SS8282 - There are actually a number of reasons not to drink alcohol when taking any medication, whether taking that medication for the short term (eg. antibiotics; analgesics for acute pain ) or whether taking the medication on a long term basis (eg. high blood pressure; many psychiatric conditions). Actually, with many psychiatric medications there are more reasons not to be drinking alcohol.

Alcohol inhibits (ie. inactivates) a hormone that acts in the kidneys called ADH (anti-diuretic hormone) and stops it from working as it should. ADH is involved in concentrating the urine during the kidney's process of filtering toxins from the blood. ADH causes water to be reabsorbed by the body from the kidney, thus leaving behind the waste products of metabolism of food, drugs, and bodily functions (eg. breakdown products of proteins, enzymes, neurotransmitters, etc.). Some intact molecules are also eliminated by the kidneys (eg. Neurontin - gabapentin; lithium).

Alcohol stops (or at least slows) the concentrating of urine leading to dehydration of the body if enough alcohol is consumed. I'm sure that you have noticed that after several wobbly pops (or whaever your favorite cocktail may be) that you need to pee ... er, urinate; and that after that first trip to the loo, the frequency of said trips increases. This is due to alcohol inactivating ADH. The same effect is seen with the consumption of caffeinated beverages, though to a much lesser extent. ADH inhibition is one of the factors in the production of a hangover.

Think of your body as a container (or glass) of water. That water saturates all bodily tissues, and is what dissolves all the enzymes, hormones, proteins, neurotransmitters, etc. It is the water, via the circulatory system, that allows these bodily constituents to travel from where they are produced to their site of action, thus enabling them to interact with each other, producing the myriad of chemical reactions that make our body function. When you decrease the amount of water in the body (ie. dehydration) the enzymes (etc.) become more concentrated, and do not move throughout the body, nor interact with each other as efficiently as when the body is fully hydrated. One can look at the body as a full glass of water when normally hydrated, and less than full (eg. 3/4 full or 1/2 full) when dehydrated.

This can effect medications in a number of ways. For a drug to work there must be a high enough concetration in the bloodstream to cause the desired medicinal effect. This is called the "minimum effective concentration" (MEC). Conversely, if the concentration of the drug in the bloodstream is too high it can cause toxic effects, commonly called an overdose, and the lowest blood level at which this can occur is called "minimun toxic concentration" (MTC).

The range of blood concentrations of a drug between MEC and MTC is called the "therapeutic window" (or "therapeutic index"). For most medications taken for a chronic condition to work properly the concentration of drug in the bloodstream should always be maintained within that drug's therapeutic window. Fortunately, most drugs have a very wide therapeutic window, so missing one dose is not normally a problem. Lithium and Tegretol (carbamazepine) are examples of a drugs with a narrow therapeutic window. Frequent blood tests are required when initiating treatment with these drugs in order to determine the appropriate dose (for that individual) needed to keep the blood level of the drug over MEC, but below MTC.

Alcohol consumption effectively raises the concentration of most drugs in the bloodstream. This increases the risk of the blood level of certain drugs to exceed MTC, potentially leading to an overdose. As I said before, most medications do have a very wide therapeutic window, but any increase in drug concentration in the bloodstream can, and often does, increase the incidence and severity of the side effects associated with that drug.

This increase in side effects due to increased blood levels of a drug are what causes accidental (and deliberate) deaths due to cardiotoxicity in the older tricyclic antidepressants (TCAs) (eg. Elavil - amitriptyline; Sinequan - doxepin) and many of the conventional antipsychotics (tAPs) (eg. Mellaril - thioridazine; Orap - pimozide).

Many medications (especially those that are more water soluble) are peed off (excreted) after ADH is inhibited due to alcohol consumption.This drops blood levels of the drug below MEC and thus the drug is no longer therapeutically active. In psychiatric medicine it is this drug-alcohol interaction is a real concern, as most psych meds (psychotropics) are given in doses that are close to MEC. The reason that most psychotropics are dosed to provide blood levels close to that of the drug's minimum effective concentration is to minimize the extent and severity of those adverse side effects that interfere with everyday activities (eg. excessive drowniness, incoordination, cognitive problems, nausea, etc.), and have the potential to decrease one's quality of life. So, if alcohol does have a tendency to cause the excretion of a certain psychotropic in a particular person, that person will not be benefiting for the therapeutic effect of the drug, and cosequently will be at risk of suffering a relapse. Depending upon the person's diagnosis this means that there is an increased risk of a relapse of their depression, psychosis, or mania, or an increase in the number and severity of panic or anxiety attacks, etc.

In a majority of psychiatric medications both of the above effects occur at the same time, but in varying and unpredictable degrees. Whether a psych med is more likely to be excreted (and blood levels drop below MEC) or if most is reabsorbed (and blood levels rise) after alcohol consumption depends on many factors. Some of these include the person's genetically-determined reaction to alcohol (ie. how well the metabolize both the drug and alcohol; the extent to which their levels of ADH are affected by alcohol; etc.), how well their kidneys function, the specific drug involved, the "normal" blood concentration of that drug (which is related to the drug dose), the amount of alcohol consumed and over what time frame, the number of other medications the person is concurrently taking, and several other factors that just don't come to mind at the moment. This is why it is difficult to determine just what effect alcohol consumption will have on a particular psych med. The only thing that is certain is that one or more pharmacokinetic and therapeutic parameters will be altered; it is just the degree of that alteration that is in question.

Another significant psychotropic-alcohol interaction occurs due to the fact that many psychotropics are central nervous system (CNS) depressants. CNS depression is the mechanism of action of many psychotropics as they reduce anxiety, are used as sleeping pills, and inhibit psychosis.

The central nervous system processes information to and from the peripheral nervous system (the nerves functioning outside the brain and spinal cord) and is the main network of coordination and control for the entire body. The CNS controls the functions and sensations of the body, including emotions, sleep, muscular movement, pain sensation, sexual activity, memory, thirst, and hunger.

Drugs like the benzodiazepines (eg. Rivotril/Klonopin - clonazepam; Xanax - alprazolam; Ativan - Lorazepam) and opiates (codeine; Oxycontin - oxycodone; MS Contin - morphine) cause significant CNS depression. Alcohol also cause a significant amount of CNS depression. When taken together the amount of CNS depression is at least additive, sometimes more than additive. Death from too much CNS depression is usually a result of the muscles of the chest relaxing culminating in suffocation due to an inability to breath (ie. the chest muscles become too relaxed to be able to pull air into the lungs). Physical trauma is also more likely to occur, due to accidents cause by psychomotor incoordination (ie. clumsiness, staggering) and impaired mental function. Many people who mix these psychotropics with alcohol do not realize the extent of their impairment until too late.

Now I am not naive enough to think that everybody taking psychotropics never have a drink, or even get bent out of shape. Everyone has to try to reduce the stress in their lives from time to time, and for many people that stress reliever is alcohol. Admittedly it is not the best option, but it is one of the most available and affordable recreational drug in our society. I guarantee that there is no psychotropic on the market that hasn't been mixed with alcohol in someone's bloodstream, at one time or another. I am just saying that there are inherent risks mixing alcohol with any medication, and the effects of such combinations are at least unpredictable, and at worst fatal.

Now, to get to the reason that you were told not to drink alcohol with Risperdal. I am guessing that your doctor is concerned about a couple of the above effects. Firstly, the inhibition of ADH may lead to an increase in the blood concentrations of Risperdal, and thus increasing the magnitude of the drug's side effects. One of the side effects of Risperdal is cardiac arrythmias (increases in heart rate), which can result in a heart attack, especially in those with pre-existing heart conditions. Risperdal can also lower blood pressure possible resulting in unpredictable fainting spells or (at worst) cardiovascular collapse.

This same mechanism can cause increases in prolactin levels, which can play havoc with the sexual hormones, possibly resulting in menstrual problems and milk production in females and breast enlargement (with milk production - rare) in men.

Although with lower blood levels of Risperdal the risk of a movement disorder called extrapyramidal syndrome (EPS) is fairly low, but is much more likely to occur at higher blood levels of the drug. EPS is a fairly common side effect of the traditional antipsychotics and when these drugs were used over long periods of time (which they had to be in people who were afflicted with disorders such as schizophrenia) EPS often worsened into to a condition of irreversible movement disorder called tardive dyskinesia.

Also, Risperdal is a CNS depressant, so the above remarks regarding CNS depression should be noted.

Granted, the above outcomes are rare when only occasionally mixing small amounts of alcohol with Risperdal, and chances are that none of the would occur. The reality is is that the potential for problems does exist and the risk of a serious problem occurring, though relatively remote, is still much, much higher than if you did not consume alcohol while taking Risperdal. Drug interactions are a "crap shoot" at the best of times; ya pays your money and ya takes your chances.

Sorry for the long post, I just got carried away. I have this pet peeve with society's perception of alcohol. People do not believe that is as dangerous a substance as it is. I am not against recreational drug use, and I feel that no one should be able to mandate what you can and cannot put into your own body. The criteria that I use to determine how damaging a recreational drug is to a person is to look at how much it can disrupt a person's life. I just find that, for me, alcohol is probably one of the worst recreational drugs available, just under injected crystal methadrine and sniffing solvents (on my list, anyway).

I hope that this is of some help. I also hope that there are not too many spell/gramatical errors in this post, because I didn't proof read it; I've spent far too long on it as it is. - Cam