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jake-head-shot.jpgJake Young is a MD/PhD student at Mount Sinai School of Medicine focusing in Neuroscience. He is due to graduate in 2032. He received a BS and a MS in Biological Sciences from Stanford University -- where he spent most of his time drinking heavily and building vegetable catapults instead of learning information that would now be eminently useful. When he is not failing terrifically to perform his sworn duties, he enjoys watching bad movies, ethnic food, and running.

Pure Pedantry is a blog about science -- social sciences and otherwise -- as well as academic and scientific culture. No one can live on science alone, so I also like to dwell on pop culture, periodically explore the humanities, and indulge in other types of geeky goodness.

Jake is joined periodically by two wonderful guest bloggers: Kara Contreary and Kate Seip. See the About Page.

DISCLAIMERS: 1) Jake Young is not a licensed physician (yet). He is merely a medical student. The information published on this site is not intended for use in medical decision making. Please seek advice from a licensed, medical professional before making any health decisions. 2) The opinions expressed are my own or those of my co-bloggers. They do not represent the views of SEED magazine or the educational establishments we currently attend.

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On the Merits of Postponing Your Alcoholism

Category:
Posted on: July 6, 2006 12:14 PM, by Jake Young

The New York Times has a interesting article about the long term consequences to adolescent brains of early drinking. To whit:

In experiments conducted by the Duke team, the reformed rat drinkers learned mazes normally when they were sober. But after the equivalent of only a couple of drinks, their performance declined significantly more than did that of rats that had never tippled before they became adults. The study was published in 2000 in the journal Alcoholism: Clinical and Experimental Research. Other research has found that while drunken adolescent rats become more sensitive to memory impairment, their hippocampal cells become less responsive than adults' to the neurotransmitter gamma-amino butyric acid, or GABA, which helps induce calmness and sleepiness.

This cellular mechanism may help explain Jack London's observation, in "John Barleycorn: Alcoholic Memoirs," that when he was a teenager he could keep drinking long after his adult companions fell asleep.

"Clearly, something is changed in the brain by early alcohol exposure," Dr. Swartzwelder said in an interview. "It's a double-edged sword and both of the edges are bad.

"Teenagers can drink far more than adults before they get sleepy enough to stop, but along the way they're impairing their cognitive functions much more powerfully."

Alcohol also appears to damage more severely the frontal areas of the adolescent brain, crucial for controlling impulses and thinking through consequences of intended actions -- capacities many addicts and alcoholics of all ages lack.

In 2000, Fulton Crews, a neuropharmacologist at the University of North Carolina, subjected adolescent and adult rats to the equivalent of a four-day alcoholic binge and then autopsied them, sectioning their forebrains and staining them with a silver solution to identify dead neurons.

All the rats showed some cell die-off in the forebrain, but the damage was at least twice as severe in the forebrains of the adolescent rats, and it occurred in some areas that were entirely spared in the adults.

Although human brains are far more developed and elaborate in their frontal regions, some functions are analogous across species, Dr. Crews said, including planning and impulse control. During human adolescence, these portions of the brain are heavily remolded and rewired, as teenagers learn -- often excruciatingly slowly -- how to exercise adult decision-making skills, like the ability to focus, to discriminate, to predict and to ponder questions of right and wrong.

Basically what I heard from this article is that there is concern that early alcohol abuse may cause long lasting receptor, particularly GABA receptor, changes and possibly increased neurotoxicity in adolescent brains. (I am not certain I buy the neurotoxicity bit...I haven't read the paper but I don't think that silver staining is a particularly good way to detect apoptosis in neurons.)

Alcohol induced changes may have lasting behavioral consequences due to their direct effects on areas of the brain which are directly responsible for preventing more drinkning. Thus, they drink on, against the current of neurological determinism, borne back ceaselessly into their alcohol soaked pasts.

It makes me kind of happy I was a goody-goody in high school. Now I can drink knowing that as opposed to direct neurotoxicity, I only have to worry about liver failure, vitamin deficiency, Wernicke-Korsakoff syndrome, ulcers, aspiration pneumonia, social dysfunction...

UPDATE: Some of the commenters have expressed some skepticism as to the good intent of this research. Quitter has the folllowing:

So, when they say, 14-year-olds who drink are more likely to be alcoholic it is also quite likely that 14-year-olds who seek out alcohol and binge drink might have a genetic predisposition for that behavior. Any other conclusion kind of defies common sense because it requires you to compare people who start drinking at early ages to those who wait until they're 21. Now, anyone who has grown up and been to college knows what those who wait until 21 are like. Of course they will never become alcoholics, they're prudes! Always have been, probably always will be.

I am not quite willing to question the good intent of the researchers yet. I imagine the researchers were people who like most of us raised their hell in college, came very close to loosing something or someone, and would like to see children be safe. Likewise, I don't think many of them would advocate complete prohibition of alcohol.

But genetics and a slowly declining middle school use of alcohol (as daksya showed) do not in my mind take away from the wisdom in having some programs to encourage kids to delay and limit their drinking. Everything that we know about behavioral genetics particularly behavioral genetics of disease -- this IS in part what I study -- shows that genetic effects on behavior are important only in particular environmental contexts. It is important to identify biological and environmental risks and try to prevent them to limit behavioral disorders. This does not involve sweeping kids into anti-alcohol camps gestapo-style, but it does involve acknowledging that if they drink early that will have lasting consequences. Similarly, a declining rate is not a zero rate -- even 6% of 8th graders hurting their own brains can be a cost on society.

UPDATE: Corpus Callosum adds in reference to quitter's comment:

There probably is some truth to that (although I personally would not phrase it so stridently). It sure is a lot easier to get funding for a study that might deter substance abuse, than it is to get funding for a study on medical uses of cannabis.

My own cynicism leads me to comment of the conclusion in the abstract of the JPAM article: "There is a need to screen and counsel adolescents about alcohol use and to implement policies and programs that delay alcohol consumption."

It would be hard to argue with those points. However, the article does not really support the last point. While they do show that earlier onset of drinking is associated with a worse prognosis, that does not show that getting a kid to delay the onset of drinking will improve the prognosis. A completely different kind of study would be needed to show that.

Comments

Eh,
I read the science funded by the anti-alcohol and anti-drug agencies with more and more skepticism and disgust. There are many better hypotheses that fit this data.

For instance, I've been arguing with that silly piece of data that those who start drinking earlier are more likely to become alcoholics since it came out. This may be true, but it doesn't necessarily say what they think it says. For instance, there was no attempt to identify, eliminate or control for those who would be predisposed to alcoholism in the study. Genetic studies of alcoholism are clear, there is a definite genetic component that leads some individuals to seek out drugs and alcohol more readily and become addicted. You are more likely to be an alcoholic if you have an alcoholic parent or other first degree relative, even if you are adopted and weren't raised by them, for instance. Alcoholism is not purely environmental

So, when they say, 14-year-olds who drink are more likely to be alcoholic it is also quite likely that 14-year-olds who seek out alcohol and binge drink might have a genetic predisposition for that behavior. Any other conclusion kind of defies common sense because it requires you to compare people who start drinking at early ages to those who wait until they're 21. Now, anyone who has grown up and been to college knows what those who wait until 21 are like. Of course they will never become alcoholics, they're prudes! Always have been, probably always will be.

Then theres these freaking receptor studies. What a load of crap those have been. For years they've been trying to freak kids out about MDMA by showing them PET scans of X users compared to a normal control. And it's totally misleading! Of course if you use a drug that increases serotonin levels in the brain you're going to see a concommitant decrease in receptor density! Does that mean anything? Maybe, maybe not, but it certainly doesn't mean those areas of the brain are dead or have disappeared, which is what showing those images are meant to suggest.

The whole field is just filled with prohibitionists in disguise, overinterpreting data to freak people out rather than rationally determining what would probably be some really interesting results.

Posted by: quitter | July 6, 2006 12:45 PM

I am not certain I buy the neurotoxicity bit...I haven't read the paper but I don't think that silver staining is a particularly good way to detect apoptosis in neurons.

I'm not going to look up the actual paper either, but remember, apoptosis isn't the only kind of cell death. For this kind of study, the authors would want to see as broad a representation of toxicity as possible.

Posted by: Brian | July 6, 2006 7:27 PM

I find the comments to this piece disturbing. Are they written as scientists or people with NO children?
The problem in our high schools, colleges and our MIDDLE schools is increasing exponentially.
Even incidental and anecdotal science has some value. Prohibition is never going to work, but careful education and training in moderation can make a difference.
To those who want to divorce science from clinical alcohol treatment and education, sophistry and narcissistic babble about poor science serves no useful purpose other to see one's own writing in print(and marvel at it's elitist, unhelpful message).

Posted by: JT Young MD | July 7, 2006 1:28 AM

It's not that it's incidental or anecdotal. It's just wrong or at the very least sloppy. I believe they are coming to erroneous conclusions. Sorry if that drives my ire and isn't appropriately puritan for your taste, but I stand by my assertion that bullshit is bullshit, even if you don't want to hear it.

I tell you what's even more unhelpful to those trying to prevent immoderation in kids, lying and exaggerating to get the party line of "drugs are bad m'kay" across. Kids can smell it, and once they learn they've been lied to, your entire message is lost.

Think about the study showing 14-year-olds that drink are more likely to be alcoholic. Rather than blaming the kids youthful activities for their adult alcoholism, what about addressing the very reasonable hypothesis that this reflects a predisposition to drinking that is more genetic? If you could prospectively identify those that are more likely to be alcoholic, that wouldn't only be useful for understanding the mechanism of alcoholism but might be useful for identifying and targeting teens at risk for adult alcoholism with a preventative treatment and education. Instead the interpretation is "early drinking makes you an alcoholic" and that's probably BS, or at least unproven by this study design.

Further where is your evidence that the problem is increasing exponentially? I smell bullshit there. Every generation thinks the next one is out of control, and the data on kids today doesn't show an increase in drinking and drug use over, say, kids in the 70s. That and drugs they use vary a great deal. Cocaine, heroine and alcohol are down right now, but pills inhalents and marijuana are up. An overview of illicit drug use may be found here, more updated data here .. This data indicates things appear to be trending downwards, including alcohol. Why don't you try looking at some data before saying things are increasing EXPONENTIALLY.

Posted by: quitter | July 7, 2006 2:55 AM

The problem in our high schools, colleges and our MIDDLE schools is increasing exponentially.

Cite?

As per the MTF surveys, percentage who have been drunk in the month prior to the survey

8th grade
1999: 9.4
2000: 8.3
2001: 7.7
2002: 6.7
2003: 6.7
2004: 6.2
2005: 6.0

10th grade
1999: 22.5
2000: 23.5
2001: 21.9
2002: 18.3
2003: 18.2
2004: 18.5
2005: 17.6

12th grade
1999: 32.9
2000: 32.3
2001: 32.7
2002: 30.3
2003: 30.9
2004: 32.5
2005: 30.2

Posted by: daksya | July 7, 2006 4:36 AM

Thanks for posting that daksya.

I actually linked to that data last night in a post (from 1970 the drop in drinking and drug use is even more dramatic) but was censored for some reason.

Posted by: Quitter | July 7, 2006 12:24 PM

Here is the source of that data set by the way. See in particular this table which shows the trends downwards since the 70s of every drug (except those which didn't exist) including alcohol.

The problem is actually getting better, but I don't think it's from scare tactics. My problem with this paper isn't that it's incidental or anecdotal, and would also argue with your assertion that anecdotal information is valuable. My problem is that this data is being misread to suggest early drinking is causative of alcoholism, which is missing the point, and comparing two very different groups of kids inappropriately. I would like this kind data to instead be used to identify behaviors prospectively, such as early drinking, which might be predictive of an alcoholic susceptibility in kids. Eventually we could even consider genetic screening for susceptibility. Simply saying drinking before 14 increases your susceptibility to alcoholism is a bit glib, reading causation where it probably doesn't exist.

I don't see how that makes me a horrible person. Sorry that you read my writing as elitist, narcissistic and nasty, but bad science tends to piss me off, and I'm saying that as a scientist, so chill out. You also haven't been reading the full canon of stuff that comes out of the anti-drug abuse funding, it is pretty ridiculous at times. Think, the scientific equivalent of Reefer Madness.

Posted by: quitter [TypeKey Profile Page] | July 7, 2006 1:05 PM

Woah, I can't say that I agree with this.


Even incidental and anecdotal science has some value. Prohibition is never going to work, but careful education and training in moderation can make a difference.

Proposing to base treatment on studies that offer only anecdotal evidence is just a bad idea. There was anecdotal evidence in the not-so-distant past that suggested that only gays got AIDS. Clearly, running with that line of evidence would not have helped the problem.

Good science aside, what happens if you tell kids that drinking puts them at risk for XYZ, and then several months later, another, more comprehensive study proves that you were pretty convincingly wrong? Whoops - there goes your credibility...

Posted by: Chris | July 10, 2006 2:41 AM

Not to nitpick, but... You always spell "To whit" wrong.

It's "to wit". Related to "wissen" in German, "wit" in English, these roots have to do with "knowing".

"Whit" is used in the phrase "not a whit" meaning "not even a little bit".

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