Ethanol perverts the effects of drugs: it can increase or decrease their effectiveness, potentiate unwanted adverse reactions. At the same time, some drugs can aggravate the toxic effects of alcohol.

The interaction may be at the level of pharmacodynamics. For example, alcohol combined with a number of drugs can mutually increase the effect on CNS. Pharmacokinetic interaction may occur at the stage of absorption. For example, low-alcohol beverages may accelerate medication penetration into the blood, resulting in a sharp increase in concentrations of the latter can manifest as symptoms of overdose. This is possible when the interval between the intake of alcohol and the pill is small.

Alcohol can alter the pharmacokinetics of drugs by interfering with their metabolism, which occurs with the participation of the cytochrome P450 system.

When the concentration of ethanol in the blood reaches more than 1% (150 ml of vodka drunk), cytochrome system enzymes are involved in ethanol utilization. This means that the load on the enzymes increases and the elimination time of harmful substances, which the body considers to be both drugs and alcohol, increases. This leads to a longer effect of both drugs and alcohol on the body.

On the other hand, alcohol itself affects the P450 system. And the nature of the effect depends on the dose of alcohol and the body’s tolerance to alcohol. Alcoholic drink drunk by a non-drinker in a large dose inhibits functioning of all cytochrome enzymes. This means that the elimination period of the drug is longer, and its pharmacological effects and side effects are intensified. Regular consumption of alcohol in small and medium doses increases cytochrome P450 system activity. The opposite process occurs. The medication is metabolized faster and loses its effect.

In addition to the dose and the nature of alcohol consumption, other circumstances influence how alcohol behaves together with the medication in the body:

What kind of medication the patient is taking and its dose
strength of the drink, its type, and time of ingestion
overall condition of the patient, the severity of the illness
individual characteristics of body chemistry
gender, age, weight, comorbidities and others.

It is difficult to predict in advance the consequences of combining a drug with alcohol, since targeted studies involving people on this issue are not conducted, and too many factors play a role. However, certain combinations of drugs with alcohol are known to have clinically significant adverse effects that are definitely worth avoiding.

A number of medications inhibit alcohol dehydrogenase, which neutralizes the toxic breakdown product of alcohol, acetaldehyde. Accumulation of acetaldehyde in the body is expressed by symptoms of fever, shortness of breath, tachycardia, nausea, vomiting, general malaise, increased sweating, tremors, chest pain, heaviness in the head, a feeling of fear for life, and blood pressure may drop.

Alcohol and drugs used in cardiology

Ethanol is able to interact with many cardiology drugs, namely antianginal, antihypertensive, antiarrhythmic, cardiotonics. In almost all cases, the combination of alcohol and drugs of these pharmacological groups will lead to adverse effects, whether it is a change in pharmacological efficacy, the manifestation of adverse reactions or toxic effects.

Alcohol and agents affecting blood clotting
Ethanol in combination with indirect oral anticoagulants (syncoumar, warfarin) may both decrease and increase their effect. Reaction to alcohol intake is individual and depends on the dose, the nature of alcohol consumption, and the state of the liver. It is possible to neutralize the effect (in the form of thrombosis), and its enhancement (in the form of badly stopped serious bleeding in injuries, surgeries). In combination with acetylsalicylic acid, a dose-dependent potentiation of its antiaggregant effect by ethanol has been established.

Alcohol and hypoglycemic agents
Alcohol has an adverse effect in the treatment of diabetes mellitus. Ethanol, when entering the body, first causes an increase in glucose levels, and then a fall. Fluctuations in blood glucose concentration adversely affect the patient’s condition, and also invert the picture at control measurements. When drinking alcohol during treatment with antidiabetic drugs, especially sulfonylurea derivatives (glibenclamide, gliclazide, glimepiride), the risk of hypoglycemia increases. In turn, sulfonylurea antidiabetic agents slow down alcohol metabolism. Sucrose-lowering effect of insulin can be both enhanced and weakened by alcohol. Patients taking metformin are at increased risk of lactoacidosis with chronic use of alcoholic beverages.

Alcohol and drugs affecting the CNS
Opioid analgesics (fentanyl, promedol, tramadol, buprenorphine, as well as codeine, a component of combined analgesics and anti-cough drugs), neuroleptics (aminazin etc.), tranquilizers (especially benzodiazepines), sleeping pills (barbiturates) have a depressing effect on the CNS. Alcohol increases sedation, may cause impairment of memory, coordination, loss of consciousness, and depression of the respiratory center.

First generation antiallergic drugs (dimedrol, tavegil, suprastin, ketotifen, diazolin, pipolfen) with alcohol exhibit sedative properties more pronounced. Headache, drowsiness, lethargy, lethargy, loss of consciousness may occur.

Administration of alcohol and antidepressant monoamine oxidase inhibitors (nialamide, iproniazide) can lead to “tyramine syndrome”, which is expressed by increased heart rate, vasoconstriction, increased BP with a risk of hypertensive crisis.