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alcoholic_liver_disease [2018/03/14 08:02] (current)
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 +======= Alcoholic Liver Disease =======
  
 +[[Alcohol]] consumption has a long history in human civilization,​ dating back to the early neolithic, with references to the problem of [[alcoholism]] noted in the ancient medical texts of India and other cultures. At one time it was thought that [[wp>​alcoholic liver disease]] (ALD) was solely related to the nutritional deficiencies caused by using alcohol as the primary source of dietary calories, but it is now understood that excessive alcohol consumption promotes specific degenerative changes in the liver that are responsible for the clinical manifestations of ALD, which progresses from [[wp>​fatty liver]], to [[wp>​alcoholic hepatitis]],​ and finally [[wp>​cirrhosis]]. Only about 15% of people with [[wp>​alcoholism]] however will go on to experience [[cirrhosis of the liver]]. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +The pathogenesis of ALD relates primarily to the quantity of [[wp>​alcohol]] consumed and the duration of consumption,​ as well as the patient'​s overall nutritional status and a number of genetic and metabolic characteristics. Consuming as little as 20 grams of ethanol, equal to 60 mL of 40% whiskey, 200 mL of 12% wine, or 500 mL of 5% beer can produce liver injury when consumed daily over a period of years. In cases of alcoholic hepatitis a patient will consume up to 80 grams of alcohol daily for almost a decade, whereas cirrhosis is typically seen with the consumption of 160-200 g daily over the same period. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +Alcohol is a potent source of carbohydrates,​ and thus decreases the appetite, promoting malabsorption through its toxic effects on the gut and pancreas. The net result of this is malnutrition,​ which tends to hasten the negative effects of alcohol, and promoting aging and susceptibility to other diseases. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +When ingested alcohol is quickly absorbed from the GI tract, and directed to the liver where it is metabolized by oxidative mechanisms that involve alcohol dehydrogenase and the microsomal ethanol oxidizing system. Alcohol dehydrogenase produces acetaldehyde as the major catabolite, which is toxic to both the liver and other organs, and is further oxidized to acetate. This process increases the redox state of the liver, which interferes with normal functions, inhibiting gluconeogenesis and protein synthesis, and increasing fatty acid synthesis and lipid peroxidation (seen in fatty liver). Alcohol metabolism also induces a local hypermetabolic state that promotes hypoxic damage, as well as induces microsomal P-450, which is involved in drug metabolism. As a result of this, alcoholics tend to acquire an increased tolerance to alcohol and drugs, often leading to multiple drug abuse patterns. Women in particular appear to be more susceptible to alcohol, thought to be because females tend to produce less alcohol dehydrogenase in the gastric mucosa than males. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +Fatty liver or steatosis is the initial manifestation of acute or chronic excess alcohol consumption,​ the liver becoming enlarged and yellowed from the accumulation of fat droplets that can coalesce as larger cysts. These fatty changes to the liver however are completely reversible, and usually presents no more symptoms that the malaise and discomfort of the typical symptoms of ‘hangover’ experienced the next day. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +If ethanol is consumed on a regular basis and to excess however, the injury to the liver persists and the result is alcoholic hepatits, which is usually superimposed upon the fatty changes. The swollen and injured hepatocytes undergo degeneration and a localized inflammatory reaction develops in response. Cellular necrosis and hypoxia stimulates fibrosis, often around the central vein, and in severe cases can be totally obliterated,​ surrounded by dense fibrous tissue called central hyaline sclerosis. Clinically, the effects of alcoholic hepatitis are noted by malaise, anorexia, right upper quadrant pain and jaundice, with laboratory investigation revealing leukocytosis and elevated serum aminotransferase activity. In about 10-30% of the cases the result is death. In those that survive and persist in drinking the acute illness will eventually be followed by chronic hepatitis, usually resulting in cirrhosis within a few years. Even for those patients that abstain from drinking at this point only about 25% fully recover by 6 months, and 20% will continue on to experience cirrhosis regardless of abstinence. For most patients recovery is very slow, and will show some degree of liver disease even after a year of abstinence. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +
 +Cirrhosis represents the end-stage disease of ALD, with hepatocellular necrosis and generalized fibrosis that surrounds the few remaining hepatocellular nodules. Essentially,​ the liver becomes shrunken and fibrotic, and patients will often die from esophageal hemorrhage (secondary to portal hypertension) or from complete hepatic failure. (Berkow 1992; Rubin and Farber 1990, 412-415)
 +Treatment of alcoholism
 +
 +There are a variety of approaches undertaken in the treatment of alcoholism, but none are effective until the patient is faced with the realization of the impact of the disease, and fortified with the resolve to make healthy changes. This process is greatly assisted by a loving, compassionate and respectful group of peers that the patient can turn to for advice, reassurance,​ and encouragement. In many cases the 12-Step program initiated by Alcoholic Anonymous is undertaken:
 +
 +Step 1. We admitted we were powerless over alcohol - that our lives had become unmanageable.
 +
 +Step 2: We came to believe that a Power greater than ourselves could restore us to sanity.
 +
 +Step 3: We made a decision to turn our will and our lives over to the care of God, as we understand him.
 +
 +Step 4: We made a searching and fearless moral inventory of ourselves.
 +
 +Step 5: We admitted to God, to ourselves and to another human being the exact nature of our wrongs.
 +
 +Step 6: We were entirely ready to have God remove all these defects of character.
 +
 +Step 7: We humbly asked Him to remove these shortcomings.
 +
 +Step 8: We made a list of all the persons we had harmed, and became willing to make amends to them all.
 +
 +Step 9: We made direct amends to such people wherever possible, except when to do so would injure them or others.
 +
 +Step 10: We continued to take personal inventory and when we were wrong promptly admitted it.
 +
 +Step 11: We sought through prayer and meditation to improve our conscious contact with God as we understand him, praying only for knowledge of his will and the power to carry that out.
 +
 +Step 12: Having had a spiritual awakening as a result of these steps, we tried to carry this message to others, and to practice these principles in all our affairs.
 +
 +While many have found the 12-Step promulgated by Alcoholic Anonymous (AA), which is supported by a large community that maintains regular meetings in almost every city and town, not all people find the 12-Steps outlined to be necessarily helpful. The 12-Step program has a fairly strong Judeo-Christian ethic, and thus may discourage participation by people of other faiths, rationalists and agnostics. Some people are able to give up alcohol simply through the act of gumption, others with fairly intensive psychotherapy,​ or some with the help of family and friends. Former alcoholics often believe that alcoholism is a disease, a perspective which is fostered by the AA and has now more or less become enshrined as truth. Some critics perceive this notion has divested alcoholics of personal responsibility,​ and therefore the need for balance and moderation in all activities. For example, many former alcoholics continue to abuse their bodies, such as by smoking or drinking large volumes of coffee: in such cases the addictive response has not been addressed. Some former alcoholics that have learned to control their desires find that they can continue to drink in small amounts on special occasions, after a period of abstinence and self-reflection,​ without guilt or depression. In large part the success of either method entirely depends upon the patient.
 +
 +It is important when initiating a program for an alcoholic patient to ensure that alcohol consumption is tapered off slowly, over a period of a week. Quitting alcohol “cold turkey” may give rise to delirium tremens, a potentially fatal form of ethanol (alcohol) withdrawal. Symptoms include tremors, irritability,​ insomnia, nausea/​vomiting (frequently secondary to gastritis or pancreatitis) hallucinations (auditory, visual, or olfactory), confusion delusions, severe agitation, and seizures, which can begin between 6 to 48 hours after the last drink. The condition appears to be caused by the direct effect that ethanol has on the benzodiazepine-GABAa-chloride receptor complex, leading to the down-regulation of GABA and an unopposed increase in sympathetic activity. Ethanol also acts as an N-methyl D-aspartate receptor antagonist.
 +
 +Beyond specific treatments to the hepatobiliary system, the treatment of alcoholism in herbal medicine consists of:
 +
 +1. Restoring proper nutrition. The high carbohydrate,​ high calorie nature of regular alcohol consumption can have a major effect upon metabolic and cardiovascular health. Furthermore,​ an assessment of hepatic detoxification should also be undertaken at some point to establish guidelines for hepatotrophorestoration,​ or at least, the usage of hepatorestorative botanicals. A variety of nutrients in supplemental form can be seen to be helpful, including:
 +
 +    Vitamin A, 25,000 IU daily
 +    Vitamin B complex, 100 mg daily
 +    Vitamin C, 2-3 g daily
 +    Vitamin E, 400 IU daily
 +    Magnesium, 250 mg twice daily
 +    Selenium, 200 mcg daily
 +    Zinc, 30 mg daily
 +    EFAs, EPA/DHA, 1000 mg each daily
 +    Glutamine, 1 g daily
 +    MSM, 2-3 g daily
 +    Probiotics
 +
 +2. Addressing symptoms of withdrawal.
 +
 +    Oral rehydration
 +    Antispasmodics,​ e.g. Black Cohosh (Cimicifuga racemosa), Wild Yam (Dioscorea villosa), Cramp Bark (Viburnum opulus), Hing (Ferula foetida)
 +    Relaxing nervines, e.g. Milky Oats (Avena sativa), Valerian (Valeriana officinalis),​ Skullcap (Scutellaria lateriflora),​ Passionflower (Passiflora incarnata)
 +    Trophorestoratives,​ e.g. Damiana (Turnera diffusa), American Ginseng (Panax quinquefolium),​ Ren Shen Ye(Panax ginseng leaf), Bai Shao (Paeonia lactiflora),​ Ashvagandha (Withania somnifera), Amalaki (Phyllanthus emblica), Draksha (Vitis vinifera), Punarnava (Boerhavia diffuse)
 +    Sedatives, e.g. California Poppy (Eschscholzia californica),​ Himalayan Blue Poppy (Meconopsis spp), Yan Hu Suo (Corydalis yanhusuo)
 +    Aromatherapy,​ e.g. EO of lavender, rose, geranium, neroli, vetivert, rosemary, lemon balm, peppermint, basil, sweet marjoram, bergamont, hyssop, lemon, clary sage, myrrh, frankincense,​ sandalwood
 +    Massage
 +    Steam bath, sweat lodge, after weaning and no indication of delirium tremens
 +    ​
 +[[Fair Use]] Source: http://​www.toddcaldecott.com/​index.php/​healing/​conditions/​176-alcoholic-liver-disease
 +
 +http://​www.ayurveda-california.com/​distance_learning/​index.php/​diseases-treatment-with-ayurveda-chinese-medicine/​alcoholic-liver-disease
alcoholic_liver_disease.txt · Last modified: 2018/03/14 08:02 (external edit)