Mitigating the harms of alcohol dependence

Why do some drinkers become dependent while others don’t?

It’s the familiar story of environment interacting with genes. There is a clear genetic risk: in most samples, 60-70% of people with alcohol dependence have a family member with the same problem. Some people who had a dependent parent will actively not drink. Others may drink and follow a more than usually rapid trajectory into dependence.

People probably have different sensitivities to alcohol and so a different capacity for drinking; and you have to drink a lot to become dependent. Perhaps those with a low sensitivity need to drink more to get the same effect. That is one model. Other people take one drink and find it so psychologically reinforcing that they want to carry on.

What is the impact of dependence?

The problem is the classic iceberg. There are a few people at the top whose whole life is spent acquiring, drinking and recovering from alcohol. They will probably have lost functional relationships, their job and their home and can’t engage with anyone who isn’t drinking just as heavily. They have a very narrow repertoire of behaviour. Nothing is positively reinforcing – not even alcohol since it is being drunk to prevent withdrawal.

Then there is the much larger proportion who are still working but for whom most things outside work are alcohol-related. But because they are not drinking spirits, or they are not drinking in the morning, or because they still have a job they may not consider themselves dependent. Yet they may have a drink when they come home and consume two bottles of wine during the evening. People can do that for ten or fifteen years. And they don’t realise that first drink at seven, when they are feeling a bit agitated, is treating early withdrawal.

These people run all sorts of risks – of destroyed family relationships, poor work performance, and of their children growing up thinking that ubiquitous alcohol is the norm. Of course they also risk   high blood pressure, obesity, depression and fatty liver. If they can reduce their drinking enough, the risk of hypertension and low mood and excess weight may go away.

The costs to society are substantial. The UK enquiry into preventable deaths suggested that 84% of liver mortality is attributable to alcohol. Yet treating alcohol dependence is not part of our management of liver disease. We need some more joined-up thinking.

Given the scale of the problem, why are so few patients in treatment?

We are coming to realise the potential value of “starting where the patient is”. Alcohol is a pro-amnestic drug.  A lot of people don’t know they have a problem, or deny it. Others recognise the problem but won’t go for treatment because alcohol and drug services are often provided together and they don’t want the stigma of being seen as “one of them”.  Because alcohol is reinforcing, some people think they can do nothing about it. They can’t imagine living without drink. And the perception that abstinence is the only option is a barrier.

Unlike in the US, that view is now slowly changing in the UK. There are many alcohol dependent people who do not want to abstain but are prepared to try cutting down. That idea at least gets them through the door. And professionals in the field are seeing the potential value of “starting where the patient is.”

Why is early treatment important?

To try and avoid the state in which people are drinking five hundred units a week and have destroyed much of their liver. At that point, the patient may feel the pit is too deep to get out of. And this is why we see high suicide rates.

Earlier intervention has a chance of preventing accrual of that level of damage. And it may be helpful to view alcohol use disorder as something like depression – as a chronic and potentially relapsing condition, but one with is treatable and whose harms can be mitigated.