This topic was presented by Thomas TenEyck on October 21, 2007 at
West Hills Unitarian Universalist Fellowship, Portland, Oregon, at the
invitation of WHUUF’s Addressing Addictive Behaviors Committee.

Rigorous academic scientific enquiry into what causes addictions had its earliest funding started in earnest about 1970 when congress created the National Institute of Alcoholism And Alcohol Abuse – called NIAAA (“n-i-triple-a”). This was followed a few years later with the creation of the National Institute of Drug Abuse – NIDA (“ny-da”). Both of these federal agencies, housed in the National Institute of Health (NIH), gave researchers the ability to open new directions of inquiry into the etiology of drug addictions.

This led to a new definition of the term “psychoactive substance.” Previously it simply meant “drug.” Now a psychoactive drug was any substance that when injected into a rat gave rise to a scientific paper.1

So significant academic careers began to be built, and the result has been an explosion of knowledge not only about alcoholism, but all drug abuse and other behaviors that can become addictive, like gambling or shopping.

Today the science focuses mainly on the chemistry of the brain itself. Briefly, here are some things we have learned.

1) Some individuals (possibly as high as 30% of the American population) are at a higher risk than others to become addicted due to what is called “genetic predisposition.” This is true for both drug addictions and behavioral addictions.

2) The younger an individual starts using a drug the higher the risk of ultimately becoming addicted. 2

3) Drug taking or some other behaviors, when repeated frequently or compulsively, result in fundamental and long-lasting changes in the brain itself.

4) Ultimately, one reaches a point when deciding to engage in the behavior is no longer voluntary. It is now a “compulsion.”

5) The neurobiology of drug addiction is the same as the neurobiology of behavioral addictions, like pathological gambling or compulsive shopping or sex addiction.

So what is the brain chemistry of addiction, of compulsion? How does the brain change as the result of prolonged use of addictive drugs or behaviors that become compulsive? And, why do perfectly nice, seemingly rational individuals in most other areas of their lives, continue destructive behaviors despite overwhelming negative consequences.

The best way to approach these questions is to think of the brain in its evolutionary sense.

We have an “old brain” which runs our body functions, is our emotional center, and imprints survival memories. Note this again since it will be very important later: the old brain imprints survival memories. All animals have most of this old brain, which is why we share such a huge percentage of genes with fruit flies, slugs and kittens.

However, we humans have evolved over millennia a “new brain” which covers over the top of the “old brain.” This new brain allows us to speak, to reason, to create, and to consciously remember. It is what makes us uniquely human in the animal kingdom, different from fruit flies, slugs and kittens.

Think of the old brain as being the home of our “instincts” or “appetites,” and the new brain as housing our “rational selves.” The old brain, for the most part, operates below consciousness, below language.

The two brains do communicate with each other. There is a feedback loop that moves from the old brain to the new brain and back again to the old brain, which allows us (to a certain degree) to override some of our instincts or appetites. But this can be difficult at times because the old brain is very, very powerful. Remember, it houses our survival instincts.

A side note here. The area of the new brain that reasons, makes judgments and decides to override certain impulses from the old brain is not fully developed until we reach our early twenties.

Teenagers impulsive? Do dangerous and “stupid” things? “If it feels good, do it!” You bet!

And this is one reason that when youth do psychoactive drugs at an early age, they are more vulnerable to harm and more at risk of becoming addicted. First, they are not able to connect the behavior with the possible consequences. They don’t “think it through” because they don’t have the biology to effectively do that kind of thinking yet.

Furthermore, the early drug use itself stunts the growth of the parts of the new brain that ultimately would become the areas of rationality, of cause-and-effect thinking, of judgment. So the new brain doesn’t fully develop the necessary “adult” strength to better override old brain impulses.

But, back to the old brain.

In the center of the old brain is a small almond-shaped organ called the Amygdala. It produces dopamine, a powerful neurotransmitter, that when released from the Amygdala into a brain pathway called the mesolimbic dopaminergic reward pathway, it causes us to feel good, to feel pleasure, to feel satiated. Scientists also call it the “reward/reinforcement pathway.” To keep it simple, let’s call it the “on switch.”

It is basic to our survival. Indeed, when mothers tell us of the powerful surge of pleasure when their tiny baby first makes meaningful eye contact, we now know this feeling results from the surge of dopamine in this area of the brain, not only in the mother’s brain, but also in the infant’s brain!

This is the neurobiology of connection, of attachment. It is very powerful and underpins the bonding that is necessary for the infant to survive, not to mention the at times heroic selflessness required to care for infants. Parents of colicky babies know exactly what I mean!

This dopamine surge then imprints a powerful memory of the connection between the behavior and the surge of pleasure. Since it led to a good feeling, we tend to repeat the behavior. All this resides below consciousness, so we perceive these behaviors as instinctive.

Psychoactive drugs and some behaviors also stimulate the release of dopamine in this same area. There is a feeling of pleasure, of fullness, of “okay-ness,” of satiation: think of enjoying a nice glass of wine. But after feeling satiated, most individuals discontinue the behavior before it becomes maladaptive and they return to their “baseline” state of dopamine.

However, some don’t. A glass of wine has a very different meaning to them. These individuals typically have an insufficient amount of dopamine in this area. Some may have been born this way – e.g., those mentioned above who are genetically predisposed to develop addictions – and some may have damaged their ability to manufacture sufficient amounts of dopamine due to being exposed to high stress situations or living in stressful environments for prolonged periods of time. In either case, this condition of insufficient dopamine is now called the “dopamine reward/deficiency syndrome.”

When this individual who has low dopamine first experiences a drug or behavior that causes a huge surge of dopamine, the experience is not just of pleasure or satiation, but of euphoria, or of a “rush,” an extreme “high,” a “WOW!”

Then when the drug wears off, or the behavior is stopped, the person drops back to their baseline, which is actually deficient in dopamine. What before was felt as their usual state is no longer accepted as “normal” since they have now felt what it is like to have a sufficient amount of dopamine. Their usual state is now experienced as dysphoria, a feeling of emptiness, of feeling “not so good.”

Furthermore, when they are not engaged in the behavior or taking the drug, they slowly lose the ability to feel much pleasure at all – a state called anhedonia. This sets up a strong desire to continue taking the drug or repeating the behaviors again, and again, and again, and again, and on and on it goes, until it becomes a true compulsion.

Here is the kicker. The old brain now has imprinted in its memory that the way to lift the dopamine to “normal” levels is to do the drug or the behavior again. It interprets these drugs or behaviors to be connected to its natural survival mechanisms. Consequently, if the behavior is not repeated, it can end up being interpreted as anti-survival.

I can’t emphasize this enough. This is why an individual, who seems reasonable enough most of the time, compulsively continues behaviors that we see are becoming more and more dangerous to their well being, but don’t stop. The words “Just say no!” land in the new brain, but the old brain doesn’t hear them the same way. It hears “Just say yes!” This part of the brain has been hijacked, and the repetition of the drug or the behavior has actually subverted the brain’s survival mechanisms.

So now the “on switch” has become the “more and more switch.” This is the essence of craving.

Another side note here. New brain research has shown that when some of us see a piece of chocolate cake – think Rose’s Deli 24 layer chocolate cake oozing with dark, dark frosting… – when we see that gorgeous piece of cake, we have already made the decision to buy it BEFORE we engage our conscious mind in internal argument over whether we should, or should not indulge. All this thinking may be good intentions, but it is mostly useless and ends in rationalization. So much for free will!

What this tells us is how difficult it is for some of us to rationally override our old brain appetites. Ever had only one potato chip? Only one peanut? For some, only one drink?

Now here is the double whammy. Along with the old brain thinking it might not survive without doing that drug or that behavior, the “off switch” mentioned earlier in the person prone to addictions is defective either due to genetic issues or to damage from drug use or the compulsive behavior itself. The off switch is weak and doesn’t kick in soon enough. Its action is delayed so even though the individual feels satiated, s/he continues the behavior anyway.

So the on switch becomes the more and more switch and the off switch is so weak it can’t do its job very well.

This is, in short, the neurobiology of addictions. The old brain is fundamentally changed so that it feels the use of the drug or the repetition of the behavior is necessary for optimal re-balancing of a deficiency in brain chemistry, and the feedback loop that moderated pleasurable behaviors is weak and defective.

1 This observation is by Daryl S. Inaba, Pharm.D., CADC III, co-author of Uppers, Downers, All Arounders, Sixth Edition (2007).
2 From age 13 to age 21, for each year that a youth postpones the initial use of alcohol (and most likely other psychoactive drugs like nicotine), s/he reduces the risk of abuse by 8% and the risk of addiction by 14%! If abstinent until 21, the genetic predisposition is completely nullified so the risk of addiction is extremely low. (B.F. Grant & D. Dawson, “National Longitudinal Alcohol Epidemiological Survey” in Journal of Substance Abuse, 9:103.110.)


Thomas G. Ten Eyck, MA, CADC II, CGAC II, is an addictions specialist with emphasis on co-occurring disorders and pathological gambling. He has presented at international, regional, and state-wide conferences and institutes. He is adjunct faculty at Lewis & Clark College Graduate School of Counseling Psychology, Mount Hood Community College, and Chemeketa Community College. He also serves as one of Oregon's Approved Clinical Consultants to problem gambling counselors and their supervisors. Tom can be reached at teneyckt@dishmail.net