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Physical Impacts of Alcohol Abuse

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Published: Tue, 05 Jun 2018

Alcohol use and abuse can affect the liver, central nervous system and the kidneys. The result of the constant use of alcohol can be noted and examined in patients using numerous methods. These methods utilize the body’s reaction towards alcohol using biochemical markers like γ-glutamyl tranferase (GGT), high density lipoprotein cholesterol (HDL-C) and aspartate aminotransferase (AST). Although biochemical markers can easily tell the clinician about the use and abuse of alcohol, genetic markers may also contribute to the dependence of alcohol.

Alcohol use and abuse is associated with multiple illnesses such as cirrhosis and alcoholic hepatitis. Alcohol consumption has many negative effects that increase with age, ranging from short term reactions like dehydration and ethanol poisoning to chronic reactions like liver failure and alcoholic fatty liver disease. The result of alcohol consumption is reactive changes in the body such as an increase of enzymatic activity and concentration as well as the decrease of enzymatic activity and concentration due to tissue destruction.

The enzyme γ-glutamyl tranferase (GGT) activity is one of the most sensitive tests for alcohol use. The enzymes activity rises when there is acute hepatocellular damage present commonly is patients with alcoholic liver disease (G. Bbosa, D. Kyegombe, W. Anokbonggo, A. Lubega, A. Mugisha and J. Ogwal-Okeng, 2014). GGT is such a sensitive marker that the levels will also be increased even if no hepatic or biliary damage is present in the patient suffering from alcoholism. GGT levels increase drastically in the serum of patients abusing alcohol chronically, an increase of 2-3 times the normal value is most commonly present (S. Kavitha, V. Venkatraman and K. Jeyaprakash, 2013). GGT serum levels can also be raised in patients with digestive disorders and mostly only indicates alcoholism in patients who abuse the substance excessively.

High density lipoprotein cholesterol (HDL-C) levels are more commonly decreased in older patients suffering from alcoholism than in younger patients and are used rather as a confirmation marker than an initial indicator. The HDL-C levels in the serum will be decreased in the patients presenting with alcohol abuse (S. Kavitha, V. Venkatraman and K. Jeyaprakash, 2013).

The enzyme aspartate aminotransferase (AST) can be used to indicate alcoholic liver disease and cirrhosis, but proves difficult to provide accurate results in the absence of liver damage. The enzyme is also found in multiple other organs like the brain and the kidneys and is more likely to be used as a confirmation of liver disease than a definitive diagnosis (D. Adler, 2013). The levels of AST in the patients’ serum will be increased up to 4 times the normal ranges in cases of liver damage. The increased AST levels, when indicating alcoholic liver disease, is most likely due to cellular necrosis due to excessive alcohol consumption.

Alanine aminotransferase (ALT) is overly produced in patients with hepatic injury and in alcoholic patients (M. Hyder, M. Hasan and A. Mohieldein, 2013). The disadvantage of this test in that the levels only significantly increases if severe hepatic damage is already present, but the major advantage is that ALT is only present in the liver (R. Van Dyke, 2012). ALT will be increased 4-6X in cases of alcoholic cirrhosis and 7-10X in cases of alcoholism with alcoholic liver disease.

The ratio of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) can also indicate alcoholic liver disease with a ratio greater than 2:1 with respect to AST:ALT. This result is mostly due to low ALT levels in the serum because of hepatic necrosis, pyridoxal-5’-phosphate deficiency or mitochondrial AST leakage (M. Adak, A. Thakur and K. Adhikari, 2012). The ratio is mostly used as an affirmative test as the ratio only rises above 2 in severe cases of alcoholic liver disease.

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Genetic predispositions to alcoholism have not been completely identified, but studies have indicated genes that may be responsible. These genes are known as the Mpdz, the Kcnj9 and the GABRA2 genes. Although these genes are used theoretical markers rather than actual indicator to alcohol dependence there is a correlation between the severity of the withdrawal symptoms and the risk of alcohol dependence (K. Buck, L. Milner, D. Denmark, S. Grant and L. Kozell, 2012).

The GABRA2 gene is located on chromosome 4p12 and regulates the production of gamma-amino butyric acid (GABA) which acts as an inhibitory neurotransmitter (U.S. National Library of Medicine, 2014). Alcohol can affect the signalling pathway of the GABA system if a variation is present in the GABRA2 gene increasing the pleasure derived from the consumption of alcohol above normal levels which can greatly increase the risk of alcoholism in the persons who have this variation (D. Dick and A. Agrawal, 2008).

Alcoholism poses a serious health threat to the medical community causing many serious complications in a healthy lifestyle. Testing for GGT is seen as the most sensitive test, but has the one drawback of having quite a bit of interferences, which can be cancelled out if brought into the equation. ALT and AST tests the livers general homeostasis and should rather be handled as a complimentary test along with a test such as GGT in order to confirm a diagnosis. Genetic markers for alcohol abuse have not been fully discovered as of yet, although a variation in GABRA2 is known to increase the risk of alcohol dependence due to its effects on the GABA pathway when alcohol is consumed.

References:

  1. G. Bbosa, D. Kyegombe, W. Anokbonggo, A. Lubega, A. Mugisha and J. Ogwal-Okeng. (2014). Chronic Alcohol Consumption Affects Serum Enzymes Levels in the HIV-Infected Patients on Stavudine (d4T)/Lamivudine (3TC)/Nevirapine (NVP) Treatment Regimen. Pharmacology & Pharmacy. 1 (5), 181-194.
  2. M. Adak, A. Thakur and K. Adhikari. (2012). Study of Biochemical Markers in Alcoholic Liver Disease: Hospital-Based Case Control Study. Research Journal of Pharmaceutical, Biological and Chemical Sciences. 3 (3), 987-995.
  3. S. Kavitha, V. Venkatraman and K. Jeyaprakash. (2013). Biochemical Markers and Age Onset Involved In Heavy Alcoholism. Asian Journal of Biochemical and Pharmaceutical Research. 4 (1), 80-87.
  4. D. Adler. (2013). The Difficulty of using a Biological Marker for Alcohol Use: A Recent Historical Overview. Sound Neuroscience: An Undergraduate Neuroscience Journal. 1 (1), 1-8.
  5. K. Buck, L. Milner, D. Denmark, S. Grant and L. Kozell. (2012). Discovering genes Involved in Alcohol Dependence and other Alcohol responses Role of Animal Models. Alcohol Research: Current Reviews. 367-374.
  6. U.S. National Library of Medicine. (2014). GABRA2. Available: http://ghr.nlm.nih.gov/gene/GABRA2. Last accessed 02 September 2014.
  7. D. Dick and A. Agrawal. (2008). The Genetics of Alcohol and Other Drug Dependence. Alcohol Research & Health. 31 (2), 111-118.
  8. R. Van Dyke. (2012). Liver Tests: Use and Interpretation. Open Michigan. 1 (1), 1-60.
  9. M. Hyder, M. Hasan and A. Mohieldein. (2013). Comparative Levels of ALT, AST, ALP and GGT in Liver associated Diseases. European Journal of Experimental Biology. 3 (2), 280-284.

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