Alcoholic Cirrhosis as a Syndrome

Abstract: This paper introduces the proposition that alcoholic cirrhosis is not a disease, and certainly not a fatal one. It is my purpose to demonstrate that alcoholic cirrhosis is a cluster of reversible deficiency diseases. By not treating the actual disease processes, conventional treatment is counterproductive and leads to a progressive decline in the patient’s condition. 


"You see only what you know"—Goethe
 

Introduction

Alcohol does not cause cirrhosis. It is estimated that 10% of the population is alcoholic; that would be 28 million people. Since only 25,000 die each year (0.1%), something else must be at cause. Alcoholic cirrhosis is not itself a disease. The cirrhotic liver is merely the largest organ showing damage inflicted systemically. Although the acute symptoms are treated, the cirrhotic liver itself is not treated by contemporary medical practice.

Alcoholic cirrhosis is a collection of symptoms of other diseases, primarily vitamin deficiency diseases, identified in the first half of the 20th century. What was cutting edge medicine only 50 years ago has now become such old news that many physicians do not recognize the symptoms, even when they present in themselves or close family members. In fact, to those whose loyalties lay with pharmacological intervention, the use of vitamins is considered "alternative medicine". Thus has modern medicine abandoned its proud heritage.

In reading this paper, there are a number of questions to keep in mind. 

  • Why don’t all heavy consumers of alcohol get cirrhosis?
  • Why does the cirrhotic condition not resolve after alcohol consumption stops?
  • Why is there no accepted remedial treatment of the liver itself?
  • Why does the liver lose its amazing ability to regenerate when being treated for cirrhosis?
  • Why does conventional intervention not result in cure?
  • Why is there no consistent prognosis for patients with alcoholic cirrhosis?
  • Why do many advanced cirrhotic patients appear to have an unidentified wasting disease?
Catabolic wasting

Catabolic wasting or cachexia is a clinical wasting syndrome that is characterized by unintended and progressive weight loss, weakness, and low body fat and muscle. Oxidative stress is well known to be a complicating factor in chronic diseases. Pro-oxidant free radicals, formed continuously to be available to destroy invading microorganisms, when not blocked by anti-oxidants, lead to cellular destruction and a wasting process. This wasting occurs not just in muscle tissue, but in organ tissue as well, and releases additional free radicals. Symptoms of catabolic wasting may include vision problems, problems with balance, depression, apathy, acquired hemophilia, and dropsy. The loss of weight seen in patients with starvation or clinical wasting profiles has been widely accepted as detrimental to disease management efforts and requires treatment for reversal. When found in an alcoholic, it is called cirrhosis of the liver, and the patient is sent home to die of it. Conventionally, no medical effort is made to treat cachexia in the patient with alcoholic cirrhosis.
 


Etiology of cirrhosis

In the case of alcoholic cirrhosis, the condition is created gradually, while the alcoholic continues with his/her daily life. This stage is referred to as compensated cirrhosis, meaning that few symptoms are causing lifestyle changes in the patient-to-be. When the condition of the liver deteriorates, the person begins to have symptoms, and this is termed decompensated cirrhosis. Decompensated cirrhosis is much more common in those who drink hard liquor than in those who drink beer or wine, probably due to greater availability of vitamins in fermented drink versus distilled alcohol.

Heavy drinkers frequently have poor nutritional habits; missing meals, eating unbalanced diets and heavily processed foods. In addition, binge drinkers are frequently nauseated by the food they do eat, especially while drinking, and may throw up what they have eaten. And if the food stays down, it may be poorly processed, leading to diarrhea. Alcohol has a diuretic effect, which causes frequent urination, with an extra loss of  minerals and the water-soluble vitamins. All of these things lead to poor absorption of nutrients, shortages of which may then lead to further problems with absorption. Thus, the syndrome could be said to be a disease of diarrhea and diuretics.

Health Status

Alcoholic patients have been widely studied and their body chemistry measured. (Ref. Research ) As a group, alcoholics who drink distilled spirits are usually deficient in vitamins B1, B2, B3, B5, B6, B-12, C, D, and K. Except for D and K, these are water-soluble vitamins. In addition, they are usually low in calcium, magnesium, potassium, zinc, and selenium. In patients with advanced, but still compensated cirrhosis, muscle loss and weakness from malnutrition may be noticed.

Alcoholics frequently suffer from pancreatitis, as alcohol seems to damage the pancreas before it damages the liver.  Selenium deficiency has been shown to cause pancreatitis, and supplementation to prevent it.

Cirrhotic symptoms
Acute:

  • Portal hypertension
  • Esophageal varices
  • Ammonia toxicity and acidosis
  • Hepatic coma
  • Gastrointestinal hemorrhage
  • Kidney failure.
Chronic symptoms of cirrhosis include:  
Nausea and vomiting  Spider angiomas 
Chronic dyspepsia (indigestion) Varicosities (varicose veins)
Constipation or diarrhea Nosebleeds and bleeding gums
Anorexia (loss of appetite) Internal and external bleeding
Dyspnea (labored breathing) Easy bruising
Weight loss (cachexia) Extreme dryness of skin
Ascites (dropsy) Extreme paranoia
Light-colored stools Confusion
Ataxia or unsteadiness of balance Loss of memory
Weakness Apathy
Dull abdominal aching Depression
Diabetes Pancreatitis
Osteomalacia (adult onset rickets) Osteoporosis (loss of bone mass)

Customary Treatment of Decompensated Cirrhosis

There is no accepted treatment for cirrhosis itself. Only various symptoms are treated. No attempt is made to reverse the damage to the liver.

The common management of ascites is to restrict fluids and to give the patient diuretics to encourage the body to remove excess fluid from the organs.

To manage portal hypertension, diuretics may be prescribed, or a portal shunt installed.

To protect the esophageal varices from acid reflux, which can lead to further damage and scarring of the blood vessels, a drug which blocks the secretion of stomach acid is prescribed.

To protect against ammonia toxicity, Neomycin and Lactulose will be prescribed. The primary source of ammonia is thought to be from bacterial action on protein, particularly animal protein, in the intestines. The purpose of the Neomycin is to sterilize the intestines, so there will be no bacteria to act upon the protein and produce ammonia. Lactulose is a lactose derivative that is indigestible by the human digestive system. But in the colon, bacteria will break it down, producing an acid condition that draws ammonia from the blood into the colon where it can be eliminated. A secondary effect of the Lactulose is to promote frequent bowel movements, said to be beneficial for elimination of the ammonia that it has attracted.

A restricted diet will be prescribed, with special limits on animal protein to lessen the ammonia production in the bowel.

For the formation of fibrous tissue and scarring of the liver, there is no specific treatment, except liver transplant.

For the kidney disease, treatment is confined to dietary restriction or kidney transplant.
 


Deficiency Symptoms

A review of the symptoms of the various vitamins and minerals follows. Many of these deficiencies will produce the symptoms noted above. (When making bread, if you leave out yeast, you will not get bread, so yeast is the critical ingredient. But, if you have yeast, but leave out the water, you do not get bread, so water is the critical element. But if you have yeast and water, but no flour, you do not get bread, so flour is the critical element. No! You have to have it all, and in proportion.)

Vitamins

Vitamins are not building blocks of the body; they are consumed in the biochemical fire of life. For proper function of the body, the vitamins consumed must be replaced. If they are not, degenerative diseases begin to manifest, and will lead to death if the shortage is uncorrected.

A serious vitamin B1 (thiamine) deficiency goes by the name of beriberi, a serious disease of the central nervous system. It was common until the early part of the 20th century, when thiamine deficiency was discovered to be the cause and supplementation its cure. B1 deficiency symptoms include mental confusion, ascites, dyspnea, loss of physical coordination (ataxia), and vision weakness, hypothermia, hypotension and coma. Thiamine is required for the production of hydrochloric acid in the stomach, for the formation red blood cells, and has a critical role in the metabolism of carbohydrates.

Alcohol is destructive of thiamine, as are antibiotics and bicarbonate of soda. Malabsorption, malnutrition, diarrhea, and low folate levels can all contribute to B1 deficiency. Antacids and other medicines that reduce stomach acidity can destroy it. Magnesium is a necessary co-factor of thiamine metabolism.

When B2 (riboflavin) is deficient, there will be various skin problems, cracks around the mouth, problems with red blood cells, and a weakened immune system. B2 is used in the metabolism of fats, carbohydrates, and proteins, and a deficiency leads to weakness and lack of energy. Riboflavin deficiency can develop within a week. Compazine, or prochlorperazine (used for nausea, which is common in the cirrhotic patient) as well as some other drugs can contribute to a riboflavin deficiency.

B3 (niacin, niacinamide, or nicotinic acid) has profound effects on the higher functions of the brain. Its deficiency has been implicated in schizophrenia and psychosis. A severe deficiency results in a disease called pellagra, a serious, potentially fatal, disease of the nervous system. Symptoms include depression, dementia, gastrointestinal upset and diarrhea.

Niacin is required for the production of insulin, the sex hormones, metabolism of fats, carbohydrates and proteins, and the production of hydrochloric acid.

B5 (pantothenic acid) is required for metabolism of fats, carbohydrates, and proteins. It is needed to make various hormones, steroids, cortisone, and neurotransmitters in the brain. It is required for production of antibodies, cholesterol, red blood cells, vitamin D, and bile. When adequate levels of B5 are missing, one will find depression, hypoglycemia, fatigue, and lack of coordination (ataxia).

B6 (pyridoxine) is actually a group of substances. B6 is required in more than 300 processes in the body, including all the functions mentioned for other B vitamins as well as the formation of serotonin and cholesterol regulation. Deficiency symptoms include nausea, vomiting, anemia, asthma, arthritis, depression, lethargy, and a weakened immune system. Deficiency can develop in two or three weeks.

B-12 (cyanocobalamin) is a water-soluble vitamin, which is normally stored in the liver and kidneys. It is a coenzyme that is required for the synthesis of DNA, and hence the formation of healthy cells throughout the body. A deficiency can result in a disease known as pernicious anemia, a condition of poorly formed blood cells. Also found is a condition where the myelin sheath that insulates nerve cells is progressively destroyed. Symptoms include disorientation, delusions, confusion, memory loss, eye disorders, diarrhea, fatigue, enlargement of the liver, loss of appetite, labored breathing (dyspnea), and moodiness.

Biotin is a member of the B-complex family of vitamins and is essential for cell growth and the production of fatty acids, and the activation of other members of the B family. Biotin is produced by bacterial action in the small intestine and a deficiency is rare unless other intestinal problems are present, or unless antibiotics taken by mouth destroy the bacteria which manufacture it.

Choline is a member of the B vitamin family and is the precursor of the neurotransmitter acetylcholine and is involved in control of homocysteine. It, along with B-12, is necessary for myelin formation. Choline also plays a role in gall bladder regulation, liver function, and lecithin formation, and aids in hormone production and in fat and cholesterol metabolism.

Folic acid is a coenzyme required for the formation of RNA and DNA, red blood cells, proper functioning of the intestinal tract, as well as metabolism of fats, carbohydrates, and proteins. Alcohol is a special villain in the life of folate. It blocks folate absorption, and people who regularly use substantial amounts of alcohol are often seriously deficient. A deficiency is first found in rapidly growing cells such as red blood cells and liver cells, suggesting a cause for the liver to fail to repair cirrhotic damage. Other symptoms include diarrhea, malnutrition, weakness, labored breathing, and apathy.

Inositol, a water-soluble vitamin, is found in cell membranes throughout the body and is involved in the metabolism of fatty acids and cholesterol. It is part of a number of enzymes. Inositol deficiency has been shown in animal studies to produce irritability, mood swings, fatty liver, intestinal disorders and nerve damage.

Co-Q10 is a vitamin made in the body from the B vitamins, amino acids, and minerals. It is necessary for the production of energy at the mitochondrial level. It has a profound effect on energy levels and fatigue.

Vitamin C (ascorbic acid) is important in wound healing due to its role in making collagen (connective tissue), a vital component throughout the body. The scarring of the liver occurs in the connective tissue, and blood vessel walls maintain their structure due to collagen. Vitamin C is involved in the manufacture of hormones, steroids, and neurotransmitters and is necessary for the conversion of folate into its active form. It also assists in iron absorption.

The need for, and use of, vitamin C increases in the presence of infection or injury. Serious burns increase requirements by a factor of one hundred. In the case of malabsorption, one must take in a lot to get in a little. Vitamin C deficiencies are common in alcoholics, where its deficiency manifests as poor wound healing, easy bruising and bleeding, anemia, and varices.

Scurvy is the name for vitamin C deficiency and it is characterized by bleeding gums, easy bruising, hemorrhaging of skin capillaries (spider angiomas), and, untreated, leads to death. Late-stage scurvy has not just serum, but actual blood, leaking through the walls of the blood vessels.

Vitamin K is a necessary factor for blood clotting. Vitamin K deficiency will be found in those with malabsorption or after long-term use of powerful antibiotics, which sterilize the gut. In the cirrhotic patient, it will contribute to varices. It may be difficult to treat, as the damaged liver does not handle it well.

Vitamin A deficiency results from malabsorption of fats, laxatives, antibiotics, and from excess alcohol use. Dry eyes, night blindness, and other eye conditions are symptoms of vitamin A deficiency. In extreme cases, blindness can result. Also there is an adverse impact on white cells and red blood cells, and resistance to infection is impaired. Vitamin A deficiency can result in more, and more severe, diseases of many types and has been shown to increase the risk of pneumonia and severe diarrhea. It is required for metabolizing protein.

Vitamin E (tocopherol), an anti-oxidant, is absorbed in and with fat; it requires pancreatic and biliary enzymes for absorption. Effects of vitamin E deficiency include peripheral neuropathy, poor positional orientation, and balance (ataxia).


Minerals Calcium is critical to the transfer of nerve impulses, formation of connective tissue and, of course, bone. It is involved in buffering the pH of the blood. Its deficiency (common in cirrhosis) can result in more than a hundred diseases, the best known being osteoporosis, essential hypertension, and irregular heart beat. Hypoalbuminemia should be considered as a cause of calcium deficiency.

Magnesium plays an active role in the metabolism of sodium, potassium, and calcium. It acts on the heart and blood vessels, nerves, muscles, and intestines. High alcohol use reduces the body’s supply of magnesium, possibly through diuretic action. Diuretics decrease the renal threshold for magnesium reabsorption in addition to flushing of potassium and calcium. A magnesium deficiency (common in cirrhosis) will lead to a calcium deficiency, tremors of the hands and extremities, and combativeness. Magnesium is a required cofactor in thiamine metabolism.

Zinc is poorly absorbed by healthy persons; those with poor intestinal absorption will get significantly less than 25% of intake. Zinc is necessary for the function of the immune system and its deficiency will be seen in poor wound healing and maintenance of tissue, unclear thinking, and protein metabolism will be impaired. Diarrhea can be both a cause and a result of zinc deficiency. The sense of taste is dependent on zinc so its deficiency affects both appetite and absorption. Zinc deficiency interferes with hormone production, leading to a loss of sexual desire. The ability to create lean body mass is impaired.

Research done in 1992 shows that supplementation of zinc lessens the effects of fibrogenesis in rats with induced cirrhosis. German research shows that zinc deficiencies are implicated in liver cirrhosis.

Selenium is almost always seriously deficient in alcoholics. Selenium levels correlate with albumin levels, with lean body mass, and with total lymphocyte count -- all markers of immune function. Selenium deficiency is associated with heart disease, pancreatitis, AIDS, hepatitis, and with anemia. In agricultural veterinary medicine, cirrhosis can be induced by withholding selenium, and cured by supplementation.

Chromium is required in the utilization of insulin. Thus when it is deficient, blood sugar levels can be elevated as well as cholesterol and triglyceride levels. Peripheral neuropathy and weight loss have been reported.

Copper is a necessary mineral in a number of metabolic processes. Deficiencies contribute to osteoporosis and weakened blood vessels. Symptoms of deficiency will include hemorrhoids and aneurysm.

Potassium is required for the regulation of nerve impulses and its deficiency results in muscle weakness, fatigue, abdominal distension, heart and kidney damage, mental confusion, and apathy. Has been implicated in nutritional edema. While not ordinarily a problem for healthy individuals, diuretics, laxatives, vomiting, chronic diarrhea, and diabetic acidosis can produce the deficiency. It can also be brought on by magnesium deficiency.

Essential Fatty Acids (EFAs)
There are three common essential fatty acids; omega-3 (fish oil & flaxseed oil), omega-6 (grain oils, such as corn oil, cottonseed oil, safflower oil), and omega-9 (olive oil).  Omega-3 oils are anti-inflammatory; omega-6 oils are pro-inflammatory, and omega-9 oils are neutral.  It is believed that the optimum ration of omega-3 to omega-6 is 1:1.  The modern diet is reported to be 1:15 or even 1:20.  There is little research on what effect this has on cirrhosis, but what there is suggests that lowering the ration would be beneficial.  There is much research that shows just that in heart disease, diabetes and arthritis.
  Pancreatic enzymes The pancreas is responsible for producing the enzymes that complete the digestion of all food as well as the production and release of insulin. The enzymes are released through a duct that empties into the gallbladder, while insulin is released directly into the blood. Failure of the pancreas to produce lipase results in fat not being digested, resulting in diarrhea. Failure to produce protease will prevent protein from being digested to a point where it can be absorbed through the intestinal walls. And, of course, failure of the pancreas to produce insulin will cause diabetes.

There is another, probably more serious result of the impairment of the pancreas, and that is the cirrhosis itself. In a cirrhotic liver, normal tissue is replaced by fibrotic tissue. The loss of normal tissue impairs the liver’s ability to produce the 500 or so compounds that are it’s normal responsibility. The fibrin that is produced and laid down at the site of injuries throughout the body is removed as healing continues by pancreatic enzymes. The enzymes are found in normal blood after being recovered from the lower portion of the intestine. If the pancreas is not producing sufficient enzymes, and/or the intestine is not able to recover sufficient enzymes, fibrin will not be removed.

While this line of thought is a bit speculative, there is support for the idea from those who have Cystic Fibrosis, a congenital defect of the pancreas that results in excess fibrotic tissue throughout the body, including the liver. One of the treatments for this condition is supplemental pancreatic enzymes delivered orally.


Protein There are many proteins and amino acids involved in the symptoms of alcoholic cirrhosis, but they will not be discussed here. Instead, consider the totality of protein starvation, Kwashiorkor. In our pride, we consider it a disease of Africa and India, not one of middle-class Americans. Cancer patients, AIDS patients, and cirrhotic patients often meet the criteria to be included in this diagnosis, although it is seldom made.

Body cell mass is catabolized (consumption by the body of protein stores, including organs and muscle tissues) to provide amino acids in support of immune cell and other protein-mediated processes required for life to continue in the short term. The destruction of cells releases free radicals, which may cause further tissue damage. Thus the actual cause of the edema found in hypoalbuminemia may be a vitamin C deficiency.

Attention is called to the symptom of extreme protein deficiency (hypoalbuminemia), dropsy. Dropsy is the old term for abdominal edema, called ascites when considering cirrhosis. While the ascites is believed to be caused by portal hypertension, the presence of dropsy is rarely considered or treated.


 
Table 1. Symptoms and Deficiencies Relevant to Cirrhosis

Symptom                   Description                             Deficiency

Liver fibrosis Replacement of connective tissue with abnormal connective tissue Biotin     Folic Acid Selenium Glutamine Vitamin C Choline  Zinc 
Protease
Encephalopathy Altered brain function, nerve damage Vitamin B-1 Vit  B-12  Vitamin B-3 Magnesium
Encephalopathy Ammonia poisoning (blood is alkaline, not acidic) Vitamin B-2  Vitamin C
Encephalopathy Altered brain function (acidosis, not enough buffering) Vitamin B-2  Calcium
Ascites (Dropsy) Abdominal edema Vitamin B Protein  Vitamin C Magnesium
Varices Enlarged, weakened blood vessels Vitamin C Vitamin K Copper Vitamin E Calcium 
Ataxia Loss of coordination, loss of balance Vitamin B-1 Vit  B-12  Vitamin B-5 Vitamin E
Confusion Vitamin B-1 Vitamin B-3 Vitamin B-6 Potassium  Vitamin B-2 Vitamin B-5 Vitamin B-12 Zinc
Cachexia Catabolic wasting (progressive weight loss, weakness, and low body fat and muscle)  Vitamin B-1 Vitamin B-3 Vitamin B-6 Co Q-10 Vitamin C Potassium  Vitamin B-2 Vitamin B-5 Vitamin B-12 Chromium Zinc
Dyspepsia Indigestion Vitamin B-1 Hydrochloric Acid Vitamin B-3 
Osteomalacia  Adult onset rickets Vitamin D  Calcium
Diarrhea Loose, watery stools Vitamin A Vitamin B-6 Folic Acid  Vitamin B-3 Vitamin B-12 Zinc
Nausea, vomiting Vitamin A Folic Acid  Vitamin B-6 Folic Acid 
Pancreatitis Selenium

 
 
Table 2. Summary of Deficiencies Relevant to Cirrhosis
Deficiency
Symptoms
Vitamin B1 Wernicke's encephalopathy, ataxia, confusion, cachexia, dyspepsia, beriberi, lactic acidosis, abdominal edema
Vitamin B2 Confusion, cachexia, metabolic acidity
Vitamin B3 Encephalopathy, confusion, cachexia, dyspepsia, diarrhea, pellagra
Vitamin B5 Ataxia, confusion, cachexia, fatigue
Vitamin B6 Confusion, cachexia, diarrhea, nausea
Vitamin B-12 Encephalopathy, confusion, cachexia, diarrhea, ataxia
Biotin Fibrosis, nausea
Folic Acid Fibrosis, nausea, diarrhea
Vitamin C Fibrosis, varices, ammonia toxicity, free-radical damage
Vitamin D Osteomalacia (Adult onset rickets)
Vitamin E Ataxia, varices, free-radical damage
Vitamin K Varices, anemia, bleeding
CoQ-10 Cachexia, weakness, fatigue
Calcium Acidosis, varices, osteomalacia
Copper Varices, ascites
Chromium Cachexia, weakness, fatigue
Magnesium Wernicke's encephalopathy, tremors, nausea
Potassium Cachexia, nausea
Selenium Fibrosis, pancreatitis
Zinc Fibrosis, confusion, cachexia, diarrhea
Protease Fibrosis

 
"Truth emerges more readily from error than from confusion." -- Francis Bacon


Discussion

A patient with alcoholic cirrhosis comes to the decompensated stage with a long history of low to very low levels of the water-soluble vitamins. The intestine is likely to be damaged and not able to properly absorb vitamins and minerals when they are present. Consequently, most patients also have significant mineral deficiencies. Customary medical practice may not address the nutritional problem either on the macro-nutrient or on the micro-nutrient level. The trauma interventions common to medical emergencies in the cirrhotic patient seriously aggravate the deficiencies. Customary palliative care may also.

Few patients get to end-stage cirrhosis except under a doctor’s care. This is because the degenerating liver leaves a person incapacitated, unable to function without support from family or friends. That patients reach end-stage cirrhosis is itself an indication that contemporary medicine does not have the answer.

It is a matter of seeing the symptoms and connecting the dots. If one connects the dots to depict a devil, one names it cirrhosis and is at the effect of the monster. If one connects the dots to depict degeneration due to multiple nutrient deficiencies, an obvious, effective, and well-documented treatment plan is waiting.

 


Ill-Advised Standard Interventions

For the management of ascites, diuretics to remove fluid from the body are prescribed. With the fluid goes water-soluble vitamins, perhaps some protein, and the kidneys have a heavier load. In extreme situations, fluid will be withdrawn directly.

For encephalopathy there are three predominant interventions:

  1. Restricted protein intake: When thinking of protein restriction, think of Kwashiorkor, dropsy, and starving children. Why would one be tempted to prescribe such a slow and lingering death?
  2. Lactulose: One of the side effects that is promoted as a benefit is its laxative action. But with three to six bowel movements per day, how can the small intestine extract the nutrient that a starving patient needs? The fluid loss in the resulting diarrhea may help the ascites by removing fluid, but it also removes every mineral, vitamin, fat, carbohydrate, and protein that is desperately needed.

  3.  

     
     
     
     
     

    And why is the laxative action wanted anyway? Ammonia is an alkaline. When the Lactulose is working, it is producing an acid condition, which is what is required to create the osmotic pressure to move the ammonia from the blood to the bowel. But the moment an alkaline molecule encounters an acid, it is neutralized. There is really no way for a bowel to force a reverse chemical reaction and split the resulting salt back into ammonia and acid.

    But for the Lactulose to work, it has to be retained long enough for bacterial action to break down the sugars to produce acid. But the laxative action washes it out. Shouldn’t indigestible fiber (psyllium husks) be used to slow down the flushing?

    But there is an even worse problem. Recall that the small intestine needs to have an alkaline solution (pH of 8 to 9) in order to produce the osmotic pressure to move nutrients into the blood (pH of ~7.5). To do this, the liver produces bile, which empties into the intestine to neutralize the acid from the stomach (normally pH 1 to 3). But even a healthy liver cannot produce a day’s worth of bile each day. Instead, 95% of the bile acids are recycled from the lower small intestine to the liver via the portal vein in the healthy person. But not when there is persistent diarrhea. (While it is not part of the customary care for cirrhotic patients, shouldn’t bile salts be prescribed for the invalid?)
     

  4. Neomycin: Neomycin will sterilize the gut, but at what cost to a critically malnourished patient? How will any but the simplest of carbohydrates be assimilated? Will the intestines have the bacteria to manufacture biotin and vitamin K? What about the adverse affect on thiamine. Note that both biotin and thiamine deficiencies produce the symptoms of encephalopathy without any ammonia being present. (Consider Wernicke's encephalopathy: A neurological disorder of acute onset due to a deficiency of thiamine, characterized by ocular abnormalities, ataxia, and a global confusional state. Wernicke)
Then, reading the literature that comes with Lactulose, there are cautions about using it with oral antibiotics. That’s because Lactulose needs bacterial action in the colon to create the acidic condition that is its reason to be used.

Of course, it would be irresponsible to allow the ammonia to build up in the blood until the patient is comatose. So, before that happens the first time, consider treating the scurvy. The varices occur not because the liver has failed, but because the connective tissue that forms the elastic blood vessel wall have been weakened in the absence of copper, inositol and ascorbic acid. As long as we’re talking about ascorbic acid and ammonia, let’s remember the chemistry of the meeting of an acid and a base. They neutralize to form a salt; something that does not cause a coma.

Acid Blockers: Consider the consequences of using Prilosec. Protein, particularly animal protein, cannot be broken down without the action of acid in the stomach. In the absence of sufficient acid, the intestine will not see amino acids nearly ready for assimilation, but instead will see indigestible chunks of meat, the perfect setup for intestinal bacteria to produce ammonia.
Bicarbonate of soda: Sodium bicarbonate is contra-indicated in lactic acidosis as it creates metabolic acidosis. Further, it destroys thiamine, and thiamine deficiency is often associated with lactic acidosis. The patient needs calcium, not sodium.
 

Possible Interventions For ammonia toxicity, varices, and fibrosis, vitamin C by mouth throughout the day could be considered. If the blood pH is maintained by the presence of ascorbic acid, ammonia will be neutralized as fast as it is encountered. The symptoms of scurvy will also be resolved. For those wishing to undertake a more aggressive therapy, consideration may be given to intravenous administration of sodium ascorbate. See References.

For encephalopathy, intravenous administration of thiamine has repeatedly been reported to be the treatment of choice. See References.

For ascites, balanced amino acids are indicated. For the patient with adequate digestion, diets as prescribed for the starving can be considered. For those with inadequate digestive capability, a brief course of intravenous feeding might be appropriate.

The next time a cirrhotic patient is brought in to the hospital in a comatose state, why not test those wild claims made for intravenous administration of ascorbic acid? Other doctors have reported, in peer-reviewed journals, the injection of more than 200 grams of sodium ascorbate in twenty-four hours for such infections as pneumonia and hepatitis. Two hundred grams should neutralize quite a bit of ammonia. How little might be required to resolve the ammonia toxicity?
 

Summary

It has been shown that alcoholics are deficient in many vital nutrients before cirrhosis is diagnosed. The effects of the various deficiencies are sufficient to create all of the symptoms associated with the syndrome known as cirrhosis of the liver. The deficiencies create the syndrome; there is no "disease" creating the deficiencies and the symptoms. And there is no disease absent the deficiencies.

There is no reason not to prescribe vitamins to the "entry-level" cirrhotic patient, as there has never been a recorded fatality from vitamin consumption. For the advanced cirrhotic patient, intravenous administration of B-complex and C have been shown in study after study to alter the outcome.

The B-complex vitamins are water-soluble and easily washed out of the body. In fact, deficiency can be detected in as little as five days for riboflavin, and 14 days for folate. Their deficiency causes mental problems (encephalopathy, confusion, depression, and apathy), problems with physical coordination (ataxia and dizziness), and a host of others found in cirrhotic patients such as anemia, nausea, vomiting, diarrhea, catabolic wasting, and the failure of the liver to replace its own cells.

Vitamin C deficiency creates a myriad of problems ranging from connective tissue disease, including the blood vessel wall elasticity and liver fibrosis, and fragility of blood vessels. It is beyond the scope of this paper to document all the research showing that free-radical damage can produce all the organ degeneration found in alcoholic cirrhosis, or that the antioxidant properties of vitamin C prevent them. And, of course, vitamin C deficiency seriously weakens the immune response.

Vitamins A and E, and selenium have been shown in published research to have powerful antioxidant properties and to protect against damage to liver and kidneys.

Customary crisis care for the cirrhotic patient aggravates the loss of any of the vital nutrients that may have been left. So in the process of saving the patient, the treatment is killing him.

This paper does not suggest that vitamin and mineral supplementation is an alternative, complementary, or adjunctive therapy. It is sound, mainstream, medical treatment of acute vitamin deficiency diseases that have been known for years. They’ve gone by names such as scurvy, beriberi, pellagra, and pernicious anemia. When they are all present at once, they have not been recognized for what they are: Easily treated, historical, deficiency diseases.
 

 

References
1. An extensive listing of research trials of issues related to alcohol and cirrhosis. Perhaps the best single source of current information on the topic. Forty-one pages of published studies. http://www.healthy.net/library/books/werbach/part1/alcohol.htm
2. Excerpted from www.emedicine.com. The complete article is available at: http://www.emedicine.com/EMERG/topic642.htm. Authored by Philip Salen, MD, Research Director, Clinical Assistant Professor of Medicine, Department of Emergency Medicine, St. Luke's Hospital

Edited by Peter M.C. DeBlieux, MD, Associate Professor of Clinical Medicine, Section of Emergency Medicine and Section of Pulmonary and Critical Care, Charity Hospital; Francisco Talavera, PharmD, PhD, Creighton University, Department of Pharmacy; J Stephen Huff, MD, Associate Professor, Departments of Neurology and Emergency Medicine, University of Virginia Health Sciences Center; John Halamka, MD, Executive Director, Center for Quality and Value, Instructor, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; and Scott H. Plantz, MD, Research Director, Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center

Wernicke's Encephalopathy
Background: Wernicke's encephalopathy is a neurologic disorder of acute onset due to a deficiency of thiamine, characterized by ocular abnormalities, ataxia, and a global confusional state.

Pathophysiology: Wernicke's encephalopathy results from a deficiency in vitamin B1 and thiamine, an essential coenzyme in intermediate carbohydrate metabolism. Alcohol interferes with active GI transport of thiamine. Additionally, in states of chronic liver disease, activation of thiamine pyrophosphate from thiamine is decreased and the capacity of the liver to store thiamine is diminished. Intracellularly thiamine is converted to its active form, thiamine pyrophosphate, which acts as a coenzyme for enzymes involved in the pentose-phosphate pathway (transketolase) and the tricarboxylic acid cycle (pyruvate decarboxylase and alpha-ketoglutarate). Proposed mechanisms for the development of Wernicke's encephalopathy include altered cerebral energy metabolism resulting from decreases in transketolase, pyruvate and acetylcholine, diminished nerve impulse transmission at synapses and impaired DNA synthesis.

Frequency:
In the U.S.: Wernicke's encephalopathy is most commonly associated with chronic alcohol abuse. However, it can occur in any subject suffering from a poor nutritional state.
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Mortality/Morbidity:
Recent studies have confirmed the fact that Wernicke's encephalopathy is poorly recognized by clinicians even when features of the classic triad of symptoms are evident. Recognition of the progressive nature of the disease is critical, since the mortality rate is 10-20% and treatment may correct all the abnormalities.
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Medical/Legal Pitfalls:
Acute Wernicke's encephalopathy may be precipitated rapidly after institution of IV therapy with glucose-containing solutions in high-risk patients, causing postoperative coma after general anesthesia and a rapid change in cognitive function and ocular characteristics in patients being evaluated in the ED. The fact that the development of Wernicke's encephalopathy may be iatrogenic cannot be overemphasized.
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  • Excerpted from www.emedicine.com. The complete article is available at:
    1. http://emedicine.com/emerg/topic291.htm

      Thiamine deficiency may be associated with cardiovascular compromise and lactic acidosis. The response to thiamine (given as 50-100 mg IV followed by 50 mg/d orally for 1-2wk) may be dramatic and potentially life saving.

      The use of sodium bicarbonate is controversial and generally should be avoided (see "Medications" section below). Sodium bicarbonate administration results in the production of carbon dioxide, which leads to subsequent intracellular acidosis. Prospective studies of bicarbonate use in lactic acidosis have shown no improvement in outcome, even in the case of severe acidosis. Toxic etiologies of lactic acidosis, such as methanol, ethylene glycol, and cyanide poisoning may justify administration of bicarbonate (see topics "Toxicity Cyanide," "Toxicity, Ethylene Glycol," and "Alcohols").


  • Massive thiamine dosage in the treatment of acute alcoholic psychoses.
  • Cade JF
    Aust N Z J Psychiatry 1972 Dec;6(4):225-30
    PMID: 4511361, UI: 73134334
    No abstract available.
    -----------

    A quote attributed to this paper from a book in the following context:

    In 1945-50, before thiamine treatment was used, eighty-six patients died of alcoholism complications. In 1956-60, eight people died, but no deaths have occurred from 1966 to now. Cade concluded "that because the mode of death was identical with that in beriberi, because

    thiamine deficiency has been demonstrated in a significant proportion of sick alcoholics, because deaths no longer occur when they are given thiamine, and because there have been no other discernible significant changes in treatment which are likely to have been responsible, thiamine is the therapeutic agent which is literally lifesaving in a significant proportion of patients.
     


    From The Life Extension Foundation http://www.lef.org/protocols/prtcl-065a.shtml
    At the University of Illinois College of Medicine …
    The kidneys can be protected from free-radical damage, a major factor in renal health, by supplementing with vitamin E. Vitamin E has been shown to restore tubular flow to rats with severe kidney disease by suppressing the free radicals that cause tubulointerstitial damage.

    Homocysteine can be very damaging to kidneys. Dialysis patients often require high levels of homocysteine-lowering nutrients such as folic acid, vitamin B12, TMG (also known as betaine or trimethylglycine), and vitamin B6. Folic acid was used in an important study conducted on 82 patients undergoing dialysis (70 used hemodialysis and 12 used peritoneal dialysis) 3 times a week for 4 weeks. The results showed that both groups had homocysteine concentration reduced by 35% after taking 2.5 to 5 mg folic acid after each dialysis treatment. Although dialysis had the effect of lowering homocysteine levels, folic acid further reduced homocysteine levels and, more importantly, had long-term effects even after folic acid supplementation was withdrawn. "Homocysteine concentrations remained decreased in 20 patients four weeks after withdrawal of folic acid supplementation."

    The established dosages for these critical nutrients are as follows:
    Folic acid (800 mcg)
    TMG or betaine (500 mg ) taken twice each day
    Vitamin B12 (300 mcg)
    Vitamin B6 (150 mg minimum) taken throughout the day
     


    According to Roger J. Williams, "Vitamin C is essential for the building of collagen, the most abundant protein built in our bodies and the major component of connective tissue. This connective tissue has structural and supportive functions which are indispensable to heart tissues, to blood vessels, -- in fact, to all tissues. Collagen is not only the most abundant protein our bodies, it also occurs in larger amounts than all other proteins put together. It cannot be built without vitamin C. No heart or blood vessel or other organ could possibly perform its functions without collagen. No heart or blood vessel can be maintained in healthy condition without vitamin C."
    The AIDS Reader June - Volume 10, Number 6 Reversal of Cachexia in Patients Treated
    With Potent Antiretroviral Therapy CME
    Daniele Scevola, MD; Angela Di Matteo, MD; Filippo Uberti, MD;
    Guia Minoia, MD;Federica Poletti, MD; Angela Faga, MD

    Puott and colleagues[citation below] evaluated the association between liver fibrosis and CD4+ lymphocyte depletion in HIV/HCV. A significant independent association was found between fibrosis and CD4+ lymphocyte depletion (<500 cells/mm3). In contrast, the fibrosis score did not correlate with HIV infection itself. The authors suggested that the influence of CD4+ lymphocyte depletion might be mediated via cytokines associated with chronic inflammation.

    [Puoti M, Bonacini M, Govindarajan S, et al. Liver fibrosis progression is related to CD4+ cells depletion in patients with hepatitis and human immunodeficiency virus coinfection. Program and abstracts of the XIII International AIDS Conference; July 9-14, 2000; Durban, South Africa. Abstract TuPeB3175.]
     


    Drug-Induced Nutrient Depletion Handbook, 1999-2000, Ross Pelton, et al, Lexi-Comp, Inc. 1999 ISBN 091658979X

    McCloy R.  Chronic pancreatitis at Manchester, UK. Focus on antioxidant therapy.
    Digestion. 1998; 59 Suppl 4: 36-48    Abstract

    Kuklinski B, Buchner M, Schweder R, Nagel R.  [Acute pancreatitis--a free radical disease. Decrease in fatality with sodium selenite (Na2SeO3) therapy]  Z Gesamte Inn Med. 1991 Apr; 46(5): 145-9  Abstract
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