Effects of Alcohol on Digestive System, Stomach and Intestines

By: Mark J. Occhipinti, M.S., Ph.D., N.D.c

William Silkworth, wrote in the preface of The “Big Book” the following: “The action of alcohol on chronic alcoholics is a manifestation of an allergy: that the phenomenon of craving is limited to this class and never occurs in the average temperate drinker.” Alcoholics

often eat poorly, limiting their supply if essential nutrients and affecting both energy supply and structure maintenance. Furthermore, alcohol interferes with the nutritional process by affecting digestion, storage, utilization, and excretion of nutrients.

Background Studies

Several studies have shown that alcoholic patients have an unusually high degree of allergic responses: both to “classic allergens such as pollen and to various foods. Multiple studies have compared the allergic responses of alcoholics, depressive, and schizophrenic patients, and found that the alcoholic group was significantly more allergic to a variety of food allergens. A similar study compared patients admitted to an inpatient alcoholism hospital with a matched control group of patients with no history or evidence of alcohol abuse who have been admitted to a general hospital for elective surgery. Most alcoholics are allergic to a wide range of foods as well as environmental-mental allergens. Among foods, grains (the primary ingredient of many alcoholic beverages) are highly reactive. It is well known that that particular foods and/or certain chemicals-can become an addiction.

In these individuals, the body adapts to the presence of the allergic substance by suppressing the immune response and altering its allergen.

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Alcohol Effects on the Gastro-Intestinal System

When alcohol passes through the stomach and intestinal tract it causes subtle cellular damage in the linings of these crucial digestive organs. Over time , alcohol damages these delicate tissues to the point that they become increasingly porous, allowing large, incompletely digested food particles to pass directly into the bloodstream. As these improperly digested food particles enter into the blood stream, immune cells identify them as foreign and attack them with specially designed antibodies.

Once these antibodies have come into existence they remain in the body waiting to be released by the offending food, etc. Unfortunately, food particles “invade” all the time -every time the alcoholic eats. This continuous assault is an ideal environment for the allergy-addiction cycle. The immune system is in a state of perpetual hyper-reactivity-fending off “invaders” that are actually part of the food supply, including Alcoholic Beverages.

Impairment of Nutrient Digestion and Utilization

Alcohol inhibits the breakdown of nutrients into usable molecules by decreasing secretion of digestive enzymes from the pancreas. Alcohol impairs nutrient absorption by damaging the cells lining the stomach and intestines and disabling transport of some nutrients into the blood. In addition, nutritional deficiencies themselves may lead to further absorption problems.

For example, folate deficiency alters the cells lining the small intestine, which in turn impairs absorption of water and nutrients including glucose, sodium, and additional folate. Even if nutrients are digested and absorbed, alcohol can prevent them from being fully utilized by altering their transport, storage, and excretion. Decreased liver stores of vitamins such as vitamin A, and increased excretion of nutrients such as fat, indicate impaired utilization of nutrients by alcoholics.

Alcohol and Energy Supply

Some alcoholics ingest as much as 50 percent of their total daily calories from alcohol, often neglecting important foods. Even when food intake is adequate, alcohol can impair the mechanisms by which the body controls blood glucose. In non-diabetic alcoholics, increased blood sugar, or hyperglycemia-caused by impaired insulin secretion-is usually temporary and without consequence.

Decreased blood sugar, or hypoglycemia, can cause serious injury even if this condition is short lived. Hypoglycemia can occur when a fasting or malnourished person consumes alcohol. When there is no food to supply energy, stored sugar is depleted, and the products of alcohol metabolism inhibits the formation of glucose from other compounds such as amino acids. As a result, alcohol causes the brain and other body tissue to be deprived of glucose needed for energy and function.

Although alcohol is an energy source, how the body processes and uses the energy from alcohol is more complex than can be explained by a simple calorie conversion value. For example, alcohol provides an average of 20 percent of the calories in the diet of the upper third of drinking Americans,. Chronic drinking triggers an inefficient system of alcohol metabolism, the microsomal ethanol-oxidizing system (MEOS). Much of the energy from MEOS-driven alcohol metabolism is lost as heat rather than used to supply the body with energy.

Alcohol and the maintenance of cell structure and function structure

Because cells are made mostly of protein, and an adequate protein diet is important for maintaining cell structure, especially if cells are being damaged. Research indicates that alcohol affects protein nutrition by causing impaired digestion of proteins to amino acids in the small intestine, and the liver. This interference of amino acid metabolism in the liver compromises all bodily functions.

Vitamins and Minerals

Vitamins

Vitamins are essential in the growth and maintenance of all physiological processes. Chronic heavy drinking is associated with deficiencies in many vitamins (especially the B-vitamins), due to both the decrease in food ingestion, impaired absorption, metabolism, and utilization of all macro and micro-nutrients.

For example, alcohol inhibits fat absorption, which impairs absorption of vitamin E, A and D that are normally along with dietary fats. Vitamin A deficiency is associated with night blindness, and vitamin D deficiency is associated with softening of the bones.

Vitamins A, C, D, E, K, and the B vitamins, also found highly deficient in many alcoholics, are all involved in wound healing and cell maintenance. Vitamin K is necessary for blood clotting, and alcohol related deficiencies can result in delayed clotting, and excessive bleeding. The deficiency of B vitamins associated with alcohol consumption lead to severe neurological damage.

Minerals

Deficiencies of minerals such as calcium, magnesium, iron and zinc are common in alcoholics due to the affect on absorption of these critical minerals/electrolytes.

1. There is a decrease in calcium absorption due to fat malabsorption:
2. Magnesium deficiency due to decreased intake in the diet.
3. Increased Urinary Excretion.
4. Vomiting and Diarrhea
5. Iron deficiency related to Gastrointestinal Bleeding
6. Zinc Malabsorption
7. Mineral deficiencies can cause a variety or medical consequences from calcium-related bone disease to zinc-related night blindness and skin lesions.

Alcohol and Women

There are several considerations when discussing women and alcohol. The first point is:

Woman have lower total water content than men of comparable size. After alcohol is consumed, it diffuses uniformly into all body water, both inside and outside cells. Due to their smaller quantity of body water, women achieve higher concentrations of alcohol in their blood than men after drinking equivalent amounts of alcohol.

Second, diminished activity of alcohol dehydrogenase (the primary enzyme involved in the metabolism of alcohol) in the stomach, which leads to a heightened vulnerability of women to physiological conditions that typically lead to pathological conditions. There is a phenomenon called “first pass metabolism” regarding alcohol breakdown and absorption that takes place in the stomach. This is a defense mechanism that protects the body to some degree from excessive alcohol entering into the system. Due to the decreased amount of the primary enzyme that breaks down alcohol in a woman’s body there is virtually no first pass breakdown in the stomach of alcohol. This results in increased levels of alcohol reaching the system in a woman as opposed to a man.

Third, fluctuations in estrogen hormone levels during the menstrual cycle may affect the rate of alcohol metabolism, making a woman more susceptible to blood alcohol concentrations at different points in the cycle. Chronic alcohol abuse exacts a greater physical toll on women than on men. Female alcoholics have death rates 50 to 100 percent higher than those of male alcoholics. A greater percentage of women die from suicides, alcohol-related accidents, circulatory disorders, and cirrhosis of the liver. Research has found that women develop more cases, with greater severity of liver disease, including cirrhosis and hepatitis after a comparatively shorter period of heavy drinking than men.

Menstrual disorders (painful menstruation, heavy flow, premenstrual discomfort, and irregular or absent cycles) have been associated with chronic and heavy drinking due to a depletion of vital electrolytes (potassium, magnesium, sodium, and calcium). Chronic drinking has been linked strongly to early menopause, and decreased fertility, while increasing the incidence of breast cancer. The increased risk of developing breast cancer was found to be directly related to the amount of alcohol consumed according to studies performed by Longnecker and associates as reported in the Journal of the American Medical Association in 1988.

Conclusion: Free Radical Damage and Alcohol Consumption

Much of the cell damage that occurs during liver degeneration is caused by free radicals, that are highly reactive and destructive molecular fragments liberated during alcohol metabolism. the damage caused by free radicals can include the destruction of essential components of cell membranes. The liver produces natural anti-oxidants (free radical fighters), including the most powerful: Glutathione. The function of GHS (glutathione) and certain vitamins that are taken in the diet (vitamin E, C, and Beta Carotene), which are all anti-oxidants is impaired in alcoholics. Acetaldehyde, the primary metabolic product of alcohol in the liver appears to be a key generator of free radicals. Due to its reactivity, acetaldehyde can promote membrane damage an can stimulate the synthesis of collagen to form scar tissue.

The immune system is affected in many ways from alcohol ingestion, including the breakdown of liver proteins from acetaldehyde. These altered proteins trigger various immune response, including the further depletion of adrenaline, and the release of cortisol (this hormone causes a loss of proteins; including, smooth, cardiac, and skeletal muscle.) Toxins released from cells of the body cause a dramatic release of white blood cells, thereby further weakening the body’s defenses. Please refer to the following comprehensive list of references for further information.

There are many excellent Medical Doctors who have devoted their life to correcting the problems created by alcohol on a cellular level utilizing nutrients, not drugs, in concert with counseling and proper diet.

References; Nutrients & Efficacy in Treatment of Alcoholism

These Studies Discuss Essential Fatty Acids in reducing cravings for alcohol among alcoholics.

1. Essential Fatty Acids and Immunity in Mental Health, Dr. Charles Bates American College of Advancement in Medicine Conference, Washington DC, May, 1990
2. The Major Psychoses and Neuroses as Omega-3 Essential Fatty Acid Deficiency Syndrome: Substrate Pellagra D. Rudin. Biological Psychiatry, vol. 16, No. 9. 1981
3. Glenn I. et al. Possible pharmacological approaches to the prevention and treatment of alcohol-related CNS impairment: Results of a double blind trial of essential fatty acids in G Edwards, J. Littleton, Eds. Pharmacological Treatments for Alcoholism, London, pp. 331-350.,1884.
4. Horrobin,DF, A biochemical basis for alcoholism and alcohol-induced damage including the fetal alcohol syndrome and cirrhosis: Interference with Essential Fatty Acid and Prostaglandin Metabolism. Med.Hypotheses 6:929-42, 1980.
5. Horrobin,DF, Prostaglandin’s and Essential Fatty Acids: A New Approach to the Understanding and Treatment of Alcoholism. Psychiatry in Practice, pp. 19-21.,August, 1984.
6. Seganick DJ, et al. Gamma Linolenic acid inhibits the development of the ethanol-induced fatty liver. Prostaglandin’s Leukotrienes Med., 17:277-82, 1985.
7. Essential Fatty Acids Increase Prostaglandin Production and Decrease Withdrawal Syndrome
8. Wilson, D. et al. Clinical Research 1973; 21:289.
9. Rotroeen J. et al. Life Science. 1980;26: 1867-76.
10. Lee,T.H. et al. Effect of Dietary Enrichment with Eicosapentaenoic and Docosahexaenoic Acids on In Vitro Neutrophil and Monocyte Leukotriene Generation and Neutrophil Function, N. Engl.J. Med., 312, pp.1217-1224, 1985.
11. Fehily, A.M., et al. The Effect of Fatty Acids on Plasma Lipid and Lipoprotein Concentrations Am J. Clin. Nutr., 38, pp. 349-351.,1983.
12. Fats that Heal, Fats that kill, Section Six: New Research-New Fats Fat Finding Missions, Breakthroughs, Applications, Udo Erasmus, 1993.
    These studies discuss GLUTAMINE in reducing cravings in alcohol among alcoholics.
13. GLUTAMINE: Physiology, Biochemistry and Nutrition in Critical Illness, Wiley W. Souba, R.G. Landes Company Austin, 1992.
14. Neuro-Nutrition as an Adjunct to Therapy for Addictive Diseases, J. M. Larson,Ph.D. Health Media of America, June, 1989.
15. A Primer on Neurotransmitters and Cocaine, J. of Psychoactive Drugs, Jul.-Sept., 1988.
16. Strategic Precursor and Co-Factor Loading for Neurotransmitters Depleted by Cocaine Abuse
17. Rogers LL, et al. Quart. J. Studies on Alcohol, 18(4):581-7, 1957
18. Rogers LL. et al. Voluntary alcohol consumption by rats following administration of L-glutamine. J. Biol. Chem. 220(1):321-3, 1956.
19. Werbach,M. MD, Nutritional Influences on Mental Illness, A source book of clinical research. 1991.
20. Kappus H. et al. Lipid peroxidation induced by ethanol and halogenated hydrocarbons in vivo as measured by ethane exhalation, in H Sies & A Wendel Eds. Functions of Glutathione in Liver and Kidney. Berlin, Springer-Verlag, 1978.
21. Volkow, N. et al. et al. Changes in Brain Glucose metabolism in Cocaine Dependence and Withdrawal, Am. J. Psychiatry, 148:5, May 1991.
22. These studies discuss PANTETHINE interaction with acetaldehyde (the primary metabolite of alcohol) among alcoholics.
23. Myer RD. Tetr-hydro-isoquinolines in the brain: The basis of an animal model of addiction. Alcohol Clinical Exp. Res. 2:145, 1978.
24. Cohen G.et al. Alkaloids from catecholamines in adrenal tissue: Possible role in alcoholism. Science 167:1749-51, 1970.
25. Davis VE, et al. Alcohol, amines and alkaloids: a possible biochemical basis for alcohol addiction. Science 167:1005-7, 1970.
26. Watanabe A. et al. Lowering of blood acetaldehyde but not ethanol concentrations by pantethine following alcohol ingestion: Different effects of flushing and nonflushing subjects. Alcoholism (NY) 9(3): 272-76, 1985.
27. Smimuzu et al. A Biochemical Study of Pantethine. Chem. Pharm. Bull. 13(2), 1965.
28. Pantethine, Treatment of Hyper-lipidemia, Clin. Ther., 8:537, 1986.
    These Studies Discuss AMINO ACIDS in reducing cravings in alcoholic’s.
29. Blum K. et al. Enkephalinase Inhibition and Precursor Amino Acid Loading Improves Inpatient Treatment of Alcohol and Polydrug Abusers: double-blind Placebo-Controlled Study of Nutritional Adjunctive Therapy. Alcohol. Vol. 5, pp. 481-493. 1989 (article contains 99 additional references on micro-nutrient therapy in the treatment of alcohol and polydrug abuse).
30. Effects of Taurine on Alcohol Withdrawal, The Lancet, Sept. 1977.
31. Jaffe, R. MD, et al. The Biochemical-Immunology Window: A Molecular view of Psychiatric Case Management, J. Appl. Nutr. Vol. 44(2), 1992.
32. Tyrosine for the Treatment of Depression. Am J. Psychiatry 137:5, May, 1980.
33. Phenylalanine in Affective Disorders. Ad. Biol. Psych. vol. 10. pp. 137-147, 1983.
34. GIBSON C, et al. Tyrosine for the Treatment of Depression. Ad. Bio.Psychiat.10:148-154, 1983.
35. Watanabe, A. et al. Lowering of liver acetaldehyde but not ethanol concentrations by pretreatment with taurine in ethanol-loaded rates. Experientia 41(11): 1421-22, 1985.
36. Ikeda H. Effects of taurine on alcohol withdrawal. Lancet 2:509, 1977.
37. Nasrallah SM, et al. Amino acid therapy of alcoholic hepatitis. Lancet 2:126-7, 1980.
38. These studies discuss VITAMINS in reducing cravings in alcoholics.
39. Baines M. Detection and incidence of B and C vitamin deficiency in alcohol-related illness. Ann. Clin. Biochem. 15:307-12, 1978.
40. Blocker DE et al.. Alcohol reduces folate absorption, Am. J. Clin. Nutr. 46:503, 1987.
41. Cleary JP. Niacinamide and addictions. J. Nutr. Med. 1:83-84, 1990.
42. Lumeng L. The role of acetaldehyde in mediating the deleterious effect of ethanol on pyridoxal 5-phosphate metabolism. J. Clin. Invest. 62:286-93, 1978.
43. Majumdar SK The influence of ethanol on intestinal absorption and utilization of nutrients. Clin. Gastro-enterol. 10(2):263-93, 1981.
44. Sikic BI. et al. Effects of Dietary Ascorbic Acid Supplementation on Hepatic -Metabolizing Enzymes in the Guinea Pig, Bio Pharm. 26:2037-41.,1977.
45. Leo MA, Interaction of ethanol with vitamin A Alcoholism: Clin. Exp. 7:15, 1983.
46. Hoffer, A. Niacin therapy in Psychiatry, Charles Thomas, Springfield, Ill. 1962.
47. Wilson, Bill, The Vitamin B-3 Therapy, A Second Communication to AA Physicians, February, 1968.(containing 55 references world-wide regarding human clinical studies using vitamin therapy in reducing cravings for alcohol).
48. Brown JR., et al. Neurodynamics of Relapse Prevention: A Neuronutrient Approach to Outpatient DUI Offenders. J. Psych. Drugs, vol. 22(2) April-June, 1990.(85 references citing intervention of micro-nutrients in reducing cravings of alcohol among alcoholics.
49. Susick RL et al. Effect of ascorbic acid on the consequences of acute alcohol consumption in humans. Clin. Pharmacol. Ther. 41(5):502-09, 1987.
50. These Studies Discuss Minerals Ability to Reduce Cravings in Alcoholics.
51. O’Brien CC. Experimental evidence in the treatment of alcoholism by intensive calcium therapy. J. Am. Osteopath. Assoc. 51(8):393-94,428, 1952.
52. Flink EB, Magnesium deficiency in alcoholism. Alcoholism (NY) 10(6): 590-94,1986.
53. Pall HS, et al. Hypo-magnesemia causing myopathy and hypocalcemia in an alcoholic. Postgrad Med. J. 63:665-67, 1987.
54. McClain CJ, et al. Zinc deficiency in the alcoholic: A review Alcoholism: Clin. Exp. 7:5, 1983.