Monday, March 12, 2007

Alcohol, neuroscience, genetics & public policy

I earlier presented a liberal-rational choice model of alcohol use and policy. In that model problem drinkers were a ‘nuisance’ minority. Although this soothed the wounds I had experienced from being described on this blog as ‘illiberal’ on drugs policy it really is a limited way of looking at what is a serious social problem. I drafted the notes below that concentrate on 'problem drinkers' for a larger study I am working on – comments are very welcome.

Background.

According to a recent ABS survey (discussed here):

  • Levels of risky drinking have increased 50% over the past 10 years. 15% of male adults and 12% of female adults in Australia drink at 'risky' levels. Women are catching up.
  • Alcohol is the second largest cause of drug-related deaths and hospitalisations in Australia - tobacco beats it - and alcohol is the main cause of deaths on Australian roads.
  • In 2004, the age-standardised rate for male deaths due to alcoholic liver disease was 5.5 per 100,000 and 1.5 per 100,000 for females.
  • In 2004, the age-standardised rate for male deaths with mental and behavioural disorders due to alcohol was 1.9 per 100,000 and 0.4 per 100,000 for females.
  • From 1998-99 to 2004-05, the overall number of hospital separations with principal diagnosis of mental and behavioural disorders per 1,000 population increased by 39% for all ages (by 41% for those under 20 years).
  • Most of the alcohol-related hospital separations among both men and women in 1998 was due to alcoholism and alcoholic liver cirrhosis. The second-largest number was due to road injuries for men and cancer for women.
  • 31,132 died from alcohol-caused disease and injury from 1992-2001; of these 75% were male and 25% female. From 1993-94 to 2000-01, there were over half a million hospitalisations due to risky and high-risk drinking.

Alcohol is not an ordinary consumer good and its consumption cannot be analysed purely using a rational choice model of behaviour. As these statistics indicate people do get addicted to alcohol in an unconscious process that can eventually take over and ruin their lives.

Neuroscience and genetics

Most alcoholics start drinking as adolescents. Here standard motivations associated with specific adolescent behaviour (risk-taking, novelty seeking and peer pressures) increase the probability of experimenting with alcohol. At this age it is thought the desire to drink could be linked to incomplete development of certain brain regions involved in the processes of executive control and motivation. Studies suggest that the neuroadaptions that occur in adolescents exposed to certain drugs are different from those that occur in adulthood. Certainly there is a greater vulnerability to alcoholism in individuals who start using alcohol early in life.

Those who abuse alcohol have a higher incidence of mental disorders (depression, anxiety, ADHD and schizophrenia) than do the general population and those with these disorders have a much higher incidence of alcohol abuse. Those with mental disorders may use alcohol and other drugs to self-medicate.

There are also definite genetic influences on the propensity to consume alcohol. These genetic influences may partially underlie certain personality traits such as impulsivity, risk-taking and stress responsivity. Family and twin epidemiological studies suggest estimates of heritability of vulnerability to addictive diseases of between 30-60%.

Like other addictive drugs (opioids, stimulants, nicotine, marijuana) and natural rewards (food, sex, water) alcohol produces euphoria by activating pleasure centres in the brain. Like these other drugs it releases extracellular dopamine levels in the shell of the nucleus accumbens. These pleasure centres have evolved to ensure survival but get ‘hijacked’ by alcohol.

It is this euphoria – particularly if it is enhanced by a genetic predisposition – which encourages repeat use. Like sex you don’t want to just do it once! Over time however alcohol can disrupt these reward circuits and produce dysphoric states such as withdrawal and craving. These negative reinforcements alternate with the positive reinforcement of euphoria to drive a cycle of addiction that becomes etched into the midbrain and frontal structures. This etching reinforces the pursuit of survival-related behaviours by dominating attention and decision-making.

Alcoholics face particular difficulties limiting the number of drinks they consume during a particular episode. The first drink leads to uncontrolled drinking during that episode.

These compulsions to use are not only short-term. Cues associated with alcohol (people, places, an alcohol advertisement) can trigger intense cravings among the alcohol addicted which can trigger relapse into use even after a protracted abstinence of months, years or even indefinitely. These cue-induced cravings can be measured using neuroimaging studies and show dramatic limbic responses that correlate with the degree of the reported craving.

Where does this lead to for public policy?

According to the neuroscience-genetic view excessive alcoholic consumption is due to mistakes that will often be initiated in adolescence. People who initiate consumption at this age may gain short-term pleasures from it but driven by genetic factors, neuroadaptions and alternating positive and negative reinforcements they become dependent on alcohol and find it difficult to control its consumption.

From this perspective alcoholism (contrary to the beliefs of liberals) is probably best viewed as partly a disease.

1. Liberal-rational choice modelling need not be thrown out the window entirely with respect to problem drinkers. Information of the type outlined above can be provided to consumers. There is some controversy over the specific implications of having alcoholic parents for the chance that progeny will develop alcoholism but there is enough evidence to suggest a warning might reasonably be given. If you are male and your (birth) father is an alcoholic you are very likely to face problems managing alcohol consumption should you choose to drink. Information concerning alcohol’s risks needs to specifically target youth while information that targets problem drinkers needs to address issues of problem-recognition, denial and treatment options.

2. Tax policies on alcohol sales are less likely to significantly reduce consumption among addicted users who have markedly inelastic alcohol demands. High taxes may encourage the decision to quit entirely but, given an alcoholic’s compulsion to not stop at one drink, will not reduce the intensity of drinking during a particular consumption episode. High taxes will have their major effects in restricting alcohol consumption among adolescents – these effects are very strong.

3. Restrictions on advertising are very effective in limiting drinking – particularly among youth. They are also useful for curbing drinking among abstaining alcoholics who are subject to cue-driven responses. This points generally to a case for limiting cues in the media, in movies and in public life that provide cues to drink.

4. Supply control measures on the number of outlets and on opening hours are known to limit alcohol consumption and the social damages associated with excessive consumption. Such measures limit the number of cues and also promote the ability of individuals to control their own drinking. Keeping away from cues and knowing that beyond a certain time drinking will be impossible helps people with self-control problems to limit the number of drinks they have.

5. Treatment options emerge as a major way of addressing excessive use. Local GPs can be effective people in cautioning people concerning alcohol problems. Promoting a variety of behavioural and cognitive therapies makes sense as do traditional routes to controlling use such as Alcoholics Anonymous. Given that there are social costs associated with alcoholism there is a case for publicly-subsidising the costs of such services.

6. Treatment options should include pharmacotherapies using drugs such as naltrexone. Naltrexone reduces daily drinking and diminishes alcohol-induced cravings. It even reduces alcohol cravings after a priming drink of alcohol and therefore reduces the tendency of alcoholics to lose control once they begin to drink. Again given the external social costs of alcoholism there is a case for publicly-subsidising such drugs.

10 comments:

conrad said...

Three independent things:

1) You can now go and see a psychologist for free if you have these sorts of addictions. Its more than likely that these guys will employ much better methods than a GP for helping you, and most of them are not going to have religious biases like AA.

2) At least for alcohol, when you talk "genetic" components, you are missing people's differences in the ability to assimilate alcohol (which has nothing to do with personality factors). There's are reason Southern China has extremely low rates of alcoholism -- people simply can't assimilate it well enough to become addicted easily. Three beers is a lot for many Southern Chinese -- 30 is a lot for many Northern Europeans.

3) I still can't get to grips with how to evaluate genetic susceptibilities and individual responsibility well (even if we could estimate the first well). All behavior presumably has some genetic component, so should I treat drug susceptibility like a distribution, or should I treat it like a line in the sand (as done with violence)? Also, do I really need to worry about it to come to the conclusion you do? Even if there were no genetic differences in alchol susceptibility, would it change your argument?

Francis Xavier Holden said...

harry - I think you'll find that hospital separations and etc figures are very very under estimated. Most coding/ reporting doesn't drill down far enough although there is a movement to change this a bit.

Unless someone is dishevelled and obviously pissed then a broken arm from falling off the trampoline at a BBQ after a gutfull of beer won't appear anywhere as alcohol related. Similar for lots of other breaks, cuts, bruises etc.

There is some evidence that many falls of elderly (large cause of admissions in older) are alcohol related but rarely recorded as such. Too far down the coding ladder - at least 3 rung.

hc said...

Conrad, There ios lots of evidence that GPs are very e3ffective at early interventions. Google 'GP early intervention alcohol'. They tend to be believed perhaps because they are known.

I think being borne with the wrong genes is not an out. But I think information about genetic susceptibilities can be given.

conrad said...

HC -- I agree -- I just think that the new government regulations for mental health will mean that we will see better outcomes than just GPs alone.

Being an economist, you might like to do an analysis of it some time, and see whether the extra money spent on psychologists trades off with money not lost on alcoholism and the like. It would be interesting to know if there is an advantage purely on a monetary level.

Mike said...

Hi. nice blog.I've actually never tried drugs and don't plan on it. I've had an uncle that was addicted to marijuana and he lost part of his one leg in a car accident due to drugs. It's scary and I don't understand why someone would want to waste their life doing drugs. drug treament

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Anonymous said...

hi this is anil. I still can't get to grips with how to evaluate genetic susceptibilities and individual responsibility well (even if we could estimate the first well). All behavior presumably has some genetic component, so should I treat drug susceptibility like a distribution, or should I treat it like a line in the sand (as done with violence)? Also, do I really need to worry about it to come to the conclusion you do? Even if there were no genetic differences in alchol susceptibility, would it change your argument?

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