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Alcohol use has been going since prehistory; even apes will go out of their way to ingest fermented fruits. About 30 % of the population is problem drinkers, 10 % are alcohol dependent and 2-3% are significantly impaired by their disease. One way to screen for the disease is the CAGE questionnaire: Have you tried to Cut down. Do you get Angry when your drinking is criticized? Do you feel Guilty about your drinking? Do you have an Eye-opener? Two yes questions equal a 90% risk of alcohol dependence
The effects of alcohol in the brain are many. It produces euphoria by releasing B-endorphin. It produces a depressant effect by both increasing the effects of GABA (an inhibitor of the brain function) and antagonizing the effects of glutamate (a stimulator of brain function). Other area of the brain are also affected.
We know that alcohol affects the liver, can cause stomach inflammation, can cause muscle weakness including that of the heart. It contributes to cancer and nutritional issues as well. However, I want to focus on the brain and withdrawal so as to review treatments.
With steady use of alcohol, the brain adapts to its' chronic depressant effect by increasing its own baseline excitability. This leads to tolerance and some normalization of function initially but it has consequences. When we can no longer get enough alcohol, the brain will become over excited. The alcoholic will then go into withdrawal with a rapid pulse, high BP, tremors, and anxiety. This will last up to 3-4 days. In severe cases there can be seizures, confusion, and/or hallucinations. The most severe form is delirium tremens (DTs) which is potentially fatal and needs ICU level treatment. Even after the acute phase, mild increases in brain over activity seem to result is long term anxiety, irritability, and triggered cravings. This goes on for months.
We also know that people will develop abnormalities in their endorphin physiology which also leads to increased cravings, depression and the absence of motivation for non alcohol activities. This also seemingly lasts weeks to months.
The risk of alcoholism has a strong genetic component which occurs in two patterns. Early onset alcoholics (before age 25) tend to be male, are involved with multiple drugs and tend to have more impulsive behaviors. Later onset alcoholics tend to be equally split between sexes. It is interesting that medications, such as anti-depressants, which benefit the older group, are known to cause the younger group to drink more often.
The first order of business is detoxification. While many patients choose to do this in a hospital setting, there are protocols for outpatient detoxification which are successful in the great majority of cases. \Sedatives and anti-seizure drugs are the cornerstone of treatment. Vitamin replacement is important.
However, after the acute detoxification, the real challenge begins. Chronic depression and irritability, cravings and wavering of motivation are all a part of the abnormal brain function. This can often heal in time; the trick is putting together enough time. Naltrexone, Vivitrol, topirimate, Neurontin, N acetyl cysteine, low dose ondansetron, bupropion, Chantix and disulfiram (Antabuse) can relieve these symptoms by affecting endorphin, dopamine, serotonin or other types of physiologic imbalances. All have complementary roles and can be mixed and matched
I do not mean to minimize the role of AA and/or counseling. Many alcoholics in recovery swear that AA was the only thing that allowed them to get sober. If these work and are sufficient, that's great. However, even by AA's reckoning, only about 10% of all people who walk into the rooms find benefit solely from AA. I consider addiction to be primarily a biological disease with behavioral manifestations. Therefore, the treatment needs to be biological when behavioral interventions don't suffice. My role as a doctor is to find the treatment for the 90% of alcoholics that AA does not help, not just tell them they are not ready to be helped.
There are different types of diabetes, different types of Herpes Simplex and different types of Alcoholism. The different types of disease demonstrate different causes, different disease progressions and different responses to treatment.
Back in the 1980s, Dr Cloninger noted that there were two different patterns of inheritance of alcoholism. There was the alcoholic who developed his disease slowly. He may have drank heavily as a young adult but did not become clinically alcoholic until his mid-30s or 40s. First degree family members of this person would have a 30-40% chance of being alcoholic. If they did develop alcoholism, the presentation was similar in that it developed relatively later.
However, if you were a male who was drinking alcoholically by your early 20s, than you had a 90% chance of having a son with the same early onset of alcoholism. Clearly, there seemed to be two different abnormalities being passed on that predisposed to alcohol abuse.
The two groups were better characterized in the 90s. The older onset, or Type One, had isolated alcohol problems. They tended to work more and develop problems after the age of 25. Type two alcoholics, on the other hand, were drinking heavily before age age 25. They had more psychiatric problems, more conduct issues and more use of illicit drugs.
The different types of patterns suggest there might be separate abnormal physiologies that led alcoholism. It is still unclear what the exact nature of these abnormalities are. Abnormalities of serotonin receptors have been postulated to be one source of disease but this is still being worked out. However, the important question remains: Should we treat both types of alcoholism the same way.
The short answer is NO!!!.
A famous alcohol treatment study, the COMBINE study, was done looking at treatment responses to naltrexone. Naltrexone was found to have some mild benefit. However, when the population was separated by subtype- type I alcoholics had a more significant benefit and type IIs had no benefit.
By the early 90s, it had been demonstrated that antidepressants had no benefit in treating alcoholism unless there was an independent diagnosis of depression. But that was also wrong. More recent research shows that that Zoloft helps reduce alcohol use in type I. However, alcohol use goes up in type IIs when they when prescribed antidepressants. . I cannot tell you how many young alcoholics are prescribed this type of medication without any thought that the drug might be causing harm. When they subsequently relapsed, we blamed toe patient and not the treatment. Ongoing alcohol use has always been blamed on the alcoholic, blaming anything else, we are told, is shirking responsibility. However, maybe we should also blame the medication. After all, bipolar gets worse with antidepressants, so why should we be surprised that one type of alcohol dependence also gets worse.
Zofran, in the low doses that are used for craving, has been found to be more helpful for type II alcoholics and of uncler benefit for type I. Perhaps this demonstrates that abnormal serotonin and/or abnormal learning is more of an issue with type II alcoholism.
My biggest question is whether this disease sub-type can be generalized to other classes of drug use. I believe it does though few studies have been done exploring this.