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A Little-Known Fact: Alcohol is a Carcinogen!

November 2005

By Dale Kiefer

People associate excess alcohol ingestion with liver cirrhosis and brain cell damage. Alcohol, however, inflicts a more insidious effect.

Epidemiological studies clearly show that those who consume large amounts of alcohol have sharply increased risks of certain cancers.

Especially troubling are esophageal and brain cancers, both of which are increasing in frequency at an alarming rate. In women, even moderate alcohol consumption is linked with higher breast cancer incidence.

In this article, we reveal what most of the public does not know about the carcinogenic effects of excess alcohol ingestion. We then provide some guidance as to what one may do to reduce alcohol’s damaging effects.

Despite its widespread use and social acceptance, alcohol is one of the 10 leading causes of death and injury in developed countries, according to the Institute for Alcohol Studies in Cambridgeshire, England.1 The World Health Organization (WHO) estimates that alcohol causes 1.8 million deaths worldwide each year, with the highest proportions occurring in the Americas and Europe.

“Alcohol was estimated to cause, worldwide, 20–30% of esophageal cancer, liver disease, epilepsy, motor vehicle accidents, and homicide and other intentional injuries,” the WHO noted in its 2002 World Health report.2 An estimated 63% of US adults drank alcohol in the past year. Alcohol abuse occurs in approximately 6% of Americans, and may affect 10-20% of the population at some point in their lives.3 Untreated alcoholism has been estimated to reduce life expectancy by as much as 15 years.4

In its 2000 Report on Carcinogens, the US Department of Health and Human Services listed alcohol as a known human carcinogen that can cause cancers of the mouth, pharynx, larynx, and esophagus. The risk is greatest among smokers and heavy drinkers. Cancers of the oral cavity and upper airway frequently go undiscovered until their latter stages, when the death rate is very high; surgical treatment of these malignancies can cause disfigurement and difficulties with speech, chewing, and swallowing. The Report on Carcinogens further noted that evidence suggests a link between alcohol consumption and cancers of the liver and breast.5

South American scientists reported in 2003 that Chileans who are heavy drinkers (defined as consuming more than 402 grams of alcohol per week) are significantly more likely to develop hemorrhagic stroke, “a major cause of disability and death worldwide.” The more than fourfold increase in risk was independent of other factors, such as high blood pressure, cigarette smoking, or liver disease.6

The use and misuse of alcohol may also wreck havoc with the brain and the nervous system. Peripheral neuropathy—marked by pain, tingling, and loss of sensation and muscle strength in the extremities—is often the first sign of alcohol dependence.7 Alcoholic neuropathy may result from alcohol’s toxic effects on nerve tissue or may be related to alcohol-induced nutritional deficiencies.8 Alcohol can also have extensive and far-reaching effects on the brain, including contributing to memory lapses and cognitive impairment.9

Clearly, alcohol is a major toxin that can contribute to cancer, stroke, and neurodegenerative decline. Guarding against the effects of this lethal chemical is crucial to promoting optimal well-being.

While the history of alcohol use dates back thousands of years, the chemistry of alcohol metabolism—what actually takes place in the body when we imbibe—is only now becoming clear. Indeed, our understanding of alcohol’s toxic effects is still evolving. We know, for example, that the liver is uniquely susceptible to injury from alcohol, as it is the organ primarily responsible for metabolizing toxins entering the bloodstream. While evidence suggests that drinking in moderation may confer modest cardiovascular benefits,10,11 make no mistake—generally speaking, alcohol is toxic to living cells.

Consumed in excessive quantities, alcohol can cause acute liver injury resembling that caused by viral hepatitis. Long-term abuse may result in chronic liver disease, cirrhosis, and increased risk of developing cancers of the liver, esophagus, mouth, larynx, breast, prostate, and colon.10-18 Other conditions, such as infection with the hepatitis B or C virus, obesity, type II diabetes, or exposure to toxins such as aflatoxin or vinyl chloride, may increase alcohol’s carcinogenic effects in a synergistic manner.16

One should avoid consuming alcohol in quantities sufficient to produce a morning-after hangover. Described as a “constellation of unpleasant physical and mental symptoms that occur between 8 and 16 hours after drinking alcohol,”19 a hangover may be nature’s way of telling us that we have overindulged. In fact, recent research associates morning-after hangovers with diminished memory, cognition, and visual functions, even with blood alcohol levels at or near zero.19-21 Other studies have associated alcohol dependence with significantly elevated levels of interleukin-6, an inflammatory cytokine.22

When abstinence is impractical or undesirable, it is possible to counteract some of the harmful effects of alcohol consumption. Scientists have identified several natural agents that counteract alcohol’s adverse effects on the liver.

Liver cirrhosis.

How the Body Detoxifies Alcohol

Once ingested, alcohol must be eliminated by the body. Like other toxins, however, it must be transformed within the body before it can be safely removed. This transformation, or metabolism, of alcohol involves two major steps. First, it is oxidized to an intermediary compound, acetaldehyde, through the action of an enzyme called alcohol dehydrogenase, or a secondary enzyme, catalase. This initially takes place, to a small extent, in the stomach, and then, to a much greater extent, in the liver. After ethanol (alcohol) is converted to acetaldehyde—a compound even more toxic than alcohol—another enzyme, aldehyde dehydrogenase, converts acetaldehyde to acetate, which is eventually converted to harmless carbon dioxide and water.23,24

A secondary alcohol detoxification system involves a family of detoxifying proteins known as the cytochrome P450 enzymes, which also help metabolize alcohol. Known as the microsomal ethanol oxidizing system (MEOS), this second metabolic pathway also transforms alcohol to acetaldehyde. A highly reactive free radical known as 1-hydroxyethyl is created as a byproduct of this conversion.23,25-32

Another metabolic byproduct produced during the breakdown of acetaldehyde is a chemical called diacetyl. This previously overlooked metabolite may play an important role in generating oxidative stress that can eventually lead to the development of diseases such as Alzheimer’s and cancer, as well as genetic mutations.33

Women at Special Risk

Because men produce more alcohol dehydrogenase in their stomachs and livers than women, they metabolize more alcohol during first-pass metabolism than women. Women, on the other hand, rely more heavily on the detoxification capacity of their livers. Due to this gender-related difference, women are affected more profoundly than men by equivalent doses of alcohol,34-37 and are also more susceptible than men to the threat of developing fatty liver, cancer, cirrhosis of the liver, and brain damage when they drink.

CT scans of sections through the body of a female patient with liver cancer. The dark blobs in the red/orange liver are tumors.

Recent studies suggest that some Asians—who demonstrate genetic polymorphisms, or variability in the genes that code for the enzymes alcohol dehydrogenase and aldehyde dehydrogenase—are at elevated risk of developing alcohol- related liver disease, as are African-Americans of either sex.38,39 In fact, African-Americans have been dying of liver cirrhosis at a greater rate than whites of comparable age for the last 40 years.40 However, neither men nor women enjoy any relative advantages when it comes to protecting against the toxic effects of the powerful 1-hydroxy-ethyl radical.

Because alcohol has substantial caloric value (7.1 calories per gram), it may displace ordinary nutrients in the diet, including antioxidants such as vitamin C, thereby causing primary malnutrition.23 Secondary malnutrition can occur later in the course of chronic alcohol use, when food is no longer properly digested and absorbed by the gastrointestinal tract.30,41-43

Long-term alcohol abuse often leads to a condition known as cirrhosis, which is responsible for the high rate of mortality among heavy drinkers. While liver disease was long thought to be caused by malnutrition, scientists eventually demonstrated that alcohol causes liver cirrhosis even in the absence of nutritional deficiencies. Liver cirrhosis was the twelfth leading cause of death in the US in 2000.35,44

The correlation between alcohol intake and cirrhosis is confirmed in epidemiological data gathered in the last century. For example, Canadian scientists recently analyzed alcohol consumption and cirrhosis incidence in the US before, during, and after Prohibition. The data provide striking evidence of the close correlation between drinking and incidence of the disease. As alcohol consumption plummeted during the Prohibition era, cirrhosis closely followed suit. With the repeal of Prohibition, drinking resumed with gusto, as did diagnoses of fatal liver cirrhosis. The nefarious cause-and-effect relationship between alcohol consumption and deadly cirrhosis continues to this day.35