ALCOHOL HAS TAKEN MORE LIVES, DESTROYED MORE  FAMILIES, CRIPPLED THE ECONOMY WITH ENORMOUS MEDICAL AND unneeded EXPENSES, surpassED THE HORRORS OF ANY WAR, IS THE ULTIMATE WEAPON OF MASS DESTRUCTION, A TSUNAMIC DISASTER IS JUST ANOTHER WAVE, ADD PLAGUES AND EARTHQUAKES......

 ALCOHOL USE AND ITS MEDICAL CONSEQUENCES

The Biochemistry, Pharmacology and Toxicology of Alcohol

Most of the acute pharmacological effects of ethyl alcohol are manifestered through the central nervous system (CNS). Ethanol can be described as a primary, functional, irregularly descending CNS depressant. Depression of the mid-brain functions interferes with spinal reflexes and temperature regulation. Ultimately, the medulla also succumbs and death results from a paralysis of the medullary centers.

 

As the blood alcohol concentration (BAC) rises so also does the concentration in the CNS resulting in a continuous spectrum of effects. The euphoric stage of intoxication is the goal of the social drinker. It is characterized by talkativeness, increased self confidence, decreased inhibitions (but not increased sexual appetite per se), diminution of attention and judgement and loss of efficiency in finer performance tests. The excitement phase begins for most individuals at the BAC accepted as the legal criterion of intoxication. The individual now exhibits emotional instability, impairment of memory and concentration, and some muscular incoordination. In the stage of confusion the individual may be disoriented, dizzy, have exaggerated emotional states (fear, anger, grief), diplopia, ataxia and slurred speech. In the stage of stupor there is marked muscular incoordination with an inability to stand or walk, the response to sensory stimuli is markedly decreased, vomiting and incontinence are common. In the stage of coma, reflexes may be totally abolished. This stage of general anesthesia may progress to the terminal event which is death in respiratory failure.

Ethanol does enhance cutaneous blood flow, and a flush is a common sign of mild intoxication. This effect will accelerate heat loss. In addition the thermoregulatory center is impaired in severe intoxication. Thus, drinking when one is exposed to cold is irrational and dangerous. Ethanol should never be given to victims of hypothermia. In addition, chronic abuse may, by unknown mechanisms, produce myocardiopathy. A skeletal muscle myopathy may also be a consequence of chronic ethanol abuse. Ethanol stimulates the secretion of gastric juices by complex mechanisms, that may involve psychic, neural and humoral factors. Alcohol abuse is etiologically associated with acute and chronic pancreatitis, fatty changes in the liver, inflammation of the liver, cirrhosis and esophagitis. Heavy users of alcoholic beverages have an increased incidence of carcinoma of the pharynx, larynx and esophagus.

Alcohol may aggravate or reactive peptic ulcer. It may exacerbate pre-existing liver disease, and patients with liver disease may be especially sensitive to ethanol because of an impaired ability to metabolize it. Ethanol may trigger seizures in epileptics. Ethanol can potentiate the CNS depressant effects of other drugs, and such combinations should be avoided.

Hypoglycemia may occur in people who drink heavily after a period of not eating. Their hepatic glycogen stores are already depleted, and the increased ration of NADH/NAD as a consequence of ethanol oxidation decreases gluconeogenesis from alpha-glycerophosphate, lactate and pyruvate, and amino acids via oxalacetate. The hypoglycemia may be severe and rarely even fatal. Intoxicated persons may pass from intoxication into hypoglycemic coma. Eventually with chronic excessive abuse of ethanol, physical dependence will develop to the point where an unambiguous withdrawal reaction can be recognized. Minor withdrawal reactions are characterized by insomnia, irritability and tremor whereas major withdrawal reactions include anxiety, agitation, sweating delirium and disorientation. Withdrawal seizures ("rum fits") may occur in the 12 to 48 hour period after the start of abstinence. The combination of delirium with tremor gave rise to the name delirium tremors (DT's) which in its most serious form includes vivid, terrifying hallucinations, tachycardia, fever, sweating and a profoundly hyper metabolic state.

 ALCOHOL AND THE LIVER

Alcohol is the major cause of liver cirrhosis in developed nations. Ingestion of large quantities of ethanol may be associated with damage to many cells and organs. Chief among these are liver cells which are primarily responsible for ethanol metabolism. Liver damage clearly is related to the degree and duration of ethanol use, even though other environmental and genetic factors may modulate development of cirrhosis or other serious liver injury. Classically, three major categories of liver change or damage have been recognized in association with heavy ingestion (five drinks per day) of ethanol - Fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. The fatty change is completely reversible. Therefore, if alcoholic hepatitis or cirrhosis has not supervened, the prognosis is excellent as long as abstinence or moderation (Three drinks per day) can be maintained. Alcoholic hepatitis is a disease which takes a fairly long time to develop (months to years of excess ethanol) and which is characterized by smoldering necrosis and inflammation. The cornerstones of therapy for alcoholic hepatitis are abstinence, rest and good nutrition. It is not surprising that abstinence might favorably affect the sequella of alcoholic hepatitis. Some authorities say that 80 percent of patients who continue to drink will develop cirrhosis in 1-12 years. Alcoholic cirrhosis, simply states, is a cirrhosis caused by prolonged heavy ingestion of ethanol. Its seems probable that alcoholic hepatitis is a necessary precursor of alcoholic cirrhosis. Because fatty infiltration and active alcoholic hepatitis so often accompany alcoholic cirrhosis, the liver of the alcoholic cirrhotic is more likely to be enlarged, at least at the earlier stages of disease.

At the later stages, the liver may shrink and become indistinguishable from the liver of post-necrotic cirrhosis, due to viral hepatitis or drug-induced liver injury. The principles of management of alcoholic cirrhosis are similar to those for cirrhosis of any etiology, with the added proviso that patients should abstain from further ethanol intake. The complications of alcoholic cirrhosis are due mainly to diminished liver cell function and to marked abnormalities in portal and liver blood flow. This may lead to development of varices and hemorrhoids, as there is enlargement of alternative collateral channels between the splanchnic and systemic circulations. These dilated collaterals may rupture, producing GI bleeding. The bleeding may be exacerbated by accompanying defects in blood coagulation due to liver cell failure or to consumptive coagulopathy (DIC). Other complications of cirrhosis include ascites, edema, renal tubular acidosis, functional renal failure, increased incidence of peptic ulcer, increased incidence of pigment gallstones, diabetic-like glucose intolerance, increased absorption of iron from the GI tract, coagulopathy, impaired immune function, impaired leukocyte function, hypersplenism, and development of hepatoma. Alcoholic cirrhosis is a serious disease; particularly if the cirrhosis is "decompensated" as evidence by jaundice, acites, functional renal insufficiency, and/or variceal hemorrhage. The prognosis can be improved by abstinence, especially if the disease is not already far advance.

 

 HEMATOLOGIC COMPLICATIONS OF ALCOHOL

Alcohol affects virtually all products of the hematopoietic system. Its effects on erythropoiesis leads to anemia. Folic acid deficiency results from decreased ingestion, impaired absorption and abnormal folate metabolism. Patients with alcoholism have an increased susceptibility to infection. Such infections are usually more severe than in the non-alcoholic patient and are associated with higher mortality. Although the lung is the most common site of infection, there is an increased incidence of other life-threatening infections such as septicemia, septic arthritis, meningitis, and peritonitis.

 ALCOHOL AND THE ALIMENTARY TRACT

Heavy ethanol consumption and cigarette smoking significantly increase the risk of developing esophageal cancer. Evidence is inconclusive on whether ethanol alone is carcinogenic or whether it enhances the carcinogenic effect of tobacco. There may be a direct damaging effect on the mucosa exposed to high concentrations of ethanol. Nutritional deficiencies associated with chronic alcoholism may induce metaplasia in the esophageal mucosa, making it more sensitive to carcinogenic stimulation. Other substances in the alcoholic beverage, such as Nitrosomonas and polycyclic hydrocarbons, may also play a role. One of the most important consequences of alcoholic cirrhosis is the development of portal hypertension and esophageal varices. Bleeding from esophageal varices may be life threatening. Chronic ethanol use may lead to varying degrees of chronic gastritis. The frequency may be influenced by other factors such as cirrhosis, age, malnutrition, medications, and concomitant systemic disease.

 ALCOHOL AND THE PANCREAS

The precise incidence of ethanol-related pancreatitis varies depending on the population studied. In the U.S.A. and other developed countries the etiology is about 1/3 from ethanol, 1/3 from gallstones and 1/3 from all other causes. The typical patient with alcoholic chronic pancreatitis is a middle-aged man who has drunk heavily for 10-25 years. Blood and urine glucose may be increased. Other signs of chronic alcoholism (hematologic, neurologic, hepatic, etc.,) may be apparent. Some people are constitutionally resistant to the development of alcoholic pancreatitis despite years of heavy drinking. 50 percent of chronic heavy drinkers at post mortem will have evidence of chronic pancreatitis. A minority of patients suffer clinically overt chronic pancreatitis and even smaller portion die from pancreatitis per se.

 ALCOHOL: PREGNANCY AND THE FETAL ALCOHOL SYNDROME

"Behold, thou shalt conceive and bear a son: and now drink no wine or strong drinks." (Judges, 13:7)

"Foolish, drunken and hair-brained women most often bring forth children like unto themselves, morose and languid." (Aristotle) Since earliest times, maternal alcohol use during pregnancy has been suspected to have an adverse effect on the developing fetus. Drs. Kenneth L. Jones and David W. Smith reported that they had identified a "characteristic pattern of malformation" in 8 children of alcoholic women. This pattern was characterized by a concurrent triad of signs: growth deficiency, altered morphagenesis (especially facial), and mental retardation. The pattern was termed "fetal alcohol syndrome" (FAS). Since FAS was first identified, maternal drinking has been linked to a broad spectrum of fetal effects that range from subtle to severe. These include not only the full fetal alcohol syndrome, but intrauterine growth retardation, increased risk of anomalies, effects on behavior and intelligence and increased mortality. Major effects of ethanol by trimester of pregnancy are, trimester: (1) major morphologic abnormalities, (2) increased risk of spontaneous abortion, (3) decreased fetal growth. No "safe" dose of alcohol in pregnancy has been identified. Further more, there does not appear to be a "safe" period of pregnancy. Rapid fetal growth, especially of the brain, in the third trimester makes this a vulnerable period as well. FAS children are generally below the third percentile in height, weight, and/or head circumference. They often eat poorly, with poor sucking in infancy. They may be hospitalized for failure to thrive. Other physical findings often seen in FAS are: eye anomalies such as ptosis and strabismus, ear anomalies, prominent palatine ridges, cardiac defects, pictus excavatum, external genital anomalies (labial hypopiasia), aberrant palmer creases, and hemangiomas. Mental retardation is the most debilitating feature of fetal alcohol syndrome. The average IQ score for children with FAS is around 2 standard deviations (30 points) below the normal mean IQ of 100. The mental deficiency and microcephaly seen in children with FAS have been attributed to diminished brain growth. In general, the more severe the physical signs of FAS, the more profound is the accompanying mental retardation. The monetary cost of providing life-time medical and custodial care and remedial education for the cohort of expected FAS and FAE cases in the State of New York in 1978 was estimated to be over $155 million. When this estimate was extrapolated to the country as a whole, these direct costs of all FAS and FAE cases in the United States exceed a billion dollars each year. Added to this are huge social costs, including lost productivity, permanent physical, mental and behavioral disabilities, and the enormous burden on the child and the family associated with fetal alcohol effects. Yet these effects are completely preventable.

 ENDOCRINE AND METABOLIC EFFECTS OF ALCOHOL

Both acute and chronic ingestion of alcohol often have distinct effects on various endocrine and metabolic systems. Liver disease and malnutrition associated with alcoholism may also have adverse endocrine effects.

Male alcoholics may complain of decreased libido and/or impotence. Gynecomastia is often found. Examination also frequently reveals atrophy of testes. Other sexual characteristics are usually intact, although some patients may develop a female escutcheon. In one study of 50 hospitalized men with alcoholic liver disease, over half had testicular atrophy and even more had a female escutcheon. Both a decreased sperm count and decreased serum testosterone concentration are common findings. The chronic alcoholic woman may have infrequent periods or even total cessation of cyclic menstrual flow. Decreased fertility has also been reported. It is thought that alcohol may have a direct toxic effect on the ovaries as well as on the secretion of gonadotropin by the pituitary gland. In addition, both malnutrition and chronic disease may cause amenorrhea, probably via a hypthalmamic effect.

 CONCLUSION

Alcoholism, like crime and mental illness, seems to run in families. Few who have known an alcoholic are likely to argue that an alcoholic's behavior will have no impact on his or her family. Partly for this reason, the relatively high rate of alcoholism found among children of alcoholics has often been interpreted in social-psychological terms. Over the last two decades, however, evidence has mounted to suggest a genetic component in the development of alcoholism. Whether genetic factors placing a person at risk for alcoholism will produce alcoholism seems to depend, at least in part, on the environment.

As stated in the beginning of this action, 10 to 15 million American people were documented as being alcoholics and another 35 million are affected as family members or other victims. Other statistics are as follows:

a- There are approximately 500,000 men and women in local, state, and federal prisons. 50 to 70% are incarcerated because of alcohol related crimes. Homicide - 64%; Assaults - 41%; Rape - 34%; Robbery - 72%.

b- Suicide - 30%; Child abuse - 60%; Fire fatalities - 53%; Drowning - 68%.

c- Alcohol is responsible for the majority of family breakups.

d- Alcohol is responsible for the majority of battered women and children. 38% of child abusing parents have a history of drinking problems.

Each and every statistic is or was a family member: THE FAMILY IS AMERICA!

"THEY KNEW OR SHOULD HAVE KNOWN", the burden, responsibility, and accountability should be that of the alcohol beverage industry. The primary financial responsibility is that of the alcohol beverage industry to reimburse society for the devastation their product generates. Not only does the alcohol beverage industry have the duty to warn and reimburse, they must also provide the public with the facts about the true, scientific consequences of drinking alcoholic beverages. The consumer has not been properly informed and has been denied his or her right to know. Any member of our American Society, hurt by alcohol consumption, has a right to be paid for his or her damages.