Alcohol, also known as ethanol, is made through a process called fermentation.

During
fermentation, yeast breaks sugar down into ethanol and carbon dioxide. This process is done
without any air present and once complete, the carbon dioxide gas bubbles out into the air,
leaving ethanol and water behind. Distilled spirits, such as vodka, rum, gin, and whiskey, are
fermented and then distilled to separate the ethanol from the water.

Various sources of sugar are used in these processes, resulting in different forms of alcohol. The
sugar from crushed grapes is used to make wine; malted barley is used to make beer; sugar cane
or molasses makes rum; grain, potatoes, beets, molasses, and a variety of other plants are used to
make vodka.

The technique used to make the beverage will determine the alcohol content. You will see the
percentage of alcohol per volume listed on the bottle, as well as the proof of the drink. The proof
of a beverage is twice the alcohol content, so a drink with 12% alcohol per volume is 24 proof.
Generally, a 12-ounce glass of beer, a 5-ounce glass of wine, and a 1.5-ounce shot of liquor all
contain a ½ ounce of pure alcohol and are considered one drink.

Have you ever wondered why you feel the way that you do after drinking alcohol? Many people
will admit that they drink to get that feeling, but not many know exactly what is going on to
cause it. The effects that alcohol has on your health start with how it's metabolized. Once alcohol
is in your system, your body makes metabolizing it a priority. That means that it will stop
metabolizing anything else in order to first get the alcohol metabolized. The reason for this is
because unlike protein, carbohydrates, and fat, there is nowhere for alcohol to be stored in our
body so it has be metabolized first.

Once alcohol enters your stomach, up to 20% of it can be absorbed there and go directly into
your bloodstream. Within minutes, alcohol will reach your brain and give the feeling of being a
stimulant. No other nutrient is able to do this. The remaining alcohol goes to your intestines and
is absorbed there with the rest of the nutrients. A small amount of alcohol is excreted through
sweat, saliva, urine, and your breath, which is how it is detected by a Breathalyzer.

Your liver is the primary site for alcohol metabolism; this is why you can have liver problems
from consuming too much alcohol. Alcohol is detoxified and removed from the blood through a
process called oxidation. Oxidation prevents the alcohol from accumulating and destroying cells
and organs. A healthy liver oxidizes pure ethanol at the rate of about ¼ to ⅓ of an ounce per
hour, which is less than 1 ounce of hard liquor.

When you drink alcohol, your blood alcohol concentration (BAC) will rise rapidly. Within five
minutes of having a drink, there's enough alcohol in your blood to measure. The BAC is
determined by how quickly alcohol is absorbed, distributed, metabolized, and excreted. The
following factors can influence the BAC:

 Gender
  Race
 Food consumed with the alcohol
 Chronic alcohol consumption
 Drinking pattern
 Medications

The consumption of one standard drink will result in a peak in BAC within 35 to 45 minutes. A
150-pound person with normal liver function metabolizes about 7 to 14 grams of alcohol per
hour, which is approximately 100 to 200 mg/kg of body weight per hour. This is comparable to 8
to 12 ounces of beer or half of an alcoholic drink. Controlling the rate of consumption will give
your liver time to metabolize the alcohol and limit your BAC. Once you stop drinking, your
blood alcohol level decreases by about 0.01% per hour. You are legally intoxicated with a blood
alcohol concentration of 0.8. Time is the only way to eliminate alcohol from your system, so
cold showers and coffee will not sober you up. Trying to get someone who is drunk to feel and
appear more alert can cause a false sense of sobriety to the person drinking and everyone around
them.

Alcohol Metabolism: An Update

Drinking heavily puts people at risk for many adverse health consequences, including
alcoholism, liver damage, and various cancers. But some people appear to be at greater risk than
others for developing these problems. Why do some people drink more than others? And why do
some people who drink develop problems, whereas others do not?

Research shows that alcohol use and alcohol-related problems are influenced by individual
variations in alcohol metabolism, or the way in which alcohol is broken down and eliminated by
the body. Alcohol metabolism is controlled by genetic factors, such as variations in the enzymes
that break down alcohol; and environmental factors, such as the amount of alcohol an individual
consumes and his or her overall nutrition. Differences in alcohol metabolism may put some
people at greater risk for alcohol problems, whereas others may be at least somewhat protected
from alcohol’s harmful effects.

This Alcohol Alert describes the basic process involved in the breakdown of alcohol, including
how toxic byproducts of alcohol metabolism may lead to problems such as alcoholic liver
disease, cancer, and pancreatitis. This Alert also describes populations who may be at particular
risk for problems resulting from alcohol metabolism as well as people who may be genetically
―protected‖ from these adverse effects.

THE CHEMICAL BREAKDOWN OF ALCOHOL

Alcohol is metabolized by several processes or pathways. The most common of these pathways
involves two enzymes—alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).
These enzymes help break apart the alcohol molecule, making it possible to eliminate it from the
body. First, ADH metabolizes alcohol to acetaldehyde, a highly toxic substance and known
carcinogen (1). Then, in a second step, acetaldehyde is further metabolized down to another, less
active byproduct called acetate (1), which then is broken down into water and carbon dioxide for
easy elimination (2).

Other enzymes—
The enzymes cytochrome P450 2E1 (CYP2E1) and catalase also break down alcohol to
acetaldehyde. However, CYP2E1 only is active after a person has consumed large amounts of
alcohol, and catalase metabolizes only a small fraction of alcohol in the body (1). Small amounts
of alcohol also are removed by interacting with fatty acids to form compounds called fatty acid
ethyl esters (FAEEs). These compounds have been shown to contribute to damage to the liver
and pancreas (3).

The Chemical Breakdown of Alcohol

The chemical name for alcohol is ethanol (CH3CH2OH). The

body processes and eliminates ethanol in separate steps.
Chemicals called enzymes help to break apart the ethanol
molecule into other compounds (or metabolites), which can
be processed more easily by the body. Some of these
intermediate metabolites can have harmful effects on the
body.

Most of the ethanol in the body is broken down in the liver by

an enzyme called alcohol dehydrogenase (ADH), which
transforms ethanol into a toxic compound called acetaldehyde
(CH3CHO), a known carcinogen. However, acetaldehyde is
generally short-lived; it is quickly broken down to a less toxic
compound called acetate (CH3COO-) by another enzyme
called aldehyde dehydrogenase (ALDH). Acetate then is
broken down to carbon dioxide and water, mainly in tissues
other than the liver.

Acetaldehyde: a toxic byproduct—Much of the research on alcohol metabolism has focused on

an intermediate byproduct that occurs early in the breakdown process—acetaldehyde. Although
acetaldehyde is short lived, usually existing in the body only for a brief time before it is further
broken down into acetate, it has the potential to cause significant damage. This is particularly
evident in the liver, where the bulk of alcohol metabolism takes place (4). Some alcohol
metabolism also occurs in other tissues, including the pancreas (3) and the brain, causing damage
to cells and tissues (1). Additionally, small amounts of alcohol are metabolized to acetaldehyde
in the gastrointestinal tract, exposing these tissues to acetaldehyde’s damaging effects (5).

In addition to its toxic effects, some researchers believe that acetaldehyde may be responsible for
some of the behavioral and physiological effects previously attributed to alcohol (6). For
example, when acetaldehyde is administered to lab animals, it leads to incoordination, memory
impairment, and sleepiness, effects often associated with alcohol (7).

On the other hand, other researchers report that acetaldehyde concentrations in the brain are not
high enough to produce these effects (7). This is because the brain has a unique barrier of cells
(the blood–brain barrier) that help to protect it from toxic products circulating in the
bloodstream. It’s possible, however, that acetaldehyde may be produced in the brain itself when
alcohol is metabolized by the enzymes catalase (8,9) and CYP2E1 (10).

nsport chain.

3
In other words, CYP2E1 has a high Km for ethanol of 8–10 mM, compared with a Km of 0.05–
40 mM for hepatic ADH.
Figure 4 Oxidative pathways of alcohol metabolism. Alcohol is metabolized mainly in the
cytosol by alcohol dehydrogenase (ADH) to produce acetaldehyde. At high levels of alcohol
consumption, an enzyme in the endoplasmic reticulum, cytochrome P450 IIE1 (CYP2E1),
becomes involved in metabolizing alcohol to acetaldehyde; this enzyme also is induced by
chronic drinking. A catalase-mediated reaction in the peroxisomes is considered a minor
metabolic pathway of alcohol metabolism. Acetaldehyde is further metabolized to acetate in the
mitochondria. Alcohol metabolism results in the formation of NADH and thus changes the redox
state of hepatocytes (i.e., increases the ratio of NADH/NAD+). Both alcohol metabolism by
CYP2E1 and the re-oxidation of NADH via the electron transport chain in the mitochondria
results in the formation of reactive oxygen species (ROS).

THE GENETICS BEHIND METABOLISM

Regardless of how much a person consumes, the body can only metabolize a certain amount of
alcohol every hour (2). That amount varies widely among individuals and depends on a range of
factors, including liver size (1) and body mass.

In addition, research shows that different people carry different variations of the ADH and
ALDH enzymes. These different versions can be traced to variations in the same gene. Some of
these enzyme variants work more or less efficiently than others; this means that some people can
break down alcohol to acetaldehyde, or acetaldehyde to acetate, more quickly than others. A fast
ADH enzyme or a slow ALDH enzyme can cause toxic acetaldehyde to build up in the body,
creating dangerous and unpleasant effects that also may affect an individual’s risk for various
alcohol-related problems—such as developing alcoholism.
The type of ADH and ALDH an individual carries has been shown to influence how much he or
she drinks, which in turn influences his or her risk for developing alcoholism (11). For example,
high levels of acetaldehyde make drinking unpleasant, resulting in facial flushing, nausea, and a
rapid heart beat. This ―flushing‖ response can occur even when only moderate amounts of
alcohol are consumed. Consequently, people who carry gene varieties for fast ADH or slow
ALDH, which delay the processing of acetaldehyde in the body, may tend to drink less and are
thus somewhat ―protected‖ from alcoholism (although, as discussed later, they may be at greater
risk for other health consequences when they do drink).

Genetic differences in these enzymes may help to explain why some ethnic groups have higher
or lower rates of alcohol-related problems. For example, one version of the ADH enzyme, called
ADH1B*2, is common in people of Chinese, Japanese, and Korean descent but rare in people of
European and African descent (12). Another version of the ADH enzyme, called ADH1B*3,
occurs in 15 to 25 percent of African Americans (13). These enzymes protect against alcoholism
(14) by metabolizing alcohol to acetaldehyde very efficiently, leading to elevated acetaldehyde
levels that make drinking unpleasant (15). On the other hand, a recent study by Spence and
colleagues (16) found that two variations of the ALDH enzyme, ALDH1A1*2 and ALDH1A1*3,
may be associated with alcoholism in African-American people.

Although these genetic factors influence drinking patterns, environmental factors also are
important in the development of alcoholism and other alcohol-related health consequences. For
example, Higuchi and colleagues (17) found that as alcohol consumption in Japan increased
between 1979 and 1992, the percentage of Japanese alcoholics who carried the protective
ADH1B*2 gene version increased from 2.5 to 13 percent. Additionally, despite the fact that
more Native American people die of alcohol-related causes than do any other ethnic group in the
United States, research shows that there is no difference in the rates of alcohol metabolism and
enzyme patterns between Native Americans and Whites (18). This suggests that rates of
alcoholism and alcohol-related problems are influenced by other environmental and/or genetic
factors.

HEALTH CONSEQUENCES OF ALCOHOL USE

Alcohol metabolism and cancer—Alcohol consumption can contribute to the risk for developing
different cancers, including cancers of the upper respiratory tract, liver, colon or rectum, and
breast (19). This occurs in several ways, including through the toxic effects of acetaldehyde (20).

Where Alcohol
Metabolism Takes Place
Alcohol is metabolized in the
body mainly by the liver. The
brain, pancreas, and stomach
also metabolize alcohol.

Many heavy drinkers do not develop cancer, and some people who drink only moderately do
develop alcohol-related cancers. Research suggests that just as some genes may protect
individuals against alcoholism, genetics also may determine how vulnerable an individual is to
alcohol’s carcinogenic effects (5).

Ironically, the very genes that protect some people from alcoholism may magnify their
vulnerability to alcohol-related cancers. The International Agency for Research on Cancer (21)
asserts that acetaldehyde should be classified as a carcinogen. Acetaldehyde promotes cancer in
several ways—for example, by interfering with the copying (i.e., replication) of DNA and by
inhibiting a process by which the body repairs damaged DNA (5). Studies have shown that
people who are exposed to large amounts of acetaldehyde are at greater risk for developing
certain cancers, such as cancers of the mouth and throat (5). Although these individuals often are
less likely to consume large amounts of alcohol, Seitz and colleagues (5) suggest that when they
do drink their risk for developing certain cancers is higher than drinkers who are exposed to less
acetaldehyde during alcohol metabolism.

Acetaldehyde is not the only carcinogenic byproduct of alcohol metabolism. When alcohol is
metabolized by CYP2E1, highly reactive, oxygen-containing molecules—or reactive oxygen
species (ROS)—are produced. ROS can damage proteins and DNA or interact with other
substances to create carcinogenic compounds (22).

Fetal Alcohol Spectrum Disorder (FASD)—Pregnant women who drink heavily are at even
greater risk for problems. Poor nutrition may cause the mother to metabolize alcohol more
slowly, exposing the fetus to high levels of alcohol for longer periods of time (23). Increased
exposure to alcohol also can prevent the fetus from receiving necessary nutrition through the
placenta (24). In rats, maternal malnutrition has been shown to contribute to slow fetal growth,
one of the features of FASD, a spectrum of birth defects associated with drinking during
pregnancy (23). These findings suggest that managing nutrition in pregnant women who drink
may help to reduce the severity of FASD (25).

Alcoholic liver disease—As the chief organ responsible for the breakdown of alcohol, the liver is
particularly vulnerable to alcohol metabolism’s effects. More than 90 percent of people who
drink heavily develop fatty liver, a type of liver disease. Yet only 20 percent will go on to
develop the more severe alcoholic liver disease and liver cirrhosis (26).

Alcoholic pancreatitis—Alcohol metabolism also occurs in the pancreas, exposing this organ to
high levels of toxic byproducts such as acetaldehyde and FAEEs (3). Still, less than 10 percent of
heavy alcohol users develop alcoholic pancreatitis—a disease that irreversibly destroys the
pancreas— suggesting that alcohol consumption alone is not enough to cause the disease.
Researchers speculate that environmental factors such as smoking and the amount and pattern of
drinking and dietary habits, as well as genetic differences in the way alcohol is metabolized, also
contribute to the development of alcoholic pancreatitis, although none of these factors has been
definitively linked to the disease (27).

SIDEBAR

TRENDS IN RESEARCH
Investigators are studying factors that influence alcohol metabolism, such as variations
in the study subjects’ gender and ethnicity, genetic variations in alcohol-metabolizing
enzymes, and even the food subjects consumed that day. Two methods that are helping
researchers gain a better understanding of how alcohol is metabolized are the alcohol
clamp method, in which alcohol is given intravenously, and the use of specially grown
cells.

The alcohol clamp method. The speed at which people absorb, distribute, and
metabolize alcohol varies as much as three or four times between individuals (1,2).
The alcohol clamp is a method of administering alcohol intravenously to subjects,
allowing researchers to circumvent variations in alcohol absorption. This technique
enables researchers to administer precise doses of alcohol to achieve an exact breath
alcohol concentration (a measure of how much alcohol is in the body) (3,4). The actual
dose of alcohol is calculated for each individual based on his or her specific alcohol
elimination rate, controlling for factors like gender and body mass. This allows
researchers to compare the alcohol elimination or metabolism rates without
complicating factors. For example, using the alcohol clamp method researchers were
able to determine that male volunteers eliminated alcohol at significantly faster rates
than did female volunteers (5–8). The alcohol clamp method also helps researchers
study the genetics of alcohol metabolism, including differences in how volunteers who
carry different versions of the ADH and ALDH genes metabolize alcohol (9).

Cultured cells. Cells that are grown in the laboratory (i.e., cultured cells) are an
important tool in studying how alcohol damages the liver on a molecular level.
Cultured cells can help to clarify the processes associated with alcohol metabolism that
damage cells by allowing researchers to investigate individual metabolic pathways; to
control the cells’ exposure to alcohol and its byproducts; and to work with uniform, or
cloned, cells (10). Additionally, because large quantities of cells can be cloned,
researchers are able to repeat experiments many times in order to confirm findings.

REFERENCES

(1) ) Friel, P.N.; Baer, J.S.; and Logan, B.K. Variability of ethanol absorption and
breath concentrations during a large-scale alcohol administration study. Alcoholism:
Clinical and Experimental Research 19:1055–1060, 1995. PMID: 7485816 (2) ) Li,
T.-K.; .; Beard, J.D.; Orr, W.E.; et al. Gender and ethnic differences in alcohol
metabolism. Alcoholism: Clinical and Experimental Research 22:771–772, 1998. (3)
O’Connor, S.; Morzorati, S.; Christian, J.; and Li, T.-K. Clamping breath alcohol
concentration reduces experimental variance: Application to the study of acute
tolerance to alcohol and alcohol elimination rate. Alcoholism: Clinical and
Experimental Research 22:202–210, 1998. PMID: 9514308 (4) Ramchandani, V.A.;
O’Connor, S.; Neumark, Y.D.; et al. The alcohol clamp: Applications, challenges and
new directions. Alcoholism: Clinical and Experimental Research 30:155–164, 2006.
PMID: 16433744 (5) Kwo, P.Y.; Ramchandani, V.A.; O’Connor, S.; et al. Gender
differences in alcohol metabolism: Relationship to liver volume and effect of adjusting
for body mass. Gastroenterology 115:1552–1557, 1998. PMID: 9834284 (6) Li, T.-
K.; Beard, J.D.; Orr, W.E.; et al. Variation in ethanol pharmacokinetics and perceived
gender and ethnic differences in alcohol elimination. Alcoholism: Clinical and
Experimental Research 24:415–416, 2000. PMID: 10798571 (7) Sato, N.; Lindros,
K.O.; Baraona, E.; et al. Sex difference in alcohol-related organ injury. Alcoholism:
Clinical and Experimental Research 25:40S–45S, 2001. PMID: 11391047 (8)
Ramchandani, V.A.; Bosron, W.F.; and Li, T.-K. Research advances in ethanol
metabolism. Pathologie Biologie 49:676–682, 2001. PMID: 11762128 (9) Neumark,
Y.D.; Friedlander, Y.; Durst, R.; et al. Alcohol dehydrogenase polymorphisms
influence alcohol-elimination rates in a male Jewish population. Alcoholism: Clinical
and Experimental Research 28:10–14, 2004. PMID: 14745297 (10) Clemens, D.L.
Use of cultured cells to study alcohol metabolism. Alcohol Research & Health
29(4):291–295, 2006.

END OF SIDEBAR

CONCLUSION
Researchers continue to investigate the reasons why some people drink more than others and
why some develop serious health problems because of their drinking. Variations in the way the
body breaks down and eliminates alcohol may hold the key to explaining these differences. New
information will aid researchers in developing metabolism-based treatments and give treatment
professionals better tools for determining who is at risk for developing alcohol-related problems.
REFERENCES
(1) Edenberg, H.J. The genetics of alcohol metabolism: Role of alcohol dehydrogenase and
aldehyde dehydrogenase variants. Alcohol Research & Health 30(1):5–13, 2007. (2) National
Institute on Alcohol Abuse and Alcoholism. Alcohol Alert: Alcohol Metabolism. No. 35, PH
371. Bethesda, MD: the Institute, 1997 http://pubs.niaaa.nih.gov/publications/aa35.htm. (3)
Vonlaufen, A.; Wilson, J.S.; Pirola, R.C.; and Apte, M.V. Role of alcohol metabolism in chronic
pancreatitis. Alcohol Research & Health 30(1):48–54, 2007. (4) Zakhari, S. Overview: How is
alcohol metabolized by the body? Alcohol Research & Health 29(4):245–254, 2006. (5) Seitz,
H.K., and Becker, P. Alcohol metabolism and cancer risk. Alcohol Research & Health 30(1):38–
47, 2007. (6) Deitrich, R., Zimatkin, S., and Pronko S. Oxidation of ethanol in the brain and its
consequences. Alcohol Research & Health 29(4):266–273, 2006. (7) Quertemont, E., and
Didone, V. Role of acetaldehyde in mediating the pharmacological and behavioral effects of
alcohol. Alcohol Research & Health 29(4):258–265, 2006. (8) Aragon, C.M.; Rogan, F.; and
Amit, Z. Ethanol metabolism in rat brain homogenates by a catalase–H2O2 system. Biochemical
Pharmacology 44:93–98, 1992. PMID: 1632841 (9) Gill, K.; Menez, J.F.; Lucas, D.; and
Deitrich, R.A. Enzymatic production of acetaldehyde from ethanol in rat brain tissue.
Alcoholism: Clinical and Experimental Research 16:910–915, 1992. PMID: 1443429 (10)
Warner, M., and Gustafsson, J.A. Effect of ethanol on cytochrome P450 in the rat brain.
Proceedings of the National Academy of Sciences of the United States of America 91:1019–1023,
1994. PMID: 8302826 (11) Hurley, T.D.; Edenberg, H.J.; Li, T.-K. The Pharmacogenomics of
alcoholism. In: Pharmacogenomics: The Search for Individualized Therapies. Weinheim,
Germany: Wiley–VCH, 2002, pp. 417–441. (12) Oota, H.; Pakstis, A.J.; and Bonne-Tamir, B.
The evolution and population genetics of the ALDH2 locus: Random genetic drift, selection, and
low levels of recombination. Annals of Human Genetics 68(Pt. 2):93–109, 2004. PMID:
15008789 (13) Bosron, W.F., and Li, T.-K. Catalytic properties of human liver alcohol
dehydrogenase isoenzymes. Enzyme 37:19–28, 1987. PMID: 3569190 (14) Ehlers, C.L.; Gilder,
D.A.; Harris L.; and Carr L. Association of the ADH2*3 allele with a negative family history of
alcoholism in African American young adults. Alcoholism: Clinical and Experimental Research
25:1773–1777, 2001. PMID: 11781511 (15) Crabb, D.W. Ethanol oxidizing enzymes: Roles in
alcohol metabolism and alcoholic liver disease. Progress in Liver Disease 13:151–172, 1995.
PMID: 9224501 (16) Spence, J.P.; Liang, T.; Eriksson, C.J.; et al. Evaluation of aldehyde
dehydrogenase 1 promoter polymorphisms identified in human populations. Alcoholism: Clinical
and Experimental Research 27:1389–1394, 2003. PMID: 14506398 (17) Higuchi, S.;
Matsushita, S.; Imazeki, H.; et al. Aldehyde dehydrogenase genotypes in Japanese alcoholics.
Lancet 343:741–742, 1994. PMID: 7907720 (18) Bennion, L.J., and Li, T.-K. Alcohol
metabolism in American Indians and whites: Lack of racial differences in metabolic rate and
liver alcohol dehydrogenase. New England Journal of Medicine 294:9–13, 1976. PMID:
1244489(19) Bagnardi, V.; Blangiardo, M.; La Vecchia, C.; and Corrao, G. Alcohol
consumption and the risk of cancer: A meta-analysis. Alcohol Research & Health 25(4):263–
270, 2001. PMID: 11910703 (20) Koop, D.R. Alcohol metabolism’s damaging effects on the
cell: A focus on reactive oxygen generation by the enzyme cytochrome P450 2E1. Alcohol
Research & Health 29(4):274–280, 2006. (21) International Agency for Research on Cancer
(IARC). Re-evaluation of some organic chemicals, hydrazine and hydrogen peroxide. In:
Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Acetaldehyde
No. 77. Lyon, France: IARC, 1999, pp. 319–335. (22) Seitz, H.K., and Stickel, F. Risk factors
and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress.
Biological Chemistry 387:349–360, 2006. PMID: 16606331 (23) Shankar, K.; Hidestrand, M.;
Liu, X.; et al. Physiologic and genomic analyses of nutrition-ethanol interactions during
gestation: Implications for fetal ethanol toxicity. Experimental Biology and Medicine 231:1379–
1397, 2006. PMID: 16946407 (24) Dreosti, I.E. Nutritional factors underlying the expression of
the fetal alcohol syndrome. Annals of the New York Academy of Sciences 678:193–204, 1993.
PMID: 8494262 (25) Shankar, K.; Ronis, M.J.J.; Badger, T.M. Effects of pregnancy and
nutritional status on alcohol metabolism. Alcohol Research & Health 30(1):55–59, 2007. (26)
McCullough, A.J., and O’Connor, J.F. Alcoholic liver disease: Proposed recommendations for
the American College of Gastroenterology. American Journal of Gastroenterology 93(11):
2022–2036, 1998. PMID: 9820369 (27) Ammann, R.W. The natural history of alcoholic
chronic pancreatitis. Internal Medicine 40(5):368–375, 2001. PMID: 1393404

Resources

Source material for this Alcohol Alert originally appeared in

a special two-part series of Alcohol Research & Health that examines the topic of alcohol
metabolism.

 Alcohol Research & Health, Vol. 29, No. 4, 2006: This issue describes alcohol’s
metabolic pathways, their genetic variation, and the effects of certain byproducts, such as
acetaldehyde, on a range of organs and tissues.
 Alcohol Research & Health, Vol. 30, No. 1, 2007. This issue examines how differences
in metabolism may lead to increased or reduced risk among individuals and ethnic groups
for alcohol-related problems such as alcohol dependence, cancer, fetal alcohol effects,
and pancreatitis.
 Full-text articles from each issue of Alcohol Research & Health are available on the
NIAAA Web site at www.niaaa.nih.gov

Subscriptions to Alcohol Research & Health are available from the Superintendent of
Documents for $25. Write to New Orders, Superintendent of Documents, P.O. Box
371954, Pittsburgh, PA 15250–7954; or fax 202-512-2250.

All material contained in the Alcohol Alert is in the public domain and may be used or
reproduced without permission from NIAAA. Citation of the source is appreciated.
Copies of the Alcohol Alert are available free of charge from the
National Institute on Alcohol Abuse and Alcoholism Publications Distribution Center
P.O. Box 10686, Rockville, MD 20849–0686.

Print version

Site Map

Accessibility

Privacy

FOIA

Contact Us

Material en Español

USA.gov—Government Made Easy

U.S. Department of Health and Human Services

National Institutes of Health

NIAAA: Understanding the impact of alcohol on human health and well-being