Alcohol Use Causes Increased Inhibitions

Alcohol Res Health. 1999; 23(1): 40–54.

Alcohol and Medication Interactions

Abstract

Many medications can interact with alcohol, thereby altering the metabolism or effects of alcohol and/or the medication. Some of these interactions can occur even at moderate drinking levels and result in adverse wellness effects for the drinker. Two types of booze-medication interactions exist: (1) pharmacokinetic interactions, in which alcohol interferes with the metabolism of the medication, and (2) pharmacodynamic interactions, in which alcohol enhances the furnishings of the medication, particularly in the key nervous organization (eastward.thou., sedation). Pharmacokinetic interactions mostly occur in the liver, where both alcohol and many medications are metabolized, ofttimes past the same enzymes. Numerous classes of prescription medications can interact with alcohol, including antibiotics, antidepressants, antihistamines, barbiturates, benzodiazepines, histamine H₂ receptor antagonists, musculus relaxants, nonnarcotic pain medications and anti-inflammatory agents, opioids, and warfarin. In addition, many over-the-counter and herbal medications tin can cause negative effects when taken with alcohol.

Keywords: moderate AOD use, prescription drug, adverse drug interaction, drug metabolism, ethanol metabolism, cytochromes, liver, alcohol dehydrogenases, antibiotics, antidepressants, histamine H1 receptor blockaders, barbiturates, benzodiazepines, histamine H2 receptor blockaders, anti-inflammatory agents, opioids, warfarin, over-the-counter drug, literature review

Nigh people who consume booze, whether in moderate or large quantities, also have medications, at least occasionally. Every bit a effect, many people ingest alcohol while a medication is present in their body or vice versa. A big number of medications—both those available only by prescription and those bachelor over the counter (OTC)—have the potential to interact with alcohol. Those interactions can change the metabolism or activity of the medication and/or alcohol metabolism, resulting in potentially serious medical consequences. For instance, the sedative effects of both alcohol and sedative medications can raise each other (i.due east., the effects are additive), thereby seriously impairing a person's ability to drive or operate other types of mechanism.

Almost studies assessing alcohol-medication interactions focus on the effects of chronic heavy drinking. Relatively limited information is bachelor, however, on medication interactions resulting from moderate alcohol consumption (i.e., i or two standard drinks^ane per 24-hour interval). Researchers, physicians, and pharmacists must therefore infer potential medication interactions at moderate drinking levels based on observations fabricated with heavy drinkers. In add-on, moderate alcohol consumption may direct influence some of the disease states for which medications are taken (meet sidebar, pp. 52–53, for further discussion of alcohol's influences on various disease states). This article discusses alcohol absorption, distribution, and metabolism within the body; the sites where potential alcohol-medication interactions can occur; and possible agin effects from various alcohol-medication combinations, including OTC or herbal products.

Alcohol's Influences on Various Disease States

Many people who are being treated for chronic wellness issues, such as diabetes and high blood pressure (i.e., hypertension), swallow alcohol, whether occasionally or regularly. As described in the main article, booze consumption, fifty-fifty at moderate levels, may interfere with the activities of many medications prescribed for such weather condition. In add-on, all the same, alcohol use may contribute to or exacerbate certain medical conditions.

Diabetes

In people with diabetes, command of the levels of the sugar glucose in the blood is severely impaired, either because these people lack the hormone insulin, which plays a central role in claret carbohydrate regulation, or considering their body does non answer appropriately to the insulin they produce. Alcohol consumption in diabetics can result either in college-than-normal blood sugar levels (i.due east., hyperglycemia) or in lower-than-normal blood carbohydrate levels (i.eastward., hypoglycemia), depending on the patient'due south nutritional condition (Emanuele et al. 1998). Thus, long-term (i.due east., chronic) alcohol consumption in well-nourished diabetics tin lead to hyper-glycemia. Conversely, alcohol consumption in diabetics who have not eaten for a while and whose glucose resources are exhausted (i.e., who are in a fasting state) tin induce hypoglycemia. Both hyperglycemia and hypoglycemia can accept serious health consequences. Diabetes medications that substitute for or stimulate the torso's own insulin production (e.g., insulin or sulfonylureas) likewise may pb to hypoglycemia.

Alcohol-induced hypoglycemia occurs in the fasted state, when the diabetic's blood sugar levels are already low and the torso depends on the production of new glucose molecules (i.eastward., gluconeogenesis) to maintain sufficient claret glucose levels. Gluconeogenesis, which occurs in the liver, requires certain compounds whose levels are regulated by a substance called reduced nicotinamide adenine dinucleotide (NADH). Booze metabolism in the liver generates excessive NADH levels and thus reduces the levels of the compounds needed for gluconeogenesis, thereby contributing to a farther drop in blood carbohydrate levels. This response is particularly critical in diabetics taking medications that tin can crusade hypoglycemia. Consequently, these patients should be advised to drink alcohol simply with or presently after meals.

Diabetics who consume booze as well must exist alert to the fact that the symptoms of mild intoxication closely resemble those of hypoglycemia. Accordingly, diabetics should bank check their blood glucose levels whenever they are uncertain about whether their symptoms are acquired by hypoglycemia or alcohol intoxication (for additional recommendations for diabetics who eat booze, run into the textbox). Finally, patients using certain diabetes medications (east.k., chlorpropamide) should exist cautioned that the medications tin crusade a disulfiram-similar reaction when booze is consumed.

Preventing Booze-Induced Hypoglycemia

Booze-consuming diabetic patients should consider the following general suggestions for preventing alcohol-induced hypoglycemia:

Never eat alcohol without nutrient or while in a fasting land.
Consume only moderate amounts of alcohol (i.e., one or 2 bottles of beer, spectacles of vino, or mixed drinks at one sitting), and drink no more than once or twice weekly.
Permit 1.5 to 2 hours between drinks.
Avert sugar-containing drinks, and consume simply light beer, dry out wine, or drinks mixed with nutrition sodas.
Check blood sugar levels if unsure whether certain torso sensations (e.g., low-cal-headedness) result from hypo-glycemia or alcohol furnishings.
Be on the alarm for alcohol hidden in prescription and over-the-counter medications.

Hyperlipidemia

In people with hyperlipidemia, the levels of fatty molecules in the blood—particularly molecules called triglycerides—are higher than normal. This condition can be associated with an increased risk of diverse health bug, the near serious of which is cardiovascular illness. Booze consumption may exacerbate hyperlipidemia, because the same metabolic alcohol effects that inhibit gluconeogenesis also inhibit fat metabolism. As a result, the production of certain molecules called very depression density lipoprotein (VLDL) particles is increased. Thus, people with elevated triglyceride levels in the claret should probably abstain from alcohol to determine if alcohol consumption is contributing to their elevated lipid levels.

Hypertension

Elevated claret pressure is a run a risk factor for cardiovascular disease, including middle attacks. Alcohol is known to crusade a dose-dependent top in blood pressure level (Beilin 1995). Researchers practise non nevertheless know exactly what levels of alcohol consumption cause hypertension (for more than information, run into the commodity by Klatsky, pp. 15–23). However, all patients who are diagnosed with high blood force per unit area should exist questioned regarding their booze intake earlier beingness started on antihypertensive therapy. In some of those patients, cessation of drinking lone may reduce blood pressure and thus obviate the need for pharmacological treatment. Furthermore, patients taking certain kinds of cardiac medications (e.g., isosorbide [Isordil^® and Ismo^®], terazosin [Hytrin^®], doxazosin [Cardura^®]) should be warned that alcohol consumption in combination with those medications may cause lower-than-normal blood pressure. These of import potential risks associated with even moderate alcohol consumption (i.e., i or two standard drinks^one per day) must be considered when discussing the cardiovascular benefits associated with moderate drinking (e.g., reduced run a risk of heart attacks and sure kinds of strokes.)

Hepatitis C Infection

Infection with the hepatitis C virus, which tin outcome in serious and even fatal liver damage, is common in the United States and around the world. The only effective treatment to date involves a substance called interferon-α, often in combination with an agent called ribavirin, and has a cure rate of approximately 40 percent. Heavy alcohol utilise in patients infected with hepatitis C accelerates the charge per unit of liver impairment and increases the gamble of cirrhosis. Moreover, heavy alcohol use appears to reduce the number of hepatitis C-infected people who respond to treatment with interferon-α. Researchers do not all the same know how alcohol consumption exacerbates disease progression and interferes with treatment. Still, people infected with the hepatitis C virus probably should avoid using alcohol, particularly during interferon-α treatment.

— Ron Weathermon and David Due west. Crabb

¹A standard drink is divers as one 12-ounce tin can of beer or bottle of vino cooler, 1 v-ounce glass of vino, or i.5 ounces of distilled spirits and is equivalent to approximately 0.v ounce, or 12 grams (yard), of pure alcohol.

References

Beilin LJ. Alcohol and hypertension. Clinical and Experimental Pharmacology and Physiology. 1995;22:185–188. [PubMed] [Google Scholar]
Emanuele NV, Swade TF, Emanuele MA. Consequences of alcohol use in diabetics. Booze Health & Research World. 1998;22(three):211–219. [PMC complimentary commodity] [PubMed] [Google Scholar]

Alcohol Assimilation, Distribution, and Metabolism

Gastrointestinal Assimilation and Metabolism

When alcohol is ingested through the oral cavity, a small amount is immediately broken down (i.east., metabolized) in the stomach. Well-nigh of the remaining alcohol is then captivated into the bloodstream from the gastrointestinal tract, primarily the tum and the upper small-scale intestine. Alcohol absorption occurs slowly from the tum merely apace from the upper small intestine. In one case absorbed, the alcohol is transported to the liver through the portal vein. A portion of the ingested alcohol is metabolized during its initial passage through the liver; the residual of the ingested alcohol leaves the liver, enters the general (i.e., systemic) circulation, and is distributed throughout the body'south tissues.

Alcohol metabolism (or the metabolism of whatever other substance) that occurs in the gastrointestinal tract and during the substance's initial passage through the liver is called " first-pass metabolism" (run into figure ane). For example, the mucosa lining the stomach contains enzymes that can metabolize alcohol as well as other substances; some of those enzymes, including booze dehydrogenase (ADH) and cytochrome P450 are described in more detail in the section "Alcohol Metabolism in the Liver."

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Schematic representation of showtime-pass metabolism. (A) Alcohol ingested through the mouth reaches the breadbasket, where a portion is metabolized by the enzyme booze dehydrogenase (ADH). The remaining alcohol enters the intestine, where nearly of the rest is absorbed into the bloodstream and enters the portal vein that leads to the liver. In the liver, part of the alcohol is metabolized by ADH or cytochrome P450. The remaining alcohol enters the general (i.east., systemic) circulation and eventually is transported back to the liver and metabolized in that location. The metabolism of alcohol in the stomach or during the first passage through the liver subsequently absorption from the intestine is called first-pass metabolism. (B) Changes in blood alcohol levels (BALs) after oral booze ingestion and after intravenous administration of the same booze dose. The difference in BALs accomplished with both administration routes (i.e., the amount past which the BAL is lower afterward oral ingestion) represents that portion of the ingested alcohol that has been broken down by first-pass metabolism before reaching the systemic circulation.

The contribution of stomach (i.due east., gastric) enzymes to outset-pass alcohol metabolism, however, is controversial. Whereas some researchers have proposed that gastric enzymes play a major role in showtime-pass metabolism (Lim et al. 1993), other investigators consider the liver to be the primary site of kickoff-pass metabolism (Levitt and Levitt 1998). Furthermore, some gender differences announced to exist in the overall extent of, and in the contribution of, gastric enzymes to starting time-laissez passer metabolism. For example, the extent of first-pass metabolism is less in women than in men and some studies as well accept found lower gastric ADH activity in women (Thomasson 1995).

First-pass metabolism is readily detectable after consumption of depression alcohol doses^two that get out the tummy slowly (eastward.g., considering they have been consumed with a meal). Thus, under such conditions of delayed gastric emptying, more than alcohol can be metabolized in the tum or absorbed slowly from the stomach and transported to the liver for kickoff-laissez passer metabolism.

In general, probably only a small fraction (mayhap 10 pct) of ingested booze is eliminated from the body past first-pass metabolism subsequently consumption of low doses of alcohol. As booze ingestion increases, the corporeality of alcohol eliminated by beginning-pass metabolism becomes an even smaller fraction of the total amount of alcohol consumed. Some researchers have suggested, however, that some medications tin block first-pass metabolism, resulting in claret alcohol levels (BALs) that are higher than normal for a given booze dose. For instance, people taking medications that tin inhibit ADH activity—such as aspirin and certain medications used to treat ulcers and heartburn (i.east., H₂ receptor antagonists, such as cimetidine [Tagamet^® ], nizatidine [Axid^® ] and ranitidine [Zantac^® ])—experience reduced first-pass metabolism (Caballaria et al. 1991; Roine et al. 1990). Similarly, medications that advance gastric emptying (due east.g., the tummy medications metoclopramide [Reglan^® ] and cisapride [Propulsid^® ] and the antibody erythromycin) may reduce outset-laissez passer metabolism in the stomach.

The contribution of bacteria living in the large intestine (i.e., colon) to gastrointestinal alcohol metabolism is all the same controversial. Laboratory experiments have demonstrated that these bacteria can metabolize alcohol. In add-on, a breakdown production of alcohol (i.due east., acetaldehyde) is generated in the colon after alcohol administration. Finally, studies in rats found that animals treated with an antibiotic to reduce the number of bacteria in the colon showed a reduced alcohol emptying rate compared with untreated rats (Nosova et al. 1999). If these enquiry findings also apply to humans, alcohol elimination may exist delayed in people taking certain antibiotics that are active against colonic leaner.

Booze's Distribution in the Body

Alcohol that has non been eliminated past beginning-pass metabolism enters the systemic circulation and is distributed throughout the body water (i.e., the claret and the watery fluid surrounding and inside the cells). Alcohol does not dissolve in fat tissues. The proportion of body h2o and torso fat differs between men and women and between young and former people; women and older people generally have more body fat and less trunk water than do men and younger people. Equally a result, alcohol distribution throughout the body depends on a person's gender and age.

Differences in alcohol distribution patterns likewise impact the BALs accomplished with a given alcohol dose (Thomasson 1995). Thus, women, whose lower torso h2o creates a smaller fluid volume in which the alcohol is distributed, tend to accomplish higher BALs than practice men later consuming the aforementioned amount of alcohol. The normal loss of lean body weight and increment in trunk fat that occurs with aging has a like upshot on BALs. The potentially higher BALs can exaggerate alcohol-medication interactions in both women and older people. Bated from this effect of gender and age on BALs, researchers have not reported any other major gender- or age-related differences in susceptibility to booze-medication interactions. However, this issue all the same requires further investigation.

Alcohol Metabolism in the Liver

The liver is the primary site of alcohol metabolism. Alcohol circulating in the blood is transported to the liver, where it is broken downwards by several enzymes, the nigh important of which are ADH and cytochrome P450 (figure 2). The activities of these enzymes may vary from person to person, contributing to the observed variations in alcohol elimination rates amid individuals (Martin et al. 1985).

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Booze metabolism in the liver. Alcohol is broken downwards to acetaldehyde either by alcohol dehydrogenase (ADH) or cytochrome P450 (CYP). The acetaldehyde then is broken downwardly to acetic acrid and water by two variants of the enzyme aldehyde dehydrogenase (ALDH). Alcohol metabolism by ADH generates a byproduct called reduced nicotinamide adenine dinucleotide (NADH). Excessive NADH levels can inhibit glucose product (i.e., gluconeogenesis) and breakdown (i.due east., oxidation) of fat molecules equally well as stimulate product of fatty molecules.

ADH converts alcohol into acetaldehyde in a reaction called oxidation. Acetaldehyde, which is a toxic substance that may contribute to many of booze'due south adverse effects, is cleaved downwards further by an enzyme called aldehyde dehydrogenase (ALDH). (The office of ALDH is discussed in more detail in the following section.) Several ADH variants (i.e., isozymes) exist, which differ in their activity when studied in the laboratory. In humans, however, the event of different ADH isozymes on alcohol elimination is small (Thomasson 1995). Although different ADH variants are associated with different risks of developing alcoholism, no studies to date take researched the effects of these isozymes on a person's susceptibility to alcohol-medication interactions.

In contrast to ADH, the alcohol-metabolizing enzyme cytochrome P450—also called microsomal ethanol oxidizing system (MEOS) (Lieber 1994)—plays a cardinal role in booze-medication interactions. Cytochrome P450 actually is a arrangement consisting of two enzymes, one called cytochrome P450 reductase and another i called CYP2E1, which are both embedded in the membrane of a cell component called the endoplasmic reticulum.³ In addition to booze, CYP2E1 can metabolize numerous compounds, including acetaldehyde, the pain medication acetaminophen, the antibiotic isoniazid, and the barbiturate phenobarbital. Accordingly, CYP2E1 plays an of import role in many alcohol-medication interactions.

In people consuming alcohol simply occasionally, CYP2E1 metabolizes just a small fraction of the ingested booze. Chronic heavy drinking, however, tin can increase CYP2E1 activeness up to tenfold, resulting in a substantial increment in the proportion of booze that is metabolized by this enzyme rather than by ADH (effigy 3) (Lieber 1994). The effect of lower levels of alcohol consumption on CYP2E1 activity is unknown. Considering CYP2E1 also metabolizes several medications, alcoholics, in whom CYP2E1 activity is enhanced, exhibit increased metabolic rates for those medications when they are sober. When those alcoholics are intoxicated, however, the alcohol in their system competes with the medication for metabolism past CYP2E1. Equally a issue, the breakup of the medication is slowed. With many medications, increased or decreased metabolic rates tin accept agin or even fatal consequences. With increased metabolic rates, the medication'south concentration in the trunk may be likewise low or may decline too fast for it to be effective. Conversely, decreased metabolic rates may result in the aggregating of higher drug concentrations over longer periods of times, which may result in harmful overdoses.

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Potential alcohol-medication interactions involving cytochrome P450 enzymes (CYP) in the liver.

Broad variation exists among people in both CYP2E1 action and metabolic rates for medications broken downward by this enzyme (eastward.g., acetaminophen and chlorzoxasone, a medication used to salve muscle hurting). Some of this variation may exist genetically adamant, although the specific underlying mechanism is unknown (Carriere et al. 1996). A person's CYP2E1 activity level, nonetheless, could influence his or her susceptibility to booze-medication interactions involving this enzyme. For instance, in a person with innately low metabolic rates, a further decrease in metabolism when alcohol is consumed would bear upon medication levels (and thus the potential for adverse effects or interactions with alcohol) to a greater extent than in a person with innately loftier metabolic rates.

In addition to CYP2E1, at least 2 other cytochrome enzymes that metabolize various medications (i.e., CYP3A4 and CYP1A2) also tin break down alcohol (Salmela et al. 1998). Moreover, the amounts of various enyzmes of the cytochrome CYP3A family unit (including CYP3A4) can increment from alcohol consumption (Niemela et al. 1998). Thus, potential interactions also exist betwixt booze and medications metabolized by these cytochromes.

Acetaldehyde Metabolism in the Liver

As mentioned in the previous section, alcohol breakdown by ADH generates acetaldehyde, which, in turn, is metabolized farther past ALDH. Two major types of ALDH (i.east., ALDH1 and ALDH2) be, which are located in different regions of the cell. ALDH1 requires relatively loftier acetaldehyde concentrations in the prison cell to be agile, whereas ALDH2 is agile at extremely low acetaldehyde levels. Appropriately, ALDH2 may play a specially of import function in acetaldehyde breakdown after moderate alcohol consumption.

The significance of ALDH2 activity in booze and acetaldehyde metabolism is further supported by an inborn variation in alcohol metabolism that occurs primarily in people of Asian heritage simply which is rare amidst Caucasians. After consuming alcohol, many Asian people experience an unpleasant " flushing" reaction that can include facial flushing, nausea, and airsickness. These symptoms are caused by acetaldehyde accumulation in the body. Thus, following alcohol consumption, acetaldehyde levels in people susceptible to the flushing reaction may be x to twenty times higher than in people who do not experience flushing. Researchers have noted that approximately 40 percent of Asians lack ALDH2 activity considering they have inherited ane or ii copies of an inactive variant of the cistron that produces ALDH2 (Goedde et al. 1989). Almost of these individuals flush when they swallow booze. These observations imply that ALDH2 plays a crucial role in maintaining low acetaldehyde levels during alcohol metabolism. Consequently, fifty-fifty inadvertent alcohol assistants to people of Asian heritage (who may have inherited an inactive ALDH2 gene) can cause unpleasant reactions. Thus, the potential flushing response should be an important business organization for physicians and patients, considering many prescription and OTC medications contain substantial amounts of booze (meet table ane). Physicians and pharmacists therefore must be warning to the possibility that Asian patients may be intolerant of these medications.

Table 1

Alcohol Content of Prescription and Over-the-Counter Medications

Product	Alcohol Content (%)
Betadine (mouthwash, gargle)	8.8
Cepacol (mouthwash, gargle)	fourteen.0
Cheracol Sore Pharynx	12.five
Chlortrimeton syrup	seven.0
Cimetidine Oral Solution	2.8
Cyclosporine Oral Solution	9.5–12.5
Cyproheptadine	5.0
DentSure (denture rinse, peppermint)	14.iv
Dr. Tichenor's Antiseptic	70^*
Digoxin Elixir	ten.0
Entex	v.0
Furosemide Liquid	11.five
Intensol (diazepam)	19.0
Listerine	26.ix
Listerine Absurd Mint or Freshburst	21.6
Lomotil Liquid	15.0
Mellaril/Thioridiazine	3.0–four.2
Mentadent Mouthwash	10.0
Oral-B Anti-Plaque Rinse	eight.0
Plax-Advanced Formula	8.7
Peri-colace	ten.0
Phenobarbital Elixir	14.0
Promethazine/Phenergan	7.0
Ranitidine	7.5
Telescopic, Baking Soda	9.9
Scope, Cool Peppermint	fourteen.0
Senokot Syrup	seven.0
Targon Smokers' Mouth Wash, Clean Gustation	fifteen.six^*
Targon Smokers' Mouth Wash, Original	xvi.0^*
Tavist Oral Solution	v.5
Theophylline Elixir	20.0
Viadent Oral Rinse	10.0

Several medications can inhibit even active ALDH molecules (both ALDH1 and ALDH2), thereby inducing a flushing reaction in all people who eat booze after taking those medications. In fact, this medication outcome is exploited in alcoholism handling. The medication disulfiram (Antabuse^® ), which inhibits mainly ALDH1 but also ALDH2, is given to alcoholics trying to quit drinking. If the alcoholic drinks alcohol after taking disulfiram, he or she will experience a severe flushing reaction. The experience of such an unpleasant reaction, or even the expectation that this reaction volition occur if alcohol is consumed, can help many alcoholics achieve and maintain abstinence. Moderate drinkers are not likely to exist treated with disulfiram; all the same, many other medications (and certain toxic substances) likewise can induce disulfiram-like reactions when combined with booze (encounter table two). For example, the commonly prescribed diabetes medication chlorpropamide and the antibiotics cefotetan and metronidazole tin can induce disulfiram-like reactions, fifty-fifty after ingestion of only small booze amounts. These reactions not only are unpleasant only besides can event in serious medical consequences. For case, flushing is associated with a widening (i.e., dilation) of the blood vessels, low blood pressure level, and rapid heartbeat, all of which tin can be dangerous in patients with coronary avenue illness. Patients taking medications that tin induce disulfiram-like reactions therefore should be brash non to drink alcohol.

Tabular array 2

Usually Used Medications That Cause Disulfiram-Similar Reactions (i.e., Flushing, Nausea, Vomiting, Sweating) After Alcohol Consumption

Type of Medication	Generic Names	Brand Names
Analgesics (NSAIDs)	Phenacetin	various
Analgesics (NSAIDs)	Phenylbutazone
Antibiotics	Cefamandole	Mandol
	Cefoperazone	Cefobid
	Cefotetan	Cefotan
	Chloramphenicol	various
	Griseofulvin	Fulvicin, Grifulvin,Grisactin
	Isoniazid	Nydrazid, Rifamate, Rifater
	Metronidazole	Flagyl
	Nitrofurantoin	Furadantin, Macrodantin
	Sulfamethoxazole	Bactrim, Septra
	Sulfisoxazole	Pediazole
Cardiovascular medications (nitrates)	Isosorbide dinitrate	Dilatrate, Isordil, Sorbitrate
Cardiovascular medications (nitrates)	Nitroglycerin	Nitro-Bid, Nitrostat
Diabetes medications (sulfonylureas)	Chlorpropamide	Diabinese
	Glyburide	DiaBeta, Glynase, Micronase
	Tolazamide	generic
	Tolbutamide	generic

Alcohol's Effects on Liver Metabolism

In addition to influencing the metabolism of many medications by activating cytochrome P450 enzymes in the liver, alcohol and its metabolism cause other changes in the liver'southward ability to eliminate various substances from the body. Thus, alcohol metabolism affects the liver'south redox land and glutathione levels. The term "redox state" refers to the concentrations of ii substances in the cells—nicotinamide adenine dinucleotide (NAD⁺) and reduced NAD⁺ (NADH)—that are needed for the performance of many enzymes. Alcohol metabolism by ADH results in the conversion of NAD⁺ into NADH, thereby increasing the liver'south NADH levels (see effigy 2). Elevated NADH levels, in turn, stimulate the generation of fat molecules and interfere with the ability of other liver enzymes to intermission down fatty molecules and produce the carbohydrate glucose. Through these metabolic changes, alcohol metabolism tin substantially affect the torso's general metabolism and functioning. Furthermore, elevated NADH levels may prevent the liver from generating UDP-glucuronic acid, a substance that must be attached to various medications before they tin be excreted from the body.

Glutathione is an antioxidant, an agent that prevents certain highly reactive, oxygen-containing molecules (i.e., reactive oxygen species) from damaging the cells. Both alcohol metabolism and the metabolism of certain medications can generate reactive oxygen species, thereby inducing a state chosen oxidative stress in the cells. At the same time, heavy alcohol consumption reduces the corporeality of glutathione in liver cells, particularly in the mitochondria (i.e., the cell components where nearly of the prison cell's energy is generated). Consequently, the cell'due south protective mechanisms against oxidative stress are dumb, and prison cell decease may result. Furthermore, reduced glutathione levels increase the liver's susceptibility to damage caused past toxic breakdown products of some medications (due east.g., acetaminophen and isoniazid).

Common Alcohol-Medication Interactions

Mechanisms of Alcohol-Medication Interactions

Interactions betwixt alcohol and a medication can occur in a diversity of situations that differ based on the timing of alcohol and medication consumption. For instance, such interactions can occur in people who consume booze with a meal shortly before or after taking a medication or who have hurting medications after drinking to prevent a hangover. Alcohol-medication interactions fall into two general categories: pharmacokinetic and pharmacodynamic. Pharmacokinetic interactions are those in which the presence of alcohol directly interferes with the normal metabolism of the medication. This interference can accept 2 forms, as follows:

The breakdown and excretion of the affected medications are delayed, because the medications must compete with alcohol for breakup by cytochrome P450. This type of interaction has been described more often than not for metabolic reactions involving CYP2E1, just it as well may involve CYP3A4 and CYP1A2 (Salmela et al. 1998).
The metabolism of the affected medications is accelerated, because booze enhances the activity of medication-metabolizing cytochromes. When booze is not present simultaneously to compete for the cytochromes, increased cytochrome activeness results in an increased elimination charge per unit for medications that these enzymes metabolize.

Pharmacodynamic alcohol-medication interactions do not involve enzyme inhibition or activation, but rather refer to the condiment effects of alcohol and sure medications. In this type of interaction, which occurs well-nigh commonly in the key nervous system (CNS), alcohol alters the effects of the medication without changing the medication's concentration in the claret. With some medications (e.g., barbiturates and allaying medications chosen benzodiazepines), alcohol acts on the aforementioned molecules inside or on the surface of the cell every bit does the medication. These interactions may be synergistic—that is, the effects of the combined medications exceed the sum of the furnishings of the private medications. With other medications (eastward.g., antihistamines and antidepressants) alcohol enhances the sedative effects of those medications merely acts through different mechanisms from those agents.

Specific Alcohol-Medication Interactions

This section describes different classes of medications and their interactions with alcohol (see tabular array three). The potential for the occurrence and relevance of booze-medication interactions in moderate drinkers may differ, however, betwixt pharmacokinetic and pharmacodynamic interactions. The number of potential pharmacokinetic interactions with alcohol is bully, because the various cytochrome P450 enzymes metabolize many medications.⁴ Still, many of the pharmacokinetic interactions discussed here were first discovered in heavy drinkers or alcoholics or were studied in animals given big alcohol doses in their nutrition. Although the potential for such effects certainly exists even after low booze consumption, researchers accept not nevertheless demonstrated the occurrence and relevance of those effects in moderate drinkers. Conversely, pharmacodynamic interactions can occur with intermittent alcohol consumption and fifty-fifty after a single episode of drinking. Appropriately, those interactions clearly pertain to moderate drinkers.

Table 3

Interactions Between Alcohol and Various Classes of Medications

Drug Course (Conditions for which they are used)	Generic Name	Brand Proper noun	Availability	Type of Interaction
Analgesics (pain relief)	Aspirin	various	Rx and OTC	Aspirin increases gastric emptying, leading to faster booze assimilation in the small intestine; may also inhibit gastric ADH. Alcohol enhances acetaminophen metabolism into a toxic production, potentially causing liver damage.
Analgesics (pain relief)	Acetaminophen	e.m., Tylenol
Antibiotics (microbial infections)	Erythromycin	various	Rx	Erythromycin may increase gastric elimination, leading to faster booze absorption in the small intestine. Alcohol increases the risk of isoniazid-related liver affliction.
Antibiotics (microbial infections)	Isoniazid	Nydrazid, Rifamate, Rifater
Anticonvulsants (seizure disorders)	Phenytoin	Dilantin	Rx	Chronic alcohol consumption induces phenytoin breakdown.
Antihistamines (allergies, colds)	Diphenhydramine	e.g., Benadryl	Rx and OTC	lcohol enhances the effects of these agents on the central nervous arrangement (CNS), such every bit drowsiness, sedation, and decreased motor skills. The interactions are more pronounced in elderly people. No documented interactions exist with nonsedating antihistamines (i.e., certrizine, hismanal, loratidine).
	Chlorpheniramine Clemastine	various
	Hydroxyzine	Atarax, Vistaril
	Promethazine	Phenergan
	Cyproheptadine	Periactin
Anticoagulants (prevention of blood clots)	Warfarin	Coumadin	Rx	Acute booze intake may increment anticoagulation by decreasing warfarin metabolism; chronic alcohol ingestion decreases anticoagulation past increasing warfarin metabolism.
Antidiabetic agents (claret sugar regulation)	Chlorpropamide	Diabinese	Rx	Alcohol consumption by diabetic patients taking these medications increases the adventure of lower-than-normal blood sugar levels (i.e., hypoglycemia). Chlorpropamide, glyburide, and tolbutamide can cause disulfiram-like interactions afterward alcohol ingestion. Metformin may cause increased levels of lactic acrid in the claret afterward alcohol consumption.
	Glipizide	Glucotrol
	Glyburide	DiaBeta, Glynase, Micronase
	Tolbutamide	Orinase
	Metformin	Glucophage
Barbiturates (anesthesia, pain relief)	Phenobarbital	diverse	Rx	Chronic alcohol intake increases barbiturate metabolism by cytochrome P450. Alcohol enhances the sedative and hypnotic effects on the CNS.
Benzodiazepines (sedative agents)	Alprazolam	Xanax	Rx	Alcohol enhances the furnishings of these agents on the CNS, such as drowsiness, sedation, and decreased motor skills.
	Chlordiazepoxide	Librium
	Clonazepam	Klonopin
	Clorazepate	Tranxene
	Diazepam	Valium
	Lorazepam	Ativan
	Midazolam	Versed
	Oxazepam	Serax
	Temazepam	Restoril
	Triazolam	Halcion
Histamine H₂ receptor antagonists (ulcers, heart fire)	Cimetidine	Tagamet	Rx and OTC	The agents inhibit ADH in the stomach, thereby reducing alcohol first-pass metabolism (run into figure one), as well every bit increase gastric emptying. As a event, BALs are college than expected for a given booze dose; this outcome increases over time.
	Nizatidine	Axid
	Ranitidine	Zantac
Immune modulators (rheumatoid arthritis)	Methotrexate	Rheumatrex	Rx	Allowed modulators (i.e., medications that affect immune cell office) are associated with a risk of liver impairment, which is increased in combination with alcohol.
Musculus relaxants	Carisoprodol	Soma	Rx	Booze consumption enhances damage of physical abilities (e.yard., driving) and increases sedation. Carisoprodol produces an opiate-like high when taken with booze; it is metabolized to meprobamate and sometimes driveling as a street drug.
Musculus relaxants	Cyclobenzaprine	Flexeril
NSAIDs (pain relief and inflammation)	Ibuprofen	eastward.yard., Motrin	Rx and OTC	Booze consumption increases the associated risk of gastrointestinal bleeding.
	Flurbiprofen	various
	Fenoprofen	Nalfon
	Ketoprofen	Orudis
	Naproxen	Naprosyn
	Diclofenac	Voltaren
Opioids (pain relief)	Codeine	various	Rx	Alcohol enhances the effects of these agents on the CNS, such as drowsiness, sedation, and decreased motor skills.
	Hydromorphone	Dilaudid
	Fentanyl	generic
	Morphine	various
	Meperidine	e.g., Demerol
	Propoxyphene	Darvon, Wygesic
Sedatives and hypnotics	Chloral hydrate	Noctec	Rx	Alcohol inhibits the metabolism of these agents and produces a depressant effect on the CNS that includes sleepiness, disorientation, incoherence, and confusion.
Sedatives and hypnotics	Meprobamate	Equanil, Miltown
Tricyclic antidepressants (depression)	Amitriptyline	Elavil, Endep	Rx	Alcohol consumption increases the risk of sedation and a sudden drop in blood pressure level when a person stands upwardly (i.e., orthostatic hypotension).
	Clomipramine	Anafranil
	Desipramine	Norpramin
	Doxepin	Adapin, Sinequan
	Imipramine	Tofranil
	Nortriptyline	Aventyl, Pamelor
	Trimipramine	Surmontil
Herbal medications (slumber aids)	Chamomile	diverse	OTC	Booze may accentuate the drowsiness that is associated with these herbal preparations.
	Echinacea	preparations
	Valerian

Antibiotics

The bundle inserts for most antibiotics include a alert for patients to avoid using alcohol with those medications. The rationale for these warnings is not entirely clear, however, because simply a few antibiotics appear to interact with alcohol. For instance, although some antibiotics induce flushing, almost antibiotics do not. The antibiotic erythromycin may increment alcohol assimilation in the intestine (and, consequently, increase BALs) by accelerating gastric emptying. Furthermore, people taking the antituberculosis drug isoniazid should abstain from booze, considering isoniazid tin cause liver damage, which may be exacerbated by daily alcohol consumption. Bated from these effects, however, moderate alcohol consumption probably does not interfere with antibiotic effectiveness. Possibly, concerns regarding the concurrent utilize of alcohol and antibiotics grew from inquiry findings indicating that heavy booze utilise can impair the function of sure allowed cells and that alcoholics are predisposed to certain infections. These effects, however, are unlikely to occur in moderate drinkers.

Antidepressants

Several classes of antidepressant medications exist, including tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase (MAO) inhibitors, and atypical antidepressants. These classes differ in their mechanism of action in that they affect different brain chemicals. All types of antidepressants, however, have some sedative as well every bit some stimulating activeness.

TCAs with a higher ratio of sedative-to-stimulant activity (i.e., amitriptyline, doxepin, maprotiline, and trimipramine) will crusade the most sedation. Alcohol increases the TCAs' sedative furnishings through pharmacodynamic interactions. In addition, alcohol consumption can cause pharmacokinetic interactions with TCAs. For example, booze appears to interfere with the outset-laissez passer metabolism of amitriptyline in the liver, resulting in increased amitriptyline levels in the claret. In addition, alcohol-induced liver disease further impairs amitriptyline breakup and causes significantly increased levels of active medication in the torso (i.e., increased bioavailability). High TCA levels, in plough, can lead to convulsions and disturbances in heart rhythm.

SSRIs (i.due east., fluvoxamine, fluoxetine, paroxetine, and sertraline), which are currently the about widely used anti-depressants, are much less sedating than are TCAs. In addition, no serious interactions appear to occur when these agents are consumed with moderate alcohol doses (Matilla 1990). In fact, SSRIs have the best safety contour of all antidepressants, fifty-fifty when combined in large quantities with alcohol (east.yard., in suicide and overdose situations).

Conversely, people taking MAO inhibitors or atypical antidepressants can feel adverse consequences when simultaneously consuming alcohol. Thus, MAO inhibitors (eastward.m., phenelzine and tranylcypromine) can induce severe high blood force per unit area if they are consumed together with a substance called tyramine, which is nowadays in cerise vino. Accordingly, people taking MAO inhibitors should be warned confronting drinking red wine. The singular antidepressants (i.e., nefazodone and trazodone) may cause enhanced sedation when used with booze.

Antihistamines

These medications, which are available both by prescription and OTC, are used in the direction of allergies and colds. Antihistamines may cause drowsiness, sedation, and depression blood pressure (i.due east., hypotension), especially in elderly patients (Dufour et al. 1992). Through pharmacodynamic interactions, alcohol can substantially enhance the sedating effects of these agents and may thereby increment, for example, a person'due south risk of falling or impair his or her ability to drive or operate other types of mechanism. As a result of these potential interactions, alarm labels on OTC antihistamines caution patients about the possibility of increased drowsiness when consuming the medication with alcohol. Newer antihistamines (i.east., certrizine and loratidine) have been adult to minimize drowsiness and sedation while still providing constructive allergy relief. However, these newer medications may still be associated with an increased risk of hypotension and falls amongst the elderly, especially when combined with booze. Consequently, patients taking nonsedating antihistamines withal should exist warned confronting using alcohol.

Barbiturates

These medications are sedative or sleep-inducing (i.e., hypnotic) agents that are often used for anesthesia. Phenobarbital, which is probably the most commonly prescribed barbiturate in modernistic do, also is used in the treatment of seizure disorders. Phenobarbital activates some of the aforementioned molecules in the CNS as does alcohol, resulting in pharmacodynamic interactions between the 2 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 crave alertness, such every bit driving or operating heavy machinery, particularly after simultaneous alcohol consumption.

In improver to the pharmacodynamic interactions, pharmacokinetic interactions between alcohol and phenobarbital exist, because alcohol inhibits the medication's breakup in the liver. This inhibition results in a slower metabolism and, mayhap, higher claret levels of phenobarbital. Conversely, barbiturates increase total cytochrome P450 activity in the liver and accelerate booze elimination from the blood (Bode et al. 1979). This acceleration of alcohol elimination probably does not take whatsoever agin upshot.

Benzodiazepines

Like barbiturates, benzodiazepines (BZDs) are classified as allaying-hypnotic agents and act through the aforementioned brain molecules as do barbiturates. Appropriately, as with barbiturates, concurrent consumption of BZDs and moderate amounts of alcohol can cause synergistic sedative effects, leading to substantial CNS damage. It is worth noting that both barbiturates and benzodiazepines can impair memory, equally can booze. Consequently, the combination of these medications with alcohol would exacerbate this retention-impairing outcome. In fact, this effect sometimes is exploited by mixing alcoholic beverages with BZDs, such as the rapid-acting flunitrazepam (Rohypnol^® ), an agent implicated in date rape (Simmons and Cupp 1998). In addition, the metabolism of sure BZDs involves cytochrome P450, leading to the booze-induced changes in metabolism described earlier in this article.

Histamine H₂ Receptor Antagonists (H₂RAs)

Equally mentioned earlier in this article, H₂RAs (eastward.g., cimetidine, ranitidine, nizatidine, and famotidine), which reduce gastric acid secretion, are used in the treatment of ulcers and heartburn. These agents reduce ADH activity in the tummy mucosa (Caballeria et al. 1991), and cimetidine also may increment the rate of gastric emptying. As a issue, alcohol consumed with cimetidine undergoes less starting time-pass metabolism, resulting in increased BALs. For example, in a study of people who consumed three or 4 standard drinks over 135 minutes while taking cimetidine, BALs rose higher and remained elevated for a longer period of fourth dimension than in people not taking cimetidine (Lieber 1997; Gupta et al. 1995). Not all H₂RAs, however, exert the same effect on BALs when taken with alcohol. Thus, cimetidine and ranitidine have the almost pronounced event, nizatidine has an intermediate effect, and famotidine appears to have no consequence (i.e., appears not to interact with booze).⁵ In add-on, because women mostly appear to have lower first-pass metabolism of booze, they may exist at less risk for adverse interactions with H₂RAs.

Muscle Relaxants

Several muscle relaxants (e.m., carisoprodol, cyclobenzaprine, and baclofen), when taken with booze, may produce a certain narcotic-like reaction that includes farthermost weakness, dizziness, agitation, euphoria, and confusion. For example, carisoprodol is a commonly abused and readily available prescription medication that is sold as a street drug. Its metabolism in the liver generates an anxiety-reducing agent that was previously marketed every bit a controlled substance (meprobamate). The mixture of carisoprodol with beer is popular amongst street abusers for creating a quick state of euphoria.

Nonnarcotic Pain Medications and Anti-Inflammatory Agents

Many people frequently utilise nonnarcotic hurting medications and anti-inflammatory agents (e.g., aspirin, acetaminophen, or ibuprofen) for headaches and other minor aches and pains. In improver, arthritis and other disorders of the muscles and bones are among the most common problems for which older people consult physicians (Adams 1995). Nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., ibuprofen, naproxen, indomethacin, and diclofenac) and aspirin are commonly prescribed or recommended for the treatment of these disorders and are purchased OTC in huge amounts. Several potential interactions be between alcohol and these agents, every bit follows:

NSAIDs have been implicated in an increased take a chance of ulcers and gastrointestinal haemorrhage in elderly people. Alcohol may exacerbate that risk by enhancing the ability of these medications to harm the stomach mucosa (Adams 1995).^vi
Aspirin, indomethacin, and ibuprofen cause prolonged bleeding by inhibiting the function of sure blood cells involved in blood jell formation. This result too appears to be enhanced by concurrent alcohol use (Deykin et al. 1982).
Aspirin has been shown to increase BALs after modest alcohol doses, maybe by inhibiting first-pass metabolism (Roine et al. 1990).

An important pharmacokinetic interaction between booze and acetaminophen can increase the take chances of acetaminophen-related toxic effects on the liver. Acetaminophen breakdown by CYP2E1 (and possibly CYP3A) results in the germination of a toxic product that can crusade potentially life-threatening liver harm. As mentioned earlier, heavy alcohol utilize enhances CYP2E1 activeness. In plough, enhanced CYP2E1 activity increases the germination of the toxic acetaminophen product. To prevent liver damage, patients generally should non exceed the maximum doses recommended by the manufacturers (i.e., 4 grams, or up to viii extra-force tablets of acetaminophen per day). In people who drink heavily or who are fasting (which also increases CYP2E1 action), all the same, liver injury may occur at doses every bit depression as 2 to 4 grams per day. The specific drinking levels at which acetaminophen toxicity is enhanced are still unknown. Because acetaminophen is easily bachelor OTC, however, labels on the packages warn people virtually the potentially dangerous booze-acetaminophen combination. Furthermore, people should be aware that combination cough, cold, and flu medications may contain aspirin, acetaminophen, or ibuprofen, all of which might contribute to serious health consequences when combined with alcohol.

Opioids

Opioids are agents with opium-like effects (e.g., sedation, pain relief, and euphoria) that are used every bit pain medications. Alcohol accentuates the opioids' sedating effects. Accordingly, all patients receiving narcotic prescriptions should exist warned virtually the drowsiness caused past these agents and the condiment effects of alcohol. Overdoses of alcohol and opioids are potentially lethal because they can reduce the coughing reflex and animate functions; every bit a result, the patients are at risk of getting foods, fluids, or other objects stuck in their airways or of being unable to breathe.

Certain opioid pain medications (e.g., codeine, propoxyphene, and oxycodone) are manufactured as combination products containing acetaminophen. These combinations can exist specially harmful when combined with alcohol because they provide " hidden" doses of acetaminophen. As described in the previous department, booze consumption may result in the accumulation of toxic breakdown products of acetaminophen. Therefore, patients using opioid-acetaminophen combination products should be cautioned about restricting the total amount of acetaminophen they ingest daily (i.e., they should non take regular acetaminophen in addition to the combination product).

Warfarin

The anticoagulant warfarin is used for the prevention of blood clots in patients with irregular eye rhythms or artificial centre valves; it is besides used to treat clots that course in extremities such as legs, artillery, or sometimes the lungs. Its anticoagulant effect is acutely altered by fifty-fifty small amounts of alcohol. In people taking warfarin and ingesting a few drinks in 1 sitting, anticlotting effects may be stronger than necessary for medical purposes, placing these people at risk for increased bleeding. This excessive warfarin activity results from alcohol-related inhibition of warfarin metabolism by cytochrome P450 in the liver (Lieber 1994). Conversely, in people who chronically drinkable booze, long-term alcohol consumption activates cytochrome P450 and, consequently, warfarin metabolism. Equally a upshot, warfarin is broken down faster than normal, and higher warfarin doses are required to achieve the desired anticoagulant effect. Thus, alcohol consumption can issue in dangerously high or insufficient warfarin activeness, depending on the patient'south drinking pattern. Therefore, patients taking warfarin more often than not should avoid alcohol.

Moderate Alcohol Consumption and OTC or Herbal Medications

Use of OTC medications is widespread amid the general population. According to a contempo survey, 85 percent of adults ages 18 and older have used OTC pain relievers at least once, and up to 34 percent apply OTC pain relievers on a weekly basis, oft without consulting a pharmacist. Furthermore, a recent scientific panel convened by the American Pharmaceutical Association (1997) reported that although adults frequently use OTC medications, many consumers neglect to read the product warning labels. Finally, consumers frequently are unaware of the blazon of medication they take (e.g., NSAID or analgesic). For example, only one in three adults are familiar with the product names acetaminophen, aspirin, or ibuprofen and are able to link these product names to specific brand names. Equally a consequence, many consumers are not fully enlightened of the potential risks of taking these products, specially in combination with other prescription medications or alcohol.

Another factor contributing to an increasing risk of medication-medication or booze-medication interactions is that many medications that previously were available only past prescription (e.chiliad., H₂RAs and NSAIDs) are gaining OTC status. OTC marketing strategies, however, often atomic number 82 the consumer to think that these medications are safe to use on an "as-needed" basis, even though they tin can be potentially dangerous when used with booze. For example, the message that "acid blocker" medications can be used before or during a spicy meal to prevent heartburn symptoms may lead consumers to believe that this practise is also acceptable when they drink booze with their meal.

Non only the combination of booze and OTC products but likewise the amount of alcohol independent in various OTC products can be dangerous (encounter table i). Booze concentrations in these products can be substantial; mouthwashes and cough syrups tend to take the highest booze contents. In an endeavour to control the booze amounts in these products and promote safety, the Food and Drug Administration'due south (FDA's) OTC-drugs advisory committee has adopted the following limits on the corporeality of alcohol considered appropriate:

For children under age half-dozen, products should exist "alcohol free" (i.due east., take an alcohol content of 0.5 percent or less).
For children ages 6 to 12, the booze content should range between 0.5 and v percent.
For people over age 12, the alcohol content should not exceed 5 to 10 per centum.

These levels represent but guidelines, however, and are not enforced by the FDA. The manufacturers of OTC products take agreed to maintain certain standards to proceed their products equally close to these suggestions every bit possible. Yet, college alcohol concentrations are considered acceptable in certain products, such as herbal medications, because alcohol oftentimes is needed to excerpt and deliquesce organic substances from plants.

Herbal medications currently are widely used, and many people assume that considering these products are "natural," they also are safe to use. This assumption may not ever be right, however. For example, chamomile, echinacea, and valerian ordinarily are used as slumber aids, and like prescription and OTC products that cause sedation, these herbal products may produce enhanced sedative effects in the CNS when combined with alcohol. In addition, liver toxicities caused past various natural products take now been identified (Heathcote and Wanless 1995), and their combination with alcohol may enhance potential adverse effects. To date, limited documentation of such interactions exists because of a lack of scientific studies on this subject field (Miller 1998).

Conclusions

Alcohol'south effects on the metabolism and activities of diverse medications have been well documented in chronic heavy drinkers. The effects of moderate alcohol consumption, however, have non been studied every bit thoroughly. Those effects most likely to exist clinically significant are the hazard of over-sedation resulting from the combination of benzodiazepines and alcohol and the interaction of booze with warfarin. Given the diversity and complexity of observed interactions between booze and numerous medications, information technology is hard to recommend an alcohol consumption level that tin can be considered rubber when taking medications. As a rule, people taking either prescription or OTC medications should always read the product warning labels to make up one's mind whether possible interactions exist. Similarly, health care providers should be alert to the potential for moderate booze use to either heighten medication effects or interfere with the desired therapeutic deportment of a medication.

Footnotes

¹A standard drink is divers as one 12-ounce can of beer or bottle of wine cooler, ane 5-ounce drinking glass of wine, or 1.5 ounces of distilled spirits and is equivalent to approximately 0.5 ounce, or 12 grams (g), of pure alcohol.

²Depression booze doses are defined hither as 0.three 1000 per kilogram body weight, equivalent to approximately two standard drinks for a person weighing seventy kg.

³The endoplasmic reticulum is an extensive network of membrane-enclosed tubules inside the prison cell that is involved in the production of proteins and fat molecules and in the send of those molecules within the prison cell.

⁴An Internet Web site (www.accp.com/p450.html) catalogs the classes of cytochrome P450 molecules that can metabolize various medications. This resource can help place medications metabolized by CYP2E1 that may potentially interact with booze.

^vSome other grade of medications, which foreclose gastric acid production through a dissimilar machinery from the H_twoRAs (i.eastward., omeprazole and lansoprazole), also do not appear to collaborate with alcohol.

⁶Moderate booze utilise by itself, however, does non appear to be associated with an increased risk of ulcers or gastrointestinal bleeding and too is unlikely to cause a certain type of inflammation of the stomach lining (i.e., hemorrhagic gastritis) that has been observed after heavy alcohol employ.

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