Hepatitis is an inflammation of the liver. The two major types of hepatitis in North America are alcoholic hepatitis (a type of toxic hepatitis) and infectious (viral) hepatitis, usually caused by virus types A, B or C.
TOXIC HEPATITIS
Toxic hepatitis is a non-infectious conduction caused by exposure to chemicals that damage the liver. The list of harmful agents is quite extensive, but simple alcohol abuse accounts for the vast majority of cases. Alcoholism tends to be a chronic disease, and this prolonged inflammation often leads to cirrhosis (scarring) of the liver.
INFECTIOUS HEPATITIS
Infectious hepatitis is the most common of all serious infectious diseases in North America. It is estimated that perhaps a half million Americans per year contract the disease. Given the growing prevalence of a relatively new hepatitis virus - Type C - this number will likely increase. An accurate count is difficult because most cases of acute hepatitis go undiagnosed or unreported - the illness often feels no more serious than the flu. Other viruses and pathogens can cause hepatitis, but less frequently than hepatitis virus types A, Band C (see Table 19).
The course of the disease is variable. It can range from being totally asymptomatic to causing death in a small percentage of cases. Most people with infectious hepatitis suffer a few weeks of a flu-like illness, consisting of fatigue, aches and pains, mild fever, loss of appetite, abdominal pain, nausea and vomiting. More serious cases exhibit jaundice, dark colored urine, light colored stools, itching, and altered mental states, lapsing occasionally into coma. Most patients experience full recovery, but some progress to chronic hepatitis and possibly cirrhosis.
The extent of liver inflammation determines how poorly the liver works. In hepatic dysfunction it cannot normally filter and eliminate toxins, help digestion, regulate the chemical composition of the blood, process and store nutrients, and other vital functions. The extent of dysfunction can be measured by liver function tests (LFT's), a measure of certain liver enzymes in the blood. LFT's are a sensitive indicator of liver well-being.
Treatment for acute hepatitis usually follows a conservative regimen -lots of rest, good nutrition and plenty of fluids. Special care must be taken to avoid spreading the disease.
PREVENTION
The best way to deal with all forms of hepatitis is prevention - proper sanitation and hygiene, screening of blood products, vaccination, avoidance of toxins such as alcohol and intravenous drugs, and avoiding contact with the bodily fluids of infected people.
GLUTATHIONE IN THE LIVER
Hepatologists know that glutathione plays a critical role in the liver - it is that organ's most abundant antioxidant enzyme. We have already said that glutathione concentrations are higher in the liver than in any other organ. This is because it functions as a substrate for key detoxification processes in the liver.
Phase I liver detoxification transforms toxins into water-soluble forms. Glutathione is essential in Phase II, which neutralizes or conjugates these products and helps the body eliminate them through the gut or the kidneys. If these two detoxification phases are impaired for any reason, toxins will accumulate in the body and lead to disease.
Medical science has long known that a glutathione deficiency invariably accompanies liver damage. When hepatitis results from acute overdoses of hepatotoxic pharmaceutical drugs such as acetaminophen (Tylenol, Atasol, etc.), the glutathione enhancing drug NAC (N -acetylcysteine) is used to raise glutathione levels rapidly. This eliminates the toxic breakdown products of the overdose. The glutathione deficiency is critical because it further compounds the illness and can easily lead it on a downward spiral.
http://www.youtube.com/watch?v=B4Q_MNuMITM 20% OFF!!!
Decreased liver production of glutathione is seen in alcoholic cirrhosis, sicknesses caused by exposure to hydrocarbons and other toxins, viral hepatitis, fatty livers and even aging individuals. Ongoing research aims to raise glutathione levels in an attempt to support liver function in these patients. This approach is even being tried in the treatment of fulminant hepatic failure.
Alcoholic patients with lower glutathione levels are more prone to liver damage. This has prompted researchers to try to treat alcoholic liver disease by raising glutathione levels, and both clinical symptoms and liver function test results have improved with this method.
GLUTATHIONE IN THE TREATMENT OF VIRAL HEPATITIS
N.S. Weiss and his team at the Max Planck Institute demonstrated the antiviral properties of N AC in human tissue cultures. C. Watanabe found undenatured whey protein, a natural glutathione precursor, to be effective in improving liver function abnormalities and immunological parameters in hepatitis B patients. These improvements continued even after the treatment ended, reflecting the long-term benefits of such an approach.
Treatment options for chronic hepatitis C sufferers are far from ideal. Barbaro and his team in Italy eloquently described the systemic depletion of glutathione in hepatitis C patients, suggesting that this deficiency could explain their resistance to interferon therapy. O. Beloqui's team confirms this in a controlled study of hepatitis C positive individuals. By successfully raising one group'sglutathione levels with NAC therapy, they showed that interferon therapy was enhanced.
Case study
When he was young, Roger required multiple blood transfusions for hemo
philia, a bleeding disorder. As a young adult his liver was tested for abnormal
function and the results revealed that he had acquired hepatitis C, probably
from contaminated blood. Worried about the side-effects of antiviral medica
tions and their limited success, he preferred to undergo unconventional treat
ment. His protocol included milk thistle (silymarin), turmeric (curcuma),
alpha lipoic acid, methionine, N -acety/cysteine, and intravenous glutathione
as well as a low-meat diet and avoidance of alcohol, acetaminophen and
cigarettes. His liver function tests have since normalized.
http://www.youtube.com/watch?v=B4Q_MNuMITM 20% OFF!!!
CONCLUSION
The liver is the largest and most complicated organ in your body. It is intimately linked to a myriad of factors affecting health and illness. Glutathione is a key constituent of proper liver function. Low glutathione levels invite a host of toxicological and immunological diseases. High levels offer protection against these maladies.
REFERENCES
ANKRAH NA, RIKIMARU T, EKr:,BAN FA, ADDAE MM. Decreased cysteine and glutathione levels: possible determinants of liver toxicity in Ghanaian subjects. Journal of Int. Medical Research 22:171-176, 1994
BARBARO G, DI LORENZO G, SOlDINI M, ET At. Hepatic glutathione deficiency in chronic hepatitis C: quantitative evaluation in patients who are HIV positive and HIV negative and correlations with plasmatic and lymphocytic concentrations and with the activity of the liver disease. American Journal of Gastroenterology 91:2569-2573, 1996
BElOQUI 0, PRIETO J, SUAREZ M, GIL B, QIAN CH, GARCIA N, CIVEIRA MP. N-acetyl cysteine enhances the response to inteiferon.JjIJ in chronic hepatitis C: a pilot study. Journal of Interferon Research 13:279-282, 1993
BRESCI G, PICCINOCCHI M, BANTI S. The use of reduced glutathione in alcoholic hepatopathy. Minerva Medicine 82:753-755, 1991
DENTICO P, VOLPE A, BUONGIORNO R, ET At. Glutathione in the treatment of chronic fatty liver diseases.
FARINATI F, CARDIN R, DE MARIA N, ET At. Iron storage, lipid peroxidation and glutathione turnover in chronic anti-HCV positive
hepatitis. Journal of Hepatology 22:449-456, 1995
HARRISON PM, WENDON JA, GIMSON AES, ALEXANDER GJM, WILLIAMS R. Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure. New England Journal of Medicine 324:1852-1857,1991
JEWELL SA, DI MONTE D, GENTILE A, GUGLIELMI A, ALTOMARE E, ALBANO 0. Decreased hepatic glutathione in chronic alcoholic patients. Journal of Hepatology 3:1-6, 1986
LIEBER CS. Susceptibiliiyto alcohol-related liver injury. AkohoI2(supple):3IS-326,1994
LOGUERCIO C, TARANTO D, VITALE LM, BENEDUCE F, DEL VECCHIO, BLANCO C. Effect of liver cirrhosis and age on the glutathione concentration in the plasma, erythrocytes, and gastric mucosa. Free Radical Biology Medicine 20:483-488, 1996
MULDER TP,JANSSENS AR, DE BRUIN we, ET At. Plasma glutathione S-transferase alpha 1-1 levels in patients with chronic liver disorders.
N!,RDI EA, DEVITO R, CECCANTI M. Highdose glutathione in the therapy of alcoholic hepatopathy. Clinical Ter. 136:47-51, 1991
PRESSMAN AH. The GSH Phenomenon St. Martins Press, New York NY, 1997
MISCELLANEOUS Proceedings of the 16th International Congress of Nutrition. Montreal, PR514,1997
SAVOLAINEN VT, PJARINEN J, PEROLA M, PENTTIlA A, KARHUNEN PJ. Glutathione S-transferase GST M1 "null" genotype and the risk of alcoholic liver disease. Alcohol Clinical Experimental Research 20:1340-1345, 1996
WATANABE A, OKADA K, SHIMIZU Y, WAKABAYASHI H, HIGUCHI K, NIIYA K, KUWABA- RA Y, YASUYAMA T, ITo H, TSUKISHIRO T, KONDOH Y, EMI N, KOHRI H Nutritional
therapy of chronic hepatitis by whey protein (non-heated). J Med. 2000;31(5-6):283-302
WATANABE A, HIGUCHI K, YASUMURA Y, SHIMIZU Y, KONDO Y, KOHRI H. Nutritional modulation of glutathione level and cellular immunity in chronic hepatitis Band C. Hepatology 24: pt2: 597A
WEISS L, HILDT E, HOFSCHNEIDER PH. Anti-hfpatitis B virus activity of N- acetyl-L-cysteine (NAC): New aspects of a well- established drug. Antiviral Research 32:43-53, 1996
http://www.youtube.com/watch?v=B4Q_MNuMITM
Immunocal and Immunocal Platinum are the ONLY Dietary supplements, patented and scientifically PROVEN to consistentlyraise glutathione levels and enhance the human immune system! 20% OFF!!!
www.video-wellness.com
www.jrobwellness.com
No comments:
Post a Comment