I set out to remedy this when I founded the nonprofit HAMS in 2007. HAMS—an acronym for Harm reduction, Abstinence, and Moderation Support—is a lay-led, free-of-charge support group for alcohol harm reduction, which today has over 13,000 online participants. 

HAMS supports any positive change in regard to alcohol use, and supports members in goals they choose for themselves, ranging from safer drinking to reduced drinking to quitting altogether. What does success look like for HAMS members? The answer is different for every individual. Below are 10 stories by way of example—told in the person’s own words, edited for length, and shared with consent. All names are pseudonyms.

Wally

My HAMS story began around 2012. At the time I was drinking about a fifth of tequila and snorting about 2 grams of cocaine on a daily basis. I had been in and out of AA meetings for about 25 years, with mixed results. I quit trying the AA approach because of the toxic personalities there. 

It was at about this time that I came across a HAMS video online and it caught my attention. I’ve been following HAMS articles and using the HAMS Facebook group for support/education ever since. Over time I have been able to drastically reduce the amount of alcohol and cocaine that I drink/use. 

Some of the harm reduction techniques that I use are: counting the number of drinks that I have daily and recording them in the HAMS online drink tracker; only drinking at home by myself; drinking only after 4 pm; never driving while intoxicated; skipping drinking days; cost-benefit analysis, eating food when drinking; and smoking cannabis. I use the HAMS Facebook group for support/friendship daily, and find it highly useful. 

Most days I drink about eight shots of bourbon and use cocaine about twice a month. I’m happy with this number of drinks but have to abstain from coke ASAP. Trying to get there. Overall, my drinking/using is much much lower, and causes me far less trouble than they did before I started trying to change my habits with HAMS techniques.

“One of the biggest shifts for me is that I no longer see drinking as all-or-nothing. If I choose to have a drink, I do not see that as failure.”

Rachel

Before HAMS, I had been drinking daily for approximately three years. I never drank in the mornings and continued to maintain my professional responsibilities, so for a long time I did not see my drinking as problematic. During the height of my drinking, I would start drinking after seeing my last therapy client, and drank both socially and at home. Although I was not drinking heavily every day, there were periods where I drank to blackout. Over time, I realized alcohol had become automatic and something I relied on socially. It negatively affected my mood, social life and overall well-being. 

I first learned about HAMS while taking a drug and alcohol class where we discussed alternatives to traditional abstinence-based programs. What appealed to me was the focus on harm reduction, personal choice, and reducing shame rather than labels or perfection. 

Today, I am mostly abstinent. In the past seven months, I have only had a couple of cocktails. One of the biggest shifts for me is that I no longer see drinking as all-or-nothing. If I choose to have a drink, I do not see that as failure. Alcohol does not control me—it had simply become too important in my life, and I changed that relationship. 

The most helpful tools for me were the cost benefit analysis and the accountability culture within HAMS. Kenneth’s drink count posts were especially meaningful because everyone reported honestly—whether they had zero drinks or 10—without judgment. I also tried naltrexone, but it was not the right fit for me because I felt like it reduced enjoyment overall. I read the HAMS book and found it insightful (although I’m still hoping for an audiobook someday). 

Joe

My drinking before HAMS was excessive, especially around 2021 when I joined the group. I blacked out in Las Vegas, was denied access to my flight home and had to stay another night. That’s when I realized I had to change. 

My drinking now is more controlled, most of the time. I still go on benders when I’m stressed, but I’ve been leaning more into the A in HAMS, spending time alcohol-free so I can focus on fixing the problems in my life. HAMS gave me a community of like-minded people who don’t judge and don’t believe in “tough love,” but will also offer rational, logical advice. Also, HAMS, and especially How to Change Your Drinking, helped me understand what is going on with my brain and my behavior around alcohol, giving actual insights based on scientific studies and a more modern understanding of addictions and use disorders. 

My main tools for supporting my plan are definitely charting my drinks—I still notice a huge difference in the amount consumed if I don’t track and keep that number at the forefront of my mind while drinking—timing my drinks to better pace myself; not relying 100 percent on shots when drinking; taking regular alcohol-free periods of at least two weeks (usually longer at this point); and I create a cost-benefit analysis and written plan about every month, taking into account how I want my drinking to change. 

I am a huge fan of the HAMS book, and I read it about twice a year to keep myself accountable. I also am very active on the Facebook group, and I’ve found helping others has assisted in my own recovery journey. I didn’t join the Zoom meetings for my first few years in HAMS, but now they are something I look forward to, getting to share what’s been going on, and being able to connect with others about their struggles and wins. All in all I’ve struggled with life since around COVID, adding kids, losing jobs with long-term unemployment, and general mental health issues, but one thing that has remained constant is HAMS. I’ve tried a lot of the other groups and books […] but nothing I’ve experienced has gotten to the core of the apple like HAMS, and I’m eternally grateful.

Mary

I’m just about to hit four years abstinent from alcohol with my partner. We did it together after he puked blood from a day-long binge, and I lost a very dear friend from alcohol-related suicide and feared I might follow him. I’d come very close to checking out myself in 2021, and ended up in hospital three times in one week. We’d tried moderation but always failed miserably. 

We ran a harm reduction charity in the UK for 10 years, but when we lost our funding in 2014 we slowly slipped into a pattern of binge drinking ourselves, which soon became a nightmare for me due to the kindling effect, which I learned about in the HAMS group. 

HAMS helped me ground myself and not feel guilty or embarrassed about messing up, even though I knew all the dangers and pitfalls of drinking again inside out. It’s easy to help and advise others, but hard to apply that same compassion to yourself sometimes. HAMS was a safe space for me to vent and share without judgment. I’d had terrible experiences with AA in the past, so it’s wonderful that alternatives like HAMS exist now. 

“Being amongst others who shared similar struggles helped me understand that I am not alone and I am not the monster I was acting like.”

 

Martha

Before HAMS I was drinking two-to-three fifths of liquor a day. Drinking would make me act paranoid and erratically. My partner at the time was not helpful, and I was also struggling with my mental health. I’d cause bodily harm to myself and property damage around me when I’d have my paranoid fits. I ended up in the psych ward three different times in the first half of 2025. 

I found HAMS looking for a secular support group for drinking, because I knew my relationship with alcohol was not healthy and needed to change. I started scrolling HAMS, and being amongst others who shared similar struggles helped me understand that I am not alone and I am not the monster I was acting like. Reading other people’s success stories gave me hope I could also get out of this rut I found myself in. 

I met someone who was nice and kind, who didn’t drink, and didn’t enable that behavior. I moved in with him in September 2025. And now, almost a year later in August, I will be one year sober. I didn’t use any medications or tools to help with quitting. For me, it was about leaving behind the environment I was in. Not wanting to be in that survival mode state anymore… And surrounding myself with people who share my value of wanting to not drink. And willpower. 

I never experienced any withdrawal symptoms other than the hangxiety. I simply went to the psych hospital one final time and never took another sip after that. I took a Greyhound out of state and away from that environment. Drinking isn’t for me. I don’t know if there will ever be a day where I can casually enjoy a drink again. But if not, I’ve accepted that reality. 

Naomi

I became active in HAMS after suffering a life-threatening bout with alcohol last year. I was drinking vodka 24/7 and ended up in the ICU in critical condition. I had to call an ambulance for myself. 

Since then, I’ve joined HAMS Zoom meetings multiple times per week and have made real friends. Through support of my goals of not necessarily full sobriety, they’ve met me where I’m at. Today, I’m drinking far less, have regained partial custody of my kids and wouldn’t be here without my HAMS support network. They mean the world to me. The vodka is gone. The 24/7 drinking is gone. HAMS got me there, due to group accountability and work on my own. I have my life back with my children, and that’s a gift from HAMS I can never overstate. The Zoom calls are life-altering for me, and I’d recommend them to anyone struggling. 

Esther

I am one that chooses to be alcohol-free. Before I detoxed, I was in a cycle of blackout drinking, being sick throughout the workday until I could have a drink on the way home from work. Weekends were just a blur. I medically detoxed three times within a year. It was a never-ending cycle. 

I choose to be abstinent because I have too much to lose, as a single mother whose children lost their father to alcohol. I found the HAMS Facebook page after my last detox, and felt a sense of relief. HAMS has been immensely helpful to me because there is no judgment. I’m not flawed, I’m human. There is nothing wrong with me. My current plan that works for me has been bi-weekly therapy to deal with my trauma from my ex husband. I do utilize legal THC/CBD edibles at night, which helps with sleep and anxiety. I interact on the HAMS Facebook page. 

Grace

I stumbled across HAMS one night when I was completely wasted. I wanted to do something about my drinking, and I was like messing around on Facebook and that’s how I found it. At that time I was drinking about a handle (1.75 liters) of booze a night. 

I did the HAMS taper, and just having the support from other people who knew where I had been and being able to talk to people and communicate with people who had been there was so helpful. Now, I drink alcohol maybe once a month, about two drinks. Instead, I drink THC beverages, and that helps to curb my, you know, craving for alcohol. Actually, I’d rather drink those than alcohol now. I tried AA and that didn’t work for me. And I tried Antabuse and that was god-awful. I find the HAMS Facebook group and the Zoom meetings really helpful; in fact, I facilitate the Zoom meeting once a week. I’m totally happy that I’m not drinking like I was before, because it was going nowhere good, if you know what I mean. 

“I think one of the main things that HAMS taught me is that I’m not powerless. I’m in control.”

 

Theresa

I was in HAMS before there was even a Facebook group, back when we did a text-based chat. Someone sent me the link to the HAMS taper, and I tapered off of a half gallon of vodka a day. 

Now, that didn’t last and I ended up going back to AA. I was sober in AA for six years and I was miserable, and then I decided to try controlled drinking again and that’s when I found the HAMS Facebook group and I joined. So, both times that I went to HAMS, my drinking was out of control. 

What is it like now? It is non-existent now. I have been alcohol-free for over three years. I’m on daily naltrexone. I never have cravings. I don’t think about it. Alcohol is not a part of my life, but I’ve also rejected all of the AA norms and stigmas and slogans and bullshit that they taught me over the years. For example, the AA saying that “non-alcoholic beers are for non-alcoholics,” and you shouldn’t go to concerts alone. I go anywhere that I damn well please—because I’m not powerless, and I think one of the main things that HAMS taught me, even though I’m one of the people that are abstinent, is that I’m not powerless. I’m in control. I’m in control of my choices, and when I got away from AA my life actually began.

Samantha

I was going through alcohol withdrawal and searching the web for information because I thought I was going to die, and the HAMS website popped up. I learned about tapering with beer, and ordered a case of beer. It took me eight months to taper down to zero. 

I find the Zoom groups very helpful. It’s a sense of community. It’s like a family within a family, and there’s a lot of support—whether you’re going to moderate your drinking, or if you’re going to quit drinking or if you’re just going to be an active drinker. Everybody supports you where you’re at, and I’ve gotten a lot of support over the last six years and it’s definitely the way to go. 

I don’t drink at home anymore, so basically if I go out to dinner, I’ll have two cocktails. If I’m at a dinner party, I’ll have no more than four drinks. I’m only drinking once or twice a month now. I’m also on the Mounjaro shot, and they say that actually can help curtail some of the cravings. I’ve lost 81 pounds and my diabetes is well under control now. I don’t know if the Mounjaro is helping the alcohol, but like I said, I’m basically doing weeks on end without anything and no cravings or anything like that, and keeping it to a maximum of four drinks when I do partake. 

Photograph by Edward Howell on Unsplash

The post “No Judgment”—Ten Personal Stories of Alcohol Harm Reduction appeared first on Filter.

Aversion therapy—often involving pairing an alcoholic drink with an emetic, to condition an association with nausea—had proved highly effective for many patients who were voluntarily seeking abstinence, as Filter described in March 2023. By the 1980s, dozens of hospitals were offering it. 

The complete erasure of aversion therapy is disempowering, because it narrows people’s choices.

However, the advent of managed care led to ever-increasing competition for an ever-declining pool of patients whose insurance would pay for treatment. This led to the treatment wars of the 1980s, where each treatment modality claimed to be the best and denigrated the others as worthless. The Raleigh Hills chain of aversion therapy hospitals fell victim to political chicanery in that period and went out of business. Schick Shadel Hospital suffered a similar fate decades later, through a combination of mismanagement and COVID-19.

It is increasingly accepted today that there are multiple pathways to recovery. It’s not a one-size-fits-all proposition. Rather, different things work for different people. The complete erasure of aversion therapy is disempowering, because it narrows people’s choices. 

Richard St. Peter, who benefited from aversion therapy himself, is the former CEO of Schick Shadel Hospital. He’s also in the early stages of working to reopen it. Filter’s interview has been lightly edited for length and clarity.

Kenneth Anderson: How did you first get involved with aversion therapy for alcohol use disorder?

Richard St. Peter: I realized that I had a problem with alcohol by the 1970s. I tried AA, but it wasn’t really helpful for me because it did nothing for my cravings. Then a friend of mine took the aversion treatment at Raleigh Hills, which operated a chain of 28 aversion treatment hospitals, mainly on the West Coast. 

I was afraid that if he quit drinking, he wouldn’t be any fun anymore, but quite the opposite was true. He out-hunted, out-fished and out-dived all of us who were still drinking, and took our money playing poker. So in 1982, I decided to take the aversion treatment at Raleigh Hills myself.

KA: And how did that work out?

RSP: It was amazing! The aversion therapy took away all my cravings for alcohol completely! I stayed abstinent from alcohol for 11 years until 1993. My training is in finance, and during that time I served as CFO and executive vice president for a number of companies.

KA: What happened in 1993?

RSP: I was at a casino in Las Vegas playing poker, and I ordered a virgin bloody mary. It took a very long time for the drink to come, and when it finally did, I gulped it down because I was thirsty. But it didn’t taste right, and I told the waitress, “I think this tomato juice is rotten.” 

And she said, “No, that’s a bloody mary.” And I said, “A real bloody mary with alcohol?” And she said, “Yeah.” And I said, “I wanted a virgin bloody mary.” And she said, “Okay, I’ll bring you a virgin bloody mary.” 

A short while after that, for the first time in 11 years, I felt the buzz, and I said to myself, Well, that was stupid drinking that. And, the next day, for the first time in 11 years, I felt the cravings come back. And I thought since my career was going so good, my family was doing so good, everything was going so good, that I could become a social drinker.

“The Schick Shadel treatment worked for me when nothing else did … I believe in multiple pathways; different things work for different people.”

KA: How did that work out?

RSP: Badly. In less than a month, my drinking spiraled out of control. I woke up one morning in a pool of vomit with no idea where I was, and that’s when I realized that I had retriggered uncontrollable alcoholic drinking.

KA: What did you do then?

RSP: Well, I tried contacting Raleigh Hills, but I found out that they had gone out of business due to some rehab politicking. But then I found out that Shick Shadel in Seattle was in business and offering the same kind of aversion treatment. It was actually Schick Shadel that had first pioneered the aversion treatment for alcohol use disorder. So, I took two days of the conditioning treatment at Schick Shadel, and have never drank since.

KA: How did your connection with aversion treatment continue?

RSP: I did well in business; I got lucky and I retired in 1998, and I started joining pay-it-forward types of activities, like alumni associations for my schools, hospitals, and businesses that put me on their boards because they thought I would help them out. That’s when I was contacted by the Schick Shadel Hospital Foundation. 

They called me up and asked me if I would join. I said, Sure, I’d love to. I went to Seattle, and I was at a foundation meeting, and afterwards the hospital administrator got me and said, “I hear you’re a finance guy. We have a controller here, and we’re bouncing checks and I can’t understand his explanations. Could you come and talk to him?” I said, Sure. And we went to his office. 

His office had a front door and a back door, and when he saw me come in the front door, he went out the back door, and we never saw him again.

The hospital administrator asked me if I could just stay on for a little bit and kind of get things sorted out until we could get a replacement. I said I would do that, and I looked at their financial statements and saw that they were indeed in deep trouble. I figured out what their problem was and got them a positive cash flow within a month. A month later, the partners that owned Schick Shadel asked me if I would like to buy in. They had some shares left, and I said yes. After that, I started buying up any shares that anyone wanted to sell. That’s when they asked me to be their CEO. I stayed on as CEO until 2011.

“We could reopen as a nonprofit. I would like to make the Schick Shadel program available to anyone who could benefit from it.”

KA: Why did you leave?

RSP: Well, the Great Recession of 2008 hit, and the majority of the stockholders decided to sell Schick Shadel to Ascend Health Corporation in 2011 because Ascend Health was willing to pay them 14 times their original investment. Then, in 2012, a hospital mega-corporation named Universal Health Services, Inc. bought Ascend Health Corporation and replaced experienced addiction management with big corporate managers. 

When COVID-19 hit, the new management, unlike other hospitals, allowed medical staff to remain employed but not come to work. The census dropped, and that’s why Schick Shadel closed on June 30, 2022.

KA: And why do you want to reopen Schick Shadel?

RSP: The Schick Shadel treatment worked for me when nothing else did. My kids went through some of the best-known rehabs in the country without being helped, and then they tried the Schick Shadel program, and that’s worked for them. And now I’ve got grandkids, and I’d like the Schick Shadel program to be there for them, too, if they need it. 

I believe in multiple pathways; different things work for different people. Some people do great with AA, but others need a different kind of a program. 

KA: And what do you need to do to reopen Schick Shadel?

RSP: Well, I have money to invest, but not enough to do it all on my own. So I need to find some investors who are interested in a solid, steady return on their investment. Schick Shadel was a very profitable business for over 80 years, until these problems with COVID and management that I mentioned.

Or, if we could find a foundation to back us, we could reopen as a nonprofit. I would like to make the Schick Shadel program available to anyone who could benefit from it.

Photograph (cropped) via GetArchive/Public Domain

The post Could Aversion Therapy for Alcohol Use Disorder Make a Comeback? appeared first on Filter.

The first ever placebo-controlled randomized trial of Ozempic for AUD was published in February by JAMA Psychiatry. The study was carried out by the University of North Carolina at Chapel Hill, in cooperation with the National Institute on Alcohol Abuse and Alcoholism. The lead investigator was Christian Hendershot, PhD.

There were 48 subjects in the study: 21 were categorized as overweight (BMI of 23 or more but less than 30) and 27 as obese (BMI of 30 or more). All subjects met criteria for AUD according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). 

On average, the participants had moderate AUD (meeting an average of 4.2 DSM-5 criteria). They consumed an average of 4.2 US standard drinks on drinking days, and drank an average of 20.2 days per month. When drinking and non-drinking days were combined, they consumed an average of 2.9 drinks per calendar day, with an average of 9.1 heavy drinking days per month and an average alcohol craving score of 12.0. None of them were previously seeking AUD treatment. 

The Ozempic group showed significantly greater reductions than the placebo group in number of drinks per drinking day, number of heavy drinking days and alcohol craving scores.

The treatment consisted of injections of either a standard dose of Ozempic or a placebo, given once a week. Both the Ozempic group and the placebo group showed reductions in all alcohol-related variables over the nine-week experiment. However, there were significant differences between the Ozempic group and the placebo group on the amount of change shown for some of these variables. 

The Ozempic group showed significantly greater reductions than the placebo group in number of drinks per drinking day, number of heavy drinking days and alcohol craving scores. Differences in number of drinks per calendar day and number of drinking days were not significant, however. As a side note, the Ozempic group showed weight loss but the placebo group did not.

Ozempic is a member of a class of drugs known as glucagon-like peptide-1 receptor agonists (GLP-1 receptor agonists). GLP-1 receptors are found in the pancreas, the brain, the nerves that control the digestive system, and a few other places. In nature, GLP-1 receptors can be activated by the hormone glucagon and by glucagon-like peptide-1 (GLP-1). GLP-1 receptors can also be activated by synthetic drugs such as Ozempic. 

When the GLP-1 receptors in the pancreas are activated, they tell the pancreas to release more insulin. When the GLP-1 receptors in the brain are activated, they tell the brain that the stomach is full and that the person should stop eating. When the GLP-1 receptors in the nerves of the digestive system are activated, they tell the valve between the stomach and the intestine to close, among other things (the brain is also involved in issuing that instruction).

It is believed that Ozempic’s effects in the brain may cause it to reduce alcohol intake. Just as Ozempic tells the brain to be satisfied with smaller amounts of food, it seems to tell the brain to be satisfied with less alcohol. Ozempic’s effect on the valve between the stomach and the intestine might also be involved, because when this valve is closed, alcohol enters the bloodstream more slowly and people attain a lower BAC.

Although that recent study was the first ever placebo-controlled randomized trial of Ozempic for AUD, it was not the first such trial of any GLP-1 receptor agonist; the first concerned a drug named Bydureon (exenatide). 

Overall, Bydureon did not significantly reduce heavy drinking days compared with placebo. However, when the results were analyzed by weight category, there were some significant findings.

The Bydureon trial, conducted in Sweden with 127 subjects and reported in JCI Insight in September 2022, was not a success. When the results of the entire group were examined, it was found that Bydureon did not significantly reduce the number of heavy drinking days compared with placebo. 

However, when the drinking results were analyzed by weight category, there were some significant findings. Among 30 patients classed as obese, the Bydureon group did significantly better than the placebo group. For 45 patients classed as overweight, there was no significant difference between groups. And among 52 patients considered to have “normal” weight, the Bydureon group did significantly worse than the placebo group. 

It is unclear whether the contrasting outcomes of the Ozempic and Bydureon trials were due to differences in the sample of subjects tested or to differences in the efficacy of the two drugs. Ozempic has been reported to be more effective than Bydureon for weight loss and control of diabetes.

More research is clearly required, and several further trials of diabetes drugs for AUD treatment have been registered with clinicaltrials.gov. 

A Danish study is currently investigating whether Ozempic reduces alcohol intake in obese patients with AUD. A multisite trial with 86 locations is investigating the effects of Ozempic and other drugs on people with alcohol-related liver disease. And both a National Institute on Drug Abuse (NIDA) study and an Oklahoma State University study are currently recruiting subjects to investigate whether Ozempic reduces alcohol intake in patients with AUD.

The raft of upcoming studies, should enhance our understanding of how effective GLP-1 agonists are in treating AUD, and for whom.

Meanwhile, a University of Colorado study is recruiting subjects to look into whether Rybelsus (semaglutide in pill form) reduces alcohol consumption in treatment-seeking individuals with AUD. And a Swiss study, which is not yet recruiting, will investigate whether Ozempic increases alcohol abstinence in patients with obesity and fatty liver disease.

Other FDA approved GLP-1 agonists are dulaglutide (Trulicity), liraglutide (Victoza), lixisenatide (Adlyxin), and tirzepatide (Mounjaro). Of these four, only Mounjaro currently has registered clinical trials for AUD treatment—three of them, in fact. 

A Danish study is currently recruiting patients to study the effects of Mounjaro on alcohol intake in patients diagnosed with schizophrenia and AUD. A University of Southern California study, not yet recruiting, will investigate whether it reduces the number of heavy drinking days in patients with moderate-to-severe AUD. And a study at Brigham and Women’s Hospital in Boston, also not yet recruiting, will investigate whether Mounjaro decreases cue-induced cravings for alcohol in people with AUD.

At the moment, then, there’s promise but not enough evidence to go on. The raft of upcoming studies, however, should enhance our understanding of how effective GLP-1 agonists are in treating alcohol use disorder, and for whom they are effective.

Photograph via PublicDomainPictures.net

The post How Hopeful Should We Be About Ozempic for Alcohol Use Disorder? appeared first on Filter.

It’s therefore instructive to look back on an often-forgotten history of LSD, one of the most famous psychedelics, being used to treat veterans—specifically for alcohol issues—in the United States.

The first report of the use of LSD as a therapeutic drug was published in Switzerland in 1947—11 years after Swiss chemist Albert Hoffman had first synthesized the substance.  Six patients with schizophrenia were given low doses of LSD, and reportedly showed temporary improvements in their emotional states, such as reductions in depression.

In the 1950s, two forms of LSD-assisted psychotherapy were developed: Psycholytic (mind loosening) therapy involved giving patients a low dose of LSD prior to the therapy session in order to allow them to talk more freely about past traumas, which could be integrated in later sessions. Psycholytic therapy was essentially a variant of narcoanalysis (aka narcosynthesis)—a method invented by J. S. Horsley in the 1930s using sodium amytal or pentothal (“truth serum”) to put the patients into an altered state and release the subconscious. Narcoanalysis has been nicknamed “short-cut psychotherapy,” since it could be done in a matter of days.

The first paper describing the use of LSD for psycholytic therapy was published in 1950. Psycholytic therapy was used for psychiatric disorders rather than for addictions.

After Osmond and Hoffer published their results in the 1950s, a number of other facilities began experimenting with psychedelic therapy for alcohol or other drug addictions.

Psychedelic therapy, under that name, was invented in 1953 at Weyburn Mental Hospital in Saskatchewan, Canada, by psychiatrists Humphry Osmond and Abram Hoffer. 

During the 1950s, the myth that “alcoholics” had to “hit bottom” in order to recover was dominant. Osmond and Hoffer interpreted “hitting bottom” to mean experiencing delirium tremens (DTs). Moreover, in the 1950s, it was believed that LSD was a psychotomimetic drug—that it mimicked symptoms of psychosis found in patients with schizophrenia. 

Osmond and Hoffer hypothesized that delirium tremens, which included unpleasant hallucinations, was essentially similar to schizophrenia. They further hypothesized that giving an “alcoholic” a high dose of LSD (500 micrograms) would duplicate the experience of DTs, thus helping the person to “hit bottom” and recover. (I use the historical, stigmatizing terms “alcoholic” and “alcoholism” in this article because they are conceptually different to the contemporary “alcohol use disorder.”)

Much to their surprise, Osmond and Hoffer found that high-dose LSD gave their alcoholic patients a mystical, transcendental experience rather than DTs. Moreover, their patients who had these experiences lost interest in alcohol and began abstaining. 

Osmond and Hoffer dubbed this psychedelic therapy. They found a certain setting—including music, flowers, a trip guide, etc.—to be essential to consistently inducing the required psychedelic experience. 

After Osmond and Hoffer published their results, a number of other facilities began experimenting with psychedelic therapy for alcohol or other drug addictions. In the US, these included Spring Grove State Mental Hospital in Maryland, Mendota State Mental Hospital in Wisconsin, Mendocino State Hospital in California, the Lexington Narcotic Farm, UCLA and five Department of Veterans Affairs (VA) hospitals. 

VA hospitals had a long history of refusing admission for a primary diagnosis of alcoholism. Service members who were labeled alcoholics were given less-than-honorable discharges. 

It is worth noting that prior to 1962, the only drugs strictly regulated by the federal government were opioids, cocaine and marijuana; regulation of other drugs was much looser, and any therapist could easily and legally obtain LSD for use in their office. After Congress passed the Drug Efficacy Amendment in October 1962, however, LSD research was strictly limited to facilities with FDA approval.

VA hospitals had a long history of refusing admission for a primary diagnosis of alcoholism, although a few alcoholic veterans were sometimes admitted under a false diagnosis. The military rejected the idea that alcoholism was a disease, and service members who were labeled alcoholics were given less than honorable discharges. 

The Winter VA Hospital in Topeka, Kansas, was the exception to the rule, however, and had operated an alcoholism treatment program from the time it opened in 1946. What made the Winter VA Hospital different was that it operated in partnership with the famous Topeka Menninger Clinic and served as the training institute for all VA psychiatrists. Karl Menninger was the director of the hospital’s neuropsychiatric unit.

In August 1960, Samuel Kaim was appointed chief of psychiatric and neurological research for the VA Central Office, putting him in charge of psychiatric and neurological research for all VA hospitals. 

Kaim had noted that about one third of patients admitted to the VA had a secondary diagnosis of alcoholism. He began funding research into alcoholism and drug addiction at VA hospitals, and by 1965, 30 VA facilities were conducting alcoholism research. In August 1964, organic disablement due to alcohol consumption was removed from the category of misconduct. From January 1967, new regulations allowed veterans to be admitted to any VA hospital for alcoholism treatment. 

In the spring of 1963, VA psychiatrist Kenneth Eugene Godfrey initiated a trial of LSD for treating alcoholism at the Winter VA Hospital. At first, the researchers attempted a version of psycholytic therapy by giving patients small doses of LSD prior to group therapy; however, this just led to chaos in the groups.

At this point, Godfrey’s patients began having psychedelic insights—and success at quitting alcohol. 

Next, the researchers attempted giving the patients a single dose of 300-400 micrograms of LSD during the sixth week of treatment and subjecting them to psychological tests; this also proved to be a failure. Godfrey finally consulted with Hoffer, Osmond and Sanford Unger, another psychedelics expert, and learned the importance of setting for the LSD experience. 

The dose was upped to 500 mcg, and administered to patients with flowers, pleasant music and a trip guide. Psychological testing during the trip was eliminated. At this point, Godfrey’s patients began having psychedelic insights—and success at quitting alcohol. 

At least, Godfrey considered the treatment to be a success; however, he was excluded from the final write up of the experiment, which was published in 1970, and which declared the LSD treatment to be a failure. 

This paper has since been justly criticized for comparing the LSD group to an unmatched control group, and its findings may have been significantly influenced by the moral panic surrounding LSD in the late 1960s.

Around 1963 or 1964, VA psychopharmacologist Leo Hollister began conducting a trial of LSD treatment for alcoholism at the VA hospital in Palo Alto, California. Yet Hollister omitted all the setting elements that had been found necessary for inducing a suitable psychedelic experience; he simply compared a high dose of LSD (600 mcg) to a dose of amphetamine (60 mg), a common alcoholism treatment of the time. Hollister published his results in 1969; not surprisingly, there was no significant difference between the two groups.

VA psychologist Milam Tomsovic and VA psychiatrist Robert V. Edwards conducted a study of the LSD treatment of alcoholism between September 1965 and April 1968 at the VA Hospital in Sheridan, Wyoming. Results were published in 1970. There were 75 subjects in the LSD group, 75 in control group I, and 183 in control group II. Control group I consisted of patients who had volunteered for the LSD study but not been given LSD. Control group II consisted of patients who had not volunteered for the LSD study. 

Control group I did the worst, probably because they had been denied the treatment which they had volunteered to take. Nonschizophrenic subjects in the LSD group showed significantly better outcomes than the other groups at one-year follow-up.

In the Highlights of the Twelfth Annual Conference Veterans Administration Cooperative Studies in Psychiatry (1967), VA psychiatrist Murray F. Ables and VA psychologist Erling W. Eng reported on an LSD alcoholism treatment trial which had been initiated at the VA hospital in Lexington, Kentucky in August of 1965. By the time of the report, 122 patients had participated (63 LSD treated patients and 59 controls); preliminary results indicated significantly more improvement for the LSD-treated patients than for the controls in both alcoholism (67 percent vs. 13 percent) and social adjustment (67 percent vs. 25 percent). A follow-up study was published in May 1970. The Lexington study was terminated in 1971.

VA psychiatrist Isham Kimbell also conducted a trial of LSD treatment for alcoholism at the VA Hospital in Houston, Texas. This was a collaborative project with Hollister of the Palo Alto VA Hospital, but I have found few details about this trial.

1966 was the year that kicked off the LSD moral panic. Scare stories appeared in the January 1966 issue of a national Sunday supplement titled This Week Magazine; in a March 1966 issue of Life Magazine; in May and June 1966 issues of the Saturday Evening Post; and many more. 

If the future prospects of treating substance use disorders with psychedelics are as bright as they appear, we can blame moral panic for several wasted decades.

Producer Jack Webb also decided to revive the popular 1950s TV series Dragnet and use it as a propaganda weapon against drugs and the counterculture. The first episode of the new Dragnet, premiering in January 1967, was titled “The LSD Story,” and gave a lurid account of a teenage boy deranged by LSD, who painted his face blue and died of an overdose of barbiturates. The Dragnet episodes, which I remember watching as a pre-teen, hit the public between the eyes like a sledgehammer. 

Later in 1967, Paul McCartney’s public confirmation that the Beatles had used the drug only added to the attention.

Meanwhile, the March 17, 1967 issue of Science reported that LSD caused chromosome damage—a major scare when the thalidomide tragedy was still fresh in the public’s mind. Although this claim would be debunked in the April 30, 1971 issue of Science, the damage to LSD research was already done. 

Research on LSD for any usage at the VA largely ended in the early 1970s, although a few projects continued as late as 1975. 

The federal government criminalized possession of LSD in October 1968, and when it created drug scheduling two years later, LSD was placed on Schedule I.

In recent years, there has been a resurgence of research on the treatment of addictions and other conditions with psychedelics. If the future prospects of treating substance use disorders with psychedelics are as bright as they appear, we can blame moral panic for several wasted decades.

Image (cropped) of the VA hospital in Topeka, Kansas, via US Department of Veterans Affairs

The post A Brief History of LSD Treatment for Alcohol Addiction at the VA appeared first on Filter.

It is worth noting that the term “therapeutic community” was originally coined by South African psychiatrist Maxwell Jones, who created a gentle and caring environment for people with mental health conditions to support each other. 

Yet a number of programs described by this term, operating in the United States from the mid-20th century, were characterized by inflicting humiliating punishments on people with addictions, in a direct reflection of the contempt society has held for them. 

The central activity of these therapeutic communities consisted of marathon sessions of what was known as “the game.” 

In such programs, minor infractions of the rules might bring penalties such as having one’s head shaved, or being forced to dress in a diaper and wear a sign proclaiming, “I am a big baby.” If a man in the community said hello to a woman, he might be made to wear women’s clothing. Failure to empty an ashtray with even a single cigarette butt in it might result in wearing said ashtray around one’s neck for a week. 

However, the central activity of these therapeutic communities consisted of marathon sessions of what was known as “the game.” 

The game generally lasted 40 hours, with a four-hour break for sleep. It consisted of members of the group, one by one, being verbally humiliated and insulted by all the other members, in an attempt to destroy the ego. In the course of the game, you’d be targeted by any number of belittling, sexist or stigmatizing slurs—“junkie” was the least of them. Once the victim of these verbal attacks was considered sufficiently cowed, the group moved on to the next person.

The first therapeutic community of this kind for drug users was Synanon. It is unclear how it was first labeled a “therapeutic community,” despite the fact that it was quite the opposite of the community created by Maxwell Jones.

Synanon was founded in 1958 by Chuck Dederich (1913-1997), a member of Alcoholics Anonymous in Santa Monica, California, who had no training in psychology, or anything else. 

The media fell in love with Dederich and Synanon, painting him as having a magic cure for addiction.

When Dederich had joined AA a few years previously, he was homeless and isolated, as well as addicted to alcohol. He flourished in the program, however, where he soon achieved the status of a guru. After meetings, Dederich would hold hours-long bull sessions in his home, and from these the game was born.  

At a time when very little treatment was available, Dederich claimed success in addressing addictions to alcohol and other drugs via the game. He then rented a storefront and dubbed it Synanon. Tradition has it that the name was the result of one of Dederich’s followers attempting to say “seminar” and “symposium” and slurring the two together.

The media fell in love with Dederich and Synanon, painting him as having a magic cure for addiction. Synanon boasted a good success rate, attributable to the fact that only the most motivated individuals were allowed to join. 

Soon, a number of other therapeutic communities for drug users sprang up, such as Daytop Village, Phoenix House, Odyssey House and others, which originally resembled Synanon to greater or lesser degrees, though they later changed. 

Synanon’s attack therapy spread into alcoholism treatment through two principal sources.

Moreover, Synanon and the game began to attract “squares”—people who had never used drugs—who sought a personality transformation. In the early 1960s, comparable encounter groups such as those at the Esalen Institute sprang up, where well-to-do Americans paid good money to be sworn at and humiliated.  

Synanon’s attack therapy spread into alcoholism treatment through two principal sources. (I will use the stigmatizing term “alcoholism” in this article both to reflect historical usage and because it is not an exact synonym for alcohol use disorder.)  

The first of these sources was the Johnson Institute in Minneapolis, Minnesota. It was the brainchild of Episcopal priest Vernon Edwin Johnson (1920-1999). According to Forrest Richeson, Rev. Johnson underwent treatment for alcoholism at the Hazelden rehab in 1962 and decided to dedicate his own life to such work. 

From 1962 to 1966, Johnson was assigned to the Action Program at St. Martin’s by-the-Lake Episcopal Church in Minnetonka Beach, Minnesota. Johnson also served as a consultant to Hazelden during this period. It was during this time that Johnson developed what would become known as the Johnson Institute Intervention—essentially the same practice that can be seen on the television show Intervention today. Although Johnson claimed an 85 percent success rate for his family interventions, independent researchers put the rate at 30 percent, far below CRAFT, at 64 percent.

It was Johnson’s contention that an “alcoholic” had developed a complex psychic defense system, and that only by breaking this down could the person be changed, else they were doomed to death.

Johnson also established an AA “slipper’s group” at St. Martin’s, for members who were constantly “relapsing.” This group added hard confrontation methods, borrowed from the encounter groups of the era, to the 12 Steps. 

It was Johnson’s contention that an “alcoholic” had developed a complex psychic defense system consisting of denial, rationalization and delusions, and that only by breaking this down could the person be changed, else they were doomed to death.

In 1964, Johnson staged an intervention for Irene Copeland Whitney. Her husband, wealthy businessman Wheelock Whitney Jr., was so grateful that he decided to fund Johnson to create an institute to conduct interventions.

The Johnson Institute was incorporated in 1966. Its mission was threefold: to help families stage interventions; to establish confrontational treatment programs in hospitals and other facilities; and to train alcoholism counselors in confrontational counseling.

The institute established its first confrontational treatment program in St. Mary’s Hospital, in Minneapolis. It was the first time St. Mary’s had offered alcoholism treatment. The pilot program had 16 beds, expanded to 44 beds in 1970 and later to over 100 beds. Under Medical Director George Adam Mann, MD, the program became notorious for verbal abuse of patients, à la Synanon.

In 1973, Johnson published I’ll Quit Tomorrow. This book detailed his theories on alcoholism and alcoholic defense mechanisms, and gave a detailed blueprint for setting up a treatment program based on confrontational counseling. Johnson reported that he had set up programs at Miller Dwan Hospital in Duluth, Minnesota, and Lincoln General Hospital in Lincoln, Nebraska, as well as St. Mary’s. 

In the 1980 edition, he reported having established confrontational treatment programs at over three dozen facilities, including Scripps Hospital in La Jolla, California; Baton Rouge General Hospital in Louisiana; Bethesda Hospital in Cincinnati, Ohio; and Flower Hospital in Toledo, Ohio. 

This, of course, does not include programs which may have adopted confrontational counseling as a result of Johnson’s book.

The second main source of confrontational alcoholism counseling was Eagleville Hospital and Rehabilitation Center in Eagleville, Pennsylvania. The facility had been converted from a tuberculosis sanatorium to an alcoholism treatment hospital in 1966. Donald Jay Ottenberg, MD (1919-2004), was the medical director. According to Ottenberg, Eagleville initially tried treating alcoholics using conventional group therapy and broad-band behavior therapy; however, this was not successful. 

As a result, Hazelden instituted the “hot seat” as a part of its treatment regimen.

In 1967, some of the Eagleville staff visited Daytop Village in New York City and took part in a marathon. Thereafter, confrontational “marathon therapy” was adopted as the standard treatment for alcoholism at Eagleville. In 1968, it admitted its first patients with addictions to drugs other than alcohol, making it the first facility to offer combined treatment since pre-Prohibition days.

By 1970, the demographics of patients admitted to Hazelden had changed, and many were addicted to both alcohol and other drugs. Since Hazelden staff were unfamiliar with the non-alcohol addictions, they made a visit to Eagleville that year to see how its system worked. 

As a result, Hazelden instituted the “hot seat” as a part of its treatment regimen. Patients would undergo one hot seat session during their 28-day stay (originally between the 10th and 14th days but later moved up to the fifth). 

The chair of the subject would be placed in the center of a circle; all other participating patients were given a list of 23 items to use in evaluating the person in the hot seat. Twenty-two of the 23 items were “character defects.” 

In the early 1980s, the hot seat was replaced by peer evaluation, aka the “love seat.” The only change was that now the people in the circle listed both the subject’s assets and their character defects. 

In 1985, Hazelden made a statement denouncing confrontational counseling. Peer evaluation appears to have been discontinued at Hazelden in 1987.

Hazelden and the Johnson Institute, together with Willmar State Hospital in Minnesota, dominated alcoholism counselor training in the 1960 and ‘70s. Willmar’s training program was established in 1962, Hazelden’s in 1966, and the Johnson Institute’s in 1967. Their preeminence ensured that what became known as the Minnesota Model would dominate treatment nationwide.

Alternatives to the Minnesota Model did exist, however, such as the Baltimore City Health Department counselor training program, established in 1967. The VA had also begun large-scale alcoholism counselor training by 1969.

Whenever a new treatment program opened, the director was frequently a counselor trained at Hazelden or the Johnson Institute, which spread use of the hot seat and hard confrontation.

The 1970s were a period of huge growth in the number of alcoholism treatment facilities in operation in general hospitals, residential facilities, and VA hospitals (together with a major decline in the number of state mental health hospitals). A handful of programs operating in 1970 had increased to several hundred by 1980. 

And whenever a new treatment program opened, the director was frequently a counselor trained at Hazelden or the Johnson Institute, which spread the use of the hot seat and hard confrontation far and wide.

The biggest competitors to the Minnesota Model promoted by Hazelden and the Johnson Institute were CompCare Corporation, which offered hospital inpatient 12-step programs without confrontation, and Raleigh Hills, which offered aversion therapy. By 1980, CompCare operated CareUnits in 53 hospitals, operated three psychiatric hospitals specializing in treatment of addictions to alcohol and other drugs, and one alcoholism hospital. Raleigh Hills was meanwhile operating 17 aversion therapy hospitals. 

The number of Minnesota Model programs in 1980 likely numbered over 100, and all of them offered some form of confrontational counseling.

Confrontational counseling began to fall into disrepute in the late 1970s, however. On December 2, 1978, Synanon founder Chuck Dederich was arrested for attempted murder. 

Dederich was accused of ordering two Synanon members to place a rattlesnake with its rattles cut off in the mailbox of lawyer Paul Morantz, in an act of revenge after Morantz had won a $300,000 lawsuit against Synanon. Morantz was bitten when he opened his mailbox. 

The story was juicy enough to make the national news and was broadcast by all the television networks. When Dederich was arrested, he had to be carried out of Synanon on a stretcher because he was dead drunk. He was ultimately sentenced to five years’ probation after pleading no contest to a conspiracy charge.

As researchers William White and William Miller described, confrontation has no therapeutic value.

The May 25, 1979 issue of the Minneapolis Tribune ran an article exposing confrontational treatments at St. Mary’s, Chanhassen Center and other Minnesota Model alcohol programs. The article stated:

At Chanhassen Center, Robert Turpin took over as program director three years ago and promptly fired 45 counselors and therapists trained in the confrontive style. “When I came in here the patients were kicking walls and pounding pillows,” Turpin said contemptuously. “They reinforced that here. The staff wasn’t happy until people came out crying. They called it anger therapy.

“I call it destructive behavior. Alcoholics punish themselves. Why should they pay to go to a treatment center and be punished some more?” In place of the stereotype of alcoholics that was the focus of treatment by his predecessor, Turpin installed a working policy that each patient “is not only fallible but unique, deserves respect and is responsible for his or her own feelings and behavior.”

Confrontation gradually fell out of favor in alcohol treatment programs. The 1988 book Rehab: A Comprehensive Guide to Recommended Drug-Alcohol Treatment Centers in the United States lists 146 alcohol treatment programs; only 19 reported still using the hot seat or other forms of confrontation.

Therapeutic communities for adult drug users also toned down some of their abusive approaches in the 1980s, although, as Maia Szalavitz pointed out in Help at Any Cost (2006), many of the worst abuses continued to be practiced in adolescent treatment programs.

Confrontational counseling was an abhorrent practice to use against vulnerable people. And as researchers William White and William Miller described in their 2007 article “The Use of Confrontation in Addiction Treatment,” it has no therapeutic value. They found that “the more the counselor confronted, the more the client drank.”

Photograph by Andrew Kimmel via Flickr/Creative Commons 2.0

The post The Rise and Fall of Confrontational Alcohol Addiction “Treatment” appeared first on Filter.

The book was put together by her mother, Sheila Ellin (pseudonym). It combines letters, poems and other documents written by Elizabeth with her mother’s commentary. The published work has an important purpose: not only showing the damage caused by our current systems of incarceration and rehab, but also how science-based harm reduction interventions, such as medications for opioid use disorder, could have saved Elizabeth’s life.

I have known Sheila Ellin, who lives in New Jersey, for some years through harm reduction circles. I recently had the opportunity to interview her about her daughter’s story. Our interview has been edited for length and clarity.

Kenneth Anderson: Who was Elizabeth, and what happened to her?

Sheila Ellin: Elizabeth was gifted in so many areas—writing, art, music, fashion design—but she also struggled with social anxiety, depression and low self-esteem, made worse by childhood sexual abuse. She started self-medicating with several substances, and at age 19 she was arrested for possession and entered the criminal-legal system.

Elizabeth attended six 12-step rehabs, and was locked up in three county jails, the New Jersey state prison and several prison halfway houses. Elizabeth died from endocarditis at age 29.

“The 12-step model was useless to Elizabeth. In fact, it made her feel like a failure. That system, and most of the world, judged her.”

When did you first learn about Elizabeth’s drug use?

In January of Elizabeth’s junior year of high school, I found a lighter when I was cleaning her bedroom. I knew Elizabeth was strongly anti-smoking [of cigarettes], so I concluded that she was smoking marijuana. When I asked her about it, she told me she was “just experimenting,” and so that was that.

Three and a half years later, when she was 19, she called me in tears, and told me she was addicted to heroin.

What did you expect would happen when she first entered rehab?

When we arranged for Elizabeth to go to rehab the first time, after she told me she was addicted to heroin, I believed that she would spend 28 days in rehab [and that] she would have to go to AA/NA meetings, and she would no longer be able to use any drugs or alcohol. I thought after 28 days, her life would be back on track—as if her heroin use had never even happened. A minor blip.

What was the actual result of her going to rehab?

The actual result [was] that Elizabeth, and all the people around her, started viewing her as a “drug user” and college drop out.

She did meet her soulmate in her first rehab, and I am happy that she experienced true love in her shortened life. But the rehab did nothing for her.

They diagnosed her with an eating disorder and depression, but did not give her any medication, because they required a person to be abstinent from all substances before they would consider medication.

The 12-step model was useless to Elizabeth. In fact, it made her feel like a failure. She did not go to meetings after she left rehab; she did not get a sponsor. She just did not buy into the whole abstinence, 12 step-based system.

That system, and most of the world, judged her for that—they judged her a failure for her relapses, and for her not buying into what they were peddling.

How did her involvement in the criminal-legal system affect her?

Her involvement with the criminal system, obviously, affected Elizabeth in many ways, all negative. Elizabeth struggled with anger all her life, and being in prison increased her anger and resentment towards those who mistreated her in prison and out of prison. Her mental health suffered in prison, because she was separated from her baby, from her family, her friends, and everything she loved.

Upon leaving prison, Elizabeth was not eligible for assistance with housing because she had drug [convictions]. And because of her drug possession felonies, Elizabeth’s job options were limited.

“There are many things I believe could have helped Elizabeth. None of them are rehab or prison.”

How was her continuing experience in the treatment system?

The treatment system did not help Elizabeth. Elizabeth was always an “A” student, and she was an excellent student in 12-step rehab programs as well. She tried her best. She did all the work sheets; she worked the Steps. She was always optimistic—but that is because Elizabeth and I and so many others believed the culture of 12-step rehabs. We believed they would do what they said they would.

No matter how hard Elizabeth tried inside rehab, as soon as she was out, her issues led her to begin immediately self-medicating and using again. She was kicked out of two or three rehabs for “fraternization”—even though she always told the rehabs she had a sex addiction.

I think the main effect of the rehabs was to make Elizabeth feel like a failure. She wasn’t a failure; 12-step rehabs were just not a fit for Elizabeth. But they made her feel she was a failure. It was kicking her when she was down—over and over, with every relapse or arrest for possession.

We know that help with injection techniques and availability of alternatives could have reduced Elizabeth’s risk of endocarditis. What else do you think might have helped her?

There are many things I believe could have helped Elizabeth. None of them are rehab or prison. I would say harm reduction, [including] treatment with methadone or buprenorphine. Trauma-informed therapy—for her PTSD, the loss of her son [he was removed rom her care, and she was not allowed to see him], domestic violence, multiple rapes, childhood sexual abuse—evidence-based treatment such as cognitive behavioral therapy or dialectical behavioral therapy.

Something that would really have helped Elizabeth, and all people who use drugs, is reducing the stigma towards drug users. Elizabeth talked about herself as a criminal, loser, deadbeat mom, college dropout, etc. For people who are using drugs because they are struggling, stigma just makes them feel so much worse about themselves.

How has your loss affected you in the years since?

I’ve dealt with mental health issues since I was a child. Elizabeth was the light of my life. My mother died of cancer when I was 15. My mother was a wonderful person. Losing her, and then losing Elizabeth, who was the best thing by far to ever happen to me, has been a nightmare.

But almost worse than losing Elizabeth was seeing/feeling the pain that she went through and not being able to help her. It has changed me in ways too complicated to get into here, but I believe I am more compassionate, and I believe I am more open to new ideas and different ways of seeing the world.

“Harm reduction has changed the way I view the world.”

 

How did you come to learn about harm reduction?

I came to know about harm reduction in 2016, two years after Elizabeth’s death. I was in the Facebook group GRASP (Grief Recovery After a Substance Passing) and I made a post. An admin said my post wasn’t right for GRASP, but was perfect for their sister group Broken No More, which dealt with harm reduction, medication-assisted treatment, advocacy etc. I went to Broken No More. For several months, I read every single post, every single day.

Later that year, I attended the GRASP/Broken No More conference. The next year, the Reform conference, and the following year, the National Harm Reduction Conference.

How has harm reduction changed you?

Harm reduction has changed the way I view the world. I guess, growing up, I was relatively conservative, and I believed drugs were illegal because they were “bad.” I thought if people were arrested for possession of drugs—well, they broke the law.

After learning about harm reduction, I believe people should be able to use whatever substances they want, as long as they’re not hurting other people. I participated in advocacy groups in New York State for several years, and I spoke in Albany several times. I did not ever think I would be the type of person to have the desire or the capability to do that, but I felt very strongly, and I continue to feel very strongly about advocacy.

What would you say to other moms in the situation you experienced?

To moms in this situation, I guess what I would suggest is: One, be a support and love your child unconditionally and without judgment. Don’t believe what treatment centers tell you and don’t try “tough love” unless it’s a serious safety issue.

And two, educate yourself. The internet was not as big when Elizabeth was alive, and maybe things would’ve been different if I had learned about harm reduction and medication-assisted treatment when she was alive. Back then I read a lot of books, but most of the books were written by people in recovery through the 12 Steps, so they were pretty much useless.

“Harm reduction does not require abstinence as a condition to help a person make positive change in their life.”

What is wrong with the way the US treats people who use drugs?

Everything. Criminalization is wrong, mass incarceration is wrong, drug courts are wrong—because they punish participants by putting them in jail—stigma is wrong….

Our whole culture’s belief and fixation on 12-step rehabs, then AA/NA meetings and abstinence for the rest of your life, is just wrong—because it does not work for the majority. The $35 billion per year (several years ago) rehab industry is just not working. People need to understand that it is not working.

Another thing people need to understand is that most people who use drugs never have a problem. They just stop on their own or continue to use in a functional way. That’s something I learned through harm reduction, and most people don’t understand that. Before Elizabeth struggled, I just assumed that everyone who used heroin, crack, meth, etc., would get addicted and would have problems. No. Wrong.

What is wrong with the US treatment system?

I guess the main thing wrong is that no single treatment type will ever work for everyone. Individuals need different types of help with finding a safe place to live [with] poly-substance use, mental health issues, trauma—and everyone is different. There’s no way one type of treatment is going to work for everybody. And abstinence is not gonna happen for everyone.

If Elizabeth had lived, maybe she would’ve stopped some substances or moderated, but with all the trauma and her issues and her genetics, I do not believe she ever would’ve been abstinent, and I certainly would not have expected her to be. Substances were Elizabeth’s coping mechanisms, and I believe they work better than current psych medications for the most part.

Why is harm reduction a better way?

Harm reduction is a better way because it meets the person where they are at, without judgment. Harm reduction considers all aspects of the human condition and tries to help in any way to make a person’s life better, and reduce the harm of the substances they’re using or the behaviors they’re doing. Harm reduction does not require abstinence as a condition to help a person make positive change in their life.

Detail from the cover of Addicted and Convicted: Letters from a Lost Daughter, showing Elizabeth Elliot, courtesy of Sheila Ellin

The post A Daughter’s Life and Death, Seen Through a Harm Reduction Lens appeared first on Filter.

The reward center of the brain (the ventral striatum, which includes the nucleus accumbens) was discovered in 1954 by James Olds and Peter Milner. They implanted electrodes into the reward center of rats’ brains, connecting them to levers which the rats could press. Olds and Milner found that rats would spend all their time pressing the lever to stimulate the brain’s reward center to the exclusion of all else, including food and sex.

The dopamine hypothesis of drug addiction was first put forth in 1987, by Roy A. Wise and Michael A. Bozarth, and early versions framed dopamine as the “pleasure chemical” stimulating the “pleasure center” of the brain. 

Dopamine is constantly being released into the brain’s reward center, whether one uses drugs or not. But the dopamine hypothesis defined drug addiction as the brain’s association of drug use with pleasure through large releases of dopamine.  

The dopamine hypothesis, it should be noted, conveniently reinforces the capitalist-puritan notion that work is good and pleasure bad.

The hypothesis entered the popular consciousness with the publication of a 1997 story in Time magazine titled “Addicted: Why Do People Get Hooked?” Touting dopamine as the “pleasure chemical,” the article stated that all addictions—from drugs to drinking to smoking, but also non-drug activities like sex—were caused by its release into the brain’s “pleasure center.”

The dopamine hypothesis, it should be noted, conveniently reinforces the capitalist-puritan notion that work is good and pleasure bad, and that our purpose is to work to make profits for the billionaire class. We even have our modern picture of drug-hell, exemplified by the cocaine rat—which takes drugs until it dies, showing that the wages of pleasure are death.

But research by Kent C. Berridge in 2007 showed that dopamine was not a pleasure chemical at all. Dopamine is a reward chemical which causes people to “want” things, rather than a pleasure chemical which causes people to “like” things.

That, of course, doesn’t refute the dopamine hypothesis altogether. It does, though, raise the interesting question of what pleasure looks like in chemical terms. Scientific literature demonstrates no specific pleasure chemical, and researchers have identified a number of separate pleasure centers in the brain, known as “hedonic hotspots.” I would speculate that what we know as “pleasure” lumps together several components of the experience that do have separate chemical signifiers: relaxation (GABA), absence of pain (endorphins), love (oxytocin), stimulation (norepinephrine) and desire (dopamine), among others.

There are holes in the dopamine hypothesis big enough to throw an armadillo through. 

Addiction researchers quickly fell in love with the unified theory of addiction given by the dopamine hypothesis. Drug warriors added it to their weaponry in claiming that drugs, not social or psychological conditions, were the problem. And profiteering rehab centers used it as one more marketing tool to get their hands on your bank account.

But, as David J. Nutt pointed out in a 2015 article, there are holes in the dopamine hypothesis big enough to throw an armadillo through. 

There is strong evidence that stimulants such as amphetamine produce a release of dopamine in the reward center of humans compared to a control group (Drevets et al., 2001; Oswald et al., 2005; Martinez et al., 2007; Wand et al., 2007; Schneier et al., 2009; Leyton et al., 2002; Boileau et al., 2007; Narendran et al., 2010; Shotbolt et al., 2011), and fairly good evidence that alcohol produces such a release in humans (Boileau et al., 2003; Yoder et al., 2007). But there is little to no evidence that the same is true for opioids, cannabis, ketamine or nicotine.

Of two studies of heroin use in humans (Daglish et al., 2008; Watson et al., 2013), neither found any significant release of dopamine in the reward center compared to a control group. 

Ritalin is a stimulant which is similar to, but milder than, amphetamine. It is far less associated with addiction than heroin, yet Ritalin, in contrast, produces a large release of dopamine in the reward center (Volkow et al., 1999). Modafinil, another stimulant deemed to have low potential for addiction, also causes a large dopamine release (Volkow et al., 2009). 

Of two studies of THC use in humans, one (Stokes et al., 2009) found no significant release of dopamine in the reward center compared to a control group, whereas the other (Bossong et al., 2009) found a small but significant release. 

Of three studies of ketamine in humans, two (Kegeles et al., 2002; Aalto et al., 2002) found no significant release of dopamine in the reward center compared to a control group, whereas one (Vollenweider et al., 2000) found a large and significant release.

Of six studies of nicotine in humans, two (Barrett et al., 2004; Montgomery et al., 2007) found no significant release of dopamine in the reward center compared to a control group, whereas four (Brody et al., 2004; Brody et al., 2006; Brody et al., 2009; Takahashi et al., 2008) found a significant release.

The National Institute on Drug Abuse (NIDA) has continued to promote the dopamine hypothesis. 

Moreover, different people have different quantities of dopamine receptors in their brains’ reward centers. If the dopamine hypothesis were correct, one would expect that people with many such receptors would be more vulnerable to addiction than those with few. Yet there is research that indicates the opposite. Volkow (2006) found that having many dopamine receptors in the reward center was protective against developing alcohol addiction.

Despite this, the National Institute on Drug Abuse (NIDA), which is led by the author of that paper, Dr. Nora Volkow, has continued to promote the dopamine hypothesis. 

In 2020, it put out an anti-drug propaganda pamphlet titled Drugs, Brains, and Behavior: The Science of Addiction. On page 17, the pamphlet states correctly that dopamine is responsible for reinforcement, not pleasure. However, on page 18, it contradicts itself by calling the dopamine reward center the “pleasure center” and saying that addictive drugs target this pleasure center. 

Despite strong indications that dopamine plays no significant role in many addictions, the pamphlet states:

“Just as drugs produce intense euphoria, they also produce much larger surges of dopamine, powerfully reinforcing the connection between consumption of the drug, the resulting pleasure, and all the external cues linked to the experience. Large surges of dopamine ‘teach’ the brain to seek drugs at the expense of other, healthier goals and activities.”

Dopamine is found all over the brain, not just in the reward center. The chemical is essential for working memory, executive function, motor function, and many other functions. Excessive dopamine may be responsible for some psychosis. 

As we have seen, dopamine in the reward system may be involved in the genesis of some addictions. But for others, there just isn’t the evidence to show that. And one thing dopamine is definitely not is “the pleasure chemical.”

Human brains and experiences are a heck of a lot more complex than the fried eggs of anti-drug PSAs. And people experience addictions to all kinds of activities other than drug use. It’s obvious why propagandists and marketers like the dopamine hypothesis, and equally clear that we shouldn’t buy their claims.  

Image of dopamine formula via Pixabay

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Since then, for people who want to quit drinking, doctors in the United States have generally prescribed it as an anti-craving medicine and told patients to abstain while taking it.

However, it is unclear whether naltrexone is effective if you follow those instructions. Trials by John David Sinclair in Finland, Henry Kranzler in the US and others indicate that naltrexone is most effective in reducing alcohol consumption—if you drink alcohol about an hour after taking it. This is the Sinclair Method, also known as “targeted naltrexone.”

So how well does it work?

Its model views addiction as a conditioned response to dopamine being released into the brain’s reward pathway, in this case caused by an increase in beta-endorphin which results from drinking alcohol. The Sinclair Method seeks to block the effect of the beta-endorphin when alcohol is consumed, which, in turn, blocks the release of dopamine, which leads to the “extinction” of the conditioned response over a period of a few months.

So how well does it work?

The largest trials of the Sinclair Method were conducted between 2008 and 2011, using a close relative of naltrexone called nalmefene. Named ESENSE 1, ESENSE 2 and SENSE, they resulted in nalmefene being approved in Europe as a medication for the reduction of alcohol consumption.

Three Major Trials

ESENSE 1 (Mann et al., 2013; NCT00811720) was conducted in Austria, Finland, Germany, and Sweden at 39 sites with 604 subjects: 306 in the nalmefene (18 mg) group and 298 in the placebo group. It lasted six months. All subjects met DSM-IV-TR criteria for “alcohol dependence,” as it was then termed, ranging from mild to moderate to severe. All also received the BRENDA psychosocial treatment to encourage medication compliance and behavioral change.

Patients were instructed to take their medication (nalmefene or placebo) one-to-two hours prior to a high-risk drinking situation.

Between the month before initial screening and the last month of the study, the number of heavy-drinking days (60 grams of ethanol or more for men, 40 or more for women) in the nalmefene group fell from an average of 19.4 days to 8.2 per month; in the placebo group it went from 19.6 to 10.7 per month. The average amount drunk per day in the nalmefene group went from 84 grams of ethanol to 33; in the placebo group it went from 85 grams to 45. Overall, this showed significantly greater reduction in drinking in the nalmefene group.

Dropout rates were high, however, at 31 percent of subjects in the placebo group and 53 percent in the nalmefene group—a significant difference.

Notably, there were large reductions in both groups between initial screening and the beginning of treatment, one-to-two weeks later; 18 percent reduced their drinking to less than six heavy-drinking days per month in this brief period. It’s actually a common phenomenon: Once people decide to initiate treatment their habits tend to change even before it starts. Similar phenomena were noted in Project MATCH.

ESENSE 2 (Gual et al., 2013; NCT00812461) was conducted in Belgium, the Czech Republic, France, Italy, Poland, Portugal and Spain at 57 sites with 718 subjects: 358 in the nalmefene (18 mg) group and 360 in the placebo group. All other conditions were the same as ESENSE 1.

The number of heavy-drinking days in the nalmefene group went from 19.8 to 6.6 per month, and in the placebo group from 18.3 to 7.5—still a statistically significant difference between groups.

With average amount drunk per day—which went from 93 grams of ethanol to 30 in the nalmefene group, and from 89 to 33 in the placebo group—the difference was not statistically significant. However, even more participants in ESENSE 2 reduced their drinking between screening and treatment initiation; 33 percent had reduced heavy-drinking days to less than six per month. When these subjects were removed from calculations, nalmefene did have a significant effect on reducing average daily consumption.

Dropout rates were 41 percent in the nalmefene group and 38 percent in the placebo group—a much smaller difference than in ESENSE 1.

Overall, it was a significant—but far from dramatic—difference in favor of nalmefene.

The SENSE study (van den Brink et al., 2014; NCT00811941) lasted 12 months, twice as long as the two ESENSE studies. Conducted at 60 sites in the Czech Republic, Estonia, Hungary, Latvia, Lithuania, Poland, Russia, Slovakia, Ukraine and the United Kingdom, it had 675 subjects with alcohol dependence: 509 in the nalmefene group and 166 in the placebo group. All other conditions were the same as the ESENSE studies.

At six-month followup, there were no significant differences between the nalmefene and placebo groups in terms of heavy-drinking days or total consumption.

However, at 13-month followup, the nalmefene group showed better outcomes. It had gone from 15.2 heavy-drinking days per month to 4.7, a reduction of 10.5. The placebo group had gone from 14.7 heavy drinking days per month to 5.7, a reduction of 9.0. Average ethanol consumption in the nalmefene group had gone from 75 grams per day to 22.2, a reduction of 52.8 grams. The placebo group had gone from 75 grams to 28.7, a reduction of 46.3.

Overall, it was a significant—but far from dramatic—difference in favor of nalmefene.

This time, 39 percent of participants had reduced their drinking to less than six heavy-drinking days per month between screening and treatment initiation. When these patients were removed from calculations, the effect of nalmefene over placebo was also significant at the six-month followup on both measures.

Dropout rates were 38 percent in the nalmefene group and 32 percent in the placebo group—a significant difference once again. Some patients dropped out due to nalmefene’s side effects—similar in profile to those of generic naltrexone, and which some subjects in the placebo group also perceived. But the most common reason was withdrawal of consent.

Approval and Objections

In any case, those three major trials were enough to convince the European Medicines Agency, in 2012, to approve nalmefene for the reduction of alcohol consumption in adults with alcohol dependence.

However, six members of the agency objected to the approval. And a number of scholars, including Fitzgerald et al. (2016), Naudet et al. (2016), and Palpacuer et al. (2015), published papers criticizing the decision.

For one thing, generic naltrexone, which was much cheaper than nalmefene, had long been approved in Europe for supporting abstinence—but was also already being used off-label to reduce drinking. A lot of people viewed nalmefene as a money-making scheme for the pharmaceutical company which manufactured it.

Another charge was that subjects who improved greatly prior to treatment had been removed after the fact in the data reanalysis, to inflate the efficacy numbers.

Finally, the effect size when compared to placebo was very small.

The small effect size in some studies could be due to hit-and-miss medication compliance.

It is worth noting here that medication compliance was not reported in any of the three trials. The role of medication compliance has generally been badly overlooked in studies of targeted naltrexone. And it is possible that the Sinclair Method’s efficacy has been underrepresented as a result.

Advocates of the method say that total compliance—always taking the pill one hour before drinking—is essential to obtain and maintain the extinction effect. So the small effect size in some studies of targeted opioid antagonists for alcohol use disorder could be due to hit-and-miss medication compliance.

The Abstinence Question, and Individual Differences

Research priorities in the US have sometimes reflected how abstinence is culturally prized here much more than in Europe.

A 2016 study by Amy W. Helstrom et al. attempted to test whether naltrexone plus abstinence reduced craving for alcohol. Subjects were 100 patients and 100 matched controls undergoing residential treatment at the Hazelden rehab—where subjects had no access to alcohol.

This study was not blinded, not placebo-controlled, and not randomized. The patients themselves chose whether they wanted to be in the naltrexone group or the control group. Those given naltrexone all knew they were taking it, and that it was intended to reduce their cravings.

A randomized placebo-controlled trial is needed to determine whether there is a medication effect when naltrexone is taken while abstaining.

Craving was rated using the Penn Alcohol Craving Scale, from 0 to 6. At the beginning of the trial, the average craving rating in the naltrexone group was 2, compared to 1.1 in the control group—a significant difference. By the end, the figure for both groups had fallen below 1, and was not significantly different between groups.

However, it is currently impossible to know whether this drop in craving was due to the effect of naltrexone, to a placebo effect, or simply to the effect of time. A randomized placebo-controlled trial is needed to determine whether there is actually a medication effect when naltrexone is taken while abstaining. Still, this study showed that naltrexone plus abstinence does not lead to increased craving, as author Roy Eskapa had claimed it would.

Some people say they have experienced large reductions in craving by taking naltrexone while abstaining. But it is impossible to tell if this is simply a strong placebo effect, or if naltrexone causes a large craving reduction in some individuals. More and better research is needed on this topic.

We know that the craving reduction in people who drink on naltrexone is due, at least mainly, to the extinction effect. If naltrexone actually does reduce craving in abstainers, what could be the mechanism?

One hypothesis is that alcohol-related cues cause a release of beta-endorphin, which in turn releases dopamine. This theory proposes that naltrexone blocks the reaction of the opioid system to alcohol-related cues. A 2014 brain-imaging study by Mann et al. seems to confirm that naltrexone blocks cravings induced by alcohol-related cues.

There is evidence of a great deal of individual variation in response to naltrexone as a treatment for alcohol use disorder.

A 2019 brain-imaging study by Amanda Elton et al. found that naltrexone enhances the connectivity between the ventromedial prefrontal cortex (an area of the brain involved in craving) and the left frontoparietal network (an area of the brain involved in executive control). This increased connectivity appears to contribute to a reduction of craving for alcohol caused by naltrexone, according to the authors, a process which involves the kappa-opioid receptor system.

There is evidence of a great deal of individual variation in response to naltrexone as a treatment for alcohol use disorder. A 2014 paper by James C. Garbutt et al. reviewed possible factors.

One factor is genetic. A variant in the gene which codes the development of mu-opioid receptors appears significant. People who have the Asn40Asp variant of the gene respond better to naltrexone treatment for alcohol use disorder than those who don’t. This variant both increases mu-opioid receptor binding affinity and decreases the number of these receptors.

People with a family history of alcohol use disorder also appear to respond better to naltrexone treatment for alcohol than those with no such history. People with high levels of alcohol craving prior to treatment also appear to respond better. And out of left field, people who like sweets also appear to do better with naltrexone than those who dislike them.

These potential influences on efficacy are not always confirmed by other studies, however.

A 2019 study by Katie Witkiewitz et al. found that the Sinclair Method has different effects on people who drink for pleasure (high-reward drinkers) and those who drink to avoid pain (high-relief drinkers). These researchers divided drinkers into four categories: high-reward/high-relief, high-reward/low-relief, low-reward/high-relief, and low-reward/low-relief. They found that high-reward/low-relief drinkers showed the greatest response to naltrexone for number of heavy-drinking days and drinks per drinking day.

Only you can choose if naltrexone is right for you.

Nothing here is medical advice, and seeking medical advice is advisable. But evidence suggests that if you are a daily drinker, it does not really matter if you take naltrexone daily, an hour before drinking, or get the Vivitrol shot—the opioid receptors are still blocked either way, and the extinction effect still takes place. Fifty mg of naltrexone gives a near-total blockade of the opioid receptors for the first 24 hours, and it takes about four days for the blockade to be reduced by half.

If, on the other hand, you tend to spread out your drinking days, abstaining in-between, then taking naltrexone one hour before drinking, i.e., targeted naltrexone—the Sinclair Method—may be the best option.

And if you tend to abstain for multiple days, then go on multiple-day benders drinking morning to night, you might find that Vivitrol removes medication compliance concerns.

Potential side-effects may also influence such decisions.

There is some solid evidence for naltrexone to treat alcohol use disorder. But the evidence is much stronger for people whose goal is to reduce, rather than quit, drinking. And even then, its efficacy may be only somewhat better than placebo, and individual responses vary greatly.

It could be worth a try. But only you can choose if naltrexone is right for you.

If you take it and don’t like the effect on your alcohol buzz, there are many other ways to reduce alcohol-related harm.

Then again, if you take it while abstaining and your cravings go way down as you want them to, it doesn’t really matter if it is a medication effect or a placebo effect. If the Sinclair Method helps you reduce your consumption to where you want it to be, that is a win.

The biggest obstacle may be your medical provider. Unfortunately, as Jonathan Avery, MD noted in the American Journal of Psychiatry in 2022, many physicians are unaware of the research behind naltrexone and its targeted use.

Photograph by eflon via Flickr/Creative Commons 2.0

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A quick online search reveals many attestations of PAWS, primarily by rehabs and recovery organizations. But PAWS (sometimes known as protracted alcohol withdrawal syndrome, or protracted withdrawal syndrome) has never made it into the Diagnostic and Statistical Manual of Mental Disorders (DSM), the diagnostic bible of the American Psychiatric Association. So to what extent, if any, is it real?

The idea of it was introduced by Terence Gorski and Merlene Miller in their 1982 book Counseling for Relapse Prevention, and they expanded upon it in Staying Sober: A Guide for Relapse Prevention (1986). Staying Sober became an extremely popular workbook in the addiction treatment industry, and untold numbers of patients were introduced to the concept of PAWS as though it were a scientifically proven reality. 

It’s not hard to see why PAWS gained traction, in light of certain narratives that were dominant in the 1980s and have lingered since. 

Neither Gorski nor Miller was a research scientist. Both were addiction counselors, and based their description of PAWS on certain preconceived ideas about “alcoholism” and on observation. 

However, it’s not hard to see why PAWS gained traction, in light of certain narratives that were dominant in the 1980s and have lingered since. 

The idea that drugs cause permanent brain damage fed into the propaganda of an era notorious for its “This is your brain on drugs” PSAs. PAWS also fits in well with Alcoholics Anonymous, when AA’s Step 2 indicates that people with alcohol addiction require “a Power greater than ourselves” to “restore us to sanity.”

I well remember my introduction to PAWS in the mid-1990s, when I was made to watch one of Gorski’s films in treatment. My first reaction was, “No wonder these people are depressed and confused, since they are all being forced to attend AA!” 

It should be noted that PAWS is quite different from alcohol withdrawal syndrome (AWS). Acute AWS occurs shortly after long-term, daily, heavy drinkers cease consuming alcohol, and can last between two and seven days. Its duration and severity depend on how long the person has been drinking, how much they’ve been drinking, and genetic and physiological factors. Symptoms of acute AWS include tremors, sweating, rapid or uneven heartbeat, fever, seizures, hallucinations and delirium. In severe cases, if untreated, it can cause death. No one questions its existence, and the DSM duly includes it. 

PAWS, however, is another story, and people have been debating its reality ever since Gorski and Miller proposed it. The kind of observation they relied on is highly susceptible to confirmation bias: People see what they expect to see and fail to see things which don’t conform with their preconceived ideas. Scientists use blinded randomized controlled trials in order to eliminate confirmation bias.

PAWS is postulated to occur after AWS subsides—and to last for months, years or even a lifetime. 

According to Gorski and Miller, there are six types of PAWS symptoms:

1. Inability to think clearly

2. Memory problems 

3. Emotional overreactions or numbness 

4. Sleep disturbances 

5. Physical coordination problems 

6. Stress sensitivity

Gorski and Miller also gave a list of 37 warning signs of “relapse” which were a result of PAWS—including depression and a refusal to go to AA. Interestingly, University of New Mexico researcher William Miller (no relation) used Gorski and Miller’s warning signs to construct the 28-item Assessment of Warning-signs for Relapse (AWARE) scale; nine of Gorski and Miller’s warning signs were rejected as invalid by William Miller when tested experimentally.

Many of the symptoms ascribed to PAWS are also pre-existing symptoms which people may self-medicate with drugs.

The AWARE scale has proved a reliable tool for predicting resumption of drug use, but of course it tells us nothing about whether withdrawal produces prolonged psychiatric symptoms.

PAWS is difficult to study because many of the symptoms ascribed to it, such as insomnia, depression or anxiety, are also pre-existing symptoms which people may self-medicate with drugs. And unless these symptoms frequently co-occur in the same individuals, we are not justified in saying that they combine to form a syndrome.

According to DSM-5, anxiety, bipolar, depressive, neurocognitive, obsessive-compulsive, psychotic, sexual and sleep disorders can all be either substance-induced disorders or independent disorders. For all of these except neurocognitive disorder, DSM-5 uses the same criteria to distinguish the substance-induced disorders from the independent ones: If the disorder persists more than a month after substance use ceases, or if it existed prior to the substance use, it is to be diagnosed as an independent disorder. Otherwise, it is to be diagnosed as a substance-induced disorder.

Quite a number of scholars have raised objections to how DSM’s categorizations involve arbitrary hairsplitting to differentiate one diagnosis from another; that one-month time limit for substance-induced disorders is one such example.

The reason DSM-5 makes an exception for neurocognitive disorder is that Wernicke-Korsakoff syndrome, sometimes referred to as “wet brain,” is almost always classified as a substance-induced neurocognitive disorder. This rare condition results from the death of brain cells due to thiamine deficiency; in Western countries, such a deficiency is most often the result of long-term, heavy drinking. Wernicke-Korsakoff syndrome is largely irreversible and causes severe impairment. However, other less severe—and reversible—cognitive impairments sometimes occur in people who have ceased heavy drinking.

A review of substance-related cognitive impairment could easily take up several articles by itself; suffice it to say that this is a topic with many controversies and disagreements among researchers. I will limit myself to outlining a well-known 1990 paper by Fein et al. This found that in a clinical sample, one-half to two-thirds of people with alcohol addiction showed cognitive impairments in the first few months of abstinence.

Fein et al. found that distractibility, mild confusion and irritability generally subsided within two weeks after the subject ceased to drink alcohol. Problems with attention and concentration, reaction time, verbal learning ability, verbal abstract reasoning and verbal short-term memory lasted two-to-eight weeks. 

On the other hand, problems with nonverbal abstract reasoning, visuospatial abilities, mental flexibility and nonverbal short-term memory, they found, could last between two months and five years. 

But it is important to note that clinical samples—i.e., subjects taken from hospitals or treatment facilities—almost invariably show far higher co-occurrence of disorders than do cohorts taken from the general population. I have not found any kind of reliable estimate of the prevalence of cognitive impairment in a general-population sample of people with alcohol use disorder (AUD) who quit drinking. 

Meanwhile, a 1997 study by Schuckit, et al. looked at depressive disorders in 2,945 subjects with a diagnosis of alcohol dependence. This, again, was a clinical sample.

Schuckit et al. looked for depressive episodes which occurred during a three-month period of abstinence, rather than the one-month period given by DSM-5. The majority of their subjects, 58.4 percent, had no major depressive episodes, whereas 26.4 percent met criteria for substance-induced major depression, and 15.2 percent met criteria for independent major depression. According to the authors, substance-induced major depression typically goes away by itself, without treatment, after a few days or weeks of abstinence. 

Interestingly, the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), which was a general-population sample, found quite different results. Using the NESARC data, Grant et al. found that among subjects with a past-year substance use disorder, 15.15 percent had co-occurring major depression, but only 0.65 percent had co-occurring substance-induced major depression. Similar results were found with anxiety disorders.

Turning to another alleged PAWS symptom, estimates of insomnia/sleep problems in clinical samples of people with AUD range from 36-91 percent. I have found no good estimates of the prevalence of insomnia/sleep problems in people with AUD in a general-population sample; however, logic would point to its being much lower. 

Using the NESARC data, Brower and Perron found that 31.7 percent of people in the general population who were undergoing acute alcohol withdrawal reported short-term insomnia. However, NESARC says nothing about post-acute withdrawal insomnia. Insomnia also frequently precedes AUD; people with insomnia who use alcohol as a sleep aid may develop AUD as a result. But alcohol-induced insomnia/sleep problems are common, too, after one ceases drinking, and can last for weeks or months. Sleep aids and sleep hygiene are both important in treating insomnia and sleep problems which co-occur with AUD, whether induced or independent. 

Some evidence supports alcohol withdrawal as the cause of some symptoms ascribed to PAWS. But whether these can justifiably be clumped into a syndrome is not conclusively answered.

Overall, this seems to be what we can say with certainty: Cognitive impairment following alcohol withdrawal is common in clinical samples, but we simply don’t know if this is true of people with AUD in the general population. Alcohol-induced cognitive impairment tends to resolve itself with abstinence or moderate drinking; some cognitive impairments go away in weeks, while others take months or even longer. Cognitive impairment is more common and severe in former heavy daily drinkers than in those who drank less frequently or heavily.

People with AUD also often have a co-occurring depressive disorder: perhaps one-third of those in clinical samples, and perhaps one-sixth of those in general-population samples. But in most cases, the depression was present before the AUD. In some cases, however, the depression seems to be caused by drinking, in which case it tends to go away by itself within a few weeks after quitting.

People with AUD often have co-occurring insomnia, too: both independent and alcohol-induced, in both clinical and general populations. Alcohol-induced insomnia can resolve itself after a period of abstinence.

But besides depression, insomnia and cognitive impairment, the literature suggests that other alcohol-induced psychiatric disorders are really quite rare. Although anxiety, for example, is common during acute withdrawal, it appears that this is overwhelmingly independent anxiety, rather than alcohol-induced.

So to differing degrees, some evidence supports alcohol withdrawal as the cause of some of the symptoms ascribed to PAWS. But the question of whether these disorders of sleep, mood and cognition can justifiably be clumped together to form a syndrome—rather than being viewed as independent symptoms linked only by a common cause—is not conclusively answered by existing evidence.

And although it’s beyond the scope of this article to discuss substance-induced psychiatric disorders for drugs other than alcohol, it is worth noting that a 1995 paper by Heather Ashton estimated that only about 10-15 percent of subjects withdrawn from benzodiazepines, the best-evidenced drug association, manifested PAWS.

Based on all of this, I would argue that the DSM is right to exclude PAWS. There aren’t enough grounds to establish it as a multi-symptom syndrome induced by withdrawal from alcohol (and most other drugs). And doing so would carry serious risks. 

At the same time, we should not invalidate anyone’s experiences by telling them that what they are experiencing is not real, including if they ascribe it to PAWS. As always, we need to meet people “where they’re at” in helping them to deal with whatever issues they have.

PAWS has gone on to lend itself, frequently, to scare tactics. On current evidence, nobody should be hyping it.

Gorski and Miller based their idea of PAWS on the now largely debunked notion that alcohol causes permanent loss of brain function, and claimed that 75-95 percent of people who had been addicted to alcohol or other drugs were suffering from brain damage. 

For Gorski and Miller, AA was the cure for everything, including PAWS—and refusing to go to AA was itself a symptom of the brain damage behind PAWS.  

PAWS has gone on to lend itself, frequently, to scare tactics: Telling people that they can’t trust their own brains in order to make them subservient to an AA sponsor or to treatment.

Telling people who have just become abstinent that they are doomed to suffer from years of depression, insomnia and brain dysfunction is not only broadly untrue, but also potentially harmful. Suggestion is powerful, and may become self-fulfilling. It is better to deal with problems as they crop up than to induce them iatrogenically. 

On current evidence, nobody, least of all treatment and recovery organizations, should be hyping PAWS to add to the fears of stigmatized people who use alcohol and other drugs.

Photograph by Zoelle Suo via Unsplash 

The post Post-Acute Withdrawal Syndrome After You Quit Alcohol: Is It Real? appeared first on Filter.

However, the data do not bear this out. Some people with addictions have co-occurring post-traumatic stress disorder—and PTSD rates are much higher in this group than in the general population—but the majority do not. 

Living beings have a limited behavioral repertoire to respond to infinite possible environmental stimuli. In physics, we try to find a single cause for many different effects, like the law of gravitation. In biology, however, the same response is typically elicited by many different stimuli. Flight, for example, is one common biological response, but there are countless different things we may run from.

We are all different, and trying to reduce all addictions to a single cause does us a great disservice as humans.

Substance use disorder, similarly, can have many different causes. For some people, it has its roots in trauma—but for others it’s depression or anxiety, and for others still, the causes do not lie in any co-occurring disorder. We are all different, and trying to reduce all addictions to a single cause does us a great disservice as humans.

Let’s look at a number of major data sources, which measured their findings in quite different ways, to see what they tell us about addiction and co-occurring mental health disorders, which we’ll abbreviate as CMHD.

First, we’ll take SAMHSA’s annual National Survey on Drug Use and Health (NSDUH). NSDUH does not measure different mental health conditions individually, and probably fails to catch personality disorders. But it includes a general measurement of psychiatric impairment based on depression, anxiety, etc.

The survey for 2021, which we’ll focus on, had 69,850 subjects. It found that a little under half (44 percent*) of people with any substance use disorder had CMHD. However, rates varied greatly: Just under 40 percent of people with an alcohol use disorder had CMHD, whereas that applied to almost 55 percent of people with a drug use disorder (involving any drug, pharmaceutical or illicit, other than alcohol).

Interestingly, the Epidemiological Catchment Area (ECA) study, conducted from 1980-1985 with 20,291 subjects (19,182 survey completers), showed very similar rates. It found that 37 percent of people with an alcohol use disorder had CMHD, compared with 53 percent of people with a drug use disorder. 

Returning to NSDUH, we find striking variations between individual drugs. For example, almost 75 percent of people with a heroin use disorder had CMHD. I’ve illustrated the numbers in the graphic below:

Although drugs’ chemical differences might have some effect, it would be a mistake to emphasize this. The difference alone between heroin use disorder (75 percent CMDH) and opioid use disorder (just under 60 percent) points to the importance of other factors—such as legality, availability, cultures and stigmatization.    

NSDUH also measures severity of CMHD. People with alcohol use disorder were found to have the lowest rate of severe co-occurring disorders: just over 12 percent. Among people with any drug use disorder, that figure was almost 20 percent. People with methamphetamine use disorder showed the highest rate, at over 28 percent. 

Perhaps unexpectedly, people with heroin use disorder were found to have relatively low rates of severe CMHD, at just over 14 percent:

NSDUH also breaks down its figures by gender. Except for opioid use disorder, reported rates of substance use disorder are somewhat higher among men than women:

But what we see across the board—as in many other studies—are much higher rates of CMHD among women than among men. 

Among women with any substance use disorder, almost 55 percent in the 2021 NSDUH survey were found to have CMHD, compared with under 36 percent of men. For alcohol use disorder, it was just under half of women versus a little under a third of men. The gender gap persisted across all substances; for methamphetamine use disorder, almost 83 percent of women were found to have CMHD:

Since all of the studies referred to in this article were cross-sectional, it is important to note that no deductions about causality can be made. The studies all asked their subjects questions about symptoms and behaviors, and diagnoses were assigned based on the answers. The questions used varied widely from study to study, which may help explain why prevalence estimates also sometimes varied greatly.

Alvaro Castillo-Carniglia et al. published a 2019 paper which reviewed the research on CMHD in people with alcohol use disorder (AUD). According to this paper, 16 studies found co-occurring antisocial personality disorder in people with AUD. But the studies differed wildly in their estimates of the percentages—ranging from 1-56 percent, with a median value of 18 percent. Seven studies, also addressing AUD, looked at co-occurring borderline personality disorder: Their figures ranged from 6-66 percent, with a median value of 21 percent.

One study found major depressive disorder in 37 percent of people who’d had a diagnosis of alcohol use disorder at some point in their lifetimes. In people with a diagnosis of AUD in the past year, rates of major depressive disorder ranged from 4-22 percent across several studies. One study also found the prevalence of ADHD in adults with current AUD to be 33 percent.

Regarding anxiety, the ECA survey found that 19.4 percent of people with AUD had had a diagnosis of some type of anxiety disorder in their lifetime. 

Meanwhile, the National Comorbidity Survey (NCS), conducted from 1990-1992 with about 8,000 subjects, found that 8.6 percent of men with AUD had had a generalized anxiety disorder diagnosis at some point in their lives; for women, it was 15.7 percent. For diagnoses of panic disorder, the numbers were 3.6 percent for men and 12.9 percent for women. For social phobia diagnoses, it was 19.3 percent for men and 30.3 percent for women.

The NCS survey also looked at PTSD, finding that among women with AUD, 26.2 percent had a PTSD diagnosis at some point in their lives, compared with 10.3 percent of men. 

Substance use treatment providers must never assume they know best about their clients. People are the experts on their own lives.

The ECA survey found schizophrenia in 3.8 percent of people with AUD (the prevalence of schizophrenia in the general US population is estimated at between 0.25-0.64 percent). Bipolar disorder was found in 3.5-5 percent of people with a diagnosis of AUD at some point in their lives.

Finally, a 2020 paper by Elizabeth A. Evans et al. measured CMDH among people with a diagnosis of opioid use disorder (prescription or heroin) at some point in their lives, and found the following: PTSD (35.5 percent of women and 17.4 percent of men); major depressive disorder (women 59.6 percent, men 42.0 percent); anxiety disorder (women 54.6 percent, men 30.8 percent); and personality disorder, such as borderline, antisocial, etc. (women 55.1 percent, men 57.0 percent).

Very importantly, broad figures like all of these undoubtedly disguise much greater concentrations of CMHD in specific populations. Gabor Maté worked with unhoused people with heroin use disorder in Vancouver’s Downtown Eastside, and it is not surprising that he found very high rates of co-occurring trauma and PTSD. 

However, Maté’s sample doesn’t generalize to all people with substance use disorders.

People with PTSD or other co-occurring disorders deserve treatment, and sadly they too rarely get it. But people with substance use disorders who do not have PTSD will not be helped by PTSD treatment, and may even be harmed by it. 

All of which is to say that substance use treatment providers must never assume they know best about their clients. People are the experts on their own lives. How do we best match substance use treatment to the individual? The first step is to ask the person what they want. 

*Percentages were calculated using SAMHSA’s online Public-use Data Analysis System (PDAS). The following variables were used:

Photograph by Stefano Pollio via Unsplash. Graphics by Kenneth Anderson.

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