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Alcohol’s Role in

Gastrointestinal Tract

When alcohol is consumed, the alcoholic beverages first pass through the various
segments of the gastrointestinal (GI) tract. Accordingly, alcohol may interfere with
the structure as well as the function of GI-tract segments. For example, alcohol can
impair the function of the muscles separating the esophagus from the stomach,
thereby favoring the occurrence of heartburn. Alcohol-induced damage to the
mucosal lining of the esophagus also increases the risk of esophageal cancer. In the
stomach, alcohol interferes with gastric acid secretion and with the activity of the
muscles surrounding the stomach. Similarly, alcohol may impair the muscle
movement in the small and large intestines, contributing to the diarrhea frequently
observed in alcoholics. Moreover, alcohol inhibits the absorption of nutrients in the
small intestine and increases the transport of toxins across the intestinal walls,
effects that may contribute to the development of alcohol-related damage to the liver
and other organs. K EY WORDS : ethanol metabolism; AODE (alcohol and other drug
effects); mouth; esophagus; stomach; intestine; gastric mucosa; intestinal mucosa; gastric
lesion; gastric acid; gastrointestinal function; gastrointestinal absorption; muscle; neoplastic
disease; toxins; free radicals; etiology; literature review

mong the many organ systems intestinal bleeding (from lesions in the acute and chronic effects on GI-tract
that mediate alcohol’s effects on stomach or small intestine) and diar- function and structure.
the human body and its health, rhea. Third, functional changes and This article reviews some of these
the gastrointestinal (GI) tract plays a mucosal damage in the gut disturb the findings, focusing primarily on insights
particularly important part. Several digestion of other nutrients as well as gained during the past 10 years. (For
processes underlie this role. First, the their assimilation into the body, there- extensive reviews of the developments
GI tract is the site of alcohol absorption by contributing to the malnutrition and
into the bloodstream and, to a lesser weight loss frequently observed in CHRISTIANE BODE, PH.D., is professor
extent, of alcohol breakdown and pro- and chief of the Section of Physiology
alcoholics. Fourth, alcohol-induced
duction. (For more information on of Nutrition (140), Hohenheim
mucosal injuries—especially in the University, Stuttgart, Germany.
alcohol absorption, metabolism, and
upper small intestine—allow large
production in the GI tract, see sidebar,
pp. 82–83.) Second, the direct contact of molecules, such as endotoxin and other J. CHRISTIAN BODE, M.D., is professor
alcoholic beverages with the mucosa1 bacterial toxins, to pass more easily of medicine and chief of the Section
that lines the upper GI tract can induce into the blood or lymph. These toxic of Gastroenterology, Hepatology and
numerous metabolic and functional substances can have deleterious effects Endocrinology in the Department of
changes. These alterations may lead to on the liver and other organs. Internal Medicine, Robert-Bosch-
Over the past three decades, re- Krankenhaus, Stuttgart, Germany.
marked mucosal damage, which can
result in a broad spectrum of acute and searchers have made major progress 1
For a definition of this and other technical terms used
chronic diseases, such as acute gastro- toward understanding alcohol’s many in this article, see the central glossary, pp. 93–96.


Gastrointestinal Tract Disorders

in this field up to the early 1980’s, see (figure 2). As the food mass moves
Beazell and Ivy 1940; Bode 1980). through the small intestine, digestive
enzymes secreted by the intestinal Tongue
Oral cavity
THE GI TRACT—AN OVERVIEW cells complete the chemical degrad-
ation of nutrients into simple mole- Parotid
The GI tract’s functions are to physi- cules that can be absorbed through the gland
cally and chemically break down intestinal wall into the bloodstream.
ingested food, allow the absorption of What finally remains in the intestine
nutrients into the bloodstream, and are primarily indigestible waste prod- Teeth
excrete the waste products generated. ucts. These products progress into the
The GI tract can be viewed as one large intestine, where the waste is Salivary
continuous tube extending from the compacted and prepared for excretion glands
mouth to the anus (figure 1), which is through the anus. Like the small in-
subdivided into different segments testine, the large intestine can be
with specific functions. divided into three segments: the ce- Stomach
In the mouth, or oral cavity, the teeth cum; the colon, which constitutes
mechanically grind the food into small about 80 percent of the large intes-
pieces. Moreover, saliva excreted by tine; and the rectum. The following Duodenum
the salivary glands initiates the food’s sections review alcohol’s effect on the Jejunum
chemical degradation. From the oral different regions of the GI tract.
cavity, the food passes through the throat
(i.e., pharynx) into the esophagus. The THE ORAL CAVITY
coordinated contraction and relaxation AND THE ESOPHAGUS
of the muscles surrounding the esopha-
gus propels the food into the stomach. The oral cavity, pharynx, esophagus,
In the stomach, the chemical degra- and stomach are exposed to alcohol Cecum
dation of the food continues with the immediately after its ingestion. Thus,
help of gastric acid and various diges- alcoholic beverages are almost undi- intestine
tive enzymes. Excessive gastric acid luted when they come in contact with Ileum (colon)
production can irritate the mucosa, the mucosa of these structures. It is Rectum Anal canal
causing gastric pain, and result in the therefore not surprising that mucosal
development of gastric ulcers. Two injuries (i.e., lesions) occur quite
bands of muscle fibers (i.e., sphinc- frequently in people who drink large Figure 1 Schematic representation of
ters) close off the stomach to the eso- amounts of alcohol.2 the human gastrointestinal tract. The
small intestine comprises the duo-
phagus and the intestine. Weakness of Chronic alcohol abuse damages the
denum, the ileum, and the jejunum.
the sphincter separating the stomach salivary glands and thus interferes
from the esophagus allows the stom- with saliva secretion. In alcoholics this
ach content to flow back into the eso- damage commonly manifests itself as poor nutrition or reflect alcohol’s
phagus. This process, which is called an enlargement (i.e., hypertrophy) of direct effect on the mucosa. Finally,
gastroesophageal reflux, can lead to the parotid gland, although the mecha- chronic alcohol abuse increases the
heartburn as well as inflammation (i.e., nisms leading to this condition are incidence of tooth decay, gum disease,
reflux esophagitis) and even to the unknown. Moreover, alcoholics may and loss of teeth (Kranzler et al. 1990).
development of ulcers in the lower suffer from inflammation of the tongue Alcohol consumption can affect the
part of the esophagus. (i.e., glossitis) and the mouth (i.e., esophagus in several ways. For exam-
From the stomach, the food enters stomatitis). It is unclear, however, ple, alcohol distinctly impairs esophageal
the small intestine, which is divided whether these changes result from motility, and even a single drinking
into three segments: the duodenum, episode (i.e., acute alcohol consump-
the jejunum, and the ileum. Like the 2
The alcohol amount necessary to cause mucosal tion) significantly weakens the lower
esophagus and stomach, the intestine injury varies significantly among individual drinkers esophageal sphincter. As a result,
and depends, for example, on whether alcohol
is surrounded by layers of muscles, consumption occurs on an empty stomach or is
gastroesophageal reflux may occur,
the rhythmic movements of which accompanied by a meal. Thus, no clear threshold and the esophagus’ ability to clear the
help mix the food mass and push it exists above which alcohol exerts its adverse effects. refluxed gastric acid may be reduced.
along the GI tract. The intestine’s However, the risk for adverse effects such as tissue Both of these factors promote the
damage generally increases following the consump-
inner mucosal surface is covered with tion of more than 2 ounces of alcohol, which corre-
occurrence of heartburn. Moreover,
small projections called villi, which sponds to approximately four standard drinks (i.e., some alcoholics exhibit an abnormali-
increase the intestinal surface area “heavy” or “excessive” drinking). ty of esophageal motility known as a

VOL. 21, NO. 1, 1997 77

functioning in several ways. For ex-
ample, alcohol—even in relatively
Small Intestine
small doses—can alter gastric acid
secretion, induce acute gastric mucos-
al injury, and interfere with gastric
Intestinal wall and intestinal motility.
Gastric Acid Secretion
Analyses in several animal species
found that acute alcohol administration
by mouth or by direct infusion into the
Villi stomach (i.e., intragastrically) or the
Submucosa blood (i.e., intravenously) can affect
gastric acid secretion (Chari et al. 1993).
Intestinal muscles
The secretory response of the stomach
varies considerably, however, depend-
ing on the species studied and the alco-
hol concentrations used. In healthy,
nonalcoholic humans, intravenous alco-
hol administration of 0.3 to 0.5 grams
per kilogram (g/kg) body weight or
intragastric infusion of alcohol solutions
with concentrations of up to 5 percent
Submucosa stimulate gastric acid secretion, whereas
Intestinal muscles intragastric infusion of higher concen-
trations has either no effect or a mildly
inhibitory one (Chari et al. 1993). Accord-
ingly, alcoholic beverages with a low
Figure 2 Schematic illustration of the villi lining the small intestine. These villi serve alcohol content (e.g., beer and wine)
to increase the internal surface area of the intestine and thus enhance the strongly increase gastric acid secretion
absorption of nutrients.
and the release of gastrin, the gastric
hormone that induces acid secretion. In
“nutcracker esophagus,” which mim- um) that lead to abnormal acid produc- contrast, beverages with a higher alco-
ics symptoms of coronary heart dis- tion. A diagnosis of Barrett’s esopha- hol content (e.g., whisky and cognac)
ease (Bode and Bode 1992).3 gus is an important indicator of an stimulate neither gastric acid secretion
Chronic alcohol abuse leads to an increased risk of esophageal cancer, nor gastrin release.
increased incidence not only of heart- because in some patients the altered The mechanisms underlying the
burn but also of esophageal mucosal epithelial cells become cancerous. effects of alcoholic beverages on gas-
inflammation (i.e., esophagitis) and Another condition affecting alco- tric acid secretion have not yet been
other injuries that may induce mucosal holics is Mallory-Weiss syndrome, identified. Alcohol may interact direct-
defects (i.e., esophagitis with or with- which is characterized by massive ly with the gastric mucosa (i.e., topical
out erosions). In addition, alcoholics bleeding caused by tears in the mucosa stimulation); or, it may act through a
at the junction of the esophagus and the more general mechanism affecting the
make up a significant proportion of
stomach. The syndrome accounts for 5 release of hormones and the regulation
patients with Barrett’s esophagus. This
to 15 percent of all cases of bleeding in of nerve functions involved in acid
condition, which occurs in 10 to 20 the upper GI tract. In 20 to 50 percent secretion (Chari et al. 1993). More-
percent of patients with symptomatic of all patients, the disorder is caused by over, researchers have shown that after
gastroesophageal reflux disease increased gastric pressure resulting beer consumption, gastric acid secre-
(Wienbeck and Berges 1985), is char- from repeated retching and vomiting tion also is stimulated by by-products
acterized by changes in the cell layer following excessive acute alcohol of the fermentation process other than
lining the esophagus (i.e., the epitheli- consumption (Bode and Bode 1992). alcohol (Chari et al. 1993).
Chronic alcohol abuse also affects
The term “nutcracker esophagus” refers to the gastric function. Thus, alcoholics have
painful, spasmodic contractions of the esophagus that THE STOMACH
the patients who suffer the disorder describe as feeling
a significantly higher incidence of
as though the esophagus were being squeezed by a Both acute and chronic alcohol con- shrinkage (i.e., atrophy) of the gastric
nutcracker. sumption can interfere with stomach mucosa and decreased gastric secretory


Gastrointestinal Tract Disorders

capacity than do healthy control sub- inflammatory reactions—also might Therefore, alcohol’s effects on nutri-
jects of comparable age and sex (Bode contribute to the development of alco- ent absorption may vary throughout
and Bode 1992). The resulting decrease hol-induced mucosal injury (Bode and the small intestine, and tissue-culture
in acid production reduces the stomach’s Bode 1992). experiments with constant alcohol
ability to destroy the bacteria that enter concentrations may not always reflect
with food and thus favors the coloniza- Gastric and Intestinal Motility the conditions in the body.
tion of the upper small intestine with Studies in laboratory animals have
Alcohol can interfere with the activity
potentially harmful microorganisms. demonstrated that acute alcohol con-
of the muscles surrounding the stom-
Abstinence, however, can at least partly sumption can inhibit the absorption of
ach and the small intestine and thus
reverse these changes. water, sodium, glucose, and certain
alter the transit time of food through
amino acids and fatty acids in the small
Acute Gastric Mucosal Injury these organs. In humans, alcohol’s
intestine (Bode 1980; Mezey 1985).
effect on gastric motility depends on
Researchers have known for more Several studies in humans have ana-
the alcohol concentration and accom-
than 100 years that alcohol abuse can lyzed the effects of chronic alcohol
panying meals. In general, beverages
cause mucosal inflammation (for a consumption with the following results:
with high alcohol concentrations (i.e.,
review, see Beazell and Ivy 1940). In above 15 percent) appear to inhibit • Both in healthy people and in alco-
addition, alcohol abuse is an important gastric motility and thus delay the holics, chronic alcohol consump-
cause of bleeding (i.e., hemorrhagic) emptying of the stomach. As a result tion led to markedly reduced water
gastric lesions that can destroy parts of of the increased gastric transit time, and sodium absorption in the je-
the mucosa. Although low or moder- bacterial degradation of the food may junum and ileum (Bode and Bode
ate alcohol doses do not cause such begin; the resulting gases may lead to 1992; Pfeiffer et al. 1992).
damage in healthy subjects, even a feelings of fullness and abdominal
single episode of heavy drinking can • Alcoholics exhibited a reduced
induce mucosal inflammation and absorption of carbohydrates, pro-
In the small intestine, alcohol de-
hemorrhagic lesions. Nonsteroidal teins, and fats in the duodenum, but
creases the muscle movements that
anti-inflammatory drugs (e.g., aspirin not in the jejunum (Pfeiffer et al.
help retain the food for further diges-
and ibuprofen) may aggravate the 1992) (see table).
tion (i.e., the impeding wave motility).
development of alcohol-induced acute In contrast, alcohol does not affect the • Alcoholics without confounding
gastric lesions. movements that propel food through disorders, such as cirrhosis or
How alcohol damages the gastric the intestine (i.e., the propulsive wave impaired pancreatic function, ex-
mucosa has not yet been determined. motility) in either alcoholics or hibited malabsorption of fat and
Studies in both animals and humans healthy subjects. These effects may protein (see table).
have found that alcohol concentrations contribute to the increased sensitivity
of 10 percent and more disrupt the to foods with a high sugar content • Alcoholics showed malabsorption
gastric mucosal barrier and increase the (e.g., candy and sweetened juices), of xylose, a sugar frequently used to
mucosa’s permeability (Bode and Bode shortened transit time, and diarrhea study the function of the digestive
1992). The changes induced by short- frequently observed in alcoholics tract. The proportion of alcoholics
term exposure to alcoholic beverages (Bode and Bode 1992). who experienced this malabsorption
are rapidly reversible. Prolonged alco- ranged from 18 to 76 percent in
hol exposure, however, disturbs the various studies (see table). This
THE SMALL INTESTINE variation may reflect differences in
microcirculation and leads to progres-
sive structural mucosal damage. the nutritional status, the mean
As described previously, the small
Several studies have suggested that daily alcohol intake, or the presence
intestine is the organ in which most
of alcohol-related liver disease
the decreased formation of hormone- nutrients are absorbed into the blood-
among the studies’ subjects.
like substances called prostaglandins stream. Studies in humans and animals
might play a role in alcohol-induced as well as in tissue culture have • After chronic alcohol consump-
mucosal injury (Bode et al. 1996). demonstrated that alcohol can inter- tion, the absorption of thiamine
Prostaglandins protect the gastric fere with the absorption of several (vitamin B1), folic acid, and vita-
mucosa from damage by agents such nutrients. Alcohol itself, however, also min B12 was either unchanged or
as aspirin that break the gastric mu- is rapidly absorbed in the small intes- decreased (Mezey 1985; Bode and
cosal barrier without inhibiting acid tine. In the human jejunum, for exam- Bode 1992). Folic acid deficiency,
secretion. Other studies have indicated ple, the alcohol concentration can drop which frequently occurs in alco-
that an alcohol-dependent increase in from 10 percent to just 1.45 percent holics, can result in various disor-
the production of leukotrienes—com- over a distance of only 30 centimeters ders of the GI tract as well as in
pounds produced by the immune sys- (12 inches, about a quarter of the total anemia. However, this deficiency
tem that cause allergic and length of the jejunum) (Bode 1980). is more likely to result from a diet

VOL. 21, NO. 1, 1997 79

molecules that normally cannot cross
Summary of Studies on Malabsorption of Carbohydrates, Fat, and Protein in the intestinal wall intact (e.g., hemo-
Alcoholics Without Cirrhosis or Obvious Pancreatic Insufficiency globin) to travel between the gut and
the bloodstream (Bode 1980).
A. Frequency of Abnormal Absorption Among Alcoholics
Similarly, intestinal permeability was
% Subjects enhanced in nonintoxicated alcoholics
Nutrient Studied Number of Studies With Abnormal Absorption (Bode and Bode 1992). The enhanced
permeability induced by acute and
D-Xylose 5 18–76
Fata 2 35–56
chronic alcohol ingestion could allow
Proteinb 1 52 toxic compounds, such as endotoxin
and other bacterial toxins, to enter the
B. Mean Decrease in Absorption Compared With Nonalcoholic Controlsc bloodstream and subsequently reach
the liver. The presence of endotoxin in
Nutrient Studied % Decrease
the blood has been documented in
Carbohydrates 45 patients with early stages of alcohol-
Lipids 40 related liver damage and transiently,
Protein 81 after excessive alcohol consumption,
a Fat
absorption was determined by measuring fat excretion in the feces.
b Protein
in people with no evidence of liver
absorption was determined by measuring nitrogen excretion in the feces.
c The
study measured the absorption of a nutrient solution in the duodenum. disease (Fukui et al. 1991). Endotoxins
SOURCES: A: Bode and Bode 1992; B: Pfeiffer et al. 1992. can induce the release of cytokines
(e.g., tumor necrosis factor) and inter-
containing insufficient folic acid upper region of the duodenum. Even leukins from certain white blood cells
than from poor folic acid absorp- in healthy people, a single episode of and from Kupffer cells in the liver.
tion (Halstedt and Keen 1990). heavy drinking can result in duodenal These cytokines, in turn, may play a
erosions and bleeding. Animal studies role in the development of alcohol-
In summary, alcohol inhibits ab-
have indicated that several mecha- related damage to the liver and other
sorption of a variety of nutrients. The
nisms contribute to the development organs (Khoruts et al. 1991; Schäfer et
importance of these absorption disor-
of these mucosal injuries (Ray et al.
ders in the development of nutritional al. 1995) (figure 3). (For more infor-
1989) (for a review, see Bode and
disturbances in alcoholics, however, is mation on the association of endotoxin
Bode 1992). First, alcohol can directly
unclear. In alcoholics with limited and cytokines with liver damage, see
disturb the integrity of the mucosal
pancreatic function or advanced liver the article by Maher, pp. 5–12.)
epithelium. Second, alcohol induces
disease, digestion of nutrients may be
the release of noxious signaling mole-
a more significant problem than im- Intestinal Bacterial Microflora
cules, such as cytokines, histamine,
paired absorption disorders.
and leukotrienes. These substances Certain bacteria that are a major
Intestinal Enzymes can damage the small blood vessels, source of endotoxin may overgrow
or capillaries, in the intestinal mucosa the normal bacterial flora in the je-
Alcohol can interfere with the activity and induce blood clotting. Such clot-
of many enzymes that are essential for junum of alcoholics (Bode and Bode
ting may lead to an impaired transport 1992). Together with the altered per-
intestinal functioning. One of these of fluids across the capillaries; fluid
enzymes is lactase, which breaks down meability of the gut induced by alco-
accumulation under the tips of the
the milk sugar lactose; lactase defi- villi; and, eventually, destruction of hol, this process may allow an increased
ciency results in lactose intolerance. the tips of the villi. The resulting escape of endotoxin from the intestine
Alcohol also interferes with some of lesions allow large molecules, such as into the blood vessels leading to the
the enzymes involved in transporting endotoxins and other bacterial toxins, liver, thus increasing the liver’s expo-
nutrients from the intestine into the to enter the bloodstream and the lymph. sure to these toxins and, consequent-
bloodstream and inhibits important Third, as in the stomach, decreased ly, the risk of liver injury (figure 3).
enzymes that participate in the metab- prostaglandin synthesis may contribute The hypothesis that bacterial over-
olism of drugs and other foreign or- to changes in the capillaries and to the growth may be responsible for the
ganic substances in the gut (for development of mucosal injury. development of alcohol-related organ
reviews, see Mezey 1985; Bode 1980).
damage has been supported by the
Intestinal Permeability observation that sterilization of the
Intestinal Mucosal Injury intestine prevents alcohol-induced
In animal studies, alcohol administra-
Excessive alcohol consumption fre- tion increased the permeability of the liver injury in animal experiments
quently causes mucosal damage in the intestinal mucosa, allowing large (Adachi et al. 1995).


Gastrointestinal Tract Disorders

The Large Intestine

Until recently, alcohol’s effects on Small intestine
the large intestine had received only
minor attention. Studies in dogs
found that acute alcohol administra- Disturbed
tion depressed the colon’s impeding motility
Alcohol Bacterial overgrowth Disturbed absorption
motility but enhanced its propulsive
Decreased Increased formation of
motility (Mezey 1985). In healthy prostaglandin synthesis endotoxins and other toxins
humans, alcohol administration also
significantly reduced the frequency Mucosal lesions and
and strength (i.e., amplitude) of the increased permeability
muscle contractions in a segment of
the rectum (Mezey 1985). These
effects could reduce the transit time—
and thus the compaction—of the Increased release of cytokines Increased uptake of endotoxins
intestinal contents and thereby con- and other mediators from certain and other toxins into the
tribute to the diarrhea frequently white blood cells and Kupffer cells bloodstream and lymph
observed in alcoholics.

Damage to the blood vessels Liver cell injury and

MEDICAL CONSEQUENCES and disturbed microcirculation other organ injury
Alcohol-induced digestive disorders and Figure 3 Schematic presentation of the possible causes and consequences of
mucosal damage in the GI tract can mucosal injury, increased permeability of the intestinal mucosa to macro-
cause a variety of medical problems. molecules, and bacterial overgrowth in the small intestine of chronic
These include a loss of appetite and a alcohol abusers. Thickness of arrows indicates strength of association
multitude of abdominal complaints, such between phenomena. (For definitions, see glossary, pp. 93–96.)
as nausea, vomiting, feelings of fullness,
flatulence, and abdominal pain. Diseases
of the liver and pancreas may contribute Epidemiological studies also strongly heavy beer consumption, whereas
to and aggravate these complaints. Thus, indicate that chronic alcohol consump- distilled spirits appear to have no effect.
about 50 percent of alcoholics with an tion, especially of distilled spirits,
initial stage of liver damage (i.e., fatty markedly contributes to the develop-
liver) and 30 to 80 percent of patients
ment of esophageal cancer (Bode 1980;
with an advanced stage of alcohol-in- Wienbeck and Berges 1985). Thus, Alcohol consumption can interfere with
duced liver injury (i.e., alcoholic hepati- after adjusting for smoking habits, the function of all parts of the gastroin-
tis) report some symptoms of abdominal heavy beer drinkers have a 10 times testinal tract. Acute alcohol ingestion
discomfort (Bode and Bode 1992). These greater risk and heavy whisky drinkers induces changes in the motility of the
abdominal complaints can lead to re- a 25 times greater risk of developing esophagus and stomach that favor gas-
duced food intake, thereby causing the esophageal cancer, compared with troesophageal reflux and, probably, the
weight loss and malnutrition commonly people who consume less than 30 g of development of reflux esophagitis.
observed in alcoholics. alcohol (i.e., about 2 standard drinks) Alcohol abuse may lead to damage of
In addition to causing abdominal
daily. The differences between beer and the gastric mucosa, including hemor-
complaints, alcohol plays a role in the
whisky drinkers remain even if they rhagic lesions. Beverages with a low
development of cancers of the GI tract.
It is likely, however, that alcohol does consume the same amount of pure alcohol content stimulate gastric acid
not cause GI-tract cancers by itself but alcohol. In drinkers who also smoke 20 secretion, whereas beverages with a
acts in concert with other cancer-induc- cigarettes or more daily, the risk of high alcohol content do not.
ing agents (i.e., as a cocarcinogen) (for esophageal cancer increases about 45- In the small intestine, alcohol in-
reviews, see Seitz and Simanowski fold (Seitz and Simanowski 1988). hibits the absorption of numerous
1988; Garro and Lieber 1990). Alcohol Heavy alcohol consumption also is nutrients. The importance of these
abuse, like smoking, is associated with associated with the development of absorption disorders for the develop-
the development of cancers of the tongue, tumors in the colon and rectum. How- ment of nutritional disturbances in
larynx (i.e., the organ of voice), and ever, the relative risk of cancer is higher alcoholics, however, is unclear. In
pharynx; both alcohol consumption and for rectal cancer than for colon cancer. alcoholics with other digestive disor-
smoking independently increase the Moreover, the increased risk of rectal ders (e.g., advanced liver disease or
risk for these tumors (Bode 1980). cancer appears to result mainly from impaired pancreatic function), impaired

VOL. 21, NO. 1, 1997 81

digestion likely is more significant. blood cells and Kupffer cells. These alcohol consumption and the develop-
Acute alcohol consumption also dam- cytokines, in turn, exert multiple inju- ment of colorectal cancer. ■
ages the mucosa in the upper region of rious effects on membranes and the
the small intestine and may even lead microcirculation. The result is possi- REFERENCES
to the destruction of the tips of the ble cell damage and even cell death in
villi. The findings of human and ani- the liver and other organs.
AND THURMAN, R.G. Antibiotics prevent liver injury in
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The excessive consumption of
alcoholic beverages interferes with NAD+ NAD+
the normal function and structure
of the gastrointestinal (GI) tract.
Alcohol Acetaldehyde Acetate
The relationship between alcohol
and the GI tract is a two-way street,
however, and the GI tract plays a ADH ALDH
role in the absorption, metabolism, The pathway of alcohol metabolism. Once in the liver, alcohol is converted into
and production of alcohol. acetaldehyde, and the acetaldehyde is converted into acetate. The enzyme alco-
hol dehydrogenase (ADH) assists the chemical reaction in (i.e., catalyzes) the
first half of alcohol metabolism, and the enzyme aldehyde dehydrogenase (ALDH)
catalyzes the second half. NAD+ is a coenzyme that plays an accessory role in
Throughout the GI tract, alcohol enzyme catalysis.
absorption into the bloodstream
occurs through a process called temperature, the presence of certain metabolism) occurs not only in the
simple diffusion. The rate at which medications in the body, and the liver, as with most other nutrients,
this process occurs depends on types of spices in the food (Bode but also in the stomach and the small
several factors, primarily the dif- 1980). For example, alcohol absorp- intestine (Mezey 1985). The enzyme
ference between the alcohol con- tion occurs more slowly after the alcohol dehydrogenase (ADH),
centrations in the GI organs and in ingestion of beer than after the inges- which mediates the first step of alco-
the adjacent small blood vessels, tion of an equal amount of alcohol in hol degradation (see figure), is pre-
the regional blood flow, and the the form of whisky or brandy. Most sent in the mucosa of the stomach
permeability of the GI tract lining of these factors probably inhibit or and the small intestine. In fact, sever-
(i.e., the mucosa) in question. For enhance alcohol absorption by affect- al ADH variants (i.e., isoenzymes)
example, the higher the concentra- ing the movement of the stomach with different kinetic properties exist
tion of the ingested alcohol, the muscles (i.e., gastric motility) and in the mucosa of the GI tract; these
more alcohol the mucosa absorbs. small intestinal blood flow. isoenzymes permit alcohol metab-
In contrast, the presence of food in olism over a wide range of concen-
the stomach decreases the rate of trations. The ADH isoenzyme pattern
Metabolism in the GI tract differs from that found
alcohol absorption. Other factors
that may affect alcohol absorption More than two decades ago, in the liver.
include the type of alcoholic bever- research-ers found that the initial Some researchers have postulated
age, the drinker’s gender and body breakdown of alcohol (i.e., first-pass that first-pass metabolism in humans


Gastrointestinal Tract Disorders

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E2 and prostaglandin F2α biosynthesis in human AND ALLEN, J.I. Circulating tumor necrosis factor, ethanol-induced jejunal microvascular and morpho-
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