearly not the case.
When I was young I experimented with drugs myself. I’m in my sixties now, so I guess you can say I’m a product of the sixties. Back in the sixties it seemed as though everybody was doing LSD. Then there was the cocaine epidemic of the eighties and I remember doing a line of cocaine here and there and smoking pot at parties. Fortunately, I never became addicted (remaining a cucumber in our ongoing analogy) perhaps because (1) I was lucky and (2) I never had a genetic predisposition to addiction.
Addiction is a family disease because it affects everyone in the family system in which it occurs, but also because it runs in families. Addiction runs 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
www.nida.nih.gov Used courtesy of R.D. Schwartz-Bloom & G.G. de Nunez
Most mind- and mood-altering drugs generate high levels of pleasure in the reward center by increasing dopamine levels. If the nervous system can be considered a highway that transports people mentally and emotionally, dopamine functions as the car that travels the highway of the nervous system. If you’re driving and press the gas pedal to the floor, you’re going to go really fast. But if you keep your foot on the accelerator, not only are you at great risk of getting into an accident, but you will eventually run out of gas—and that’s what happens with the repetitive use of substances that takes place in addiction.
Almost all drugs of abuse exert an effect on dopamine levels, causing a release of and/or preventing reuptake of this neurotransmitter. Interestingly, in addiction treatment we don’t see too many people come in because they’re addicted to LSD and other hallucinogens because these drugs affect serotonin though not dopamine levels. Stimulants such as cocaine and crystal meth cause the biggest increase in dopamine levels, effectively flooding the brain with it. Figure 3 shows dopamine flooding the synapse between neurons subsequent to the ingestion of cocaine. Not only does cocaine stimulate the release of extraordinary amounts of dopamine, but it also inhibits the reuptake of that dopamine, effectively blocking it from entering the next neuron. As a result the dopamine remains in the synaptic space much longer. This is what creates the incredibly intense high users describe.
FIGURE 3
www.nida.nih.gov Used courtesy of R.D. Schwartz-Bloom & G.G. de Nunez
However, the massive release of dopamine also means that the brain’s supply of it is rapidly depleted, precipitating an equally intense crash as the car runs out of gas.
Cannabinoids are neurotransmitters linked to pain modulation. Cannabinoid receptors share some properties with opiate receptors in that they are involved with nociception, the ability to feel pain. So the cannabinoid receptors are anti-pain receptors and their activation can also cause sedation. Cannabinoid receptors are activated by cannabinoids, generated naturally inside the body (endocannabinoids) or introduced into the body externally as cannabis or a related synthetic compound. When people smoke marijuana, they experience sedation.
The GABA system is where the depressants or “downers” come into play. GABA is the chief inhibitory neurotransmitter, so it is involved with alcohol and tranquilizer use. Use of alcohol, Xanax, and Valium makes the individual feel calmer, sleepier, and less anxious via activation of the GABA receptor system. And GABA binds to the sub-receptors and activates secondary messengers, which have an effect on dopamine as well. Glutamate is the principal excitatory neurotransmitter, but it is also involved in the regulation of learning and memory. It binds to the NMDA receptor and is implicated in many of the excitatory chemical reactions.
Neurotransmitters can be viewed as the electrical plugs and receptors as the electrical outlets that neurotransmitters fit into. Every cell in our body has many types of receptors on it. Receptors allow substances, such as dopamine, to enter cells. Without receptors a substance can have no effect because it cannot enter the cell. An agonist is a substance that binds to a specific receptor and triggers a response in the cell. Agonists can be drugs, medications, or naturally occurring chemicals that interact with nerve cell receptors to stimulate drug actions or effects. For example, if you sprain your ankle, your body is going to release natural cannabinoids and natural opioids (known as endorphins) that bind to their specific receptors and decrease pain.
All neurotransmitters—serotonin, dopamine, glutamate, endorphins, cannabinoids, etc.—have specific receptors in the brain that they plug into. For example, opioid pain medications bind to endorphin receptors in the brain and their effects are limited by the number of receptors present. The neurotransmitter receptors that are involved in addiction are
the dopamine receptor,
the opioid receptor,
the glutamate (NMDA) receptor,
the GABA receptor,
the cannabinoid receptor, and
the adrenergic receptors.
There are three major opioid receptors. The mu receptor is the key to opiate addiction. Some of the other receptors have more to do with pain, but the mu receptor, when it’s ignited, triggers the most dramatic psychoactive response. When opioids attach to the mu receptors, dopamine is released, causing pleasurable feelings to be produced. As opioids leave the receptors, pleasurable feelings fade and withdrawal symptoms (and possibly cravings) begin.
The structures in the brain that these neurotransmitters activate and that are involved in the addiction cycle are the prefrontal cortex, the nucleus accumbens, and the ventral tegmental area (VTA). The reward pathway connects the VTA to both the nucleus accumbens and the prefrontal cortex via this pathway. The neurons of the VTA release dopamine in the nucleus accumbens and in the prefrontal cortex.
In 1953, experiments by James Olds and Peter Milner revealed first glimpses of the neuroanatomy of the reward pathway of the brain. They discovered that rats would press a bar to receive a pulse of electricity through an electrode implanted in a specific area of the brain. This electrical stimulation of the reward pathway proved to be so powerfully self-reinforcing that rats would press the bar at rapid rates for fifteen to twenty hours until exhausted, all the while ignoring food, water, and in the case of mothers their pups, in order to continue to receive the stimulation.7
Subsequent research on how drugs activate the reward pathway demonstrated that rats and monkeys will compulsively self-inject cocaine intravenously, to the neglect of food, water, and mating, even with females in heat. When access to the drug was unlimited, they would self-inject until they died. Using cocaine to stimulate the reward pathway in the brain became the animals’ highest priority in life—everything else took a backseat.8, 9
There is a substantial body of research, including stimulation studies, ablation studies, blockade studies, and neuroimaging studies that support the influence of the reward pathway in determining behavior. Stimulation studies involve exciting or arousing the test animal by placing a lead (electrode) in the reward center of the brain. Ablation means surgical destruction of anatomy of the reward pathway. When the anatomical structures of the reward pathway are taken “offline,” test animals will no longer respond to cocaine or other drugs because they can no longer stimulate the part of the brain that evokes pleasure. Pharmacological blockade involves blocking the effect of a neurotransmitter at a cell-surface receptor by a pharmacologic antagonist bound to the receptor, effectively filling the electrical outlet so the plug cannot be inserted. Blockade studies use chemicals to stop a particular receptor from firing.
Neuroimaging studies are used to provide images using brain-scanning technology to assess the effects of acute as well as long-term substance use on brain structure and functioning. A variety of brain-imaging techniques are used, such as the SPECT, MEG, PET, fMRI, and QEG. The SPECT, or Single Photon Emission Computerized Tomography, scan uses a radioisotope combined with a pharmaceutical that is injected into the patient to measure cerebral blood flow. The SPECT scan measures brain receptor activity and involves a long exposure—up to six hours—after an injection to conduct the brain scan.
With PET (Positron Emission Tomography) scans, a small amount of radioactive sugar is injected into a vein and a scanner is used to make computerized images that illuminate areas of increased glucose metabolism or receptor activity. It only requires a very short exposure.
The fMRI (Functional Magnetic Resonance Imaging) scan compares the difference in the blood flow in the brain between conditions and activity like thinking, seeing, touching, and hearing to find regions of the brain that are associated with one task and not another. It involves a very short exposure and can be repeated as often as desired because there’s no radiation.
The QEG (Quantitative Electroencephalogram) scan is also known as a “brain map.” It’s a computer analysis of a brain wave signal that’s compared against a reference database. It’s often used for research studies. A MEG (Magnetoencephalography) scan is a technique for mapping brain activity by recording magnetic fields produced by electrical currents occurring naturally in the brain. Its applications include localizing regions of pathology before surgical removal, determining the functions of various parts of the brain, and neural feedback.
To be an effective addiction therapist, you don’t have to completely understand all the subtleties of neuroanatomy and neurochemistry, but it is important to have a working familiarity with the parts and processes of the brain that are involved in the addiction cycle.
Stimulation, either electrical or chemical, of the nucleus accumbens and ventral tegmental area (VTA) is intrinsically rewarding, while stimulation elsewhere in the brain is not. The reward can be interrupted by severing the nucleus accumbens/frontal cortex fibers or by using medication like dopamine blockers. This is how researchers came to know that blocking can interrupt natural reward pathways.
There are patients in psychiatric hospitals, for example, who are on antipsychotic medications and often appear to lack emotion. Affect is the outward manifestation (facial expression, tone of voice, body language, etc.) of an emotion such as sadness, happiness, and excitement. Sometimes patients on certain psychiatric medications have very flat or unresponsive affect. Many of the psychiatric medications that block the neurochemistry that generates psychosis have an unfortunate side effect of also blocking the dopamine receptors. As a result, people on such medications may have difficulty experiencing pleasure, have a narrow emotional range, and have a very flat affect. However, without these medications, patients’ active psychosis returns.
As I mentioned earlier, dopamine is the primary transmitter that activates the brain’s reward center. It is the release and inhibition of reuptake/reabsorption of dopamine that generates experiences of pleasure and reward, and in turn, reinforces behavior. All mind- and mood-altering drugs ultimately act via the dopamine pathway. The longer someone uses alcohol or other drugs, the more of the substance(s) he or she needs to use in order to get the same high. This is the phenomenon of tolerance—a neuroadaptation wherein a substance no longer “works” and a higher dosage is required to achieve the same effect.
Neuroadaptation refers to the process whereby the brain compensates for the presence of a chemical in the body so that it can continue to function normally. The brain is always attempting to maintain a state of balance or homeostasis. The way it works is that the first time you use drugs, especially a stimulant, but with any kind of psychoactive drug, you get a big boost in your mood, you feel euphoria from the substantial release of dopamine in the brain’s reward pathway. And then the next time you do it, you still feel good, but not as high as the first time, and the third time, not as high as the second time. And then eventually, you never get the same high anymore and you start feeling lower and lower. That’s neuroadaptation.
Continued usage causes a gradual decrease in the number of receptors for the substance, along with a corresponding gradual decrease in the amount of available transmitters due to a feedback mechanism in the brain that seeks equilibrium.
The brain squirts out a certain amount of dopamine when you have sex or eat chocolate, but if you’re getting a lot more dopamine stimulation from drugs (exogenous stimulation), the brain stops making its own dopamine (from endogenous production). That is because the feedback loop is informing the brain there is more than enough dopamine “on board” already. The fact that the brain makes less dopamine explains why, when people stop using crystal meth, cocaine, or other stimulants, they generally feel depressed and lethargic for up to several weeks or even months. Their brain has been depleted of dopamine and they don’t have enough to maintain a normal mood. It’s like trying to drive a car with an empty gas tank.
The process goes like this: Continuing use creates an increased number of receptors and a decrease in the amount of available neurotransmitters. As the individual develops a tolerance to the drug, more of the drug is required to get the same high or rush. As the brain adapts to the presence of the drug through repetitive use, there is an increased need both for the drug and for greater quantities of it to maintain normalcy. These are the neurochemical dynamics of substance dependence.
Now let’s look at withdrawal from alcohol and other drugs. Addiction counselors and therapists have to help patients manage the abstinence state and help patients learn and practice recovery skills. As a physician I have to manage alcohol and other drug intoxication, and I have to manage patients in withdrawal.
How do we treat patients in various states of intoxication and withdrawal medically? The emergency rooms are full of people on all kinds of drugs. Many hospital emergency rooms just let the alcohol-intoxicated patients lie there in a subacute area and “sleep it off.” The nursing staff monitors their vital signs (blood pressure, temperature, pulse, and respiration) and makes sure that patients don’t go into acute withdrawal.
Some drugs can have a terribly uncomfortable withdrawal syndrome but they’re not medically dangerous. At least the withdrawal syndrome isn’t dangerous. A classic example is opiates/opioids. When people withdraw from heroin, Vicodin, Norco, or related drugs, the withdrawal is miserable and painful but in and of itself, it won’t kill anybody. No one dies from opiate withdrawal; they die from opiate overdose.
However, other drugs like alcohol, benzodiazepines, and barbiturates can have a very dangerous withdrawal syndrome that can lead to death. When a patient withdraws from alcohol or Xanax or Valium, especially in combination, it can become highly dangerous. Patients can suffer hallucinations, seizures, and DTs and die from alcohol and sedative-hypnotic withdrawal. The severity of the withdrawal always depends on how long someone has been taking the drug and the dosage he or she has been taking, but if the use of these kinds of drugs is discontinued abruptly, the result can be death from strokes and seizures.
Remember that tolerance is a physiological and neurological adaptation to the presence of a drug. After tolerance develops, abrupt discontinuation of the drug causes a recognized withdrawal syndrome to occur. Each class of drug results in a withdrawal syndrome that is characteristic of that class. There are recognized signs and symptoms that are very characteristic of opiate withdrawal syndrome, alcohol withdrawal syndrome, stimulant withdrawal syndrome, marijuana withdrawal syndrome, sedative-hypnotic withdrawal syndrome, nicotine withdrawal syndrome, etc. And when someone is getting off multiple substances, these withdrawal syndromes appear in combination.
All these withdrawal syndromes involve an autonomic response. In other words, they activate the autonomic nervous system. The autonomic system is the part of the peripheral nervous system responsible for regulating involuntary body functions such as blood flow, heartbeat, digestion, and breathing. This system is further divided into two branches: the sympathetic division regulates the fight-or-flight response, while the parasympathetic division helps maintain normal body functions and conserves physical resources. So the autonomic nervous system governs functions like your heart rate, pulse, temperature, and blood pressure (the so-called vital signs). Substance withdrawal causes an autonomic nervous system disturbance, which results in physical shaking, elevated blood pressure, and elevated temperatures and can be very, very serious. It causes activation of the thalamus (a structure in the limbic system that connects areas of the cerebral cortex that are involved in sensory perception and movement with other parts of the brain), the locus coeruleus (LC), and the frontal cortex (FC).
Returning to the subject of neurotransmitters and brain structures, let’s look at the example of an Asian-American male, age twenty-three. He started using tobacco at age thirteen and cannabis at age fifteen. This is not unusual. He didn’t like alcohol because it caused facial flushing (redness of the face). Asian people often lack aldehyde dehydrogenase, one of the enzymes that break down alcohol, and they get especially unpleasant side effects from drinking. On weekends he started snorting heroin, gradually progressing to using it three nights a week. Subsequently, he added crack cocaine to his using regimen, which caused rapid deterioration in a number of areas in his life. This is not an atypical progression for an addicted person.
He began to engage in low-level drug dealing to help support his addiction. Increased availability led to escalating use, and he began injecting opiates and cocaine. He was then admitted for treatment. From the standpoint of the neurotransmitters, the available supply of dopamine has been depleted from the repetitive use of stimulants. The patient had become irritable and depressed, anergic (lacking energy), and anhedonic (unable to experience pleasure), because his dopamine was so depleted. Basically, he ran out of gas and was operating on empty. The patient’s increased impulsivity, and, to an extent, his depression, were manifestations of the depletion of serotonin.
Moreover, his use of opiates resulted in his brain putting a hold on its production of endorphins (the body’s naturally occurring pain-relieving chemicals). Depleted endorphins cause poor sleep, anhedonia, and decreased pain tolerance. With a minor pain, a normal person may take a Tylenol or a Motrin. In contrast, a person addicted to opiates/opioids may end up at urgent care or in the emergency room pleading for Vicodin. This can certainly be a form of drug-seeking, but it also reflects a phenomenon known as opioid-induced hyperalgesia. When you’re on opiates for a long time it changes your perception of pain. You actually become more sensitive to pain rather than less sensitive. For people who are on opiates/opioids, including prescription pain medications, for a long time, even little things hurt like crazy. Thus the twenty-three-year-old male patient’s addiction can be traced to the action of neurotransmitters interacting with certain structures in his midbrain—the biological underpinnings of addiction.
Certain drugs are used for specific effects in particular circumstances. For instance, a lot of serious substance abusers and practicing addicts drink alcohol, smoke pot, and take benzodiazepines or opiates to bring them down from stimulants, from the “speed rush” or the “cocaine high.” Brain chemistry also appears to play a role in what types of mind- and mood-altering substances people prefer, insofar as certain groups of people seem to gravitate toward certain classes of drugs. In my experience, depressed patients seem to be attracted to depressants, including alcohol. Many patients with bipolar disorder seem to love stimulants.
Patients with attention deficit disorder (ADD) or attention deficit hyperactivity disorder (ADHD) often seem to like stimulants, too. And the curious thing about stimulants is that when “normal” people ingest them, they get stimulated, but for people with ADHD who take stimulants, the effects are paradoxical—stimulants seem to calm them down. Addiction treatment professionals sometimes hear patients say, “Whenever I did coke or meth it made me feel more normal. It leveled me out.” Sometimes the use of stimulants is a form of self-medication for ADD/ADHD.
The neurochemistry of these individuals is different from that of other people. This is why psychostimulant medications such as Ritalin and Adderall are prescribed for kids with ADHD. Now, ADHD is overdiagnosed and these medications overprescribed, but there are many kids with ADHD who have great difficulty sitting still in a classroom without Ritalin or Adderall. Paradoxically, these stimulants calm them down and help them concentrate.
People with psychotic disorders frequently use a tremendous amount of nicotine and pot. If you’ve ever worked in a psychiatric hospital or with people who struggle with psychotic disorders like schizophrenia, you’ve observed how many cigarettes they tend to smoke. Somehow, this fits with their brain chemistry, and the action of smoking and the effects of nicotine and marijuana are subjectively soothing to them. By the way, intoxication can be confused with psychiatric conditions. When somebody comes in to the emergency room wired and manic from using large quantities of meth or cocaine, even an experienced psychiatrist cannot distinguish that drug-induced state from a psychiatrically-based manic decompensation.
However, the average person with an addiction problem who goes to a treatment facility will receive treatment primarily from addiction counselors unless he or she is in a state of acute intoxication, requires medically supervised detoxification, or has a co-occurring psychiatric condition that requires medication. It’s important for addiction therapists to understand that they are going to treat the vast majority of addicted persons, whereas physicians will be involved in the treatment of a relative minority of them—though there will likely be some gradual shifts as more pharmacological options become part of the addiction treatment continuum.
As I’ll cover in detail in later chapters, there are an increasing number of approved medications being made available for use in addiction treatment and there are many more in the research and development pipeline. The development of these medications is an exciting innovation of which addiction counselors need to be aware. Although addiction counselors can’t prescribe these medications, they nonetheless have a responsibility to let clients know that these medications are available and have the potential to be beneficial. Addiction treatment can take a variety of forms, and there are many paths to recovery. Irrespective of one’s personal position on the issue of medication-assisted addiction treatment and medication-assisted recovery, withholding this kind of cutting-edge information is a form of malfeasance on the part of therapists. It’s as if a patient were to see a therapist for depression and the therapist treats the patient month after month through psychotherapy, without ever informing the patient that there are antidepressant medications that might also help. It’s unethical for addiction therapists not to let clients know what all of their options are.
Medication is certainly not always necessary, but sometimes it can make the difference between someone improving or not. I once saw a patient who went to a therapist for many years for treatment for her depression. The patient’s depression became progressively worse until she became practically vegetative. She was extremely lethargic, to the point that she wouldn’t move. She had to be psychiatrically hospitalized, at which point we did some basic blood tests and found that she had severe hypothyroidism, a condition characterized by abnormally low thyroid hormone production. We prescribed her thyroid supplements and within a few days she was significantly improved. She would not have gotten better no matter how many years of psychotherapy she underwent. It’s not that the therapist in this case was “bad,” but she didn’t have a comprehensive-enough knowledge base and didn’t think in terms of potential physiological explanations for the patient’s distress and the possible need for medical care.
One question that arises often is, is it fair to tell patients about medications that they can’t get due to lack of insurance coverage? Therapists have a responsibility to let their clients know that these resources exist. Hopefully, with the implementation of the Affordable Care Act in the United States, more people will have access to more and better insurance coverage and the care it pays for. Ideally, in my opinion, we would have a national health insurance plan like they have in all the other countries of the modern world. ASAM, the American Society of Addiction Medicine, has weighed in on this issue, and you can take a look at their position reports online.
The issue of when and how to best utilize medication in the treatment of addiction and mental health conditions can be very complex. Addictive disorders are treatable brain diseases. Research is identifying the neurobiological mechanisms that are involved, and this increasing understanding will facilitate the development of effective targeted pharmacotherapies. An understanding of the neurobiology of addiction destigmatizes both the patient and the treatment and can help everyone understand the why and how of otherwise baffling symptoms. In an optimal world, counseling and psychopharmacology are integrated. Effective addiction treatment needs both.
CHAPTER TWO NOTES
4 National Institute on Drug Abuse, “Twin studies help define the role of genes in vulnerability to drug abuse” (1999), http://archives.drugabuse.gov/NIDA_Notes/NNVol14N4/Twins.html (accessed June 13, 2013).
