Scientists have developed research-based hypotheses (explanations) about the interaction between alcoholism and various characteristics, such as aging, gender, family history, and vitamin deficiency (see Table 3.10). They have also developed explanations about how alcohol affects the brain. These explanations are based on evidence from scientific studies, brain scans, and analyses of brain tissue after death. For example, results of these studies and analyses support the ideas that alcoholism accelerates aging, that alcoholism affects women more than men, that alcoholism runs in families, and that thiamine deficiency can contribute to damage within the brain.
An example of the type of data that supports hypotheses about the interaction between alcoholism and various characteristics is shown in Figure 3.3. This figure shows that the brain of the alcoholic (left) has less tissue than the brain of the nonalcoholic (right). Both subjects are fifty-seven-year-old men, but the difference in their lifetime consumption of alcohol and their amount of brain tissue is striking. The graph on the bottom shows that older alcoholics have less cortical tissue (the "thinking" part of the brain) in almost all parts of the brain than do younger alcoholics. Only the posterior temporal lobe of the brain shows equivalent tissue. However, both the younger and the older alcoholics have less cortical tissue than nonalcoholics (control subjects).
FIGURE 3.2
The path alcohol takes after consumption
TABLE 3.8
Symptoms of a hangover
| Alertness | Laziness, fatigue |
| Clumsiness, uncoordination | Lightheadedness, dizziness |
| Dazed state | Loose bowels |
| Difficulty concentrating | Muscle aches |
| Drowsiness, mental slowness | Nausea |
| Dry mouth | Sleepiness |
| Exhaustion | Stomach pains |
| Headache | Thirst |
| Hunger | Trembling hands |
| Irritability | Tremor |
Scientists have also studied the vulnerability (susceptibility) of the various parts of the brain to alcohol. These hypotheses on brain vulnerability to alcohol are shown on the lower portion of Table 3.10. In addition, Figure 3.4 shows the regions of the brain vulnerable to alcoholism-related abnormalities.
Not all of the effects of alcohol consumption are harmful to health. Table 2.1 in Chapter 2 shows levels of alcohol consumption that can provide beneficial health effects, but notes the levels that can provide harmful health effects. The number of scientific studies that support the data listed in each row of the table are noted in the "comment" column.
Compare the data listed in Table 2.1 and Table 3.9 Table 3.9 shows that the consumption of alcohol is linked to heart disease in men and stroke in both men and women. Nevertheless, moderate consumption of alcohol can benefit the heart and blood vessels. As Table 2.1 shows, a fourteen to twenty-nine gram per day intake of alcohol (about two standard drinks) provided maximum risk reduction for coronary heart disease to the individuals in the studies that were analyzed. Nevertheless, a consumption of greater than one alcoholic drink per day for women and two for men can detrimentally affect the liver and is linked to
TABLE 3.9
Major diseases and injury conditions related to alcohol and
proportions attributable to alcohol worldwide
| Men | Women | Both | |
| Malignant neoplasms | |||
| Mouth and oropharynx cancers | 22% | 9% | 19% |
| Oesophageal cancer | 37% | 15% | 29% |
| Liver cancer | 30% | 13% | 25% |
| Breast cancer | n/a | 7% | 7% |
| Neuropsychiatric disorders | |||
| Unipolar depressive disorders | 3% | 1% | 2% |
| Epilepsy | 23% | 12% | 18% |
| Alcohol use disorders: alcohol | 100% | 100% | 100% |
| dependence and harmful use | |||
| Diabetes mellitus | −1% | −1% | −1% |
| Cardiovascular disorders | |||
| Ischaemic heart disease | 4% | −1% | 2% |
| Haemorrhagic stroke | 18% | 1% | 10% |
| Ischaemic stroke | 3% | −6% | −1% |
| Gastrointestinal diseases | |||
| Cirrhosis of the liver | 39% | 18% | 32% |
| Unintentional injury | |||
| Motor vehicle accidents | 25% | 8% | 20% |
| Drownings | 12% | 6% | 10% |
| Falls | 9% | 3% | 7% |
| Poisonings | 23% | 9% | 18% |
| Intentional injury | |||
| Self-inflicted injuries | 15% | 5% | 11% |
| Homicide | 26% | 16% | 24% |
various cancers in both men and women. Clearly, the amount of alcohol consumed is important to health and must be watched carefully to reap possible beneficial health effects without risking detrimental health effects.
Alcohol-Related Hospitalization
According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA) Surveillance Report #68, Trends in Alcohol-Related Morbidity among Short-Stay Community Hospital Discharges, United States, 1979-2002 (August 2004), about 437,000 hospital visits in 2002 resulted in first-listed (primary) alcohol-related diagnoses. Alcohol was also listed as a contributing factor in another 1.5 million hospital visits. Table 3.11 lists the alcohol-related diagnostic categories.
Alcohol dependence syndrome accounted for 35% of first-listed diagnoses related to alcohol in 2002. Cirrhosis made up 30%; alcoholic psychoses, 24%; and nondependent abuse of alcohol, 11% (see Figure 3.5). Figure 3.6 shows trends in these first-listed diagnoses related to alcohol from 1979 to 2002. The percentage of alcohol dependence syndrome as a first-listed diagnosis dropped dramatically from 1979 to 2002. Conversely, alcoholic psychoses have risen
TABLE 3.10
The consequences of alcoholism on the brain
| Hypotheses emphasizing the personal characteristics associated with vulnerability | ||
| Characteristic | Hypothesis | |
| Aging | Premature aging hypothesis: Alcoholism accelerates aging. Brains of alcoholics resemble brains of chronologically old nonalcoholics. This may occur at the onset of problem drinking ("accelerated aging") or later in life when brains are more vulnerable ("increased vulnerability" or "cumulative effects"). | |
| Gender | Alcoholism affects women more than men. Although women and men metabolize alcohol differently, it is not yet clear if women's brains are more vulnerable than men's brains to the effects of alcoholism. | |
| Family history | Alcoholism runs in families; thus, children of alcoholics face increased risk of alcoholism and associated brain changes. | |
| Vitamin deficiency | Thiamine deficiency can contribute to damage deep within the brain, leading to severe cognitive deficits. | |
| Hypotheses emphasizing the vulnerability of brain regions or systems | ||
| Region/system | Hypothesis | |
| Entire brain | Vulnerable to cerebral atrophy. | |
| Limbic system, thalamus, and hypothalamus | Vulnerable to alcohol-induced persisting amnesic disorder (also known as Wernicke-Korsakoff syndrome). | |
| Frontal lobe systems | More vulnerable to the effects of alcoholism than other brain regions/systems. | |
| Right hemisphere | More vulnerable to the effects of alcoholism than the left hemisphere.* | |
| Neurotransmitter systems (e.g., gamma-aminobutyric acid (GABA), glutamate, dopamine, acetylcholine, and serotonin systems) | Several neurotransmitter systems are vulnerable to effects of alcoholism. | |
| *The right hemisphere is also believed to be more vulnerable to the effects or normal aging than the left hemisphere, which is taken as support for the premature aging hypothesis listed above. | ||
| Note: These hypotheses are not mutually exclusive; some are interrelated. Supporting data for these models come from neurobehavioral and electrophysiological studies, brain scans, and post mortem neuropathology. | ||
FIGURE 3.3
A comparison of the brain of an alcoholic with that of a nonalcoholic
as a first-listed diagnosis about 20% during that time. Cirrhosis and nondependent use of alcohol have risen as well, but not as dramatically.
FIGURE 3.4
Regions of the human brain vulnerable to alcohol-related abnormalities
The length of hospital stays varies by diagnosis, as reported in the NIAAA's Surveillance Report #68. In 2002 the hospital stay of persons diagnosed as alcohol dependent averaged 5.5 days, down from 10.7 days in 1988. The stay of those with cirrhosis averaged 6.4 days. Those diagnosed with alcoholic psychoses stayed an average of 5 days, while those with nondependent abuse of alcohol were in the hospital for 2.2 days.
Liver Diseases
Because the liver plays a central role in removing substances from the body, it is the major organ damaged by chronic drinking. This damage is called alcoholic liver disease (ALD). The most prevalent types of alcoholic liver disease are fatty liver, alcoholic hepatitis, and cirrhosis (Mann et al., "The Epidemiology of Alcoholic Liver Disease," Alcohol Research and Health, vol. 27, no. 3, 2003).
Alcohol consumption produces changes in the meta-bolism of lipids (fats) that can cause these compounds to accumulate in liver cells, producing "fatty liver." Often there are no external signs of this ailment except in severe cases. This condition is usually reversible and improves with abstinence from alcohol but can be fatal if alcohol consumption is not reduced or stopped. About 20% of alcoholics and heavy drinkers develop fatty liver.
TABLE 3.11
Definition of alcohol-related diagnoses
| Category used in report | Classification in ICD-9-CM* |
| Alcoholic psychoses | 291.0 Alcohol withdrawal delirium 291.1 Alcohol amnestic syndrome 291.2 Other alcoholic dementia 291.3 Alcohol withdrawal hallucinosis 291.4 Idiosyncratic alcohol intoxication 291.5 Alcoholic jealousy 291.8 Other specified alcoholic psychosis 291.9 Unspecified alcoholic psychosis |
| Alcohol dependence syndrome | 303.0 Acute alcoholic intoxication 303.9 Other and unspecified alcohol dependence 265.2 Pellagra 357.5 Alcoholic polyneuropathy 425.5 Alcoholic cardiomyopathy 535.3 Alcoholic gastritis |
| Nondependent abuse of alcohol | 305.0 Alcohol abuse |
| Chronic liver disease and cirrhosis: | |
| Alcoholic cirrhosis of the liver | 571.0 Alcoholic fatty liver 571.1 Acute alcoholic hepatitis 571.2 Alcoholic cirrhosis of liver 571.3 Alcoholic liver damage, unspecified |
| Other specified cirrhosis of the liver without mention of alcohol | 571.4 Chronic hepatitis 571.6 Biliary cirrhosis 571.8 Other chronic nonalcoholic liver disease 572.3 Portal hypertension |
| Unspecified cirrhosis of the liver without mention of alcohol | 571.5 Cirrhosis of liver without mention of alcohol 571.9 Unspecified chronic liver disease without mention of alcohol |
| *ICD-9-CM=International Classification of Diseases, Ninth Revision, Clinical Modification | |
Alcoholic hepatitis is an inflammation of the liver accompanied by other changes to the liver cells. The liver becomes enlarged and tender, and jaundice (yellowing of the skin and other tissues) is usually present. The condition can be, but is not always, fatal. Some complications, however, may cause hepatitis to persist for long periods after the person stops drinking. Alcoholic hepatitis is often a precursor to cirrhosis. Women have a higher incidence of alcoholic hepatitis than do men.
Cirrhosis of the liver is the most serious form of alcoholic liver disease. It is an inflammatory condition in which functioning liver cells are replaced by scar tissue. Steady, heavy drinking (five or more drinks a day for several years) is necessary to produce enough liver damage to cause cirrhosis. An estimated 10 to 15% of people with alcoholism develop cirrhosis. Ninety percent of alcoholics with cirrhosis who stop drinking survive five years or more, while only 70% of those who do not stop drinking survive (Mann et al., "The Epidemiology of Alcoholic Liver Disease," Alcohol Research and Health).
FIGURE 3.5
First-listed alcohol-related hospital diagnoses, 2002
Figure 3.7 shows that at any given level of alcohol consumption, women are more likely to develop cirrhosis than men. One explanation for this phenomenon is that the levels of an enzyme that breaks down alcohol in the stomach may be lower in women than in men, permitting more alcohol to get into the bloodstream and from there to the liver.
Abstinence from alcohol is the treatment for fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. For those whose medical condition has greatly deteriorated, liver transplants are the only alternative.
Digestion and Nutrition
The gastrointestinal (GI, or digestive) tract is also affected by chronic heavy drinking. Alcohol interferes with the functions of all parts of the GI tract, from the mouth to the large intestine. Alcohol abuse may damage the lining of the stomach and intestines, causing the formation of bleeding ulcers and producing abdominal pain and discomfort.
Alcohol is very high in empty calories; it contains no vitamins or minerals (except for a very few in beer). A drinker who gets many calories from alcohol often has little appetite for other food. In addition, alcohol reduces the absorption of food through the lining of the small intestine and interferes with the absorption of amino
FIGURE 3.6
Trends in first-listed alcohol-related diagnoses, 1979-2002
Heavy alcohol consumption is a primary cause of chronic pancreatitis. More than 75% of patients with this disease have a history of heavy drinking, most often for five to ten years before the symptoms appear. Pancreatitis causes severe abdominal pain, often accompanied by nausea, vomiting, and fever. Medical researchers do not yet fully understand how alcohol damages the pancreas.
Cancer
Drinking alcoholic beverages has been linked to cancer, particularly cancers of the upper airway and the gastrointestinal tract. In addition, alcohol consumption has been linked to cancers of the colon and rectum, and to breast cancer in women. The association between alcohol consumption and stomach, pancreatic, prostate, and endometrial cancer is still controversial. Alcohol has not been shown (as has cigarette smoking) to cause cancer, but the consumption of alcoholic beverages increases the risk of developing some cancers.
Figure 3.8 shows the relationship between consuming increasing amounts of alcohol and the relative risk (RR) of developing various cancers. The RR for any of these cancers in nondrinkers is considered to be a baseline of 1.0. The values on the graphs show the relative risk for that cancer at various levels of alcohol consumption. For example, a person consuming 28 grams of alcohol per day (about two standard drinks) is about 1.8—a higher risk than that of a person who consumes no alcohol.
FIGURE 3.7
Alcohol consumption and incidence of cirrhosis of the liver in men and women
Results of a study by Morten Gronbaek and his colleagues, "Population-Based Cohort Study of the Association between Alcohol Intake and Cancer of the Upper Digestive Tract" (British Medical Journal, September 1998), show that intake of wine tends to decrease the risk of upper digestive tract cancer, while intake of beer and spirits significantly increases the risk. The researchers suggest that their findings are strongly supported by studies showing that resveratrol, a substance in grapes and wine, may be protective against cancer, while nitrosamines in beer and spirits may promote cancer.
The Brain
Alcohol injures the brain as it does other organs. About half of the twenty million alcoholics in the United States, however, appear to be free of cognitive impairments, note Marlene Oscar-Berman and Kasenija Marinkovic in "Alcoholism and the Brain: An Overview" (Alcohol Research and Health, vol. 27, no. 2, 2003). Nonetheless, up to two million people develop such serious debilitating brain conditions that they require life-long care. Such conditions include alcoholic dementia and Wernicke-Korsakoff syndrome.
Alcoholic dementia is characterized by physical changes in the brain along with an intellectual decline, including a loss of abstract thinking and problem-solving abilities, difficulty in swallowing, and difficulty in manipulating objects. If a person stops drinking, the deterioration may stop and, in some instances, reverse itself.
Korsakoff's psychosis, a brain syndrome caused by chronic alcohol dependency, is a permanent state of cognitive dysfunction—the inability to remember recent events or to learn new information. Previously learned information may interfere with new learning, and it may also be difficult to recall events that occurred before the onset of the psychosis. A related syndrome called Wernicke's disease manifests itself with vision problems, ataxia (loss of the ability to control muscle movement), and confusion. Unlike Korsakoff's psychosis, Wernicke's disease can be reversed with an adequate intake of thiamine (vitamin B1). Both conditions in the same patient at the same time are called Wernicke-Korsakoff syndrome.
The Heart
Chronic alcohol consumption may contribute to congestive heart failure through toxic effects on the heart muscle, producing cardiomyopathy (degeneration of the heart muscle). This damage often follows a long period (about a decade) of heavy drinking. Symptoms of damage include shortness of breath, ankle swelling, unusual fatigue, and eventual heart failure.
Heavy alcohol intake also interferes with the ability of the heart to contract, and heartbeat irregularities (cardiac arrhythmias) are common in alcoholics. Chronic alcohol consumption is also associated with a significant increase in hypertension (high blood pressure) and may be an important factor in ischemic heart disease (deficient blood circulation to the heart) and cerebrovascular disorders, including stroke.
Other Muscles
Alcohol abuse can also weaken skeletal muscles. Alcoholic myopathy (muscle disease) may be either acute (having rapid onset, severe symptoms, and short duration) or chronic (long-lasting and recurrent). Symptoms of acute myopathy include muscular pain, tenderness, and weakness, usually confined to one limb or a group of muscles. The chronic form of the disease
FIGURE 3.8
Relationships between increasing amounts of alcohol and relative risk for fourteen types of cancer
causes a slow progression of muscular weakness and atrophy (wasting). Mild symptoms occur in about one-third of alcoholics. Alcohol also affects involuntary smooth-muscle contractions, a primary reason why it was once used as a treatment for controlling the contractions of the uterus in premature labor.
The Blood and Immune Systems
Alcohol can cause blood abnormalities. Common problems are anemia, a decrease in hemoglobin in the blood, and abnormally enlarged red blood cells. When an alcohol-dependent person stops drinking, his or her red blood cells do not return to their normal size for at least four months.
FIGURE 3.8
Relationships between increasing amounts of alcohol and relative risk for fourteen types of cancer [CONTINUED]
Another common blood abnormality in alcoholics is a lowered white blood cell count. White blood cells are an integral part of the body's defense against disease, and a low white cell count leaves many alcoholics more susceptible to infectious diseases than nonalcoholics. Additionally, chronic alcohol use reduces the T-cell population in lymphoid tissue and the spleen. T-cells are white blood cells that are key to the immune response.
There is no evidence of a direct association between alcohol use and AIDS (acquired immunodeficiency syndrome); however, alcohol use may increase risk-taking behavior such as sharing drug needles or having sex without taking proper precautions to reduce the risk of contracting sexually transmitted infections.
Some evidence also shows that long-term drinking can produce irregularities in blood sugar levels, although alcoholism has not been tied conclusively to diabetes.
Sexuality and Reproduction
Many alcoholics suffer from impotence and/or reduced sexual drive. Some studies suggest that about 25% of alcoholics become impotent, even after they stop drinking. This figure may actually be much higher. Male alcoholics tend to have much lower levels of testosterone, the principal male hormone, than do nonalcoholics, while their levels of estrogen, a female hormone, are increased. Many alcoholics suffer from depression, which may further impair their sexual performance.
In premenopausal women, chronic heavy drinking can contribute to a variety of reproductive disorders. These include the cessation of menstruation, irregular menstrual cycles, failure to ovulate, early menopause, and increased risk of spontaneous miscarriages. Some of these disorders can be caused directly by the interference of alcohol with the hormonal regulation of the reproductive system. They may also be caused indirectly through other disorders associated with alcohol abuse, such as liver disease, pancreatic disease, malnutrition, or fetal abnormalities.
Fetal Alcohol Syndrome
Research has shown that alcohol consumption during pregnancy can result in severe harm to the baby. Alcohol can cause birth defects, which can begin to develop within the first three to eight weeks of pregnancy. Since the development of such defects begins so early in pregnancy, the mother-to-be may not even know she is pregnant.
Drinking during pregnancy can cause fetal alcohol syndrome (FAS), which was first described in studies in France in 1968 and in the United States in 1973. The key features of FAS are listed in Table 3.12. In addition to these features, results of recent studies show that prenatal alcohol exposure is associated with abnormalities in nerve electrical properties (De Los Angeles Avaria et al., "Peripheral Nerve Conduction Abnormalities in Children Exposed to Alcohol in Utero," Journal of Pediatrics, vol. 144, no. 3, 2004). Children with FAS also exhibit a complex pattern of behavioral and cognitive dysfunctions, which are listed in Table 3.13.
TABLE 3.12
Key features of fetal alcohol syndrome (FAS)
| Prenatal growth deficiency—decreased birthweight for gestational age |
| Postnatal growth deficiency—lack of catch-up growth in spite of adequate nutrition Low weight to height ratio |
| Characteristic facial features |
| Short palpebral fissures (opening between upper and lower eyelids) |
| Maxillary hypoplasia (incomplete development of the upper jawbone) |
| Epicanthal folds (folds of skin of the upper eyelids that partially cover the inner corners of the eyes) |
| Thin upper lip |
| Flattened philtrum (an absent or elongated groove between the upper lip and nose) |
| Central nervous system (CNS) anomalies or dysfunction |
| Microcephaly (abnormally small head)—or other structural brain abnormalities with no significant catch-up through early childhood |
| Developmental delay—social and motor performance related to mental, not chronological age |
| Intellectual disability |
| Neonatal problems including irritability and feeding difficulties |
TABLE 3.13
Characteristic behavioral and cognitive dysfunctions in partial
| Difficulties in learning |
| Poor school performance |
| Poor impulse control |
| Problems in relating to others |
| Deficits in language (understanding and speaking) |
| Poor ability for abstract thinking |
| Poor arithmetic skills |
| Problems in memory, attention, or judgement |
Research results of Philip A. May and Phillip Gossage ("Estimating the Prevalence of Fetal Alcohol Syndrome: A Summary," Alcohol Research and Health, vol. 25, no. 3, 2001) show the prevalence rate of FAS in the United States during the 1980s and 1990s to have been 0.5 to two cases per one thousand live births. Results of studies conducted by the National Center on Birth Defects and Developmental Disabilities (NCBDDD) of the CDC show FAS rates to range from 0.2 to 1.5 per one thousand live births. In addition, the NCBDDD notes that researchers believe that other prenatal alcohol-related conditions less severe than FAS, such as alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD) occur approximately three times as often as FAS. (ARND and ARBD were formerly and collectively known as Fetal Alcohol Effects or FAE.)
There is no known safe level of alcohol consumption during pregnancy. The Centers for Disease Control and
TABLE 3.14
Alcohol use in the past month among females aged 18-44, by
drinking pattern and pregnancy status, 2002
[In percent]
| Pregnancy status | Drinking patterna | % |
| Pregnant | Bingeb | 1.9 |
| Frequent usec | 1.9 | |
| Any use | 10.1 | |
| Might become pregnant | Binge | 12.4 |
| Frequent use | 13.1 | |
| Any use | 54.9 | |
| All respondents | Binge | 12.4 |
| Frequent use | 13.2 | |
| Any use | 52.6 | |
| Notes: Estimated prevalence population weighted to represent U.S. women aged 18-44 years. Population consisted of a total of 64,181 women, including 2,689 who were pregnant and 4,404 who might become pregnant. | ||
| aCategories are not mutually exclusive. | ||
| bFive or more drinks on one occasion. | ||
| cSeven or more drinks per week or binge drinking. | ||
Prevention (CDC) notes that FAS and other prenatal alcohol-related disorders are 100% preventable if a woman does not drink alcohol while she is pregnant or if she is of reproductive age and is not using birth control. Yet data show that some women who might become pregnant or who are pregnant consume alcohol and put themselves at risk for have a child with FAS, ARND, or ARBD.
Table 3.14 shows that in 2002 slightly more than 10% of pregnant women consumed alcohol and approximately 2% engaged in binge drinking or frequent use of alcohol. More than half the women who might become pregnant used alcohol, approximately 13% consumed alcohol frequently, and more than 12% engaged in binge drinking.
The prevalence of binge drinking among women of childbearing age varies from state to state. (See Figure 3.9.) In addition, greater binge drinking prevalence was reported among younger women, non-Hispanic whites, current smokers, unmarried women, and impaired drivers. (See Table 3.15.)
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