Aa history Lovers 2010 moderators Nancy Olson and Glenn F. Chesnut page

Buddy

System," issue 17.10.) And in April, a paper published in Annals of Internal

Medicine concluded that a person is 50 percent more likely to be a heavy

drinker if a friend or relative is a boozehound. Even if an alcoholic's

nonsober friends are outwardly supportive, simply being around people for

whom drinking remains the norm can nudge someone into relapse. It is much

safer to become immersed in AA's culture, where activities such as studying

the Big Book supplant hanging out with old acquaintances who tipple.

As for the steps themselves, there is evidence that the act of public

confession-enshrined in the fifth step-plays an especially crucial role in

the recovery process. When AA members stand up and share their emotionally

searing tales of lost weekends, ruined relationships, and other

liquor-fueled low points, they develop new levels of self-awareness. And

that process may help reinvigorate the prefrontal cortex, a part of the

brain that is gravely weakened by alcohol abuse.
To understand the prefrontal cortex's role in both addiction and recovery,

you first need to understand how alcohol affects the brain. Booze works its

magic in an area called the mesolimbic

pathway-the reward system. When we experience something pleasurable, like a

fine meal or good sex, this pathway squirts out dopamine, a neurotransmitter

that creates a feeling of bliss. This is how we learn to pursue behaviors

that benefit us, our families, and our species.
When alcohol hits the mesolimbic pathway, it triggers the rapid release of

dopamine, thereby creating a pleasurable high. For most people, that buzz

simply isn't momentous enough to become the focal point of their lives. Or

if it is, they are able to control their desire to chase it with reckless

abandon. But others aren't so fortunate: Whether by virtue of genes that

make them unusually sensitive to dopamine's effects, or circumstances that

lead them to seek chemical solace, they cannot resist the siren call of

booze.
Once an alcoholic starts drinking heavily, the mesolimbic pathway responds

by cutting down its production of dopamine. Alcohol also messes with the

balance between two other neurotransmitters: GABA and glutamate. Alcohol

spurs the release of more GABA, which inhibits neural activity, and clamps

down on glutamate, which stimulates the brain. Combined with a shortage of

dopamine, this makes the reward system increasingly lethargic, so it becomes

harder and harder to rouse into action. That's why long-term boozers must

knock back seven or eight whiskeys just to feel "normal." And why little

else in life brings hardcore alcoholics pleasure of any kind.

As dependence grows, alcoholics also lose the ability to properly regulate

their behavior. This regulation is the responsibility of the prefrontal

cortex, which is charged with keeping the rest of the brain apprised of the

consequences of harmful actions. But mind-altering substances slowly rob the

cortex of so-called synaptic

plasticity, which makes it harder for neurons to communicate with one

another. When this happens, alcoholics become less likely to stop drinking,

since their prefrontal cortex cannot effectively warn of the dangers of bad

habits.
This is why even though some people may be fully cognizant of the problems

that result from drinking, they don't do anything to avoid them. "They'll

say, 'Oh, my family is falling apart, I've been arrested twice,'" says Peter

Kalivas, a neuroscientist at the Medical University of South Carolina in

Charleston. "They can list all of these negative consequences, but they

can't take that information and manhandle their habits."

The loss of synaptic plasticity is thought to be a major reason why more

than 90 percent of recovering alcoholics relapse at some point. The newly

sober are constantly bombarded with sensory cues that their brain associates

with their pleasurable habit. Because the synapses in their prefrontal

cortex are still damaged, they have a tough time resisting the urges created

by these triggers. Any small reminder of their former life-the scent of

stale beer, the clink of toasting glasses-is enough to knock them off the

wagon.
AA, it seems, helps neutralize the power of these sensory cues by whipping

the prefrontal cortex back into shape. Publicly revealing one's deepest

flaws and hearing others do likewise forces a person to confront the

terrible consequences of their alcoholism-something that is very difficult

to do all alone. This, in turn, prods the impaired prefrontal cortex into

resuming its regulatory mission. "The brain is designed to respond to

experiences," says Steven Grant, chief of the clinical neuroscience branch

of the National Institute on Drug Abuse. "I have no doubt that these

therapeutic processes change the brain." And the more that critical part of

the brain is compelled to operate as designed, the more it springs back to

its pre-addiction state. While it's on the mend, AA functions as a temporary

replacement-a prefrontal cortex made up of a cast of fellow drunks in a

church basement, rather than neurons and synapses.

Finally, the 12 steps address another major risk factor for relapse: stress.

Recovering alcoholics are often burdened by memories of the nasty things

they did while wasted. When they bump into old acquaintances they

mistreated, the guilt can become overwhelming. The resulting stress causes

their brains to secrete a hormone that releases corticotropin, which has

been shown to cause relapse in alcohol-dependent lab rats.

AA addresses this risk with the eighth and ninth steps, which require

alcoholics to make amends to people they've wronged. This can alleviate

feelings of guilt and in turn limit the stress that may undermine a person's

fragile sobriety.

Bill W., as Wilson is known today, didn't know the first thing about

corticotropin-releasing hormone or the prefrontal cortex, of course. His

only aim was to harness spirituality in the hopes of giving fellow

alcoholics the strength to overcome their disease. But in developing a

system to lead drunks to God, he accidentally created something that deeply

affects the brain-a system that has now lasted for three-quarters of a

century and shows no signs of disappearing.
But how effective is AA? That seemingly simple question has proven

maddeningly hard to answer. Ask an addiction researcher a straightforward

question about AA's success rate and you'll invariably get a distressingly

vague answer. Despite thousands of studies conducted over the decades, no

one has yet satisfactorily explained why some succeed in AA while others

don't, or even what percentage of alcoholics who try the steps will

eventually become sober as a result.
A big part of the problem, of course, is AA's strict anonymity policy, which

makes it difficult for researchers to track members over months and years.

It is also challenging to collect data from chronic substance abusers, a

population that's prone to lying. But researchers are most stymied by the

fact that AA's efficacy cannot be tested in a randomized experiment, the

scientific gold standard.

"If you try to randomly assign people to AA, you have a problem, because AA

is free and is available all over the place," says Alcohol Research Group's

Kaskutas. "Plus, some people will just hate it, and you can't force them to

keep going." In other words, given the organization's open-door membership

policy, it would be nearly impossible for researchers to prevent people in a

control group from sneaking off to an AA meeting and thereby tainting the

data. On the other hand, many subjects would inevitably loathe AA and drop

out of the study altogether.

Another research quandary is how to account for the selection effect. AA is

known for doing a better job of retaining drinkers who've hit rock bottom

than those who still have a ways to fall. But having totally destroyed their

lives, the most desperate alcoholics may already be committed to sobriety

before ever setting foot inside a church basement. If so, it might be their

personal commitment, rather than AA, that is ultimately responsible for

their ability to quit.
As a result of these complications, AA research tends to come to wildly

divergent conclusions, often depending on an investigator's biases. The

group's "cure rate" has been estimated at anywhere from 75 percent to 5

percent, extremes that seem far-fetched. Even the most widely cited (and

carefully conducted) studies are often marred by obvious flaws. A 1999

meta-analysis of 21 existing studies, for example, concluded that AA members

actually fared worse than drinkers who received no treatment at all. The

authors acknowledged, however, that many of the subjects were coerced into

attending AA by court order. Such forced attendees have little shot at

benefiting from any sort of therapy-it's widely agreed that a sincere desire

to stop drinking is a mandatory prerequisite for getting sober.
Yet a growing body of evidence suggests that while AA is certainly no

miracle cure, people who become deeply involved in the program usually do

well over the long haul. In a 2006 study, for example, two Stanford

psychiatrists chronicled the fates of 628 alcoholics they managed to track

over a 16-year period. They concluded that subjects who attended AA meetings

frequently were more likely to be sober than those who merely dabbled in the

organization. The University of New Mexico's Tonigan says the relationship

between first-year attendance and long-term sobriety is small but valid: In

the language of statistics, the correlation is around 0.3, which is right on

the borderline between weak and modest (0 meaning no relationship, and 1.0

being a perfect one-to-one relationship).
"I've been involved in a couple of meta-analyses of AA, which collapse the

findings across many studies," Tonigan says. "They generally all come to the

same conclusion, which is that AA is beneficial for many but not all

individuals, and that the benefit is modest but significant . I think that

is, scientifically speaking, a very valid statement."
That statement is also supported by the results of a landmark study that

examined how the steps perform when taught in clinical settings as opposed

to church basements. Between 1989 and 1997, a multisite study called Project

Match