In connection with antidepressants, the consumption of alcohol is generally not recommended. Psychotropic drugs and alcohol do not get along very well either. Particularly in the case of active substances which have an additional sedative, i.e. calming effect, additional doses of alcohol can intensify this effect.
In addition, there is a reduced ability to react, as the mental and motor performance is restricted. Driving a motor vehicle and operating machinery, for example, are strictly prohibited in this case. Antidepressants with a sedative component are the tricyclic antidepressants (NSMRI) amitriptyline, trimipramine and doxepin as well as the tetracyclic antidepressants (?2-antagonists) mianserin and mirtazapine.
Calming agents are particularly helpful in the treatment of agitated, restless depression and sleep disorders. Under the influence of alcohol, various messenger substances and receptor systems of the brain are modulated. The concentration of dopamine, for example, is increased, which has a central influence on the emotions of the human being.
One feels more uninhibited and the mood improves because the body’s own reward system is activated more. The result is a desire for more alcohol to maintain this state. The sedative effect is mediated by GABA receptors, GABA is the strongest inhibitory transmitter in the CNS.
Its concentration is indirectly increased and motor function is impaired and physical deceleration occurs. The memory performance also decreases, this is caused by a reduced glutamate receptor function. Glutamate is the most important excitatory transmitter in the CNS.
Northern adrenalin and serotonin, two other important central transmitters, are reduced in concentration, which explains aggressive and depressive behaviour of alcoholics. In addition, enkephalins and endorphins are released in greater quantities, these promote addictive behaviour and have a pain-suppressing effect. If alcohol is now taken together with an antidepressant such as amitriptyline, unmistakable interactions can be observed.
These depend on the person’s drinking behaviour (direct or chronic alcohol abuse), age, sex and how quickly the person is able to break down drugs in the body. Pharmacodynamically, the two drugs (ethanol and amitriptyline) have a mutually reinforcing effect. As a result, those affected experience severe sedation, which can range from drowsiness to dangerous coma states.
In addition, they have to expect considerable psychomotor limitations. Other side effects observed are increased susceptibility to seizures (especially when withdrawal symptoms occur), lowered blood pressure and cardiac arrhythmia. Gastro-intestinal complaints such as constipation and intestinal obstruction are among the side effects of treatment with tricyclic antidepressants or ?2-antagonists and can also increase when alcohol is consumed at the same time.
In the case of acute alcohol poisoning, some studies have shown that the duration of action of amitriptyline in the body can be prolonged. So-called cytochromes are responsible for the breakdown of tricyclic antidepressants in the organism; alcohol is also partly broken down via this enzyme system. Excessive acute intake of alcohol therefore inhibits the cytochromes for the breakdown of amitriptyline.
Regular intake of alcohol in lower doses, however, shows a different picture: increased cytochrome formation occurs because the organism has adjusted to the fact that it has to degrade more alcohol via the cytochrome system. This also leads to an accelerated breakdown of amitriptyline and other psychotropic drugs which are metabolised via cytochromes. The duration of action of the drug is shortened and consequently higher doses are required to achieve the same therapeutic effect.
In some cases, depressive persons may also have an alcohol dependency (comorbidity), in which case the depressive phases of the patients last longer than normal and in dry alcoholics the risk of relapse increases due to phases of depression. The efficacy of various antidepressants in the context of alcohol dependence has not been sufficiently researched to date; however, good approaches succeed with a combination therapy of sertraline, a selective serotonin reuptake inhibitor (SSRI) and naltrexone, an opioid antagonist. Low-dose tricyclic antidepressants are also occasionally used to treat mild withdrawal symptoms, but here doxepin is preferable to therapy with amitriptyline.
