And another response to Dr. Johnson

From The Huffington Post

Deni Carise

Chief Clinical Officer, Phoenix House
Posted: August 16, 2010 12:00 PM

Examining the Viability of Substance Abuse Treatment Today

Earlier this week, I was more than a little put off by Bankole Johnson's Washington Post editorial, "We're Addicted to Rehab. It Doesn't Even Work." It's interesting to note that this piece comes just six months before the release of his new book on medications that "conquer alcoholism," which will join countless other tomes that also claim to have the cure.

In his searing op-ed, Johnson, chair of psychiatry and neurobehavioral sciences at the University of Virginia, argues that there is little empirical evidence to suggest that substance abuse treatment programs are effective. Making sweeping generalizations, he points a finger at our country's treatment centers, including nonprofit providers, calling them both "ruinously expensive" and "divorced from state-of-the-art medical knowledge."

I take issue with these charges first and foremost as a scientist who has dedicated her career to studying the effectiveness of substance abuse treatment. In equal measure, I disagree with Johnson's allegations as a person in long-term recovery who might not be here were it not for the treatment I received.

Johnson calls substance abuse a devastating disease, yet he fails to acknowledge the limitations of treating a condition that is chronic by nature, like diabetes and hypertension. When evaluating the effectiveness of a particular medication for diabetes, treatment providers don't expect their diabetic patients to be "cured" after one treatment, nor do they define success as never having another sugar crisis. Similarly, defining successful substance abuse treatment as one that produces 100 percent abstinence for the rest of a person's life is a naïve and useless benchmark. However, if we define success as learning to manage your condition and gaining the support needed to do so, there are literally hundreds of controlled studies documenting the effectiveness of various forms of treatment. And they meet FDA levels of effectiveness.

As for Johnson's claim that substance abuse treatment is "too costly for most people," this is simply not the case. The two programs he mentions, Promises and Hazeldon, are geared toward individuals of higher socioeconomic status. However, there are many programs in our country that serve those with more modest means. When I entered substance abuse outpatient treatment in 1984, I paid just five dollars for each counseling session I attended. I later found out that the remainder of my treatment costs had been covered by the federal block grant. At Phoenix House, where our programs receive both state and federal funding, some clients stay with us even when they have no funds to cover their care. Many other non-profits do the same. Listing two expensive programs as if they are representative examples does not convey the wide range of treatment options available to people from all walks of life.

Johnson primarily aims his criticism at AA and it's true that not every substance abuser who enters AA will achieve long-term recovery. Likewise, not every diabetic who tries a particular medication will achieve long-term recovery from diabetes. As with other chronic conditions, there are many evidence-based treatment methods for substance abuse--not just the 12-step model. To discredit an entire spectrum of care that has worked for hundreds of thousands of people--and has been backed by scientific research--is to ignore the facts. It says to those of us who work with substance abusers each day that our efforts to help them are futile. And it says to those who need treatment that there is no real help available. That's inaccurate and irresponsible.

I'm certainly not dismissing the benefits of incorporating medication into substance abuse treatment. That would be irresponsible as well. But research has shown that meds alone will not produce a cure and traditional "rehab" components such as group counseling are equally important. Dr. Johnson himself runs a treatment program that includes cognitive behavioral therapy in addition to pharmacology. So why can't he acknowledge that any and all empirically-proven methods of helping people with this disease need to be included in their treatment options?

Maybe it's simply the fact that presenting a more balanced op-ed piece wouldn't sell as many books.

More on Dr. Johnson's Critique of 12-step Programs

Letters to the editor in response:

The pros and cons of 12-step rehab

Thursday, August 12, 2010

I take issue with Bankole A. Johnson's Aug. 8 Outlook commentary, "12 steps to nowhere," which essentially devalued alcohol rehabilitation in order to sell "effective medicine" to treat alcoholism.

I have been treating alcoholism in the Defense Department and the Navy for 33 years. Alcoholics Anonymous works for us. Both the Defense Department and the Navy have used AA and Twelve Step Facilitation Treatment for 40 years and have a recovery rate five years after treatment of about 75 percent. The Navy has some experience with drinking -- and it knows how to treat alcoholism. Our lives depend on it. Marines like to go to war sober.

Dr. Johnson is paid to develop drugs as the primary treatment for alcoholism. However, he knows so little about how AA works and takes quotes from the Big Book completely out of context.

Two million sober members of AA, most not on medication, will see his article and know how wrong he is for them.

Ronald Earl Smith, Bethesda
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The writer is a captain in the Navy's medical corps and a senior psychiatrist and psychoanalyst at the National Naval Medical Center.

--

I attended 150 12-step meetings in 90 days (versus the prescribed 90 meetings in 90 days) and have not been to a meeting since, in about 12 years. I also have had no alcohol in that time. The pros and cons of 12-step rehab

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I agree with everything Bankole Johnson said about the problems with 12-step rehabilitation. However, he failed to appreciate that if AA works for only a minority of people who try it, for that group "it works if you work it." Let others try something else.

If Dr. Johnson and his colleagues find a better cure, more power to them. Only do not let them or anyone say that AA does not work. It does for countless thousands, and at virtually no cost but time and effort.

Philip Saunders, Dunn Loring

--

In his commentary, Bankole Johnson stated that "no experimental studies have unequivocally demonstrated the effectiveness" of the 12-step approach to addiction.

In an experimental study in 2006 conducted at the Veterans Affairs Palo Alto Health Care System, randomly selected addicted patients who received a structured introduction to Alcoholics Anonymous and Narcotics Anonymous had a more than 60 percent greater reduction in the severity of their substance abuse problems six months later than did patients not receiving such an introduction. In a different experimental study, also in 2006, of a 12-step-oriented sober-living home, addicted individuals were, relative to those receiving other forms of care, twice as likely to be abstaining from substance use and three times as likely to not be incarcerated.
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Both of these widely cited studies were funded by major, peer-reviewed federal research grants and were published in high-profile peer-reviewed journals.

Dr. Johnson's failure to mention them resulted in a mischaracterization of what research has established about the effectiveness of the 12-step approach.

Keith Humphreys, Palo Alto, Calif.

Controversial editorial in Washington Post

In case you missed it, Bankole Johnson wrote an op-ed for the Washington Post that appeared 2 days ago. Here's a link: http://www.washingtonpost.com/wp-dyn/content/article/2010/08/06/AR2010080602660.html

You may need to register with the Post to see this link, but it's free and they don't hassle you in any way, such as spam or solicitations.

What do you think about his piece? I'm really interested in hearing.

The Need for Medical Treatment for Addiction

It's been some time since I've blogged. For those of you who are followers or check in on the blog I'm sorry for the lack of activity. The transition to Minnesota has taken a lot of energy, but I have a lot of progress to report.

My practice here in Minnesota has really taken off. Once the other physicians in the hospital and indeed throughout the entire community have become aware of an alternative to another run through rehab the referrals have become consistent. I was just away from the hospital for a week, and I suspect that the hospitalists who take care of most hospitalized patients have missed me. Once they got a taste of getting help with complex pain patients, difficult withdrawal problems, and a physician who was willing to take their referrals for patients with addiction in conjunction with medical and psychiatric disorders, they have gotten very enthusiastic. This is similar to my experience when I first started a clinic for medically ill alcoholics at the Minneapolis VA hospital years ago. The attitude towards alcohol dependent patients admitted with liver disease, pancreatitis, withdrawal, and other problems up to then had been hopeless, nihilistic. What was the use when a consultation resulted in a nurse or counselor suggesting another run through rehab even if the patient had already had that treatment multiple times? But when there was a clinic where these patients could receive ongoing care that incorporated medical, psychiatric and addiction treatment, you could almost feel the change throughout the medical center. Staff became enthusiastic about identifying and referring patients like this to the clinic. It took about 3 years to develop the clinic and figure out how to provide this type of treatment. After that, I received a grant from the the VA to study whether this treatment was effective. In order to do that, we had to assign study participants to either this new clinic or to usual care which consisted of referral to primary care clinic. At that point, it became difficult, because staff were so enthusiastic about this new approach they were reluctant to have patients assigned to usual care. That's the hardest thing about test new treatments; although you might believe strongly in the new treatment you have to be willing to randomized and let the chips fall where they may. It turned out that the new approach was significantly more effective: mortality was reduce by 30% after two years, and more patients were able to achieve abstinence. So I'm finding that the same thing is happening where I currently work at United Hospital in St. Paul. Only it's even better: I'm providing a much broader range of services. One thing that has become apparent: there is a tremendous need for innovation in treating complex chronic pain. Chronic pain and how to appropriately use opioid (narcotic) medication is one of the most difficult and under-appreciated areas in medicine right now.

Vodka Eyeballing: The latest stupid drinking trend

or, "kids do the darnedest things"...

KTLA News (Los Angeles)
Dangerous 'Vodka Eyeballing' Popular with College Students
Eyeballing can cause damage to the optic nerve, leading to blindness.
9:11 AM PDT, May 20, 2010

LOS ANGELES -- A dangerous drinking fad known as "Vodka eyeballing" is growing in popularity on college campuses in the UK and the United States, and experts say it could leave students blind.

So-called "eyeballers" claim it's an instant high with a splash of alcohol giving them a buzz, literally, in the blink of an eye.

But, doctors say, it's a dangerous trend that could cause permanent vision damage.

Dr. Elise Brisco of the Hollywood Vision Center told KTLA that the practice creates an almost instant buzz "because it's going into the central nervous system into the brain."

The alcohol can damage the optic nerve, creating spotty vision and even complete blindness.

"If it's severe enough and there's a lot of optic nerve damage, your vision may not return," Brisco said.

Some eyeballers have posted videos of themselves online, and there are even "fan" pages for the practice on Facebook.

It's believed the dangerous trend started in the United States, but it is quickly gaining popularity at British universities, according to the UK Daily Mail.

Why do you think they call it DOPamine?

More on that infamous substance we all seem to be trying to maximize day to day:

U.S. Department of Health and Human Services
National Institutes of Health
NIH News
National Institute on Alcohol Abuse and Alcoholism (NIAAA) http://www.niaaa.nih.gov

EMBARGOED FOR RELEASE: Tuesday, May 18, 2010 @ 9:00 AM EDT
Contact: NIAAA Press Office, 301-443-3860, NIAAAPressOffice@mail.nih.gov<mailto:NIAAAPressOffice@mail.nih.gov>


Receptor Variant Influences Dopamine Response to Alcohol

A genetic variant of a receptor in the brain’s reward circuitry plays an important role in determining whether the neurotransmitter dopamine is released in the brain following alcohol intake, according to a study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health.  Dopamine is involved in transmitting the euphoria and other positive subjective effects produced by alcohol.

A report of the findings, which help explain the diverse genetic susceptibility for alcohol use disorders, will appear online in Molecular Psychiatry on May 18, 2010.

“By advancing our understanding of the neurobiology that underlies the addictive properties of alcohol, this finding helps us understand why alcohol affects people in very different ways,” says NIAAA Acting Director Kenneth R. Warren, Ph.D. “This kind of information also aids the development of personalized medications for alcohol problems.”

Receptors for brain molecules known as opioid peptides help initiate the neurochemical reactions that underlie the positive effects produced by alcohol.  Activation of the mu-subtype of opioid receptor following alcohol consumption triggers the release of dopamine from the forebrain.

“But there is much variation in alcohol-induced responses that are thought to be related to dopamine,” explains Markus Heilig, M.D., Ph.D., NIAAA clinical director and the study’s senior author.  “Previous studies by our group and others suggest that variants of opioid genes may contribute to the observed variation, possibly through effects on alcohol-induced dopamine release.”

He notes, for example, that people who carry the mu-opioid receptor variant designated as 118G report increased euphoria following alcohol consumption.  Dr. Heilig’s group has reported that a similar mu-opioid receptor variant in monkeys heightened the stimulating effects of alcohol and increased their alcohol consumption.

In the current study, first author Vijay A. Ramchandani, Ph.D., an investigator in NIAAA’s Laboratory of Clinical and Translational Studies, Dr. Heilig, and their colleagues explored whether the 118G mu-opioid receptor variant influences dopamine release from a forebrain region called the ventral striatum in response to alcohol.

Using human positron emission tomography (PET), an imaging technique that allowed the researchers to analyze dopamine activity in the brain, they compared dopamine release in two groups of people that had been given a dose of alcohol. The groups consisted of those who carried a copy of the gene for the 118G mu-opioid receptor variant, and those who carried only genes for the more common 118A variant. They found that only people with the 118G variant had a dopamine response to alcohol – no such response happened in subjects with the 118A receptor variant.

In a separate experiment, they inserted genes for the human 118G or 118A mu-opioid receptor variants into mice and then directly measured the animals’ dopamine response to a dose of alcohol.  Mice with the 118G variant showed a fourfold higher peak dopamine response to the alcohol challenge compared to mice with the 118A variant.

“Taken together, our data strongly support a causal role of the 118G variant of the mu-opioid receptor to confer a more vigorous dopamine response to alcohol in the ventral striatum,” says Dr. Ramchandani. “The findings add further support to the notion that individuals who possess this receptor variant may experience enhanced pleasurable effects from alcohol that could increase their risk for developing alcohol abuse and dependence. It may also explain why these individuals, once addicted, benefit more from treatment with blockers of endogenous opioids.”

Additional Information

Why Meds Work for Some People, but Not for Others<http://nihrecord.od.nih.gov/newsletters/2010/05_14_2010/story2.htm>
NIH Record, 5/14/2010

Alcohol’s effects on endogenous opioids in the brain<http://www.niaaa.nih.gov/Resources/GraphicsGallery/Neuroscience/31_4_endogenous.htm>


The National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health, is the primary U.S. agency for conducting and supporting research on the causes, consequences, prevention, and treatment of alcohol abuse, alcoholism, and alcohol problems. NIAAA also disseminates research findings to general, professional, and academic audiences. Additional alcohol research information and publications are available at www.niaaa.nih.gov<http://www.niaaa.nih.gov>.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

More on "process addictions"

This new study found that the same brain mechanisms that are dysregulated in drug addiction are also dysregulated in binge eating. This is not surprising, of course, since behavior is dysregulated in similar ways in both disorders. That is, the behavior already tells us that the same underlying brain regulatory systems are not working properly, so these studies help confirm what we already suspected. However, these findings are not profound or startling unless one starts with the assumption that behavior can become consistently dysregulated without the corresponding systems in the brain also becoming dysregulated. To put it simply: dysregulated behavior<=>dysregulated brain. In addition, social interactions also have a correlary dysfunction, and there are additional corresonding changes at other levels of analysis, such as gene function, metabolism, and so forth. In other words the system changes at all levels at once. The other thing to keep in mind is that a study such as this does not mean that compulsive behaviors are just and only "brain diseases," since there are correlary changes up and down the system chain of events. It also does not mean the the only appropriate place to intervene is by directly manipulating neurotransmitters, e.g. medication therapy. Although that might be a useful tool, because all of these subsystems are interconnected, it is also possible to change the brain by changing the environment, or to focus on changing behavior and so forth. In addition, the study does not demonstrate that "obese people really cannot help it," or at least it is not news that this is true. We already knew that, with hundreds of studies showing that 95% of weight loss is regained after 5 years. Finally, remember that, as technically impressive as this study is, it is still a short-term study of rodents, and humans are not rodents. Rodent models give us clues, but findings in rodents do not directly translate to humans.

MW

Compulsive Eating Shares Addictive Biochemical Mechanism With Cocaine, Heroin Abuse, Study Shows


ScienceDaily (Mar. 29, 2010) — In a newly published study, scientists from The Scripps Research Institute have shown for the first time that the same molecular mechanisms that drive people into drug addiction are behind the compulsion to overeat, pushing people into obesity.
The new study, conducted by Scripps Research Associate Professor Paul J. Kenny and graduate student Paul M. Johnson, was published March 28, 2010 in an advance online edition of the journal Nature Neuroscience.
The study's startling findings received widespread publicity after a preliminary abstract was presented at a Society for Neuroscience meeting in Chicago last October. Articles heralding the new discovery appeared in news publications around the world, focusing on the point obese patients have been making for years -- that, like addiction to other substances, junk food binging is extremely difficult to stop.
The study goes significantly further than the abstract, however, demonstrating clearly that in rat models the development of obesity coincides with a progressively deteriorating chemical balance in reward brain circuitries. As these pleasure centers in the brain become less and less responsive, rats quickly develop compulsive overeating habits, consuming larger quantities of high-calorie, high-fat foods until they become obese. The very same changes occur in the brains of rats that overconsume cocaine or heroin, and are thought to play an important role in the development of compulsive drug use.
Kenny, a scientist at Scripps Research's Florida campus, said that the study, which took nearly three years to complete, confirms the "addictive" properties of junk food.
"The new study, unlike our preliminary abstract, explains what happens in the brain of these animals when they have easy access to high-calorie, high-fat food," said Kenny. "It presents the most thorough and compelling evidence that drug addiction and obesity are based on the same underlying neurobiological mechanisms. In the study, the animals completely lost control over their eating behavior, the primary hallmark of addiction. They continued to overeat even when they anticipated receiving electric shocks, highlighting just how motivated they were to consume the palatable food."
The scientists fed the rats a diet modeled after the type that contributes to human obesity -- easy-to-obtain high-calorie, high-fat foods like sausage, bacon, and cheesecake. Soon after the experiments began, the animals began to bulk up dramatically.
"They always went for the worst types of food," Kenny said, "and as a result, they took in twice the calories as the control rats. When we removed the junk food and tried to put them on a nutritious diet -- what we called the 'salad bar option' -- they simply refused to eat. The change in their diet preference was so great that they basically starved themselves for two weeks after they were cut off from junk food. It was the animals that showed the "crash" in brain reward circuitries that had the most profound shift in food preference to the palatable, unhealthy diet. These same rats were also those that kept on eating even when they anticipated being shocked."
Lethally Simple
What happens in addiction is lethally simple, Kenny explained. The reward pathways in the brain have been so overstimulated that the system basically turns on itself, adapting to the new reality of addiction, whether its cocaine or cupcakes.
"The body adapts remarkably well to change -- and that's the problem," said Kenny. "When the animal overstimulates its brain pleasure centers with highly palatable food, the systems adapt by decreasing their activity. However, now the animal requires constant stimulation from palatable food to avoid entering a persistent state of negative reward."
After showing that obese rats had clear addiction-like food seeking behaviors, Johnson and Kenny next investigated the underlying molecular mechanisms that may explain these changes. They focused on a particular receptor in the brain known to play an important role in vulnerability to drug addiction and obesity -- the dopamine D2 receptor. The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food or sex or drugs like cocaine. In cocaine abuse, for example, the drug alter the flow of dopamine by blocking its retrieval, flooding the brain and overstimulating the receptors, something that eventually leads to physical changes in the way the brain responds to the drug.
The new study shows that the same thing happens in junk food addiction.
"These findings confirm what we and many others have suspected," Kenny said, "that overconsumption of highly pleasurable food triggers addiction-like neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating. Common mechanisms may therefore underlie obesity and drug addiction."
Consistent with common mechanisms explaining addiction and obesity, levels of the D2 dopamine receptors were significantly reduced in the brains of the obese animals, similar to previous reports of what happens in human drug addicts, Kenny noted. Remarkably, when the scientists knocked down the receptor using a specialized virus, the development of addiction-like eating was dramatically accelerated.
"This addiction-like behavior happened almost from the moment we knocked down the dopamine receptors," Kenny noted. "The very next day after we provided access to the palatable food, their brains changed into a state that was consistent with an animal that had been overeating for several weeks. The animals also became compulsive in their eating behaviors almost immediately. These data are, as far as we know, the strongest support for the idea that overeating of palatable food can become habitual in the same manner and through the same mechanisms as consumption of drugs of abuse."
The study was supported by a Bank of America Fellowship, The Margaret Q. Landenberger Research Foundation and the National Institutes of Health.