Gastrointestinal Diseases Not all of the effects of alcohol occur rapidly, as in the cases of motor vehicle crashes, pedestrian falls, and subsequent skeletal injuries. Some medical consequences of alcohol are more insidious, taking years to unfold before any significant medical consequence is detected. Among these are cell damage caused by the direct or indirect toxic effects of alcohol. The first tissue that alcohol comes into contact with is, in most instances, the upper gastrointestinal system. [The author has received anecdotal reports from clinicians and recovering alcoholics about intravenous and rectal administration of alcohol, but it is believed that such experimental drug use is rare] With the exception of minute quantities of alcohol that are directly absorbed through membranes in the buccal cavity and esophagus, when swallowed, alcohol goes directly to the stomach in high concentrations. Since the toxic effects of alcohol are directly related to dose and concentrations, one might reasonably predict that high concentrations of alcohol have potentially deleterious effects throughout the cells of the gastrointestinal system. Alcohol inhibits smooth muscle contractions in the lower esophagus, which may Read more [...]

As the majority of alcohol leaves the gastrointestinal tract, it travels via the hepatic portal vein from the small intestines to the liver, the largest organ in the body and the primary site of alcohol metabolism. Since some alcohol metabolites are toxic, and because the concentration of alcohol reaching the liver is so high and the liver is the primary site of alcohol metabolism, liver damage may be among the most likely and most serious physiological consequences of alcohol abuse. This is particularly significant because of the central role the liver plays in so many physiological activities. Epidemiolog-ical data clearly reveals that alcohol abuse is by far the leading cause of liver-related mortality in the United States. Excessive alcohol consumption leads to three serious types of liver injuries: fatty liver, hepatic inflammation (alcoholic hepatitis), and progressive liver scarring (fibrosis or cirrhosis). Chronic heavy drinking can alter normal metabolism and lead to an accumulation of fat in the liver. As a result, the liver cells become infiltrated and the liver itself becomes enlarged. The bad news is that extensive lipid infiltration may damage cells. The good news is that fatty liver is reversible with Read more [...]

The metabolism of alcohol by hepatocytes requires oxygen, a process that produces free radicals, such as hydroxyl and 1-hydroxyethyl radicals and superoxide anions. These highly reactive compounds can interact with proteins, lipids, and deoxyribonucleic acid to cause damage or death to liver cells. Chronic alcohol consumption also causes white blood cells (neutrophils) to migrate to the liver where they are activated by an inflammatory substance to release large amounts of superoxides which may contribute to liver pathology. Normal liver cells contain antioxidants that can neutralize free radicals. Chronic alcohol consumption decreases antioxidant levels in the liver resulting in a state of oxidative stress that makes liver cells more susceptible to free-radical-induced injury. One such antioxidant is glutathione, which is present at high concentrations in liver cytosol and mitochondria. Alcohol inhibits glutathione transport from the cytosol to the mitochondria of the cell, causing impaired mitochondrial functioning, which is believed to cause necrosis. Acetaldehyde is another highly reactive compound that may promote hepatic injury because high concentrations of this metabolite can become a substrate for aldehyde Read more [...]

Chronic alcohol consumption induces liver fibrosis (scarring) by stimulating the fat-storing cells of the liver to differentiate into collagen-producing stellate cells. It is believed this leads to irreversible cirrhosis. Alcoholic liver fibrosis may occur indirectly through acetaldehyde-protein adducts that can enhance collagen synthesis by stellate cells in vitro. Products of lipid peroxidation also increase collagen synthesis which may lead to fibrosis. Although there are a variety of biomechanical mechanisms through which alcohol or alcohol-metabolites may cause liver damage, the problem is more complex. Hereditary variations in enzymes may explain why only a small proportion of alcoholics develop serious liver disease. Although generic variants, polymorphisms in alcohol dehydrogenase (ADH), CYP2E1 isozyme, and aldehyde dehydrogenase (ALDH) result in various rates of alcohol metabolism among different ethnic groups, no single alcohol dehydrogenase allele has been causally linked to alcoholic liver injury. Aldehyde dehydrogenase polymorphisms may also play a role in the development of alcoholic liver injury. ALDHY, an allele which is present in about half of all Chinese and Japanese, encodes an enzyme that Read more [...]

Cardiovascular disease is the leading cause of death among Americans, followed by cancer and stroke (USDHHS). The role of alcohol as both a risk factor and a potential protective factor for cardiovascular disease has been the focus of intense investigation for many years. The results are clear: alcohol has both deleterious and beneficial effects, but the conditions under which alcohol exerts these unusual behavior effects and the mechanisms involved are complex at best. Alcohol and Heart Disease Alcohol and Blood Pressure Stroke Risk There are two relevant forms of stroke: ischemic and hemorrhagic. Ischemic stroke occurs when a blood vessel in the brain is blocked. Hemorrhagic stroke occurs when a blood vessel in the brain ruptures. Alcohol-related hypertension, or high blood pressure, may increase the risk of both forms of stroke. Yet, in people with normal blood pressure, the risk of ischemic stroke may be decreased due to the apparent ability of alcohol to lessen damage to blood vessels due to lipid deposits and to reduce blood clotting. However, whereas alcohol’s anticlotting effects may decrease the risk of ischemic stroke, alcohol-induced hypertension may increase the risk of hemorrhagic stroke. Two relatively Read more [...]

It has been known for nearly eighty years that heavy drinking decreases longevity. Pearl noted that moderate drinkers lived longer than either abstainers or heavy drinkers. Over the life span, total alcohol consumption is inversely associated with heart damage. The deterioration of heart muscle, a condition known as alcoholic cardiomyopathy, is one of the most serious consequences of chronic heavy drinking. As cardiac cells deteriorate, the unique ability of these cells to contract is impaired. This is particularly significant in the heart’s left ventricle which pumps freshly oxygenated blood throughout the body. Compensatory mechanisms result in an enlarged heart, but any benefit from such cardiac hypertrophy is temporary. Eventually the heart is unable to meet the body’s demand for oxygen. Alcoholic cardiomyopathy is the most common cause of non-ischemic cardiomyopathy in Western societies and is a major source of heart failure and death. As with other diseases, women may also be more sensitive to the toxic effects of alcohol on the heart, even though women drink less, or report drinking less, than men. Possible Beneficial Effects of Alcohol on Coronary Heart Disease Several prospective studies have reported Read more [...]

There is a well-documented association between heavy alcohol consumption and hypertension. Heavy alcohol consumption elevates blood pressure and causes or exacerbates hypertension. It is estimated that one drink per day can chronically increase blood pressure one millimeter of mercury in middle-aged individuals, and even more in the elderly and people with preexisting hypertension. Controversy remains as to whether moderate alcohol consumption has any beneficial effects on blood pressure, but reducing alcohol intake may be one means of reducing blood pressure in people with hypertension. Despite the well-recognized association between alcohol and hypertension, the cellular mechanisms of alcohol’s effect on blood pressure are not well understood and are made confusing by the fact that, initially, drinking alcohol dilates blood vessels, which lowers blood pressure. Studies looking to explain how long-term, heavy alcohol consumption reverses this effect and leads to elevated blood pressure have generally concluded that this effect is due to the actions of alcohol on the autonomic nervous system. For example, heavy alcohol consumption has been associated with increased release of the stress hormones adrenaline and norepinephrine, Read more [...]

Anslinger became the first Commissioner of Narcotics in 1930, although he had had only sporadic contact with narcotic control.1 Nonetheless, his more than ten years of government experience affected his attitude toward law enforcement and addicts. Anslinger was born in 1892 in Altoona, Pennsylvania. His father worked for the Pennsylvania Railroad, and while Anslinger went to high school and then to Pennsylvania State College, he also worked for the railroad during the summers, doing maintenance and landscaping and occasionally investigating suspicious incidents for the railroad’s captain of police. Later, when the police captain became the state fire marshal, he offered Anslinger a job compiling statistics and investigating instances of suspected arson. In 1917, after the United States declared war on Germany, Anslinger was employed in Washington in the Ordinance Division of the War Department, where his chief task was to oversee government contracts. Ordinance officers were unpopular in Washington; the public expected young men to fight abroad and, when the opportunity came, Anslinger volunteered to the State Department which was looking for reliable German-speaking employees to work in Holland. He recalls being assigned Read more [...]

Social reformers successfully initiated federal restrictions on cannabis along with alcohol, opiates, cocaine, and chloral hydrate in the first decade of this century. The Pure Food and Drug Act of 1906 required that any quantity of cannabis, as well as several other dangerous substances, be clearly marked on the label of any drug or food sold to the public.8 Early drafts of federal antinarcotic legislation, which finally emerged as the Harrison Act in 1914, also repeatedly listed the drug along with opiates and cocaine. Cannabis, however, never survived the legislative gauntlet, probably because of the pharmaceutical industry’s opposition. At that time, and for at least a decade longer, the drug trades saw no reason why a substance used chiefly in corn plasters, veterinary medicine, and nonintoxicating medicaments should be so severely restricted. Not even the reformers claimed, in the pre-World War I hearings and debates over a federal antinarcotic act, that cannabis was a problem of any major significance in the United States. Congress rarely heard any witness defend opiates or cocaine, but during the January 1911 hearings on a federal antinarcotic law before the House Ways and Means Committee, the National Wholesale Read more [...]

Fear of cannabis, or marihuana, as it was beginning to be known, was minimal throughout most of the nation in the 1920s. Nevertheless it still concerned the federal government. For example, in the January 1929 authorization of the two narcotic centers for the treatment of addicted federal prisoners, the law specifically defined “habit-forming narcotic drugs” to include “Indian hemp” and made habitual cannabis users, along with opium addicts, eligible for treatment.16 Although there seem to have been few cannabis users transferred to Lexington and Fort Worth, it is significant that congressional worry about cannabis continued after passage of the Pure Food and Drug Act and clearly was present before the Bureau of Narcotics was established in 1930. In areas with concentrations of Mexican immigrants, who tended to use marihuana as a drug of entertainment or relaxation, the fear of marihuana was intense. During the 1920s Mexican immigration, legal and illegal, rapidly increased into the region from Louisiana to California and up to Colorado and Utah. Mexicans were useful in the United States as farm laborers and, as the economic boom continued, they traveled to the Midwest and the North where jobs in factories and sugar-beet Read more [...]