Alcohol as One of the Commonest Causes of Death - Essay Example

 Alcohol is nothing but ethanol. It is mainly a central nervous system depressant. When consumed in small amounts it has a mild stimulant effect. Though alcohol is considered a social drink, there is tendency for the consumers to misuse it and become addictive and succumb to the side effects. All alcoholics are not alike. Each alcoholic experiences different degrees of impairment. The disease has different origins for different people. According to the NIAAA (2004), "Women are more vulnerable than men to many of the medical consequences of alcohol use." Harm due to alcohol comes in 3 main ways: binge drinking, addiction and chronic disease. Binge drinking has become rampant in many parts of the world including Europe (Picture-1). According to a study by Anderson & Baumberg (2006), 55 million adults are estimated to drink at harmful levels in the Europe. Harmful consumption of alcohol means more than 40g of alcohol i.e. 4 drinks a day for men and over 20g i.e. 2 drinks a day by women (Anderson & Baumberg, 2006). This project is aims to study the effects of alcohol on health. Picture-1: Binge drinking in adult population (Eurobarometer Health, Food and Alcohol and Safety, 2003) It is important to know the effects of alcohol on the health because, alcohol is the third biggest cause of early death. Picture-2: Causes of death (Anderson & Baumberg, 2006). Metabolism of ethanol To understand the effects of alcohol on the health of humans, it is important to first understand the metabolism of alcohol. The cell membranes of human body are highly permeable to alcohol. Once alcohol is absorbed from the stomach, it reaches every tissue in the body. It is mainly metabolized in the liver. The mode of metabolism is oxidation. The first step in the oxidation is conversion of ethanol to acetaldehyde and this is catalyzed by alcohol dehydrogenase. During this process, NADH (NAD, nicotinamide adenine dinucleotide) is released. The acetaldehyde is further oxidized to acetic acid which then enters the citric acid cycle and metabolized to carbondioxide and water. NADH is used up in the conversion of pyruvic acid to lactic acid, in the synthesis of lipids and in the electron transport chain (Paton, 2005). Most of the damage to cells caused by ethanol is due to acetaldehyde and NADH. Acetaldehyde causes damage due to immune response and increased NADH causes altered NADH/NAD ratio leading to increased oxygen consumption and hypermetabolic state (Tome & Lucey, 2004). Short term effects The effects of alcohol change over time. This is known as biphasic effect. The side effects depend on the level of intoxication which is again dependent on many other factors like the amount and circumstances of consumption, whether taken before or after meals and also the hydration status of the body. Consumption of alcohol after a heavy meal does not produce much intoxication while consuming on empty stomach leads to increased side effects. Similarly, good hydration produces less intoxication symptoms and signs. Initially, alcohol produces mild euphoria, stimulation of behavior and minor disturbances in performance. As the levels of alcohol in the blood increase, more severe effects, and changes in behavior are seen (Table-1). Statistics have shown that 30% of road accidents, 44% of fire injuries, 34% of falls and drowning, 16% of child abuse cases, 12% of suicides and 10% of industrial accidents are related to intoxication due to alcohol (DASSA, 2008). In addition to these, alcohol also causes loss of work productivity, increases illness and contributes to criminal behavior (DASSA, 2008). Stages   BAC   Likely Effects   Feeling of well-being   Up to .05 g%   Talkative Relaxed More confident   At-risk   .05-.08 g%   Talkative Acts and feels self-confident Judgment and movement impaired Inhibitions reduced   Risky state   .08-.15 g%   Speech slurred Balance and coordination impaired Reflexes slowed Visual attention impaired Unstable emotions Nausea, vomiting   High-risk state   .15-.30 g%   Unable to walk without help Apathetic, sleepy Laboured breathing Unable to remember events Loss of bladder control Possible loss of consciousness   Death   Over .30 g%   Coma Death   Table-1: Effects on behavior (DASSA, 2004). Source: Anderson & Baumberg, 2006 Long term effects Excessive alcohol consumption over a period of time leads to various health problems and can involve any organ in the body. The side effects include damage to the heart and blood vessels, liver disease, increased blood pressure, stroke, cancers of the digestive system and breast, sexual impotence, reduced infertility, sleeping difficulties, behavioral and psychological problems like personality changes and mood changes, difficulty in concentration, poor memory, sleeping difficulties, neurological problems such as epilepsy and certain types of vitamin deficiency (DASSA, 2008). Other than these, chronic alcohol consumption also causes to develop tolerance and dependence. Liver disease Excessive alcohol (ethanol) consumption induces pathological changes in the liver which include alcoholic fatty liver, alcoholic hepatitis, and alcohol-related cirrhosis (Ismail, 2006). Fatty liver is characterized by marked increase in the fat cells in the liver. In alcoholic hepatitis, there is inflammation of the liver. In alcoholic cirrhosis, there is replacement of normal liver tissue with scar tissue. Fatty liver and alcoholic hepatitis are reversible conditions while cirrhosis of the liver is not reversible. Many mechanisms of ethanol-induced fatty liver have been proposed. Alcohol damages liver as a dose-dependent hepatotoxin (Maddrey, 2004). The damage is mainly due to the by-products of metabolism. During the initial stages of excessive alcohol consumption, fat deposition occurs in the liver. When fat deposition occurs without any evidence of cell inflammation, it is usually reversible and benign (Maddrey, 2004). However, gradually cell inflammation occurs resulting in liver necrosis and fibrosis. Acute fatty liver is caused by increased uptake of plasma-free fattyacids which are released secondary to enhanced blood flow in the liver, activation of phosphatidate phosphohydrolase and hypermobilization of adipose-tissue fat (Badawy, 1980). The increase in hepatic blood flow is secondary to the direct stimulatory effect of alcohol on the adrenal and pituitary axis (Ismail, 2006). Chronic fatty liver occurs due to chronic ingestion of alcohol which inhibits fatty acid oxidation in the liver. There is also release of very low-density lipoprotein into the blood. As consumption of alcohol continues and increases, hypoxia ensues and there is shift in lipid metabolism leading to decreased energy stores. Depletion of energy stores also occurs due to shift in the redox reaction caused by the preferential oxidation of alcohol in the central zone (Ismail, 2006). Oxidative stress occurs which is caused by pro-oxidant formation, inadequate intake of antioxidants, antioxidant depletion and alcohol-mediated inhibition of glutathione synthesis (Tome, 2004). The pro-oxidants involved in oxidative stress are reactive oxygen species and reactive nitrogen species. Role of peroxisome proliferator-activated receptor alpha, which is crucial for the regulation of hepatic fatty acid metabolism, has also been incriminated in the development of chronic fatty liver. Another hypothesis for the deposition of fat is the role of early growth response-1 transcription factor. In chronic fatty liver, the death of liver cells occurs due to apoptosis which may be related to mitochondrial proteins that regulate apoptosis and necrosis (Ismail, 2006). Alcohol causes peroxidation whch results in the destruction of membrane phospholipid leading to cell injury (Badawy, 1980). The inflammation of the cells is further propagated by a number of inflammatory cytokines and reactive oxygen species (Maddrey, 2004). Cytokines result in fibrotic responses, direct activation of stellate cells and, inhibition of the synthesis of S-adenosyl methionine (Tome, 2004). Activation of stellate cells leads to fibrogenesis due to increased production of collagen by stellate cells (Tome, 2004). Stellate cells are activated by a number of processes like direct injury from reactive oxygen species and through expression of interleukins, such as tumor necrosis factor, IL1, IL6, IL8 and the transforming growth factors (Tome & Lucey, 2004). In a study by Keegan et al (1995), they reported that in the animal models they studied, the histologic changes due to ethanol toxicity in the liver were inflammation, hepatocyte necrosis and pericentral sclerosis. They also reported abnormal mitochondria and a marked proliferation of smooth endoplasmic reticulum in livers of animals fed ethanol as seen in electron microscopy. Along with these changes, Kono et al (2001) reported significant increases in the number of infiltrating leukocytes, which were predominantly lymphocytes in the animal models. They also reported that the leukocytic infiltration was mediated by intercellular adhesion molecule. Another important mechanism of liver damage due to ethanol is increase in the endotoxin levels after alcohol intake. These endotoxins trigger both cytokine release and oxidative stress (Tome & Lucey, 2004). Studies have shown the role of alcohol in accelerating the development and progression of liver disease in patients who have concomitant hepatitis C. This probably is due to the nuclear receptor nuclear factor kappa-B. Alcohol is proven to promote the replication of the virus. This replication is dose dependent. Also, alcohol consumption inhibits the response to interferon-based therapies (Maddrey, 2004). Genetic polymorphisms influence cytokines released in response to alcohol, lipid peroxidation, circulating endotoxin and Kupffer cell activation (Tome & Lucey, 2004). Picture-3: Cirrhosis of liver Effects of alcohol on heart The relationship between alcohol and its effects on heart is complex. For some persons, consumption of some alcohol has proven to be beneficial. Alcohol raises HDL, lowers blood pressure, inhibits formation of blood clots and prevents artery damage. It is not yet clear as to how much quantity of alcohol produces these beneficial effects. A study by Abrasom et al (2001) revealed that increasing levels of moderate alcohol consumption are associated with a decreasing risk of heart failure among older persons. Their study concluded that consumption of 21 to 70 oz of alcohol per month was associated with a 47% reduction in HF risk. However, prolonged consumption of alcohol in moderate to higher quantities does cause deleterious side effects. Heavy drinking has been associated with left ventricular dysfunction and dilated cardiomyopathy (Djousse & Gaziano, 2007). The Copenhagen City Heart Study (Mukamal et al, 2005) concluded that "heavy alcohol consumption is associated with a higher risk of atrial fibrillation, at least among men" and that "this relationship does not appear to be related to the adverse effects of heavy drinking on coronary heart disease or blood pressure." Effects of alcohol on brain Alcohol causes central nervous system stimulation initially and then depression. It causes difficulty in walking, blurred vision, slurred speech, slowed reaction times and impaired memory. When consumed on empty stomach in large quantities over a short period of time it can cause blackouts. The extent of brain damage can be assessed by advanced technology such as magnetic resonance imaging, diffusion tensor imaging, positron emission tomography, and electrophysiological brain mapping. Heavy consumption of alcohol over a long period of time may lead to shrinking of the brain and deficiencies in the white matter and gray matter of the brain. Various studies in alcoholics have detected deficits in the frontal lobes and cerebellum. This explains dysfunction of behavior, memory, action and coordination in alcoholics. Studies on the brain electroencephalogram recording amongst alcoholics revealed P3 deficit (Figure-1). However researchers are under the opinion that P3 deficits may be a marker of risk for alcohol dependence, rather than a result of alcohol use (NIAAA, 2004). Most alcoholics with cognitive impairment show at least some improvement in brain structure and functioning within a year of abstinence (NIAAA, 2004). The P3 component is reduced in alcoholics compared with control subjects. Figure-1: P3 component in EEG in alcoholics Withdrawal symptoms Persons who are physically dependent on alcohol develop certain withdrawal symptoms when they stop or decrease consumption. These symptoms usually commence 6 to 24 hours after the last drink. They may last for about 5 days. The symptoms include head ache, nausea and vomiting, tremors, anxiety and depression, sweating and difficulty in sleeping. Sleeping disorder may last for several weeks Effects of consumption of alcohol during pregnancy Consumption of alcohol during pregnancy may lead to physical abnormalities, growth retardation and developmental delay in the baby. This is known as fetal alcohol syndrome. These children are likely to have fewer number of brain cells that function appropriately. Their brain volume also is less. They also are likely to have long–term problems in learning and behavior. Safe levels of alcohol during pregnancy are not established (DASSA, 2008). Effects of consumption of alcohol while breast feeding Alcohol taken by the mother can enter the baby through breast milk and can cause irritability, poor feeding and sleep disturbance in the infant. It can also reduce the quantity of breast milk production (DASSA, 2008). Interaction between alcohol and other drugs Alcohol magnifies the effects of diazepam, cannabis, some antipsychotis, antidepressants and some pain killers (DASSA, 2008). Conclusion Alcohol is a social drink with addictive properties because of which many health related problems can occur. The problems can be short term or long term. Short term effects are due to intoxication while long term effects are due to drinking large quantities over a prolonged period. Alcohol is now one of the commonest causes of death. References Abramson, J.L., Williams, S.A., Krumholz, H.M. & Vaccarino, V., 2001. Moderate Alcohol Consumption and Risk of Heart Failure Among Older Persons. JAMA, 285, 1971-1977 Anderson, P., & Baumberg, B., 2006 Alcohol in Europe: A Report for the European Commission. Retrieved on 14th May, 2008 from: http://dse.univr.it/addiction/documents/External/alcoholineu.pdf Djousse, L., & Gaziano, J.M., 2007. Alcohol Consumption and Risk of Heart Failure in the Physicians’ Health Study I. Circulation, 115, 34-39. Drug and Alcohol Services of South Australia (DASSA), 2008. Alcohol and its Effects. Retrieved on 14th May, 2008 from: http://www.dassa.sa.gov.au/site/page.cfm?u=122 Eurobarometer Health, Food and Alcohol and Safety, 2003: Retrieved on 14th May, 2008 from http://ec.europa.eu/health/ph_determinants/life_style/alcohol/documents/ebs_186_en.pdf Ismail, M.K., 2006. Alcoholic Fatty Liver. Emedicine from web MD. Retrieved on 14th May, 2008 from: http://www.emedicine.com/med/topic99.htm Maddrey, W.C., 2004. Alcohol- Induced Liver Injury. Medscape Family Medicine. Retrieved on 14th May, 2008 from: http://www.medscape.com/viewarticle/495215 National Institute on Alcohol Abuse and Alcoholism (NIAAA), 2004. Alcohol Alert. Retrieved on 14th May, 2008 from: www.niaaa.nih.gov/ Paton, A., 2005. Alcohol in the body. British Medical Journal, 330, p.85-87. Tome, S. & Lucey, M.R., 2004. Current Management of Alcoholic Liver Disease. Aliment Pharmacol Ther., 19(7), p.707-714. Read More