Red Wine Polyphenols in Cancer Research
by Dr. Erik Skovenborg

In the eyes of science all alcoholic beverages are created equal,
however, some drinks may be more equal than others. Red wine may be one
of those beverages offering a dual action of alcohol and antioxidants.
The name of the game is Red Wine Polyphenols (RWP) – compounds derived
from grape tannins and anthocyanin pigments that belong to the most
powerful antioxidants in the world. As we absorb polyphenols, they change
the properties of blood lipids making LDL-cholesterol more resistant to
the sort of oxidation that can trigger atherosclerosis and coronary heart
disease. From Coronary Heart Disease to Cancer

For many years the overwhelming evidence that light-to-moderate
alcohol use lowers the risk of coronary heart disease has been in focus.
In 2000 Morten Grønbæk with a study of data
from 257,859 person-years of follow-up (the Copenhagen Centre for
Population Studies) was able to conclude that not only did wine drinkers
have significantly lower mortality from coronary heart disease; with a
consumption of 1-3 glasses a day wine drinkers also reduced their risk of
cancer by 20 percent compared with non-drinkers. As the number of global
cancer deaths are rising there is an urgent need of efficient methods of
cancer prevention and cancer cure. Earlier studies have found a strong
protective effect of intake of fruits and vegetables against cancer. The
potential role of red wine polyphenols in cancer prevention may turn out
to be one of the most exciting areas of current cancer research.

RWP in cancer prevention

In 2000 Elias Castanas, professor of experimental endocrinology at the
University of Crete’s School of Medicine in
Iráklion, published important papers on the inhibitory
action of Red Wine Polyphenols on human breast cancer cells and human
prostate cancer cells. In collaboration with Joseph Vercauteren,
professor of pharmacology at the Université Victor Segalen
in Bordeaux and expert in polyphenols, Elias Castanas added polyphenols
derived from from de-alcoholized red wine to cultures of breast cancer
and prostate cancer cells. The RWP had an antiproliferative effect on the
cancer cell lines in test tube experiments in the laboratory. During a
short stay in Crete in the lovely September weather we had the
opportunity to ask professor Castanas some questions about his important
cancer research.

Assisted cancer cell suicide

To professor Castanas one of the most intriguing discoveries of his
laboratory tests is the very low concentrations of polyphenols needed to
inhibit cancer cell growth. Traditional chemotherapy is based on a group
of cell poisons the success of which depend on whether the poisons kill
the cancer cells before they kill the patient. Polyphenols are non toxic
compounds; as a matter of fact it looks as if the RWP have very few side
effects. So if the polyphenols do not poison the cancer cells, how do
they manage to inhibit and eventually kill them? Castanas has an idea
that includes the phenomenon of apoptosis: programmed cell death. The
general purpose of apoptosis is to have any cell that suffers from
irreparable DNA damage kill itself. Maybe the action of RWP on cancer
cells can be described as “assisted suicide”. Elias Castanas and his
colleagues are working hard to find the answers. His laboratory is doing
some preliminary animal (mice) studies that seems to back his test tube
research on cancer cells. No studies with cancer patients has yet been
performed as far as Castanas knows, and besides he warns that such
studies are premature. “Science is five years away from proving whether
wine’s antioxidant polyphenols do kill breast and
prostate cancer cells in humans”.

Other polyphenols to look for

In his tests professor Castanas has used several different polyphenols
such as quercetin against cancer cell lines. However, an extract of total
RWP is what he favours for his experiments. So far more than 200
polyphenols have been identified in red wine, and Castanas has the
opinion that the combined group of polyphenols is more active than the
single compounds by themselves.

Professor Castanas has conducted some experiments with tea polyphenols
and the results were more or less the same as for RWP. He has not yet had
the opportunity to work with beer polyphenols, however, Castanas is
familiar with some of the polyphenols in beer. In his opinion there is no
substantial mechanistic difference between the polyphenols in wine, beer
and tea, however, based on his experience RWP millimol per millimol have
a higher antioxidant capacity than other polyphenols.

Bioavailability of polyphenols

The question of bioavailability is a crucial question: if you drink a
bottle of full-bodied red wine you consume about 2 grams of RWP; what
part of these healthy compounds is absorbed during the process of
digestion to become available to target tissues like the endothelial
cells of blood vessels or the nerve tissue of the brain? Professor
Castanas has good news to wine drinkers: alcohol protects the RWP, so a
glass of Cabernet Sauvignon is a good vehicle for polyphenols. For those
who want a steak on the plate to go with their Cabernet here is more good
news: proteins have a dual action protecting the RWP from oxidation and
increasing the bioavailability of the healthy compounds. That added bonus
leads directly to Elias Castanas’ favourite advice
concerning a sufficient daily intake of polyphenols: eat a normal meal
with a variety of foods like fruit, vegetables, legumes, olive oil, bread
and fish accompanied by moderate consumption of wine.

Polyphenols on the table or in a capsule?

Who wants to spend hours in the kitchen scraping carrots, cleaning
fish and peeling fruit? Why not relax in the sun with an exciting book
washing down a capsule of RWP with Dry Martini? No, says the Cretan
professor, the antioxidant activity of extracts of polyphenols is poor
compared to the antioxidant power of polyphenols from natural fruits and
vegetables. Besides there is always the problem of protecting the
extracted polyphenols from oxidation. With an ample supply of
antioxidants from various sources like fruit, vegetables, vegetable oils
and wine you arm the cells of your body with heavy antioxidant artillery
to face any oxidant threat.

Professor Castanas is a founder member of the Greek academy of taste.
As a bon vivant with an intimate knowledge of the best restaurants on the
island of Crete the choice between a RWP-capsule and the fine cuisine of
Crete is easy. Raising a glass of fragrant Mirambelo, a red wine from the
grape varieties Kotsifali and Mandilaria picked from the mountain
vineyards of Peza, Castanas toasts the conclusion from the landmark
article on wine and health by St. Leger and A. Cochrane (Lancet
1979;i:1017-21): “If wine is ever found to contain a constituent
protective agent against I.H.D. then we consider it almost a sacrilege
that this consituent should be isolated. The medicine is already in a
highly palatable form”.

Dr. Erik Skovenborg is a founder member of the Scandanavian Medical
Alcohol Board, a specialist in alcohol and health and a member of the AIM
Editorial Board.

Red wine is a rich source of biologically active phytochemicals,
chemicals found in plants. Particular compounds called polyphenols found
in red wine, such as catechins and resveratrol, are thought to have anti
oxidant or anti cancer properties.

What are polyphenols and how do they prevent cancer?

Polyphenols are antioxidant compounds found in the skin and seeds of
grapes. When wine is made from these grapes, the alcohol produced by the
fermentation process dissolves the polyphenols contained in the skin and
seeds. Red wine contains more polyphenols than white wine because the
making of white wine requires the removal of the skins after the grapes
are crushed. The phenols in red wine include catechin, gallic acid, and
epicatechin.

Polyphenols have been found to have antioxidant properties.
Antioxidants are substances that protect cells from oxidative damage
caused by molecules called free radicals. These chemicals can damage
important parts of cells, including proteins, membranes, and DNA.
Cellular damage caused by free radicals has been implicated in the
development of cancer. Research on the antioxidants found in red wine has
shown that they may help inhibit the development of certain cancers. What
is resveratrol and how does it prevent cancer?

Resveratrol is a type of polyphenol called a phytoalexin, a class of
compounds produced as part of a plant’s defense system against disease.
It is produced in the plant in response to an invading fungus, stress,
injury, infection, or ultraviolet irradiation. Red wine contains high
levels of resveratrol, as do grapes, raspberries, peanuts, and other
plants.

Resveratrol has been shown to reduce tumor incidence in animals by
affecting one or more stages of cancer development. It has been shown to
inhibit growth of many types of cancer cells in culture. Evidence also
exists that it can reduce inflammation. It also reduces activation of NF
kappa B, a protein produced by the body’s immune system when it is under
attack. This protein affects cancer cell growth and metastasis.
Resveratrol is also an antioxidant.

What have red wine studies found?

The cell and animal studies of red wine have examined effects in
several cancers including leukemia, skin , breast, and prostate cancers .
Scientists are studying resveratrol to learn more about its cancer
preventive activities. Recent evidence from animal studies suggests this
anti-inflammatory compound may be an effective chemopreventive agent in
three stages of the cancer process: initiation, promotion, and
progression.

However, studies of the association between red wine consumption and
cancer in humans are in their initial stages. Although consumption of
large amounts of alcoholic beverages may increase the risk of some
cancers, there is growing evidence that the health benefits of red wine
are related to its nonalcoholic components.

National Institute on Alcohol Abuse and Alcoholism

No. 19 PH 329 January 1993

———————————————————————-

Alcohol and the Liver

Alcoholic liver disease is one of the most serious medical
consequences of chronic alcohol use. Moreover, chronic excessive alcohol
use is the single most important cause of illness and death from liver
disease (alcoholic hepatitis and cirrhosis) in the United States (1).

The Normal Liver

Normal liver function is essential to life. The liver is the largest
organ of the body, located in the upper right section of the abdomen. It
filters circulating blood, removing and destroying toxic substances; it
secretes bile into the small intestine to help digest and absorb fats;
and it is involved in many of the metabolic systems of the body. Digested
food substances are carried from the intestine directly to the liver for
further processing. The liver stores vitamins; synthesizes cholesterol;
metabolizes or stores sugars; processes fats; and assembles amino acids
into various proteins, some for use within the liver and some for export.
The liver controls blood fluidity and regulates blood-clotting
mechanisms. It also converts the products of protein metabolism into urea
for excretion by the kidneys.

Alcoholic Liver Disease

The three alcohol-induced liver conditions are fatty liver, alcoholic
hepatitis, and cirrhosis.

Some degree of fat deposition usually occurs in the liver after
short-term excessive use of alcohol. However, fatty liver rarely causes
illness (2).

In some heavy drinkers, alcohol consumption leads to severe alcoholic
hepatitis, an inflammation of the liver characterized by fever, jaundice,
and abdominal pain (3). Severe alcoholic hepatitis can be confused with
many serious abdominal conditions, such as cholecystitis (inflammation of
the gall bladder), appendicitis, and pancreatitis. It is important to be
aware of this potential confusion because some of these other conditions
require surgery, and surgery is contraindicated in patients with
alcoholic hepatitis. These patients have a high death rate following
surgery.

The most advanced form of alcoholic liver injury is alcoholic
cirrhosis. This condition is marked by progressive development of scar
tissue that chokes off blood vessels and distorts the normal architecture
of the liver (2).

A patient may have only one of the three alcohol-induced conditions or
any combination of them. Traditionally, they have been considered
sequentially related, progressing from fatty liver to alcoholic hepatitis
to cirrhosis. However, some studies have demonstrated that alcoholics may
progress to cirrhosis without passing through any visible stage
resembling hepatitis. Thus, alcoholic cirrhosis can appear insidiously,
with little warning (4).

Fatty liver is reversible with abstinence. Alcoholic hepatitis may be
fatal but can be reversible with abstinence (5). While alcoholic
cirrhosis is often progressive and fatal, it can stabilize with
abstinence (3).

Complications of advanced liver disease include severe bleeding from
distended veins in the esophagus, brain disorders (hepatic
encephalopathy), accumulation of fluid in the abdomen (ascites), and
kidney failure (6).

Not all liver disease that may occur in alcoholics is caused by
alcohol. In addition, when alcohol-induced liver disease does occur, it
may be accompanied by other conditions, not related to alcohol, that also
can cause liver failure. These include nonalcoholic hepatitis and
exposure to drugs and occupational chemicals (see below).

Extent of the Problem

Alcohol-related cirrhosis is know n to be underreported. However,
about 44 percent of all deaths caused by cirrhosis in North America are
reportedly alcohol related (7).

Up to 100 percent of heavy drinkers show evidence of fatty liver, an
estimated 10 to 35 percent develop alcoholic hepatitis, and 10 to 20
percent develop cirrhosis (1).

Daily drinkers are at a higher risk of developing alcoholic cirrhosis
than are binge drinkers (8). In general, patients with alcoholic
cirrhosis have been drinking heavily for 10 to 20 years (8-10).

Mortality from cirrhosis in the United States varies significantly
with gender, race, and age. In 1988, the highest mortality from cirrhosis
occurred in nonwhite males, followed by white males, nonwhite females,
and white females (11). Most of the deaths from alcoholic cirrhosis occur
in people ages 40-65 (11). Thus, alcoholic cirrhosis kills people in what
should be their most productive years.

How Does Alcohol Damage the Liver?

Currently we do not know how alcohol causes cirrhosis. However, there
are many mechanisms by which alcohol injures the liver. Many of these
mechanisms are poorly understood, in part because no simple animal model
has been developed for cirrhosis. In addition, there is considerable
variation among individuals in susceptibility to alcoholic liver disease,
so that among people drinking similar amounts, only some develop
cirrhosis.

Diet. Before the 1970’s, alcoholic cirrhosis
was believed to arise from nutritional deficiencies common among heavy
drinkers. Overwhelming evidence subsequently proved that alcohol itself
is toxic to the liver, even when nutrition is adequate. Today, it is
believed that nutritional effects and direct alcohol toxicity interact in
such complex ways that the influence of the two cannot be separated
(12).

Genetics. Genetic differences might explain
why some heavy drinkers develop cirrhosis while others do not. The scar
tissue that forms in the cirrhotic liver is composed of the protein
collagen. It has been suggested that stimulation of collagen synthesis
resulting from activation of the collagen gene may promote liver scarring
(13). In that case, it might be speculated that differences in genes for
collagen among individual drinkers may be associated with differences in
the development of alcoholic cirrhosis.

Free radicals and acetaldehyde. Much of the
cell damage that occurs during liver degeneration is believed to be
caused by free radicals, highly reactive molecular fragments, liberated
during alcohol metabolism. The damage caused by free radicals can include
the destruction of essential components of cell membranes. The cell’s
natural defenses against free radicals include the natural chemicals
glutathione (GSH) and vitamin E.

The function of GSH and vitamin E is impaired in alcoholics. For
example, chronic alcohol ingestion decreased GSH levels in baboons and
humans (14). Similarly, chronic alcohol feeding significantly increased
damage caused by free radicals in liver cells of rats maintained on a
diet low in vitamin E (15).

Acetaldehyde, the primary metabolic product of alcohol in the liver,
appears to be a key generator of free radicals. Because of its
reactivity, acetaldehyde can promote membrane damage and can stimulate
the synthesis of collagen to form scar tissue (16-18).

Nonalcoholic hepatitis. The increased
prevalence of hepatitis C viral infection in alcoholics might explain
some of the variation in individual susceptibility to alcoholic liver
disease (19). In addition, chronic hepatitis C infection is significantly
correlated with the severity of alcoholic cirrhosis (20) and may
influence the progression of alcoholic liver disease in some patients
(21,22).

The immune system. The immune system
responds or contributes to liver cell damage in alcohol-induced liver
disease in complex ways, although a causal relationship is unclear.
Acetaldehyde has been shown to attach chemically to liver proteins. The
altered proteins may then trigger various immune responses (23). Cellular
toxins are released, causing cell damage; certain proteins are deposited
along the liver’s small blood-carrying channels; and specific white blood
cells are activated (24-27).

Liver metabolism. Chronic alcohol
administration has been found to increase the rate of oxygen metabolism
by the liver. In addition, a series of studies by Israel and colleagues
(28) demonstrated similarities in the effects of alcohol and thyroid
hormone on liver cells. They called these effects the “liver
hypermetabolic state.” As a result of these studies, propylthio-uracil, a
drug used to treat excessive production of thyroid hormone, has been
tested for the treatment of alcoholic liver disease (see Treatment
below).

Gender. Current evidence suggests that women
may be more susceptible than men to alcoholic liver disease; more
research is necessary to validate this hypothesis (8,19).

Environmental factors. Chronic alcohol
consumption markedly increases the liver toxicity of various industrial
solvents, anesthetics, medications, and vitamins (29,30). For example,
acetaminophen (Tylenol and others), a widely used over-the-counter pain
reliever, is generally safe when taken in recommended doses. However,
excessive use of acetaminophen has been associated with liver toxicity in
people drinking heavily (30-32). Alcohol also enhances the toxicity of
excess vitamin A, so care must be taken when treating an alcoholic with a
vitamin A deficiency (33).

Treatment

Alcoholic hepatitis. Mortality from
alcoholic hepatitis during the early weeks of treatment is very high.
Although the evidence is inconsistent, corticosteroid therapy may improve
survival during the early stages of the disease in patients with severe
alcoholic hepatitis (34-38). Supplemental amino acids may improve a
patient’s nutrition but not the chances of survival or progression to
cirrhosis (39).

Orrego and colleagues (40) reported that the drug propylthiouracil
(PTU) improved survival of patients with all types of alcoholic liver
disease. However, other studies have demonstrated no benefit from this
therapy in patients with alcoholic hepatitis (41,42).

Abstinence is the cornerstone of therapy for patients with prolonged
alcoholic hepatitis. Also important are careful control of diet with
correction of vitamin deficiencies, and management of medical
complications (38).

If the patient with alcoholic hepatitis lives to leave the hospital,
abstinence is essential for long-term survival. Alexander and coworkers
(43) found that more than 80 percent of those who abstained or markedly
reduced their drinking were alive 7 years later, whereas only 50 percent
who continued to drink were alive 7 years later.

Alcoholic cirrhosis. Treatment for cirrhosis
is directed at symptoms and complications, with abstinence a requirement.
For terminally ill patients, liver transplantation is the only effective
treatment. This procedure in alcoholic cirrhotic patients has
demonstrated success and survival rates equal to those for nonalcoholic
cirrhotic patients (44).

Future directions in cirrhosis therapy are suggested by a study
showing that lecithin protects against the development of alcohol-induced
liver scarring in baboons (45). This therapy has not yet been studied in
humans.

———————————————————————-

Alcohol and the Liver–A Commentary by
NIAAA Director Enoch Gordis, M.D.

Abstinence from alcohol is the single most important component of
treatmen t for alcoholic liver disease. Continued drinking will worsen
the condition of patients with this disease and greatly increase their
risk for death. Physicians who treat alcoholic liver disease, no matter
how competently, and who do not address their patients’ drinking are
practicing bad medicine, akin to treating an iron-deficiency anemia and
disregarding the colon cancer that is causing it.

Because many alcohol abusers and most alcoholics require some form of
treatment to remain abstinent, simply giving advice to “quit” drinking
often is not sufficient. Physicians who choose not to manage their
patients’ alcohol problems may refer these patients to specialized
alcohol treatment providers for evaluation and appropriate treatment. In
referring a patient to appropriate alcohol treatment, physicians should
keep informed of their patients’ progress, as relapse may further
complicate management of the alcoholic liver disease.

———————————————————————-

ACKNOWLEDGMENT: The National Institute on Alcohol Abuse and Alcoholism
wishes to acknowledge the valuable contributions of Marcus A. Rothschild,
M.D., editor of Alcohol: Clinical and Experimental Research, to
the development of this Alcohol Alert.

———————————————————————-

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 Scientific Communications Branch, Office of Scientific Affairs,
NIAAA, 5600 Fishers Lane, Room 16C-14, Rockville, MD 20857. Telephone:
301-443-3860.

———————————————————————-

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service * National Institutes of Health

NCPA: MANDATES INCREASE COST OF HEALTH INSURANCE BY 30%

08/13 1148

NEW ORLEANS, Aug. 13 /PRNewswire/ — Mandates are increasing the cost
of health insurance by as much as 30 percent, according to a National
Center for Policy Analysis report released today at the annual meeting of
the American Legislative Exchange Council. The analysis, prepared by the
actuarial firm Milliman & Robertson, estimated the costs of 12 of the
most common mandates and found that added together, those 12 mandates can
increase the cost of a family health insurance policy by as much as $700
to $1,050 a year.

“Based on the Milliman & Robertson estimates, a small business
that employs 25 people, with a standard mix of 40 percent single coverage
and 60 percent family coverage, could see its premiums rise by $20,000 a
year,” said Dr. Merrill Matthews, NCPA Vice President for Domestic
Policy.

The study analyzed the cost of health care policies when minimum stay
maternity, speech therapy benefits, drug abuse treatment benefits,
mammography screening, well child care, podiatry, pap smears, vision
exams, chiropractic care, alcoholism treatment, infertility treatment and
mental health care were included.

Assuming that a mandate-free, basic health insurance policy costs a
family about $3,500 a year, the Milliman & Robertson study found:

Several of the mandates increase the cost of a policy by less than $35
each.

Infertility treatment can increase the cost of a policy from anywhere
between $105 and $175 a year.

Mental health parity, which requires insurers to treat mental
illnesses the same as physical illnesses, adds between $175 and $350 to
the cost of a policy.

While employees tend to like health insurance mandates regardless of
cost, Matthews believes that’s because the costs are hidden, while the
benefits are apparent.

“What people need to realize is that while mandates provide more
options for those with health insurance, they also mean fewer people end
up being insured,” Matthews said. “A poll of employers who have canceled
their employees’ health insurance policies found it was because the price
was no longer affordable.”

Matthews predicts problems with mandates will only get worse. In 1965
there were only seven state-mandated health insurance benefits. Today
there are nearly 1,000. In addition, the federal government recently
joined the states by imposing two mandates of its own, a ban on
“drive-through” baby deliveries and a requirement that any cap on mental
health benefits be the same as the cap on physical health benefit.

“One or two federal mandates may not increase the cost of health
insurance significantly, but, as the states have proven, it’s almost
impossible to stop with a few mandates,” Matthews said. “When the dust
settles, policies will cost more, employers and individuals will be
canceling their polices and Congress will have to face an even bigger
uninsured ‘crisis.'” For a copy of the brief analysis “The Cost of Health
Insurance Mandates” visit the NCPA Web site at http://www.ncpa.org or
contact the NCPA.

The National Center for Policy Analysis is a public policy research
institute founded in 1983 and internationally known for its studies on
public policy issues. The NCPA is headquartered in Dallas, Texas, with an
office in Washington, D.C. Internet: http://www.ncpa.org/

SOURCE National Center for Policy Analysis -0- 08/13/97 /CONTACT: Katy
Meaker Menges, Dallas, 972-386-6272, or Joan Kirby, Washington,
202-628-6671, both of the National Center for Policy Analysis/ CO:
National Center for Policy Analysis ST: Louisiana IN: HEA SU:

No Health Insurance For DUI’s

Drunken drivers may find insurance won’t pay the bills for their
injuries

BYLINE: Lee, Louise
EST. PAGES: 1
DOCID: WSAB159782
SOURCE: WALL STREET JOURNAL ABSTRACTS; WSAB
COPYRIGHT: (Copyright 1995 UMI, Wall Street Journal Abstracts)
PAGE: B, 1:3

A growing number of companies are adding drunken-driving injuries to
the list of exclusions in their health plans, including Chief Auto Parts
Inc, Monfort Inc and Electronic Data Systems Corp. Companies that won’t
cover drunken-driving injuries are often self-insured.

REFERENCE: ISSN: 0099-9660
DESCRIPTORS: DRUNK DRIVING / HEALTH INSURANCE / INCENTIVES / EMPLOYEE
BENEFITS ; LAW ENFORCEMENT; LABOR PERSONNEL ISSUES
ORGANIZATION: CHIEF AUTO PARTS INC / MONFORT OF COLORADO INC /
ELECTRONIC DATA
SYSTEMS CORP
INDUSTRY: INSURANCE
OTHER TERMS: DOCN: 03415715

THE PHYSICIANS’ GUIDE TO HELPING PATIENTS WITH ALCOHOL PROBLEMS

CONTENTS

FOREWORD

LETTER FROM NIAAA DIRECTOR

WHAT YOUR PATIENTS SHOULD KNOW ABOUT
ALCOHOL USE

RECOMMENDATIONS TO
PATIENTS FOR LOW-RISK DRINKING

SCREENING AND BRIEF
INTERVENTION PROCEDURES

Step I. Ask About Alcohol
Use
Step II. Assess for Alcohol-Related
Problems
Step III. Advise Appropriate
Action
Step IV. Monitor Patient
Progress

WHAT TO DO ABOUT PATIENTS WHO ARE NOT
READY TO CHANGE THEIR DRINKING BEHAVIOR

———————————————————————-

FOREWORD

This Guide was developed by the National Institute on Alcohol Abuse
and Alcoholism (NIAAA) in conjunction with an interdisciplinary working
group of alcohol researchers and health professionals. The clinical
recommendations in this Guide are based on the findings of more than a
decade of research on the health risks associated with alcohol use and on
the effectiveness of alcohol screening and interven- tion methods. NIAAA
plans to update this Guide periodically to reflect continuing advances in
research.

NIAAA would like to acknowledge the contributions of members of the
Working Group on Screening and Brief Intervention, including the
following: John Allen, Ph.D.; Peter Anderson, M.D.; Thomas Babor, Ph.D.;
Kendall Bryant, Ph.D.; David Buchsbaum, M.D.; Jonathan Chick, M.D.;
Frances Cotter, M.A., M.P.H.; Michael Fleming, M.D., M.P.H.; Richard K.
Fuller, M.D.; Nick Heather, Ph.D.; Yedy Israel, Ph.D.; Cherry Lowman,
Ph.D.; William R. Miller, Ph.D.; Judith Ockene, Ph.D.; and Allen Zweben,
D.S.W.

NIAAA also would like to thank other collaborators, including the
following: Michael Fleming, M.D., M.P.H., and Frances Cotter, M.A.,
M.P.H., for their leadership in writing this Guide; the College of Family
Physicians of Canada Alcohol Risk Assessment and Intervention (ARAI)
Project Steering Committee for sharing their expertise and early drafts
of brief intervention materials; and Eve Shapiro and colleagues at CSR,
Incorporated, for their expertise in editing and designing this
Guide.

Up to Table of Contents.

———————————————————————-

Letter from
NIAAA Director

Dear Colleagues: As a primary care physician, you are in an excellent
position to identify and manage patients at risk for alcohol-related
problems. Alcohol-related problems are common in primary care practice:
An estimated 25 percent of adults in the United States either report
drinking patterns that put them at risk for developing problems or
currently have alcohol-related problems, including alcohol abuse or
dependence.1 Primary care physicians are the entry point into the
health-care system for many individuals. Furthermore, because you are
concerned with the overall health of an individual, you generally see
patients more frequently than do other health-care professionals.

Primary care physicians are busy. Yet you want to practice good
medicine and are willing to take time to address your patients’ alcohol
problems. This Guide, prepared by the National Institute on Alcohol Abuse
and Alcoholism, provides you with a step-by-step approach to identifying
and managing these problems and offers practical advice on making alcohol
screening, assessment, and brief intervention procedures a routine part
of your clinical practice. There are important reasons for doing so.
Untreated alcohol- ism results in a variety of social, economic, and
medical consequences. Alcohol use can complicate treatment for medical
problems, interfere with prescribed medications, or lead to adverse side
effects. Most importantly, left untreated, alcohol abuse and alcoholism
often result in severe or fatal outcomes.

Your patients look to you for advice about the risks and benefits
associated with drinking. Research, in fact, demonstrates that simply
dis- cussing your concerns about alcohol use can be effective in changing
many patients’ drinking behavior before problems become chronic.

We commend this Guide to your attention and hope that you will make it
an integral part of your practice.

Enoch Gordis, M.D.
Director
National Institute on Alcohol Abuse and Alcoholism

Up to Table of Contents.

———————————————————————-

WHAT YOUR PATIENTS
SHOULD KNOW ABOUT ALCOHOL USE

Most adults who drink alcohol drink in moderation and are at low risk
for developing problems related to their drinking. However, all drinkers,
including low-risk drinkers, should be aware of the health risks
associated with alcohol consumption. Provide your patients with
information and advice about the risks of drinking.

Up to Table of Contents.

———————————————————————-

RECOMMENDATIONS TO PATIENTS FOR
LOW-RISK DRINKING

Advise those patients who currently drink to drink in
moderation.

Moderate drinking is defined as follows:

• Men–no more than two drinks per day
• Women–no more than one drink per day
• Over 65–no more than one drink per day

Note: A standard drink is 12 grams
of pure alcohol, which is equal to one 12-ounce bottle of beer or wine
cooler, one 5-ounce glass of wine, or 1.5 ounces of distilled
spirits.

Advise patients to abstain from alcohol under certain
conditions:

• when pregnant or considering pregnancy
• when taking a medication that interacts with alcohol
• if alcohol dependent
• if a contraindicated medical condition is present (e.g., ulcer,
  liver disease)

If a patient is at risk for coronary heart disease, discuss
the potential benefits and risks of alcohol use:

• Light to moderate drinking is associated with lower rates of
  coronary heart disease in certain populations (e.g., men over 45,
  postmenopausal women). Infrequent or nondrinkers are not advised to
  begin a regimen of light to moderate drinking to reduce the risk of
  coronary heart disease because vulnerability to alcohol-related
  problems cannot always be predicted. Similar protective effects can
  likely be achieved through proper diet and exercise.

———————————————————————-

Clinical Notes

• Women and the elderly have smaller amounts of body water than men;
  therefore, they achieve a higher blood alcohol concentration than men
  after drinking the same amount of alcohol.
• Exposing a fetus to alcohol can cause a broad range of birth
  defects referred to as fetal alcohol syndrome (FAS) or alcohol-related
  birth defects (ARBD). Although FAS/ARBD is associated with excessive
  alcohol consumption during pregnancy, studies also have reported
  neurobehavioral deficits in infants born to mothers reporting drinking
  an average of one drink per day during pregnancy.
• Studies indicate that heavier episodic drinking (i.e., the
  consumption of more than four drinks per occasion by men and more than
  three drinks per occasion by women) impairs cognitive and psychomotor
  functions and increases the risk of alcohol-related problems, including
  accidents and injuries.

Up to Table of Contents.

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SCREENING AND BRIEF INTERVENTION
PROCEDURES

Recommended screening and brief intervention procedures include four
steps:

• Step I. ASK about alcohol use.
• Step II. ASSESS for alcohol-related problems.
• Step III. ADVISE appropriate action (i.e., set a
  drinking goal, abstain, or obtain alcohol treatment).
• Step IV. MONITOR patient progress.

Up to Table of Contents.

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Ask all patients:

• Do you drink alcohol, including beer, wine, or distilled
  spirits?

Ask current drinkers about alcohol consumption:

• On average, how many days per week do you drink alcohol?
• On a typical day when you drink, how many drinks do you have?
• What is the maximum number of drinks you had on any given occasion
  during the last month?

Ask current drinkers the CAGE questions:

• Have you ever felt that you should Cut down on your drinking?
• Have people Annoyed you by criticizing your drinking?
• Have you ever felt bad or Guilty about your drinking?
• Have you ever had a drink first thing in the morning to steady your
  nerves or get rid of a hangover (Eye opener)?

If there is a positive response to any of these questions:

• ASK: Has this occurred during the past year?

A patient may be at risk for alcohol-related problems IF:

• alcohol consumption is:
  Men:
  > 14 drinks per week or
  > 4 drinks per occasion
  Women:
  > 7 drinks per week or
  > 3 drinks per occasion

or

• one or more positive responses to the CAGE that have occurred in
  the past year

When is screening for alcohol problems appropriate?

• as part of a routine health examination
• before prescribing a medication that interacts with alcohol
• in response to presenting problems that may be alcohol-related

Up to Table of Contents.

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Patients who screen positive should be
assessed to determine the nature and extent of their alcohol-related
problems. Use the assessment procedures described below to determine
problem severity, as follows: (l) at increased risk for developing
alcohol-related problems, (2) currently experiencing alcohol-related
problems, or (3) may be alcohol dependent.

1. At Increased Risk for Developing Alcohol-Related
Problems

Indicators

• drinking above recommended low-risk consumption levels or in
  high-risk situations
• personal or family history of alcohol-related problems

Assessment procedures

• Ask about typical drinking patterns:
  How long have you been drinking this amount? How many times
  in a week (or month) do you have four or more drinks on one occasion?
  What is the most you have consumed on one occasion during the past
  year?
• Ask about personal and family history:
  Have you or anyone in your immediate family ever had a drinking
  problem?

Note: For many conditions, there is a
dose-response relationship between alcohol consumption and risk. This
applies to cirrhosis of the liver; cancers of the oropharynx, larynx,
liver, and breast; hypertension; and stroke.

2. Currently Experiencing Alcohol-Related
Problems

Indicators

• one or two positive responses to the CAGE that have occurred in the
  past year
• evidence of alcohol-related medical or behavioral problems

Assessment procedures

• Review your patient’s medical history for evidence of
  alcohol-related medical problems, such as:
  blackouts
  chronic abdominal pain
  depression
  liver dysfunction
  hypertension
  sexual dysfunction
  trauma
  sleep disorders

Note: Chronic heavy use of alcohol (i.e., three
or more drinks per day) may be associated with elevations in serum
gamma-glutamyltransferase (GGT). This can be an indicator of excessive
drinking.

• Ask about interpersonal or work-related problems:
  Has your drinking ever caused you problems, such as problems with your
  family, problems with your work (or school) performance, or
  accidents/injuries?

3. May Be Alcohol Dependent

Indicators

• three or four positive responses to the CAGE that have occurred in
  the past year
• evidence of one or more of the following symptoms: 2
  Compulsion to drink–preoccupation with drinking
  Impaired control–unable to stop drinking once started
  Relief drinking–drinking to avoid withdrawal symptoms
  Withdrawal–evidence of tremor, nausea, sweats, or mood
  disturbance
  Increased tolerance–takes more alcohol than before to get
  “high”

Assessment procedures

• Ask the following questions:
  — Are there times when you are unable to stop drinking once you have
  started?
  — Does it take more drinks than before to get “high”?
  — Do you feel a strong urge to drink?
  — Do you change your plans so that you can have a drink?
  — Do you ever drink in the morning to relieve the shakes?

Up to Table of Contents.

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State your medical
concern:

• Be specific about your patient’s drinking patterns and related
  health risks.
• ASK: How do you feel about your drinking?

Advise to abstain or cut down:

• Advise to abstain if:
  — evidence of alcohol dependence
  — history of repeated failed attempts to cut down
  — pregnant or trying to conceive
  — contraindicated medical condition or medication
• Advise to cut down if:
  — drinking above recommended low-risk drinking amounts and no
  evidence of alcohol dependence

Agree upon a plan of action:

• ASK: Are you ready to try to cut down or abstain?

Talk with patients who are ready to make a change in their drinking
about a specific plan of action.

For patients who are not alcohol dependent:

• Recommend low-risk consumption limits for your patient based upon
  the low-risk drinking recommendations and your patient’s health history
  (See Recommendations to patients for low-risk drinking).
• Ask your patient to set a specific drinking goal:
  Are you ready to set a drinking goal? Some patients choose to abstain
  for a period of time or for good; others prefer to limit the amount
  they drink. What do you think will work best for you?
• Provide patient education materials and tell your patient:
  It helps to think about your reasons for wanting to cut down and
  examine what situations trigger unhealthy drinking patterns. These
  materials will give you some useful tips on how to maintain your
  drinking goal.

For patients with evidence of alcohol dependence:

• Refer for additional diagnostic evaluation or treatment.
• Procedures for patient referral are as follows:
  — Involve your patient in making referral decisions.
  — Discuss available alcohol treatment services.
  — Schedule a referral appointment while the patient is in the
  office.

———————————————————————-

SOME PATIENT COUNSELING TIPS

• Use an empathic, nonconfrontational style.
• Offer your patient some choices about how to effect change.
• Emphasize your patient’s responsibility for changing drinking
  behavior.
• Convey confidence in your patient’s ability to change drinking
  behavior.

Up to Table of Contents.

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Monitor patient progress in the same
way you manage other chronic medical problems, such as hypertension or
diabetes. Recognize that behavior change is an incremental process that
often involves trial and error. Patient management strategies include the
following:

• Indicate that you (or designated staff) are available to provide
  ongoing assistance and support.
• Support your patient’s efforts to cut down or abstain at each
  subsequent visit by:
  — reviewing progress to date
  — commending your patient for efforts made
  — reinforcing positive change
  — assessing continued motivation
• Consider scheduling a separate followup visit or telephone call, as
  appropriate, if the patient needs additional support.
• Consider referring a selected patient whose counseling needs exceed
  the services provided in a primary care setting.

For patients who have been advised to abstain or have been
referred for alcohol treatment:

• Ask to receive periodic updates from the treatment specialist on
  your patient’s treatment plan and prognosis.
• Monitor symptoms of depression and anxiety. Such symptoms may
  occur, but they often decrease or disappear after 2 to 4 weeks of
  abstinence.
• Monitor GGT levels, when appropriate, as a means of assessing
  alcohol treatment compliance.

Up to Table of Contents.

———————————————————————-

WHAT TO DO ABOUT
PATIENTS WHO ARE NOT READY TO CHANGE THEIR DRINKING BEHAVIOR

Do not be discouraged if patients are not ready to take action
immediately. Decisions to change behavior often involve fluctuating
motivation and feelings of ambivalence. By offering your advice, you have
prompted your patients to think more seriously about their drinking
behavior. In many cases, continued reinforcement is the key to a
patient’s decision to take action. Offer the following guidance to
patients who are not ready to take action:

• Restate your concern for your patient’s health.
• Reinforce your willingness to help when the patient is ready.
• Continue to monitor alcohol use at subsequent office visits.

For patients who may be alcohol dependent, you may want to
consider some additional strategies:

• Encourage your patient to consult an alcohol specialist.
• Ask your patient to discuss your recommendation with family members
  and schedule a followup visit that includes family members/significant
  others.
• Recommend a trial period of abstinence, monitor for withdrawal
  symptoms, and review progress in a followup visit.

Up to Table of Contents.

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WHERE TO GO FOR ADDITIONAL
INFORMATION

The National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Office of Scientific Affairs
Willco Building
6000 Executive Boulevard, Suite 409
Bethesda, MD 20892-7003
301-443-3860

American Society of Addiction Medicine (ASAM)
4601 North Park Avenue
Suite 101, Upper Arcade
Chevy Chase, MD 20815
301-656-3920

National Council on Alcoholism and Drug Dependence (NCADD)
12 West 21st Street
New York, NY 10010
212-206-6770

Up to Table of Contents.

———————————————————————-

NOTES

1 Seven percent of the U.S. population–approximately 14 million
adults–meet the diagnostic criteria for alcohol abuse or dependence.

Back to Letter.

2 This selective listing of dependence symptoms is offered as an
initial assessment procedure and not for the purpose of making a
diagnosis. For a diagnostic evaluation, refer your patients to a
specialist or use the diagnostic procedures outlined in the Diagnostic
and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV).

Back to Step II, Part 3.

———————————————————————-

Prepared: January 1996

Wine Industry Urges Drinking, Driving
French Winemakers Try to Counter Anti-Drunk Driving Push

ASSOCIATED PRESS

PARIS, Nov. 15 — France’s wine industry wants
drivers to know: It’s OK to have a drink for the road.
Or three.

France’s Wine Industry Encourages Drinking and Driving

11/17/2003

In an effort to counter a government campaign against drinking and
driving, French winemakers are unveiling their own campaign saying that
it’s okay to have a drink or two before driving, the Associated Press
reported Nov. 15.

“People are so afraid of the police these days that they’re not
drinking any wine at all,” said Pascal Bobillier-Monnot, director of
France’s national wine producers’ association.

The wine industry said that since the government’s current DUI
campaign began, wine sales at restaurants have dropped 15 percent. They
said the government is overreacting by telling drivers that it’s best not
to drink at all.

“We believe the government has a duty of providing information which
it has failed,” said Pascal Rousseaux, director of Afivin, an umbrella
group for wine producers, distributors, and retailers. He said drivers
should be made aware that they can drink “two or three glasses” of wine
with their meal and still be capable of driving.

France’s blood-alcohol limit is .05. “In case of doubt, the easiest
way to be sure you don’t break the limit is to refrain from drinking,”
said Transport Ministry spokeswoman Emmanuelle Dormond.

As part of French Prime Minister Jean-Pierre Raffarin’s efforts to
improve road safety, police have increased road checks and the government
has implemented stricter punishments for drunk driving.

“There’s no question about it. The enforcement effort and the
government’s rhetoric have led to a drop in wine consumption in France,”
Bobillier-Monnot said.

Starting next year, Afivin plans to launch a $350,000 initiative that
would include distributing breathalyzer tests to restaurants throughout
the country. The purpose of the campaign is to convince motorists that
they don’t have to stop drinking altogether.

DRINKING TRIPLES ORALLY SUPPLEMENTED ESTROGEN LEVEL
Alcohol Does Not Change Level of Natural Estrogen

Science News Press Releases for the week of December 4, 1996

CHICAGO–Drinking alcohol can substantially increase circulating
estrogen in postmenopausal women taking oral estrogen, according to an
article in this week’s issue of The Journal of the American Medical
Association (JAMA).

Elizabeth S. Ginsburg, M.D., from the department of Obstetrics and
Gynecology, Brigham and Women’s Hospital, Boston, Mass., and colleagues
conducted a double-blind, crossover study of 24 postmenopausal women to
determine the effects of moderate alcohol consumption on the circulating
level of estradiol, the most important of the estrogen hormones.

The study reported that estradiol levels increased by 327 percent
following alcohol ingestion in women on estrogen replacement therapy
(ERT). Alcohol did not change estradiol significantly in women who did
not use ERT.

The researchers write: “Changes in estradiol were significantly
correlated with changes in blood alcohol levels during the ascending limb
of the blood alcohol curve as well as during the descending limb of the
blood alcohol curve. Moreover, significant increases in estradiol were
detected within 10 minutes after drinking when blood alcohol levels were
low.”

There are an estimated 37,948,000 women over the age of 50 years in
the United States, and approximately 25 percent of postmenopausal women
use some form of ERT according to information cited in the study. It is
generally acknowledged that ERT has a complex pattern of risks and
benefits. ERT may reduce risk of developing osteoporosis and heart
disease. However, ERT may also have adverse effects such as an increased
risk of cholelithiasis and breast cancer.

Moderate alcohol consumption also appears to decrease the incidence of
coronary artery disease but may increase the incidence of breast cancer.
The combination of ERT and alcohol ingestion may be additive and increase
the risk of breast cancer more than either alone. Little information is
available about the potential interactions of ERT and acute alcohol
ingestion in post menopausal women. If alcohol alters the intended
biological effects of ERT, this could shift the risk-benefit ratio in an
undesirable direction, according to the researchers.

There is also evidence to suggest that there is a cumulative effect of
regular alcohol ingestion on estradiol in postmenopausal women. One study
of 164 postmenopausal women found that serum estradiol was significantly
higher in women drinking one to 28 drinks weekly than in abstainers.

The authors conclude: “As evidence of the benefits of ERT for
postmenopausal women accumulates, it is important for the physician to
evaluate the risks and benefits for each individual on the basis of her
medical history and lifestyle. Our data indicate that women who drank
alcohol and use oral estradiol for estrogen replacement may have
significantly higher circulating estradiol levels than those reported in
studies advocating the use of ERT.”

National Institute on Alcohol Abuse and Alcoholism

No. 35 PH 371 January 1997

———————————————————————-

Alcohol Metabolism

Metabolism is the body’s process of converting ingested substances to
other compounds. Metabolism results in some substances becoming more, and
some less, toxic than those originally ingested. Metabolism involves a
number of processes, one of which is referred to as oxidation. Through
oxidation, alcohol is detoxified and removed from the blood, preventing
the alcohol from accumulating and destroying cells and organs. A minute
amount of alcohol escapes metabolism and is excreted unchanged in the
breath and in urine. Until all the alcohol consumed has been metabolized,
it is distributed throughout the body, affecting the brain and other
tissues (1,2). As this Alcohol Alert explains, by understanding alcohol
metabolism, we can learn how the body can dispose of alcohol and discern
some of the factors that influence this process. Studying alcohol
metabolism also can help us to understand how this process influences the
metabolism of food, hormones, and medications.

———————————————————————-

The Metabolic Process

When alcohol is consumed, it passes from the stomach and intestines
into the blood, a process referred to as absorption. Alcohol is then
metabolized by enzymes, which are body chemicals that break down other
chemicals. In the liver, an enzyme called alcohol dehydrogenase (ADH)
mediates the conversion of alcohol to acetaldehyde. Acetaldehyde is
rapidly converted to acetate by other enzymes and is eventually
metabolized to carbon dioxide and water. Alcohol also is metabolized in
the liver by the enzyme cytochrome P450IIE1 (CYP2E1), which may be
increased after chronic drinking (3). Most of the alcohol consumed is
metabolized in the liver, but the small quantity that remains
unmetabolized permits alcohol concentration to be measured in breath and
urine.

The liver can metabolize only a certain amount of alcohol per hour,
regardless of the amount that has been consumed. The rate of alcohol
metabolism depends, in part, on the amount of metabolizing enzymes in the
liver, which varies among individuals and appears to have genetic
determinants (1,4). In general, after the consumption of one standard
drink, the amount of alcohol in the drinker’s blood (blood alcohol
concentration, or BAC) peaks within 30 to 45 minutes. (A standard drink
is defined as 12 ounces of beer, 5 ounces of wine, or 1.5 ounces of
80-proof distilled spirits, all of which contain the same amount of
alcohol.) The BAC curve, shown on the previous page, provides an estimate
of the time needed to absorb and metabolize different amounts of alcohol
(5). Alcohol is metabolized more slowly than it is absorbed. Since the
metabolism of alcohol is slow, consumption needs to be controlled to
prevent accumulation in the body and intoxication.

Factors Influencing Alcohol Absorption and
Metabolism

Food. A number of factors influence the
absorption process, including the presence of food and the type of food
in the gastrointestinal tract when alcohol is consumed (2,6). The rate at
which alcohol is absorbed depends on how quickly the stomach empties its
contents into the intestine. The higher the dietary fat content, the more
time this emptying will require and the longer the process of absorption
will take. One study found that subjects who drank alcohol after a meal
that included fat, protein, and carbohydrates absorbed the alcohol about
three times more slowly than when they consumed alcohol on an empty
stomach (7).

Gender. Women absorb and metabolize alcohol
differently from men. They have higher BAC’s after consuming the same
amount of alcohol as men and are more susceptible to alcoholic liver
disease, heart muscle damage (8), and brain damage (9). The difference in
BAC’s between women and men has been attributed to women’s smaller amount
of body water, likened to dropping the same amount of alcohol into a
smaller pail of water (10). An additional factor contributing to the
difference in BAC’s may be that women have lower activity of the alcohol
metabolizing enzyme ADH in the stomach, causing a larger proportion of
the ingested alcohol to reach the blood. The combination of these factors
may render women more vulnerable than men to alcohol-induced liver and
heart damage (11-16).

Effects of Alcohol Metabolism

Body Weight. Although alcohol has a
relatively high caloric value, 7.1 Calories per gram (as a point of
reference, 1 gram of carbohydrate contains 4.5 Calories, and 1 gram of
fat contains 9 Calories), alcohol consumption does not necessarily result
in increased body weight. An analysis of data collected from the first
National Health and Nutrition Examination Survey (NHANES I) found that
although drinkers had significantly higher intakes of total calories than
nondrinkers, drinkers were not more obese than nondrinkers. In fact,
women drinkers had significantly lower body weight than nondrinkers. As
alcohol intake among men increased, their body weight decreased (17). An
analysis of data from the second National Health and Nutrition
Examination Survey (NHANES II) and other large national studies found
similar results for women (18), although the relationship between
drinking and body weight for men is inconsistent. Although moderate doses
of alcohol added to the diets of lean men and women do not seem to lead
to weight gain, some studies have reported weight gain when alcohol is
added to the diets of overweight persons (19,20).

When chronic heavy drinkers substitute alcohol for carbohydrates in
their diets, they lose weight and weigh less than their nondrinking
counterparts (21,22). Furthermore, when chronic heavy drinkers add
alcohol to an otherwise normal diet, they do not gain weight (21).

Sex Hormones. Alcohol metabolism alters the
balance of reproductive hormones in men and women (23-28). In men,
alcohol metabolism contributes to testicular injury and impairs
testosterone synthesis and sperm production (24,29). In a study of normal
healthy men who received 220 grams of alcohol daily for 4 weeks,
testosterone levels declined after only 5 days and continued to fall
throughout the study period (30,31). Prolonged testosterone deficiency
may contribute to feminization in males, for example, breast enlargement
(32). In addition, alcohol may interfere with normal sperm structure and
movement by inhibiting the metabolism of vitamin A, which is essential
for sperm development (30,33). In women, alcohol metabolism may
contribute to increased production of a form of estrogen called estradiol
(which contributes to increased bone density and reduced risk of coronary
artery disease) and to decreased estradiol metabolism, resulting in
elevated estradiol levels (28). One research review indicates that
estradiol levels increased in premenopausal women who consumed slightly
more than enough alcohol to reach the legal limit of alcohol (BAC of 0.10
percent) acutely (28). A study of the effect of alcohol on estradiol
levels in postmenopausal women found that in women wearing estradiol skin
patches, acute alcohol consumption significantly elevated estradiol
levels over the short term (34).

Medications. Chronic heavy drinking appears
to activate the enzyme CYP2E1, which may be responsible for transforming
the over-the-counter pain reliever acetaminophen (TylenolTM) and many
others) into chemicals that can cause liver damage, even when
acetaminophen is taken in standard therapeutic doses (3,35,36). A review
of studies of liver damage resulting from acetaminophen-alcohol
interaction reported that in alcoholics, these effects may occur with as
little as 2.6 grams of acetaminophen (four to five “extra-strength”
pills) taken over the course of the day in persons consuming varying
amounts of alcohol (35,37). The damage caused by alcohol-acetaminophen
interaction is more likely to occur when acetaminophen is taken after,
rather than before, the alcohol has been metabolized. Alcohol consumption
affects the metabolism of a wide variety of other medications, increasing
the activity of some and diminishing the activity, thereby decreasing the
effectiveness, of others (35).

———————————————————————-

Alcohol Metabolism–A Commentary by
NIAAA Director Enoch Gordis, M.D.

The study of metabolism has both practical and broader scientific
implications. On the practical side, information on how the body
metabolizes alcohol permits us to calculate, for example, what our blood
alcohol concentration (BAC) is likely to be after drinking, including the
impact of food and gender differences in the rate of alcohol metabolism
on BAC. This information, of course, is important when participating in
activities for which concentration is needed, such as driving or
operating dangerous machinery.

With respect to its broader scientific application, metabolism, which
has long been studied, is emerging with new implications for the study of
alcoholism and its medical consequences. For instance, how is metabolism
related to the resistance of some individuals to alcoholism? We know that
some inherited abnormalities in metabolism (e.g., flushing reaction among
some persons of Asian descent) promote resistance to alcoholism. Recent
data from two large-scale NIAAA-supported genetics studies suggest that
alcohol dehydrogenase genes may be associated with differential
resistance and vulnerability to alcohol. These findings are important to
the study of why some people develop alcoholism and others do not.
Studies of metabolism also can identify alternate paths of alcohol
metabolism, which may help explain how alcohol speeds up the elimination
of some substances (e.g., barbiturates) and increases the toxicity of
others (e.g., acetaminophen). This information will help health care
providers in advising patients on alcohol-drug interactions that may
decrease the effectiveness of some therapeutic medications or render
others harmful.

———————————————————————-

All material contained in the Alcohol Alert is in the public
domain and may be used or reproduced without permission from National
Institute on Alcohol Abuse and Alcoholism (NIAAA). Citation of the source
is appreciated.

Copies of the Alcohol Alert are available free of charge from
the:

NIAAAPublications
P.O. Box 34443
Washington, DC 20043
Full text of this publication is available on NIAAA’s World Wide Web
site at http://www.niaaa.nih.gov

———————————————————————-

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES

Public Health Service * National Institutes of Health

New Diabetes Test Potential

Starkville, MS-Two Mississippi State University (MSU) scientists have
developed a Breathalyzer-like device that
measures symptoms of diabetes in a person’s breath.

From just one breath, this highly sophisticated sensory device
instantly determines a person’s status: completely diabetes-free, or in
the primary or more advanced stages of the disease.

John Plodinec and Chuji Wang have applied for a patent with their
prototype and are currently seeking to pair with a commercial entity to
release the device in hospitals and clinics.

Wang, a physicist and native of China, imagines that this instrument
could be installed in public places, even a shopping mall. His partner
Plodinec told the University Relations Department of MSU that the device
could be utilized in revealing poor treatment of diabetes, or it could
serve to provide information for other diseases.

It is speculated that of the 17 million Americans suffering of
diabetes, 6 million have not been diagnosed. Obesity is the top cause of
the development of diabetes, and Mississippi ranks in the top ten states
for obesity and diabetes, according to state and federal statistics.

The Breathalyzer measures the acetone in a breath in order to
determine a person’s status with diabetes. The new, highly sensitive
technology of Cavity Ring-Down Spectroscopy makes it possible to
detect the concentration levels of the acetone, which are higher in
diabetes sufferers.

June 10, 2004

Also See:

• Low-Blood Sugar in Diabetes Patients Can Impair
  Ability to Drive
• Diabetes and DUI