Opioid painkillers, when mixed with alcohol can lead to life-threatening interactions. It is crucial for individuals to be aware of these risks and to consult with healthcare professionals before combining alcohol with any medication, including over-the-counter drugs like Tylenol. Understanding the potential health risks can prevent serious complications and promote safer consumption practices. NIAAA and other medical authorities stress the significance of education on medication interactions with alcohol to help avoid negative health outcomes. Moreover, alcohol affects the brain’s communication pathways, altering mood, behavior, and coordination. Long-term consumption can lead to neurological complications and increase the risk of developing mental health conditions such as anxiety, depression, and bipolar disorder.
Alcohol’s Distribution in the Body
Certain opioid pain medications (e.g., codeine, propoxyphene, and oxycodone) are manufactured as combination products containing acetaminophen. These combinations can be particularly harmful when combined with alcohol because they provide “ hidden” doses of acetaminophen. As described in the previous section, alcohol consumption may result in the accumulation of toxic breakdown products of acetaminophen. In addition to the pharmacodynamic interactions, pharmacokinetic interactions between alcohol and phenobarbital exist, because alcohol inhibits the medication’s breakdown in the liver. This inhibition results in a slower metabolism and, possibly, higher blood levels of phenobarbital. Conversely, barbiturates increase total cytochrome P450 activity in the liver and accelerate alcohol elimination from the blood (Bode et al. 1979).
Psychological Signs of Alcohol Abuse
The remaining alcohol enters the intestine, where most of the remainder is absorbed into the bloodstream and enters the portal vein that leads to the liver. The remaining alcohol enters the general (i.e., systemic) circulation and eventually is transported back to the liver and metabolized there. The metabolism of alcohol in the stomach or during the first passage through the liver after absorption from the intestine is called first-pass metabolism.
Acetaminophen use in patients who drink alcohol: current study evidence
Diabetics who consume alcohol also must be alert to the fact that the symptoms of mild intoxication closely resemble those of hypoglycemia. Finally, patients using certain diabetes medications (e.g., chlorpropamide) should be cautioned that the medications cocaine abuse and addiction can cause a disulfiram-like reaction when alcohol is consumed. Older people are at particularly high risk for harmful alcohol–medication interactions. Aging slows the body’s ability to break down alcohol, so alcohol remains in a person’s system longer.
As a result, many consumers are not fully aware of the potential risks of taking these products, particularly in combination with other prescription medications or alcohol. Have you ever taken an over-the-counter analgesic (such as Tylenol, Advil, or Aleve) after a night of drinking to avoid or treat an alcohol-induced headache? Otherwise, you could find yourself dealing with side effects much more serious than the typical hangover—problems like ulcers, stomach bleeding, liver damage, kidney damage, and more—from mixing painkillers and alcohol. Fortunately, educating patients about the risks of combining medications with alcohol may help them avoid negative outcomes. Here, we describe briefly how alcohol and medications can interact, and we provide a few examples of common medications that could interact negatively with alcohol. We provide links to resources to help you mitigate these risks, including a consensus-developed list of potentially serious alcohol-medication interactions in older adults.
Clinical studies have also pointed out that the highest risk period for liver damage in alcoholic patients is immediately after they discontinue alcohol intake, correlating with increased CYP2E1 induction and decreased glutathione levels. The interactions between paracetamol and ethanol are complex and many questions remain to be answered. In animals, chronic administration of ethanol causes microsomal enzyme induction with increased toxic metabolic activation of paracetamol and enhanced hepatotoxicity. Conversely, the acute administration of ethanol inhibits the potentially toxic oxidative metabolism of paracetamol and protects against liver damage. This protective effect disappears when the ethanol is eliminated and the time interval between the intake of ethanol and paracetamol is critical.
In fact, the negative consequences of combining Tylenol extra strength and alcohol should be highlighted to discourage people. Still, they should also elucidate what would happen if people with AUD whose liver is damaged take this particular medicine. At this point, not enough attention is paid in public to the habit of taking Tylenol with alcohol. Stop taking acetaminophen and call your doctor if your symptoms get worse, you develop new or unexpected symptoms, including redness or swelling, your pain lasts for more than 10 days, or your fever gets worse or lasts more than 3 days.
Phenobarbital, which is probably the most commonly prescribed barbiturate in modern practice, also is used in the treatment of seizure disorders. Phenobarbital activates some of the same molecules in the CNS as does alcohol, resulting in pharmacodynamic interactions between the two substances. Consequently, alcohol consumption while taking phenobarbital synergistically enhances the medication’s sedative side effects. Patients taking barbiturates therefore should be warned not to perform tasks that require alertness, such as driving or operating heavy machinery, particularly after simultaneous alcohol consumption. In general, probably only a small fraction (perhaps 10 percent) of ingested alcohol is eliminated from the body by first-pass metabolism after consumption of low doses of alcohol. As alcohol ingestion increases, the amount of alcohol eliminated by first-pass metabolism becomes an even smaller fraction of the total amount of alcohol consumed.
- Similarly, medications that accelerate gastric emptying (e.g., the stomach medications metoclopramide [Reglan® ] and cisapride [Propulsid® ] and the antibiotic erythromycin) may reduce first-pass metabolism in the stomach.
- Alcohol-induced hypoglycemia occurs in the fasted state, when the diabetic’s blood sugar levels are already low and the body depends on the production of new glucose molecules (i.e., gluconeogenesis) to maintain sufficient blood glucose levels.
- According to a recent survey, 85 percent of adults ages 18 and older have used OTC pain relievers at least once, and up to 34 percent use OTC pain relievers on a weekly basis, often without consulting a pharmacist.
- Ongoing addiction treatment can help minimize relapses and establish longer periods of recovery.
The paracetamol–alcohol interaction is complex; acute and chronic ethanol have opposite effects. In animals, chronic ethanol causes induction of hepatic microsomal enzymes and increases paracetamol hepatotoxicity as expected (ethanol primarily induces CYP2E1 and this isoform is important in the oxidative metabolism of paracetamol). However, in man, chronic alcohol ingestion causes only modest (about twofold) and short-lived induction of CYP2E1, and there is no corresponding increase (as claimed) in the toxic metabolic activation of paracetamol. The paracetamol–ethanol interaction is not specific for any one isoform of cytochrome P450, and it seems that isoenzymes other than CYP2E1 are primarily responsible for the oxidative metabolism of paracetamol in man. Acute ethanol inhibits the microsomal oxidation of paracetamol both in animals and man. This protects against liver damage in animals and there is evidence that it also does so in man.
Subsequent investigation at more clinically realistic concentrations indicated only a minor role for CYP2E1 and that CYP3A4 was probably more important [170]. Many isoforms of cytochrome P450 including 1A1, 1A2, 2A1, 2A6, 2B1, 2C11, 2C12, 2E1, 3A1 and 3A4 contribute to the metabolism of paracetamol [95, 97, 169, 171]. More can labs detect synthetic urine in 2024 recent studies indicate important roles for CYP1A2 and CYP3A in the metabolism of ethanol and the metabolic activation and hepatotoxicity of paracetamol in animals [87–89, 99, 100, 168, 172]. In man, CYP1A2 does not seem to be quantitatively important in the metabolism of paracetamol to a toxic intermediate [173].
It’s crucial to be aware of these risks and to practice moderation if choosing to consume both substances. However, it is generally advisable to avoid mixing alcohol with Tylenol altogether to prevent any potential harm. For those who are prescribed acetaminophen or consume it regularly for pain relief, it’s essential alcohol detox diet eating healthy during alcohol withdrawal to disclose alcohol consumption habits to healthcare providers to ensure safe use. It is very difficult to accept that single and repeated daily doses of as little as 1–3 g paracetamol could cause severe and fatal liver damage in alcoholics as claimed [9, 24, 25, 30, 32, 37, 39, 40, 42, 46, 51, 52, 55, 60].
The Centers for Disease Control and Prevention (CDC) warns that the more alcohol a person drinks, the higher their risk for cancer. Additionally, alcohol can weaken the immune system, making the body more susceptible to illnesses. Some people want to know whether there are alternatives that are safe with drinking. This is especially the case for people whose alcoholic parents had a bad habit of mixing their drinks with drugs and experienced side effects in return. The good news is that there are alternatives that don’t involve taking Tylenol PM and alcohol together.
Lastly, if you find yourself in a situation where you have combined alcohol and Tylenol, monitor yourself for any adverse symptoms and seek medical attention immediately if you experience signs of liver distress or other concerning symptoms. By following these guidelines, individuals can minimize the risks and protect their health while using alcohol and Tylenol separately. Scientific literature, such as a study published in the New England Journal of Medicine, highlights the importance of long-term data to understand the effects of medical interventions. However, due to ethical and practical limitations, long-term human studies on this topic are scarce, and much of the knowledge is derived from case studies, animal models, and observational data. Our writers and reviewers are experienced professionals in medicine, addiction treatment, and healthcare.
In one chronic alcoholic who apparently took 15–25 g paracetamol daily without liver damage, there was no evidence of increased toxic metabolic activation [128]. Indeed, all other things being equal, induction of glucuronide conjugation would actually reduce the risk of paracetamol hepatotoxicity. In another study, the plasma paracetamol half-life (based on very limited sampling) was not abnormal in chronic alcoholics and was not related to the different genotypes of CYP2E1 [166]. Chronic administration of ethanol also causes microsomal enzyme induction in animals and as expected, this increased the metabolic activation and the hepatotoxicity of paracetamol [26, 72–89]. Subsequently, many anecdotal reports appeared describing severe and sometimes fatal liver damage in chronic alcoholics taking paracetamol in overdosage [2–20], as well as after its use for therapeutic purposes [5, 9, 10, 17, 18, 21–64].
(B) Changes in blood alcohol levels (BALs) after oral alcohol ingestion and after intravenous administration of the same alcohol dose. These are important considerations to determine if there is an alcohol-related use disorder than can become progressively worse over time. Alcohol is a highly addictive substance that is highly abused and can change the chemistry of the brain.