Lynne72 wonders about the efficacy of her Loved One’s use of naltrexone and other medications to treat multiple addictions.
My son has multiple addictions- gambling, alcohol, klonopin, food. He recently stated on naltrexone and two days later he went to Las Vegas for business and says he has no cravings. How long does it take for the drug to work.
Also a psychiatrist told him that he isn’t making dopamine and is suggesting a drug to raise dopamine levels. My question – do these strategies work?
Thanks for reaching out with this question. It’s an important – and interesting – one. Let’s look at these issues separately, starting with the naltrexone.
Naltrexone does not actually reduce cravings. It works by shutting down the possibility of feeling high when you drink. The euphoria and the stress release that comes on early with the first couple drinks just doesn’t happen. The person is therefore less motivated to continue to drink. Over time, the person doesn’t bother to pick up that first drink because it is useless. It is not rewarding – it simply does not provide the pleasurable feelings they previously experienced with those first few drinks. This is the theory behind the The Sinclair Method which we reference in the Resource Supplement. For some people, simply knowing that a drug won’t work is enough to stop them from picking up that drug. I have seen this work beautifully for some. By the way, this is the theory also behind naltrexone for opioids. It shuts down the effects of the high of the opioid.
Dopamine is definitely implicated in addiction as are other neurotransmitters. A neurotransmitter is responsible for transmitting a signal in between nerve cells (neurons) in the brain. It’s a complex subject and it’s always a challenge to distill the scientific information into easily digestible language. Nora Volkow, the head of the National Institute of Drug Abuse (NIDA), recently wrote that:
Dopamine (DA) is considered crucial for the rewarding effects of drugs of abuse, but its role in addiction is much less clear. This review focuses on studies that used PET to characterize the brain DA system in addicted subjects. These studies have corroborated in humans the relevance of drug-induced fast DA increases in striatum [including nucleus accumbens (NAc)] in their rewarding effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as their subjective reinforcing effects) are markedly blunted compared with controls. In contrast, addicted subjects show significant DA increases in striatum in response to drug-conditioned cues that are associated with self-reports of drug craving and appear to be of a greater magnitude than the DA responses to the drug. We postulate that the discrepancy between the expectation for the drug effects (conditioned responses) and the blunted pharmacological effects maintains drug taking in an attempt to achieve the expected reward. Also, whether tested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in striatum (including NAc), which are associated with decreases in baseline activity in frontal brain regions implicated in salience attribution (orbitofrontal cortex) and inhibitory control (anterior cingulate gyrus), whose disruption results in compulsivity and impulsivity. These results point to an imbalance between dopaminergic circuits that underlie reward and conditioning and those that underlie executive function (emotional control and decision making), which we postulate contributes to the compulsive drug use and loss of control in addiction. (our italics) Addiction: Beyond Dopamine Reward Circuitry
It is complicated. Here is my lay opinion:
There are psycho-pharmacological drugs that increase dopamine, either by creating more dopamine or encouraging better reception of dopamine at receptor sites. Your son may want to pursue these psychiatric drugs to see if they help.
In general, however, there is a lack of study and understanding of how withdrawal – both from illicit and prescribed drugs – affects dopamine and other circuitry in the brain. This is a shortcoming within the field of treatment for Substance Abuse Disorders and the psychiatric drugs used to support non-use, and it’s a great pet peeve of mine.
Volkow says that the drop in dopamine when the drug is stopped is lower than controls (I’ve italicized the passage).
With “Dopamine Agonist Withdrawal Syndrome (DAWS)” the body has trouble getting back to normal levels of dopamine (assuming it even started at normal levels). Here’s a passage about one type of dopamine drug used to treat Parkinson’s that theorizes what is going on:
Dopamine agonist withdrawal syndrome (DAWS) is a recently described syndrome where patients withdrawn from long-term treatment with dopamine agonists experience a constellation of neuropsychiatric and autonomic symptoms. It was first described by Rabinak and Nirembergé in a cohort of patients with Parkinson’s disease (PD), where most were withdrawing DA because of the development of impulse control disorders (ICD). Others have since published larger case series of PD patients confirming the common symptoms (depression, anxiety, fatigued, dysphoria, irritability, agitation, pain, sleep disturbances, diaphoresis and orthostatic hypotension) and that the overwhelming majority of patients who develop DAWS on withdrawal of DA experienced ICD while on DA. https://jnnp.bmj.com/content/85/4/471
So, there is evidence that providing artificial bumps in dopamine levels can disrupt your own natural “production” of dopamine. My assessment….
Just to complicate things even more, note that this passage talks about withdrawing patients with Parkinson’s from anti-parkinsonian drugs (whose function was to increase dopamine) because with these drugs, the patients developed an impulse control disorder (in fact, many started to gamble for the first time). Very interesting.
Anti-parkinsonian drugs have been used “off label” to treat persistent depression, which is how I first came to be on one. What I am giving you here is what I found out when I came off that drug and ended up with the withdrawal syndrome they describe. I am now very protective of my natural dopamine production, so I avoid any drug that would alter its levels. In my opinion, I probably never had healthy levels of dopamine to start with, or lost a healthy balanced level in childhood, from the effects of trauma and persistent unrelenting fear. But the withdrawals I experienced from those drugs lasted several months!
I hope this helps. If nothing else we see from this discussion of dopamine that Substance Use Disorder affects brain circuitry in serious, unrelenting, ways.
Once caught in the cycle of drug use, dopamine levels can shift both up and down. Maybe they started “down” to begin with, or maybe they get stuck in the lower levels. There are likely individual differences in how this plays out. The effects of low dopamine sound remarkably similar to withdrawal from many drugs: “depression, anxiety, fatigue, dysphoria, irritability, agitation, pain, sleep disturbances, diaphoresis and orthostatic hypotension.”
So what does all this mean for your son? Your son wants to end his drug use, and his gambling and food addictions. Pharmacologic drugs can be immensely helpful. Dopamine is implicated in compulsive disorders, including drug misuse. It is worth addressing mental distress and addiction with the help of a psychiatrist. But go carefully and read all you can. Make sure your son talks with a professional about withdrawing from any drug he is put on so that he knows what to expect.
Recovering from drug addiction is a journey. Your son has found a path towards that recovery. We are so glad to hear this, and we are glad you are here on the site. Best wishes to you both.