As the saying goes, no wine is not a banquet. Especially during the New Year’s Eve family and friends reunion, there is no shortage of wine on the table. However, the consumption of alcohol has an effect on the efficacy of drugs. Therefore, patients who are taking medication should be more cautious. Ethanol is metabolized in the liver by 90-98% of the ethanol entering the body, and is oxidized to acetaldehyde by ADH in the hepatic cell plasma, which is then oxidized to acetic acid by acetaldehyde dehydrogenase {ALDH}, which is automatically decomposed into CO2 and H2O. Acetaldehyde is a highly toxic substance that can be covalently bonded to some proteins, phospholipids, and nucleic acids in the body. Alcohol abuse or co-administration of certain drugs can increase the concentration of acetaldehyde in the blood. Many drugs can inhibit acetaldehyde dehydrogenase. The oxidative metabolic reaction of ethanol is blocked in the acetaldehyde phase, leading to acetaldehyde accumulation in the body and disulfiram reaction. Disulfiram blocks the metabolism of acetaldehyde and causes the accumulation of acetaldehyde in the blood, resulting in nausea and vomiting, flushing, headache, abdominal pain, sweating, dyspnea, hypotension, and tachycardia. Drugs that can produce this reaction include: metronidazole, furazolidone, isoniazid, sulfonamides, methanesulfonylurea, warfarin, insulin, chloramphenicol, ashwagandha, nitroglycerin, cardiac pain, diphenhydramine, barbiturates, chlorpromazine, trifluoperazine, etc., and cephalosporins. Ashwagandha can also reduce the patient’s alcohol tolerance, abnormal mood and neurotic-like symptoms. Chlorpromazine can aggravate central depression, hypotensive coma and even death by respiratory depression, and sometimes induce epilepsy. The calcium antagonists nifedipine, verapamil, monoamine oxidase inhibitors, metoclopramide, hydrochlorothiazide, reserpine, and acetaminophen also exacerbate the central depressant effects of ethanol by preventing its oxidation.