Are You Addicted?
More than 20 million Americans have diagnosed substance dependence or abuse disorders (SAMHSA, 2010). Substance use disorders are typically chronic conditions with relapse rates of at least 60 percent across all substances of abuse (Connors et al, 1996; Mackay et al, 1990; Miller et al, 2001), and by other estimates, as high as 80-90 percent, even after years of abstinence (Finney et al, 1999; Rourke et al, 1998; New York Times, 2013).
What is an addict?
The simple answer is: someone whose life is controlled by a substance, be it alcohol, drugs or other substances. The three classic elements of addiction are:
- Chemical tolerance — increased amounts are needed to produce an effect, changes in brain chemistry result and tolerance develops
- Withdrawal symptoms (e.g., nausea, sweating, irritability, tremors, hallucinations, seizures), which develop when substance use is stopped or reduced
- Constant craving, an inability to limit substance use, and, once withdrawal has ended, relapse
Are you addicted to debugs or alcohol? If you suspect that you are, you probably are. If any of the following sound familiar, it’s probably fair to say that substance use is controlling your life…
- you continue to use despite negative consequences and awareness of the physical or psychological harm to yourself or others
- your relationships, job or school performance have suffered as a result of your drug or alcohol use
- you’ve tried to stop using and couldn’t
- you regularly conceal what or how much you use and feel defensive, guilty, or ashamed about your usage
- financially subsidizing your addiction is a higher priority than meeting your financial responsibilities
- using interferes with regular sleep or eating
What’s the difference between substance addiction and substance abuse?
The terms “substance abuse” and “substance addiction” are often used interchangeably, but, in fact, denote different conditions. Substance abuse can be thought of as misuse of a substance in ways that deviate from culturally acceptable norms. Abuse may or may not include a strong motivation to continue using the substance.
Addiction always includes abuse, of course. But addiction is a behavioral syndrome in which the person’s dominant motivation is to procure and use the substance of choice and normal attempts at self-restraint are largely ineffective (Bozarth, 1994).
In addiction, the substance acts on brain reward and motivation systems, producing neurochemical disturbances that result in the substance becoming the dominant motivational factor. The “incentive value” or attraction to the drug or alcohol reward dramatically increases and the incentive value or interest in other, normal rewards decreases. This “motivational toxicity” is an aspect of addiction that requires no pre-existing conditions or special personality types, only the neurochemical action of addictive substances on brain reward systems (Bozarth, Wise, 2009).
Addiction may or may not include physical dependence (though it usually does), but is almost invariably accompanied by psychological dependence, meaning that the person requires the substance for normal psychological functioning. (Caffeine addiction might be an example.) Physical addiction is characterized by physical dependence and symptoms of withdrawal, such as disturbances in autonomic nervous system that produce nausea, sweating, chills, tremors, hallucinations, etc..
Substance abuse is easier to kick than addiction, but both are unhealthy and dangerous. Addiction can ultimately become the endpoint of a history of abuse.
When does substance use become pathological?
Activation of brain reward systems is a normal aspect of human behavior. These same reward-motivation systems exist to direct our behavior toward goals that are beneficial and promote our survival; for example, when we’re hungry, we’re motivated to seek and eat food. The direct chemical (e.g., drugs, alcohol or nicotine) activation of these reward pathways is not in itself different from the normal control that reward systems exert over our behavior. But simple activation of brain reward systems does not constitute addiction.
The distinguishing feature of addiction is the deterioration of the ability of normal rewards to govern behavior, referred to as motivational toxicity. In other words, rewards that are normally effective in influencing our behavior lose their ability to motivate us.
Drug addicts, for example, may neglect formerly high-priority rewards (e.g., career, family) in favor of acquiring and using drugs. Direct pharmacological activation of a reward system dominates their motivational hierarchy at the expense of other rewards that promote survival. The ensuing motivational toxicity distinguishes drug addiction from simple drug activation of reward mechanisms.
How Does Addiction Become Established?
Most addicts whose lives have been destroyed by addiction would tell you that if they’d known they’d become addicted, they would never have taken that first drink or drug. So why are drugs and alcohol so alluring on a cognitive level? People drink or use drugs for their own reasons. Some start casually, at social gatherings. Some use substances as a coping mechanism when their own inner resources fail them. Drinking at social gatherings for example, can be alluring because it seems to boost confidence, lower our defenses, free us from inhibitions or break the tedium of dailiness. Some overindulge to cope and avoid pain, some to relieve stress, some just because it’s “fun.”
In reality, the confidence that drugs and alcohol provide is false and fleeting, a facade. A substance cannot enhance self-respect or self-esteem; rather, substances tend to inflate ego, which under the influence of your drug of choice, may seem like the same thing but isn’t.
While a drug or alcohol can block emotional pain and may seem like a loyal friend when others fail us, avoidance coping is only useful in the (very) short term. Whatever problems you’re avoiding will still be there tomorrow. Overindulgence almost never resolves problems, but it almost always adds to them.
So, how do cravings gain power over us? There are two types of addiction-related craving: (1) Physical, such as withdrawal-based craving; (2) Memory-based craving, which is a desire that’s triggered by strong pleasure memories associated with the substance of choice. Craving, which has an obsessive component, influences thoughts. Thoughts become cravings. What you continually think about, you bring about.
Memory-based cravings can persist long after withdrawal has subsided.
Alcoholics who have abstained from drinking for months or even years are still vulnerable to their own contextual, associative drinking memories. (Ditto for drug addicts.) Environmental stimuli that are closely associated in time and space with the effects of self-administered substances — such as feelings of pleasure or euphoria — become part of the incentive or reward we’re motivated to achieve. For example, a recovering alcoholic hanging out in his favorite neighborhood bar where he’s accepted and appreciated by his old drinking buddies can increase his craving for alcohol and trigger a relapse. But those positive pleasure memories are also easily superimposed over a negative emotional state, such as depression or anxiety. Negative emotions can trigger a “bender” or binge during which we consume an excessive amount of drugs or alcohol in a matter of minutes, even as we realize that our behavior is out of control.
Some evidence suggests that having an “addictive personality structure,” a combination of traits such as impulsiveness, a predisposition to negative emotions, and requiring greater and greater stimulation to attain pleasure, can put someone at higher risk for a wide spectrum of addiction behaviors. But the most powerful cravings are usually triggered by either internal or external stimuli or cues — or a combination of both. The most difficult cravings to kick are those triggered by strong pleasure memories combined with conditioned cues; for example, habitually “relaxing with a drink” at the end of a long workday.
From Voluntary to Habitual to Compulsive…
Here’s how conditioning and reinforcement works…
Each time you reward a craving, you reconsolidate that memory of the experience (including the emotional experience), which reinforces the relevant neural circuitry and increases the likelihood that you’ll do it again in the future. We often mentally connect the anticipation and enjoyment of our substance of choice with seemingly unrelated stimuli, and once we solder in that connection to the brain’s reward circuitry, it’s hard to disconnect it.
Cues (signals or reminders) in our environment trigger and reinforce cravings through the process of classical or Pavlovian conditioning, a process first documented by Russian physiologist Ivan Pavlov, in which a stimulus (such as a particular environmental cue) comes to elicit a conditioned response (such as drinking alcohol), after a number of pairings. Pavlov famously sounded a buzzer while giving his dogs a puff of meat powder, which triggered salivation. After a number of pairings of the buzzer and meat powder, the dogs automatically salivated to the buzzer, even without the meat powder — salivation had become a conditioned response. The dogs were now conditioned to associate the buzzer cue with a food reward. Receiving the food reward each time served as a conditioned reinforcer; it strengthened the dogs’ salivation response, just as rewarding ourselves with alcohol or drugs reinforces our anticipation of the next alcohol or drug reward. When a previously reinforced stimulus presents itself, that automatic response kicks in. In other words, the more you do it, the more you want to do it. And this is what could trigger a relapse for the recovering alcoholic in our previous example who visited his old drinking buddies at his favorite neighborhood bar.
Addiction is the endpoint in a series of transitions: from actions to habits to compulsion; that is, from voluntary use to habitual use and, finally, to compulsive use.
In the human brain, drug-seeking behaviors (triggered by conditioned cues) are motivated and reinforced by several neurobiological mechanisms that act in concert to addict us and keep us addicted. The change from voluntary substance use to more habitual and compulsive use represents transitions and interactions between Pavlovian learning and “habit” learning processes.
Operant conditioning (also known as “instrumental learning”) is also at work in addiction, acting in concert with Pavlovian conditioning. For instrumental conditioning to occur, one must perform some behavior that’s ‘instrumental’ in obtaining a goal (also known as an “outcome” or “reinforcer”). For example, a lab rat must press a bar to obtain a food pellet. The food pellet is the reinforcer. For humans with substance use problems, the reinforcer is drugs or alcohol.
The persistence of habits is crucial to establishing addiction. It becomes less about “wanting” and more about “must do!” Even if “doing” has negative consequences. In studies of cocaine and alcohol self-administration, participants continued to respond habitually, even if they had to ignore or devalue negative consequences such as gastric pain (Dickinson et al, 2002; Miles et al, 2003). The drug- or alcohol-use motivation (appetitive motivation) was valued higher than the aversive motivation to stop in order to avoid significant adverse physical consequences.
Appetitive motivation refers to behavior directed toward goals generally associated with positive, pleasant processes, such as food or sex. Aversive motivation involves escaping from some unpleasant condition; for example, cold weather or the pain of an injury. Once we have progressed beyond voluntary use to habitual or compulsive use, reinforcers continue to strengthen the stimulus-response association but don’t become encoded in the brain as a goal. Extended, repeated reinforcement is effectively “training,” which leads to the development of habits, with less involvement of the goal itself. A substance habit can ultimately conquer a substance goal. We may not even need much new motivation to drink or do drugs. Habit takes over, substance misuse runs on autopilot, and a Pavlovian-instrumental learning transfer has begun. These sequential phases of Pavlovian and instrumental learning are at work in the transition from initial substance use to substance abuse, and finally to compulsive substance-seeking and substance-taking behavior — the hallmarks of addiction. The ultimate goal of the behavior (such as “feeling a buzz”) has been devalued so much that the behavior is no longer directly under the control of the original goal.
The change from voluntary substance use to more habitual and compulsive substance use also causes changes all the way down to the neural level…
Brain Systems Involved in Addiction
Cravings and addiction have neurochemical signatures. Drug and alcohol cravings influence brain dopamine, a neurotransmitter (chemical messenger) that’s heavily involved in establishing habits, compulsion and, ultimately, addiction. Dopamine regulates our pleasure-reward-motivation circuitry, controls movement/motor activity, modulates attentional systems, enhances learning, memory and the flow of information in frontal brain regions that connect thought and emotion.
Pavlovian and instrumental learning processes act in concert with a cascading loop of neural interconnectivity…
Alcohol and drugs chemically, or pharmacologically, activate several dopamine brain systems involved in pleasure, motivation, reward and for some, ultimately, in establishing addiction. One such neurochemical interface is the ventral tegmental dopamine system (i.e., ventral tegmentum), which plays a central role in regulating appetitive motivation; that is, in controlling both normal and pathological behaviors. This system eventually dominates the behavior of an addict, leading to “habit” learning and compulsive substance-seeking and substance-taking behaviors.
Cravings increase dopamine in goal-directed reward centers of the brain, including the nucleus accumbens and the striatum. These brain structures mediate the reinforcing effects of drugs and alcohol, playing key roles in the processes leading first to drug abuse and then to addiction (Everitt & Robbins, 2005). The nucleus accumbens is a pathway from motivation to action. It sends a chemical, dopamine-mediated signal that motivates us to do something about our cravings (i.e., seek drugs or alcohol).
The insula has been found to play a specific role in the conscious urge to take drugs. The insula is responsible for integrating interoceptive (bodily) states into conscious feelings and decision-making processes that involve uncertain risk and reward (Naqvi1 & Bechara, 2013).
In two areas of the striatum, another key mechanism kicks in. fMRI studies show that the ventral striatum is involved in Pavlovian conditioning; the dorsal striatum in instrumental and habit learning. Researchers often use an “actor-critic” model to help explain how the brain automatically evaluates options in decision-making, such as deciding whether to initiate or interrupt behavior. Recent research suggests that the actor and critic may play a role not only at the time of decision, but in longer-term reinforcement learning, as well.
The ventral striatum may act as the “critic” component of reinforcement learning in addiction; the dorsal striatum, the “actor” component (O’Doherty, J. et al, 2004). The critic predicts future rewards by assigning values to options and sends a training signal to the actor so it can learn which actions to take. The actor maintains information about the reward outcomes of our actions. The actor prefers appetitive learning over aversive learning and taking action, thus is heavily biased in favor of choosing reward over no-reward, even if the reward is aversive or punishing and not aligned with the critic’s choice. After long-term substance use, despite the increasing discrepancy between the critic’s “value” signal and the actor’s preference, the critic is no longer able to direct the actor toward an optimal decision, an effect that appears to only grow stronger over time. The actor, who likes instrumental learning, especially prefers that the substance be self-administered (the equivalent of pressing the bar in an instrumental learning rat experiment). The critic is silenced and substance use has just become habitual (Piray et al, 2010).
Serial, parallel communication takes place between all these brain mechanisms, controlling the neurological “switches” between drug reinforcement, drug abuse and drug addiction (Everitt & Robbins, 2005).
Co-occurrence with other mental health disorders
One particularly fiendish aspect of substance abuse is its ability to entangle its victims in a vicious web of mental health problems. Substance abuse always worsens other mental health problems. It can be both a cause and a result of other mental health disorders.
Here are some quick statistics:
- Around 43 percent of those with substance use disorders also have co-occurring mental health disorder(s) (SAMHSA, 2010).
- Around 30 percent of people with substance abuse problems also suffer from Major Depression. In fact, alcohol abuse or dependence literally doubles the risk of Major Depression.
- Alcohol and some drugs can induce depressed mood, as well as the elevated mood state associated with Mania, and, in the extreme, psychosis (e.g., schizophrenia). Studies have found that alcohol abuse may even trigger a genetic markers that increase the risk of depression (Fergusson et al., 2009).
- Approximately half of people with Generalized Anxiety Disorder also develop a substance use disorder over their lifetimes.
- More than one-fourth of adults with severe mental health disorders also have substance use dependence.
To learn how meditation influences the mechanisms of substance abuse and addiction and promotes a substance-free lifestyle, see How Sahaja Meditation Aids Substance Abuse and Addiction Recovery.
M.A. Bozarth (1994). Pleasure systems in the brain. In D.M. Warburton (ed.), Pleasure: The politics and the reality (pp. 5-14 + refs). New York: John Wiley & Sons.
Bozarth, M.A, Wise RA,. A psychomotor stimulant theory of addiction. 2009;65:189–90.
Connors GJ, Maisto SA, Donovan DM. Conceptualizations of relapse: a summary of psychological and psychobiological models. Addiction 1996;91:S5–S13.
Dickinson, A., Wood, N. & Smith, J.W. Alcohol seeking by rats: Action or habit? Q. J. Exp. Psychol. B 55, 331–348 (2002).
Everitt, B.J. and Robbins, T.W. (2005) Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nat. Neurosci. 8, 1481–1489
Finney J, Moos R, Timko C. The course of treated and untreated substance use disorders: remission and resolution, relapse and mortality. In: McCrady B, Epstein E, editors. Addictions: a comprehensive guidebook. New York: Oxford University Press; 1999. pp. 30–49.
Jin H, Rourke SB, Patterson TL, Taylor MJ, Grant I. Predictors of relapse in long-term abstinent alcoholics. J Stud Alcohol. 1998;59:640–6.
Mackay PW, Marlatt GA. Maintaining sobriety: stopping is starting. Int J Addict 1990;25(9A–10A): 1257–1276.
Miles, F.J., Everitt, B.J. & Dickinson, A. Oral cocaine seeking by rats: action or habit? Behav. Neurosci. 117, 927–938 (2003).
Miller WR, Walters ST, Bennett ME. How effective is alcoholism treatment in the United States? J Stud Alcohol 2001;62(2):211–220.
Naqvi1, Nasir H. and Bechara, Antoine. The hidden island of addiction: the insula. Trends in Neurosciences, Volume 36, Issue 2, 110-120, 18 January 2013.
O’Doherty, J. et al. Dissociable roles of ventral and dorsal striatum in instrumental conditioning. Science 304, 452–454 (2004).
Payam Piray, Mohammad Mahdi Keramati, Amir Dezfouli, Caro Lucas, Azarakhsh Mokri. Individual Differences in Nucleus Accumbens Dopamine Receptors Predict Development of Addiction-Like Behavior: A Computational Approach. Neural Computation 22, 2334–2368 (2010).
SAMHSA. (2010). Results from the 2009 National Survey on Drug Use and Health: Mental health findings. Office of Applied Studies, NSDUH Series H-39, No. SMA 10-4609.