In 1988, two Italian researchers called Gaetano Di Chiara and Assunta Imperato showed that regardless of the class of drug, all drugs (whether sedatives, stimulants, opioids or even nicotine) released dopamine at the Nucleus Accumbens. Multiple studies since seem to concur that all drugs and behaviours that are addictive, ride off the brains reward system (which is predominantly a dopaminergic system).

(For further reference see Volkow et al, Johnson et al, Corrigal et al, Adinoff and Shaffer et al).

If a drug or behaviour does not activate the brain’s reward system, then it is generally considered to have little addictive potential. Feelings of reward facilitated by brain dopamine are the basic mechanism by which addicts becomes addicted, and so the real question is, why do some people seek vastly increased amounts of brain dopamine through drug use or other behaviours, while others do not? To put it another way, why do some people need more reward than others?

In previous articles I have explored the environmental factors that are causative of addiction. In this article, I will explore the neurophysiology that predisposes some people to addiction more than others.

Reward Deficiency Syndrome

The National Institute on Drug Abuse (NIDA) suggest that part of the answer to what causes addiction might be genetic. According to NIDA genetic factors may play a role in approximately half of all addictive disorders. Among those genes that have been the most intensively studied, are the Dopamine (D2) receptor genes.

In 1990, a professor of pharmacology at the University of Texas called Ken Blum, and Ernest Noble, a professor of psychiatry at UCLA, discovered a link between a variant of the dopamine D2 receptor gene (called the A1 Allele) and alcoholism, which they published in the journal of the American Medical Association. A number of other studies they conducted throughout the 1990s further linked the D2 receptor gene to obesity, gambling, and Post-Traumatic Stress Disorder (PTSD). 

Blum and his colleagues did go to some lengths to point out that the A1 allele was not (as many people wrongly thought) a ‘gene for alcoholism’, but rather, a gene variant that caused poor dopamine function.

According to Blum and his colleagues, this reward gene (or unrewarded gene to be more accurate) strongly predisposed people to addictive disorders and other pathologies because it downregulated their dopamine function leaving them feeling catastrophically unrewarded and unmotivated. He coined the term reward deficiency syndrome to describe this naturally occurring disability.

Below, are some of the symptoms of reward deficiency that were noted by researchers. (It should also be noted that these symptoms are often observed by lay people, such as those participating in 12 Step programmes, and that they often report symptoms BEFORE the onset of addictive drug use).

  • Restlessness, irritability and discontentedness.
  • A marked inability to deal with stress.
  • A compulsive need for novelty and reward.
  • Difficulty in finding any meaning, importance or purpose in life.
  • Mind crushing boredom (the like of which most people will never experience).

In Blum’s theory then, these debilitating symptoms came first, and the drug use came second. The drugs weren’t the symptom. The drugs were the solution. They were a way to medicate the symptoms of a primary illness THAT WAS ALREADY THERE. The listless feelings brought about by this hypo-dopaminergic state, forced the sufferer to find powerful external rewards like drugs to feel normal. In Blum’s model therefore, the object of addiction — the ‘drug’ — was less relevant than the fact that a potent source of dopamine needed to be found to medicate the sufferers poor unrewarded brain. While people’s sociological or demographic differences influenced their choice of drug, the only real criteria was that something had to be found to up-regulate their dopamine function. Thus, while the reward deficient boy from a poor housing estate may have easier access to crack, methamphetamine or heroin, and little to lose by using it, the reward deficient middle class businessman may be required to find more socially acceptable routes to dopamine activation such as alcohol or work. In the final analysis however, they stem from the same neural disability – reward deficiency.

Reward deficient people just don’t have enough brain dopamine to feel like life is worth living. While you may find reward and meaning in the ordinary pleasures of life: walking the dog, being social, or playing chess with your friend — the reward deficient person can’t work out why it is worth his while to get up out of the chair for such trifles. Consequently, by adolescence most reward deficient people will have discovered that using drugs makes life tolerable. Once they have found out how to shore up their miserable feelings (by using drugs and another potent rewards) they tend to want to repeat those experiences — for glaringly obvious reasons.

Imagine being deaf your whole life and then being given a drug which allows you to hear. Imagine that you are then swept away to the most acoustically awesome amphitheatre in the world where an orchestra are performing Wagner’s Ring cycle (or some equally talented individuals are performing genius works of death metal, if that’s more to your aesthetic preference). Then imagine that the drug is wearing off and you’re back in your lonely bubble. Well that’s what an addict’s first using experience is like.

A Critique of Dopamine Theories of Addiction

Many researchers have criticized the genetic explanation of addiction (and the dopamine theory in general) for being overly ‘reductionist’; in other words, for over-simplifying the condition. Prominent among these critics have been Professor David Nutt, the former UK Drugs Tsar for Tony Blair’s government. Nutt and his colleagues argue that viewing Dopamine as the main protagonist in driving addiction is misleading. According to Nutt, a ‘search for dopamine’ would only be relevant with reference to particular drugs, namely stimulants such as cocaine and methamphetamine (and to a lesser degree alcohol) because these are the only drugs that release brain dopamine to any significant degree. Opioids, cannabis and other drugs, they argue, do not release brain dopamine dramatically enough to medicate any hypothesized hypo-dopaminergic state. (A state of ‘low’ dopamine).

A Critique of the Critique

In light of more recent theories about addiction, particularly the incentive salience model (see my previous article here I would say this. It is not so much the ‘amount’ of dopamine that is being released by any given drug that is relevant, but only the fact that dopamine is involved in recording anything useful, and then in strongly remembering it and prioritizing it in the future. This is what really underlies the process of addiction. Addiction is a learning process. A diabolical learning process to be sure, but a learning process nonetheless. And not only is the reward itself remembered, but also all of the people, places and things that were around us when we were doing it. These associated stimuli, which on the face of it seem so irrelevant; a piece of foil, a certain song, the smell of a cigarette or the noises emanating from a pub — can become the very things that trigger us the most. These often-innocuous sights, smells and sounds bedevil addicted people in early recovery. In terms of relapse, they are as potent, if not more potent, than the drugs themselves.

And it is this function of dopamine – the laying down of useful memories – that is key. It may well turn out to be the case that addicted people are ‘low dopamine’, either by birth, or by way of catastrophically unrewarding early environments, but that is not the point. The point is, that anything we view as important (even if it isn’t) can raise dopamine tone. In the end, we are not addicted to the ‘drug’ – we are addicted to the ‘process’. We are addicted to the meaning contained in it. In a world bereft of meaning, the energy conferred by cocaine; or the body image conferred by starving yourself or taking steroids; or the sense of achievement and community amongst gamers; or the emotional safety and respite provided by an opioid – all these can be experienced as incredibly meaningful. It is this – a sense of meaning and purpose – that really lies behind addiction (and the reason dopamine is so central to it).  Addiction is a search for something important, in a world where nothing is important anymore.

To me, and to many other people with a history of addiction, the reward deficiency model rings true. We were ill before the drug use began. When we stopped, the symptoms returned. Addiction isn’t what you look like when you are using drugs. The illness is what you look like when you stop using drugs. It’s that listless, unmotivated, restless, bored an irritable mindset. A mind-set that would do almost anything to escape the hellishly unrewarding moment of ‘now’.