Beriberi - Symptoms, Causes, Treatments Beriberi Treatments What is beriberi? Beriberi is a disease caused by a lack of vitamin B1 (thiamine) in the body. Although beriberi can occur in anyone who is poorly nourished, it is very rare in the United States due to the addition of vitamins to many of the foods we eat. The most common cause of beriberi in the United States is alcoholism. Heavy alcohol use can inhibit the body’s ability to absorb thiamine, leading to a deficiency. Rarely, beriberi can be inherited. Inherited beriberi creates a dysfunction in a person’s ability to take up and use thiamine. Beriberi can also sometimes be found in nursing infants whose mothers’ diets are inadequate in thiamine and in formula-fed infants whose formula is inadequate in thiamine. Looking for a Doctor? Search Now Find a Top Neurologist Near You Beriberi generally affects the cardiovascular system (known as wet beriberi) or the nervous system (known as dry beriberi).

Wernicke-Korsakoff syndrome is a brain disorder caused by thiamine deficiency that results in a number of neurologic symptoms and can lead to psychosis, confusion and hallucinations. How HIV Can Affect Your Brain HIV can cause changes in the brain that increase the risk of behavior changes. While many of the symptoms of beriberi are reversible if treated promptly, delayed treatment may result in permanent complications and may become life threatening. Beriberi, as are other vitamin deficiencies, is a serious condition that should be treated promptly. Delayed treatment of beriberi may result in permanent complications or death. If you exhibit symptoms of beriberi, or feel that your diet may be providing inadequate amounts of thiamine, seek prompt medical care. Beriberi: Overview, Causes & Symptoms Read This Next What Is Beriberi? Beriberi is a disease caused by a vitamin B1 (thiamine) deficiency. There are two types of the disease: wet beriberi and dry beriberi. Wet beriberi affects the heart and circulatory system. In extreme cases, wet beriberi can cause heart failure. Dry beriberi damages the nerves and can lead to a loss of muscle strength and eventually, muscle paralysis.

Beriberi can be life-threatening if it isn’t treated. If you have access to foods rich in thiamine, such as beans, vegetables, meat, and whole grains, your chances of developing beriberi are low. Today, beriberi mostly occurs in people with an alcohol use disorder (alcoholism). What Causes Beriberi? Who Is at Risk? The main cause of beriberi is a diet low in thiamine. The disease is very rare in regions with access to vitamin-enriched foods (e.g., breakfast cereals and breads). Beriberi is most common in regions of the world where the diet includes a lot of unenriched white rice, which only has a tenth of the amount of thiamine as brown rice. There are a number of other factors may cause thiamine deficiency as well. These include: Alcohol abuse can make it hard for your body to absorb and store thiamine. Genetic beriberi is a rare condition that prevents the body from absorbing thiamine. Pregnant women, breast-feeding mothers, and anyone with hyperthyroidism (over-active thyroid gland) need extra thiamine.

Prolonged diarrhea or use of diuretics (medication that makes you urinate more) can lead to depletion of thiamine. Infants drinking breast milk or formula low in thiamine are at risk for thiamine deficiency. Kidney dialysis can increase your risk of beriberi by depleting your body’s stores of thiamine more quickly. What Are the Symptoms of Beriberi? The symptoms of beriberi vary depending on the type (wet or dry). The following are symptoms of wet beriberi: shortness of breath during physical activity waking up short of breath rapid heart rate The symptoms of dry beriberi include: decreased muscle function, particularly in the lower legs tingling or loss of feeling in the feet and hands pain involuntary eye movement paralysis In extreme cases, beriberi is associated with Wernicke-Korsakoff syndrome. Wernicke encephalopathy and Korsakoff syndrome are two forms of brain damage caused by thiamine deficiency. Wernicke encephalopathy damages regions of the brain called the thymus and hypothalamus.

This condition can cause confusion, memory loss, loss of muscle coordination, and visual problems such as rapid eye movement and double vision. Korsakoff syndrome is the result of permanent damage to the region of the brain where memories form. This can cause loss of memory, the inability to form new memories, and hallucinations. How Is Beriberi Diagnosed? You will need a series of medical tests to determine whether or not you have beriberi. Blood and urine tests will measure the levels of vitamin B1 or thiamine in your body, specifically erythrocyte transketolase activity. If your body has trouble absorbing thiamine, you will have a low concentration of thiamine in your blood and a high concentration in your urine. Doctors will also perform a neurological exam to look for lack of coordination, difficulty walking, droopy eyelids, and weak reflexes. Later stages of beriberi will show memory loss, confusion, or delusions. A physical exam will alert your doctor to any heart problems. Rapid heartbeat, swelling of the lower legs, and difficulty breathing are all symptoms of beriberi. How Is Beriberi Treated?

While the symptoms can be severe, beriberi is easily treated with thiamine supplements. Your doctor may prescribe a thiamine shot or pill. For severe cases, intravenous thiamine will be administered. Your progress will be monitored with follow-up blood tests to see how well your body is absorbing the vitamin. How to Prevent Beriberi dairy Many breakfast cereals come enriched with 100 percent of your daily thiamine. Pregnant and nursing mothers should be checked regularly for vitamin deficiencies. Infant formulas should also be checked to be sure they contain enough thiamine. Limiting alcohol consumption will reduce your risk of developing beriberi. Anyone who abuses alcohol should be checked routinely for B1 vitamin deficiencies. What Is the Long-Term Outlook for Someone with Beriberi? If beriberi is caught and treated early, the outlook is good. Nerve and heart damage from beriberi is usually reversible when it’s caught in the early stages. Recovery is often quick once you begin treatment. If beriberi is allowed to progress to Wernicke-Korsakoff syndrome, the outlook is poor.

While treatment can control symptoms of Wernicke encephalopathy, brain damage from Korsakoff syndrome is often permanent. Maintaining a healthy, balanced diet is important for your health, so talk to your doctor if you think you are showing signs of a thiamine deficiency or if you need advice on how to get the nutrients you need. Beriberi (Thiamine Deficiency): Background, Pathophysiology, Etiology Overview Background Thiamine deficiency, or beriberi, refers to the lack of thiamine pyrophosphate, the active form of the vitamin known as thiamine (also spelled thiamin), or vitamin B-1 (see the image below). Thiamine pyrophosphate, the biologically active form of thiamine, acts as a coenzyme in carbohydrate metabolism through the decarboxylation of alpha ketoacids. It also takes part in the formation of glucose by acting as a coenzyme for the transketolase in the pentose monophosphate pathway. (See Treatment and Medication.) Beriberi in an adult patient.

See 21 Hidden Clues to Diagnosing Nutritional Deficiencies, a Critical Images slideshow, to help identify clues to conditions associated with malnutrition. Thiamine is a water-soluble vitamin that is absorbed in the jejunum by 2 processes. When the thiamine level in the small intestines is low, an active transport portal is responsible for absorption. When the thiamine concentration is high, a passive mucosal process takes place. Up to 5 mg of thiamine is absorbed through the small intestines. The small intestine is where phosphorylation of thiamine takes place. [ 1 ] The body cannot produce thiamine and can only store up to 30 mg of it in tissues. Thiamine is mostly concentrated in the skeletal muscles. Other organs in which it is found are the brain, heart, liver, and kidneys. The half-life of thiamine is 9-18 days. It is excreted by the kidney.

[ 2 , 3 , 4 , 5 ] Persons may become deficient in thiamine by not ingesting enough vitamin B-1 through the diet or may become deficient through excess use; the latter may result from hyperthyroidism, pregnancy, lactation, or fever. Prolonged diarrhea may impair the body's ability to absorb vitamin B-1, and severe liver disease impairs its use. (See Pathophysiology, Etiology, Presentation, and Workup.) [ 6 , 7 ] Dietary thiamine References Wooley, JA. Characteristics of thiamin and its relevance to the management of heart failure. Nutr Clin Pract. Oct-Nov 2008. 23:487-93. [Medline]. Isselbacher KJ, Braunwald E, Wilson JD. Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994. 474-475. McCormick DB. Shils ME, Young VR, eds. Modern Nutrition in Health and Disease. Philadelphia, Pa: Lea and Febiger; 1988.

355-61. Rosen P, Barkin R. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, Mo: Mosby Year Book; 1998. 2138-40. Thiamine. Monograph. Altern Med Rev. 2003 Feb. 8(1):59-62. [Medline]. Beers MH, Berkow R, Bogin RM, eds. The Merck Manual. 17th ed. Whitehouse Station, NJ: Merck & Co; 1999. 45-6. Cole PD, Kamen BA. "Beriberi" interesting!. J Pediatr Hematol Oncol. 2003 Dec. 25(12):924-6. [Medline]. National Academy of Sciences. Dietary Guidance: Dietary Reference Intake Reports. USDA National Agricultural Library. Available at The National Academies Press. Nutrition - Dietary Reference Intakes: DRIs): Recommended Dietary Allowances and Adequate Intakes, Vitamins. Available at ~/media/Files/Activity Files/Nutrition/DRIs/RDA and AIs_Vitamin and Elements.pdf.

Accessed: July 27, 2011. Karuppagounder SS, Xu H, Pechman D, et al. Translocation of amyloid precursor protein C-terminal fragment(s) to the nucleus precedes neuronal death due to thiamine deficiency-induced mild impairment of oxidative metabolism. Neurochem Res. 2008 Mar 4. [Medline]. Indraccolo U, Gentile G, Pomili G, et al. Thiamine deficiency and beriberi features in a patient with hyperemesis gravidarum. Nutrition. 2005 Sep. 21(9):967-8. [Medline]. Zuccoli G, Gallucci M, Capellades J, et al. Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol. 2007 Aug. 28(7):1328-31. [Medline]. Hazell AS. Astrocytes are a major target in thiamine deficiency and Wernicke's encephalopathy. Neurochem Int. 2009 Jul-Aug.

55(1-3):129-35. [Medline]. Zuccoli G, Pipitone N. Neuroimaging findings in acute Wernicke's encephalopathy: review of the literature. AJR Am J Roentgenol. 2009 Feb. 192(2):501-8. [Medline]. Masumoto K, Esumi G, Teshiba R, et al. Need for thiamine in peripheral parenteral nutrition after abdominal surgery in children. JPEN J Parenter Enteral Nutr. 2009 Jul-Aug. 33(4):417-22. [Medline]. Matrana MR, Davis WE. Vitamin deficiency after gastric bypass surgery: a review. South Med J. October/ 2009. 102:1025-31. [Medline]. Ahmed A, Daida Y, Novotny R. PS2-02: Micronutrient Deficiencies After Bariatric Surgery: Does Ethnicity Matter?. Clin Med Res. 2011 Nov. 9(3-4):165. [Medline].

Francini-Pesenti F, Brocadello F, Manara R, Santelli L, Laroni A, Caregaro L. Wernicke's syndrome during parenteral feeding: not an unusual complication. Nutrition. February 2009. 25:142-6. [Medline]. Braverman LE, Utiger RD. Werner and Ingbar's The Thyroid: A Fundamental and Clinical Text. 7th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1996. 694, 864. Sriram K, Manzanares W, Joseph K. Thiamine in nutrition therapy. Nutr Clin Pract. 2012 Feb. 27(1):41-50. [Medline]. Al-Attas OS, Al-Daghri NM, Alfadda A, Abd Al-Rahman SH, Sabico S. Blood Thiamine and Derivatives as measured by High-Performance Liquid Chromatography: Levels and Associations in DM Patients with Varying Degrees of Microalbuminuria. J Endocrinol Invest. 2011 Nov 22.

[Medline]. Wiesen P, Van Overmeire L, Delanaye P, Dubois B, Preiser JC. Nutrition disorders during acute renal failure and renal replacement therapy. J Parenter Enteral Nutr. March 2011. 35:217-22. [Medline]. Sica DA. Loop diuretic therapy, thiamine balance, and heart failure. Congest Heart Fail. 2007 Jul-Aug. 13(4):244-7. [Medline]. Hanninen SA, Darling PB, Sole MJ, et al. The prevalence of thiamin deficiency in hospitalized patients with congestive heart failure. J Am Coll Cardiol. 2006 Jan 17. 47(2):354-61. [Medline]. Aasheim ET, Bjorkman S, Sovik TT, et al. Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch. Am J Clin Nutr. 2009 Jul. 90(1):15-22. [Medline]. Rao SN, Mani S, Madap K, et al.

High prevalence of infantile encephalitic beriberi with overlapping features of Leigh's disease. J Trop Pediatr. 2008 May 8. [Medline]. Fattal-Valevski A, Azouri-Fattal I, Greenstein YJ, et al. Delayed language development due to infantile thiamine deficiency. Dev Med Child Neurol. 2009 Aug. 51(8):629-34. [Medline]. Weise Prinzo Z, de Benoist B. Meeting the challenges of micronutrient deficiencies in emergency-affected populations. Proc Nutr Soc. 2002 May. 61(2):251-7. [Medline]. Shenoy VV, Patil PV, Nagar VS, et al. Congestive cardiac failure and anemia in a 15-year-old boy. J Postgrad Med. 2005 Jul-Sep. 51(3):225-7. [Medline]. Karaiskos I, Katsarolis I, Stefanis L.

Severe dysphagia as the presenting symptom of Wernicke-Korsakoff syndrome in a non-alcoholic man. Neurol Sci. February 2008. 29:45-6. [Medline]. Isenberg-Grzeda E, Shen MJ, Alici Y, Wills J, Nelson C, Breitbart W. High rate of thiamine deficiency among inpatients with cancer referred for psychiatric consultation: results of a single site prevalence study. Psychooncology. 2016 May 26. [Medline]. Jain A, Mehta R, Al-Ani M, Hill JA, Winchester DE. Determining the Role of Thiamine Deficiency in Systolic Heart Failure: A Meta-Analysis and Systematic Review. J Card Fail. 2015 Dec. 21 (12):1000-7. [Medline]. Angstadt JD, Bodziner RA. Peripheral polyneuropathy from thiamine deficiency following laparoscopic Roux-en-Y gastric bypass. Obes Surg. 2005 Jun-Jul. 15(6):890-2. [Medline].

Koike H, Iijima M, Mori K, et al. Postgastrectomy polyneuropathy with thiamine deficiency is identical to beriberi neuropathy. Nutrition. 2004 Nov-Dec. 20(11-12):961-6. [Medline]. Lu J, Frank EL. Rapid HPLC measurement of thiamine and its phosphate esters in whole blood. Clin Chem. 2008 May. 54(5):901-6. [Medline]. Tran HA. Increased troponin I in "wet" beriberi. J Clin Pathol. 2006 May. 59(5):555. [Medline]. Falder S, Silla R, Phillips M, Rea S, Gurfinkel R, Baur E, et al. Thiamine supplementation increases serum thiamine and reduces pyruvate and lactate levels in burn patients. Burns. 2010 Mar. 36(2):261-9. [Medline]. Donnino M. Gastrointestinal beriberi: a previously unrecognized syndrome. Ann Intern Med.

2004 Dec 7. 141(11):898-9. [Medline]. Media Gallery Beriberi in an adult patient. of 1 Beriberi | definition of beriberi by Medical dictionary Beriberi | definition of beriberi by Medical dictionary Definition Beriberi is a disease caused by a deficiency of thiamine (vitamin B1) that affects many systems of the body, including the muscles, heart, nerves, and digestive system. Beriberi literally means "I can't, I can't" in Singhalese, which reflects the crippling effect it has on its victims. It is common in parts of southeast Asia, where white rice is the main food. In the United States, beriberi is primarily seen in people with chronic alcoholism . Description Beriberi puzzled medical experts for years as it ravaged people of all ages in Asia. Doctors thought it was caused by something in food. Not until the early 1900s did scientists discover that rice bran, the outer covering that was removed to create the polished white rice preferred by Asians, actually contained something that prevented the disease. Thiamine was the first vitamin identified.

In the 1920s, extracts of rice polishings were used to treat the disease. In adults, there are different forms of beriberi, classified according to the body systems most affected. Dry beriberi involves the nervous system; wet beriberi affects the heart and circulation. Both types usually occur in the same patient, with one set of symptoms predominating. A less common form of cardiovascular, or wet beriberi, is known as "shoshin." This condition involves a rapid appearance of symptoms and acute heart failure . It is highly fatal and is known to cause sudden death in young migrant laborers in Asia whose diet consists of white rice. Cerebral beriberi, also known as Wernicke-Korsakoff syndrome, usually occurs in chronic alcoholics and affects the central nervous system (brain and spinal cord). It can be caused by a situation that aggravates a chronic thiamine deficiency, like an alcoholic binge or severe vomiting. Infantile beriberi is seen in breastfed infants of thiamine-deficient mothers, who live in developing nations. Although severe beriberi is uncommon in the United States, less severe thiamine deficiencies do occur.

About 25% of all alcoholics admitted to a hospital in the United States show some evidence of thiamine deficiency. Causes and symptoms Thiamine is one of the B vitamins and plays an important role in energy metabolism and tissue building. It combines with phosphate to form the coenzyme thiamine pyrophosphate (TPP), which is essential in reactions that produce energy from glucose or that convert glucose to fat for storage in the tissues. When there is not enough thiamine in the diet, these basic energy functions are disturbed, leading to problems throughout the body. Special situations, such as an over-active metabolism, prolonged fever , pregnancy, and breastfeeding, can increase the body's thiamine requirements and lead to symptoms of deficiency. Extended periods of diarrhea or chronic liver disease can result in the body's inability to maintain normal levels of many nutrients, including thiamine. Other persons at risk are patients with kidney failure on dialysis and those with severe digestive problems who are unable to absorb nutrients. Alcoholics are susceptible because they may substitute alcohol for food and their frequent intake of alcohol decreases the body's ability to absorb thiamine. The following systems are most affected by beriberi: Gastrointestinal system.

When the cells of the smooth muscles in the digestive system and glands do not get enough energy from glucose, they are unable to produce more glucose from the normal digestion of food. There is a loss of appetite, indigestion , severe constipation , and a lack of hydrochloric acid in the stomach. Nervous System. Glucose is essential for the central nervous system to function normally. Early deficiency symptoms are fatigue , irritability, and poor memory. If the deficiency continues, there is damage to the peripheral nerves that causes loss of sensation and muscle weakness, which is called peripheral neuropathy . The legs are most affected. The toes feel numb and the feet have a burning sensation; the leg muscles become sore and the calf muscles cramp. The individual walks unsteadily and has difficulty getting up from a squatting position. Eventually, the muscles shrink (atrophy) and there is a loss of reflexes in the knees and feet; the feet may hang limp (footdrop). Cardiovascular system. There is a rapid heartbeat and sweating. Eventually the heart muscle weakens. Because the smooth muscle in the blood vessels is affected, the arteries and veins relax, causing swelling, known as edema , in the legs. Musculoskeletal system.

There is widespread muscle pain caused by the lack of TPP in the muscle tissue. Infants who are breastfed by a thiamine-deficient mother usually develop symptoms of deficiency between the second and fourth month of life. They are pale, restless, unable to sleep, prone to diarrhea, and have muscle wasting and edema in their arms and legs. They have a characteristic, sometimes silent, cry and develop heart failure and nerve damage. Diagnosis A physical examination will reveal many of the early symptoms of beriberi, such as fatigue, irritation, nausea, constipation, and poor memory, but the deficiency may be difficult to identify. Information about the individual's diet and general health is also needed. Key terms B vitamins — This family of vitamins consists of thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6), biotin, folic acid (B9), and cobalamin (B12). They are interdependent and involved in converting glucose to energy. Coenzyme — A substance needed by enzymes to produce many of the reactions in energy and protein metabolism in the body.

Edema — An excess accumulation of fluid in the cells and tissues. Enzyme — A protein that acts as a catalyst to produce chemical changes in other substances without being changed themselves. Metabolism — All the physical and chemical changes that take place within an organism. Peripheral neuropathy — A disease affecting the portion of the nervous system outside the brain and spinal chord. One or more nerves can be involved, causing sensory loss, muscle weakness and shrinkage, and decreased reflexes. Thiamine pyrophosphate (TPP) — The coenzyme containing thiamine that is essential in converting glucose to energy. There are many biochemical tests based on thiamine metabolism or the functions of TPP that can detect a thiamine deficiency. Levels of thiamine can be measured in the blood and urine and will be reduced if there is a deficiency. The urine can be collected for 24 hours to measure the level of thiamine excreted. Another reliable test measures the effect of TPP on red blood cell activity since all forms of beriberi affect the metabolism of red blood cells. An electroencephalogram (EEG), which measures electrical activity in the brain, may be done to rule out other causes of neurologic changes.

Observing improvements in the patient after giving thiamine supplements will also confirm the diagnosis. Treatment Treatment with thiamine reverses the deficiency in the body and relieves most of the symptoms. Severe thiamine deficiency is treated with high doses of thiamine given by injection into a muscle (intramuscular) or in a solution that goes into a vein (intravenously) for several days. Then smaller doses can be given either by injection or in pill form until the patient recovers. Usually there are other deficiencies in the B vitamins that will also need treatment. The cardiovascular symptoms of wet beriberi can respond to treatment within a few hours if they are not too severe. Heart failure may require additional treatment with diuretics that help eliminate excess fluid and with heart-strengthening drugs like digitalis. Recovery from peripheral neuropathy and other symptoms of dry beriberi may take longer and patients frequently become discouraged. They should stay active; physical therapy will also help in recovery. Infantile beriberi is treated by giving thiamine to both the infant and the breast feeding mother until levels are normal.

In Wernicke-Korsakoff syndrome, thiamine should be given intravenously or by injection at first because the intestinal absorption of thiamine is probably impaired and the patient is very ill. Most of the symptoms will be relieved by treatment, though there may be residual memory loss. Excess thiamine is excreted by the body in the urine, and negative reactions to too much thiamine are rare. Thiamine is unstable in alkali solutions, so it should not be taken with antacids or barbiturates . Alternative treatment Alternative treatments for beriberi deal first with correcting the thiamine deficiency. As in conventional treatments, alternative treatments for beriberi stress a diet rich in foods that provide thiamine and other B vitamins, such as brown rice, whole grains, raw fruits and vegetables, legumes, seeds, nuts, and yogurt. Drinking more than one glass of liquid with a meal should be avoided, since this may wash out the vitamins before they can be absorbed by the body. Thiamine should be taken daily, with the dose depending on the severity of the disease. Additional supplements of B vitamins, a multivitamin and mineral complex, and Vitamin C are also recommended.

Other alternative therapies may help relieve the person's symptoms after the thiamine deficiency is corrected. Prognosis Beriberi is fatal if not treated and the longer the deficiency exists, the sicker the person becomes. Most of the symptoms can be reversed and full recovery is possible when thiamine levels are returned to normal and maintained with a balanced diet and vitamin supplements as needed. Prevention A balanced diet containing all essential nutrients will prevent a thiamine deficiency and the development of beriberi. People who consume large quantities of junk food like soda, pretzels, chips, candy, and high carbohydrate foods made with unenriched flours may be deficient in thiamine and other vital nutrients. They may need to take vitamin supplements and should improve their diets . Dietary requirements The body's requirements for thiamine are tied to carbohydrate metabolism and expressed in terms of total intake of calories. The current recommended dietary allowances (RDA) are 0.5 mg for every 1000 calories, with a minimum daily intake of 1 mg even for those who eat fewer than 2,000 calories in a day.

The RDA for children and teenagers is the same as for adults: 1.4 mg daily for males over age eleven, and 1.1 mg for females. During pregnancy, an increase to 1.5 mg daily is needed. Because of increased energy needs and the secretion of thiamine in breast milk, breast feeding mothers need 1.5 mg every day. In infants, 0.4 mg is advised. Food sources The best food sources of thiamine are lean pork, beef, liver, brewer's yeast, peas and beans, whole or enriched grains, and breads. The more refined the food, as in white rice, white breads, and some cereals, the lower the thiamine. Many food products are enriched with thiamine, along with riboflavin, niacin, and iron, to prevent dietary deficiency. During the milling process, rice is polished and all the vitamins in the exterior coating of bran are lost. Boiling the rice before husking preserves the vitamins by distributing them throughout the kernel. Food enrichment programs have eliminated beriberi in Japan and the Phillipines. Like all B vitamins, thiamine is water soluble, which means it is easily dissolved in water.

It will leach out during cooking in water and is destroyed by high heat and overcooking. Resources Ryan, Ruth, et al. "Beriberi Unexpected." Psychosomatics May-June 1997: 191-294. beriberi [ber″e-ber´e] an endemic form of polyneuritis due to an unbalanced diet, chiefly a lack of thiamine (vitamin B1). It is more common in areas where refined rice is the main staple in the diet; however, improved refining processes, enrichment and fortification of grain and cereal products, and improved dietary habits have now decreased its incidence. In the United States, mild forms sometimes occur in persons on extremely restricted diets. Alcoholics, who tend to decrease food intake drastically during periods of drinking, may show signs of beriberi. See also alcoholism.

ber·i·ber·i , beri beri (ber'ē-ber'ē), A specific nutritional deficiency syndrome occurring in endemic form in eastern and southern Asia, sporadically in other parts of the world without reference to climate, and sometimes in alcoholic patients, resulting mainly from a dietary deficiency of thiamin; the "dry" form is characterized by a painful polyneuropathy that involves both large and small somatic nerve fibers, as well as autonomic nerve fibers, the initial symptom is burning feet, and later symptoms consist of painful parasthesias in the distal upper limbs as well, weakness and atrophy of the feet and hands, and distal atrophic skin and hair loss; the "wet" form is characterized by edema resulting from a high output form of heart failure, but usually there is evidence of a coexisting polyneuropathy as well.

ber·i·ber·i (ber'ē-ber'ē) A nutritional deficiency syndrome occurring in endemic form in eastern and southern Asia, sporadically in other parts of the world, and sometimes in alcoholic patients, resulting mainly from a dietary deficiency of thiamine; characterized by painful polyneuritis, diarrhea, weight loss, fatigue, poor memory, and edema resulting from a high-output form of heart failure. [Singhalese, extreme weakness] beriberi polyneuritis (distal sensory neuropathy of feet, and later hands) due to chronic dietary thiamine (vitamin B1) deficiency ber·i·ber·i (ber'ē-ber'ē) A specific nutritional deficiency syndrome occurring in endemic form in eastern and southern Asia, sporadically in other parts of the world without reference to climate, and sometimes in alcoholic patients, resulting mainly from a dietary deficiency of thiamin.

[Singhalese, extreme weakness] beriberi (asjike, athiaminosis, endemic multiple neuritis, endemic polyneuritis, hinchazon, inchacao, kakke, loempe, panneuritis endemica, perneiras) (ber´ēber´ē), n a nutritional disease resulting from a deficiency of thiamine. Classically it is characterized by multiple neuritis, muscular atrophy, weakness, cardiovascular changes, and progressive edema. beriberi the name given to thiamin deficiency in humans. See thiamin nutritional deficiency. Beriberi disease - Vitamin B1 deficiency | Nutrition, deficiency & diseases Nutrition, deficiency & diseases Beriberi disease - Vitamin B1 deficiency Jan 2014 Home › Nutritional deficiency › Beriberi disease is due to vitamin B1 deficiency Beriberi is a debilitating disease having devastating effects over almost all the organ systems of the human body. Beriberi disease manifests as neurological disorders, peripheral paralysis, psychosis, weakened heart and impaired circulatory system and results in heart failure and death. Causes for the occurrence of the Beriberi disease Beriberi disease is a disease caused by vitamin B1(thiamine) deficiency.

Primary cause of the disease is malnutrition in the form of reduced intake of essential nutrients by the economically weaker sections of the society. Beriberi disease also occurs in populations who take polished white rice as main staple food. Most of the cereals and grains have vitamin B1(thiamin) available in their outer skin. While refining and polishing them, the vitamin B1 is lost in the husk/bran. Food containing high levels thiaminase like polished rice, raw shellfish, raw freshwater fish, ferns may lead to depletion of thiamine. Betel nuts, tea and coffee which contain anti thiamine factors can cause deficiency of thiamin and beriberi disease. In regions of famine when the available meagre food excludes vitamin B1 sources like whole grains, green vegetables, fruits, legumes and animal sources of food like meat and milk, the whole population may suffer from the deficiency and get affected by Beriberi. In alcoholics due to their careless food habits combined with poor absorption and/or poor utilisation of thiamin Beriberi can occur. Patients who had gastric bypass surgery are predisposed to develop beriberi.

Infants who are milk dependent and are nursed by vitamin B1 deficient mothers develop infantile beriberi. Severe diseases of the liver, chronic diarrhea, long spell of febrile illness, pregnancy and diseases of thyroid glands can lead to vitamin B1 deficiency and beriberi. Patients on dialysis loose thiamine considerably and have the risk of getting beriberi if supplements are not taken. People taking diuretics are under the risk of developing deficiency of vitamin B1, as increased urination causes more loss of thiamine. Impaired digestive system (usually found in elderly persons), celiac disease and tropical sprue can lead to beriberi. Genetic beriberi (a hereditary disease) is a rare condition in which thiamin cannot be absorbed by the body. This condition sets in adults. Symptoms and signs of Beriberi Human body cannot produce vitamin B1. Thiamin being water soluble, in excess is excreted in urine. In the human body vitamin B1 is stored in small quantities in skeletal muscles, heart, kidneys, liver and brain. If thiamine intake is stopped totally, whole thiamin store will be depleted within a month.

Early symptoms are nonspecific like general weakness and fatigue and are followed by weight loss, pain and weakness in extremities, resting tachycardia (abnormally high heart beat rate even in resting condition), disturbed emotions, decreased reflex actions, peripheral neuropathy and edema. These symptoms of beriberi can start occurring just about ten days from the stopping of vitamin B1 intake in healthy persons. Effects of Beriberi disease on health If not treated the end result of beriberi is failure of heart and death. Depending on the prominent body systems affected the terms dry beriberi and wet beriberi are used. In wet beriberi, the circulatory system and the renal system are affected. Initially in wet beriberi vasodilation occurs. This leads to high cardiac output. Renal system responds to this by salt and fluid retention. This in turn leads to edema of the extremities more particularly legs. With the increased fluids the heart has high workload of pumping the increased volume of blood to reach out to all parts. This results in the weakening of heart, heart enlargement, fluids in the lungs, rapid heartbeat and heart muscle injury due to overuse. With the weakening of heart its output gets reduced.

Due to lack of oxygenated blood, cyanosis (blue colouration due to lack of oxygenated blood) of the hands and legs occurs. With poor level of oxygen in the blood heart muscles may stop functioning and heart failure may occur. In dry beriberi disease, which involves the nervous system, damage to the nerves and brain occurs. Treatment for Beriberi The immediate treatment for this disease is thiamine supplements as injections and/or oral tablets.A nutritive diet also should be given. Immediate improvement can be observed in the condition of the beriberi patient after administration of thiamin hydrochloride injections. In the initial stages heart damage is reversible when treated properly. In the later stages even if the life is saved by the treatment, the patient may have to live with impaired heart function. The damage to the nervous system is reversible if treated early. However some effects like poor memory and memory loss may remain. Prevention of Beriberi A balanced diet consisting of both animal and plant sources of food can prevent not only vitamin B1 deficiency caused disease like beriberi, but also all types of vitamin deficiency caused diseases. We should use whole cereals and whole wheat flour, as sufficient thiamin can be obtained from them.

Regular intake of potatoes, oatmeal, oranges, eggs and liver can prevent beriberi in normal healthy person. Alcoholics should give up alcohol and correct their food habits and take food rich in vitamin B1. Pregnant women should take food rich in thiamine and take vitamin B1 supplements as per doctor's advice. Lactating mothers also should take nutritive food and vitamin supplements. When infants are weaned care should be taken to ensure availability of vitamin B1 in the baby food to ward of beriberi disease. Related posts: Beriberi: MedlinePlus Medical Encyclopedia There are two major types of beriberi: Wet beriberi affects the cardiovascular system. Dry beriberi and Wernicke-Korsakoff syndrome affect the nervous system. Beriberi is rare in the United States because most foods are now vitamin enriched. If you eat a normal, healthy diet, you should get enough thiamine. Today, beriberi occurs mostly in patients who abuse alcohol. Drinking heavily can lead to poor nutrition. Excess alcohol makes it harder for the body to absorb and store thiamine. A rare condition known as genetic beriberi is inherited (passed down through families).

People with genetic beriberi lose the ability to absorb thiamine from foods. This can happen slowly over time and symptoms occur when the person is an adult. However, because health care providers may not consider beriberi in nonalcoholics, this diagnosis is often missed. Beriberi can occur in breastfed infants when the mother's body is lacking in thiamine. The condition can also affect infants who are fed unusual formulas that don't have enough thiamine. Getting dialysis and taking high doses of diuretics raise your risk of beriberi. Symptoms Symptoms of dry beriberi include: Difficulty walking The following tests may be done: Blood tests to measure the amount of thiamine in the blood Urine tests to see if thiamine is passing through the urine Treatment The goal of treatment is to replace the thiamine your body is lacking. This is done with thiamine supplements. Thiamine supplements are given through a shot (injection) or taken by mouth. Other types of vitamins may also be recommended. Blood tests may be done after you are given thiamine supplements to see how well you are responding to the medicine.

Outlook (Prognosis) Untreated, beriberi is often deadly. With treatment, symptoms usually improve quickly. Heart damage is usually reversible, and a full recovery is expected. However, if acute heart failure has already occurred, the outlook is poor. Nervous system damage is also reversible, if caught early. If it is not caught early, some symptoms (such as memory loss) may remain even with treatment. If a patient with Wernicke's encephalopathy receives thiamine replacement, language problems, unusual eye movements, and walking difficulties may go away. However, Korsakoff syndrome (or Korsakoff psychosis) tends to develop as Wernicke symptoms go away. Possible Complications Psychosis When to Contact a Medical Professional Beriberi is extremely rare in the United States. However, if you feel your family's diet is inadequate or poorly balanced, and you or your children have any symptoms of beriberi, call your health care provider. Prevention Eating a proper diet that is rich in thiamine and other vitamins will prevent beriberi. Nursing mothers should make sure that their diet contains all vitamins.

When infants are not receiving breast milk, parents need to be sure that their baby's infant formula contains thiamine. People who drink heavily should try to cut down or quit. They should take B vitamins to make sure their body is properly absorbing and storing thiamine. Alternative Names Thiamine deficiency; Vitamin B1 deficiency References Koppel BS. Nutrition and alcohol-related neurologic disorders. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 425. Sachdev HPS, Shah D. Vitamin B complex deficiency and excess. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 46. So YT, Simon RP. Deficiency diseases of the nervous system. In: Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC, eds. Bradley's Neurology in Clinical Practice. 6th ed.

Philadelphia, PA: Elsevier Saunders; 2012:chap 57. Read More Beriberi | Doctor | Patient Beriberi 603 Synonyms: thiamine deficiency, aneurin deficiency, vitamin B1 deficiency Beriberi is caused by deficiency of thiamine, also called aneurin and vitamin B1. This is a water-soluble, heat-labile vitamin that acts as a coenzyme on a number of metabolic pathways. The recommended daily intake is 1.2 mg.[ 1 ] The cardiovascular, muscular, gastrointestinal and nervous systems can be affected. The word 'beri' means weak in Sinhala, a language from Sri Lanka. Beriberi means very weak. Another translation is 'I cannot, I cannot'.[ 2 ] Epidemiology Beriberi was endemic in some areas of the world and may be related to the consumption of milled rice. The process removes the outer crust that contains the vitamin and, in Indonesia especially, the condition was very common. The disease tends to affect adults and infants between 1 and 4 months old.

Improved nutrition, health propaganda and heightened public awareness all contributed to a reduction in prevalence since the 1980s.[ 3 ] Outbreaks occasionally occur in circumstances in which there are dietary restrictions and/or intake of thiamine antagonists.[ 4 ][ 5 ] An outbreak in Israel in 2003 was traced to the use of soy-based milk formula.[ 6 ] Click to find out more » Risk factors In western societies, predisposing factors to thiamine deficiency include gastrointestinal disease and alcoholism, as the latter impairs absorption of the vitamin. Deficiency has been recorded in AIDS, after bariatric surgery and in hyperemesis gravidarum.[ 7 ][ 8 ] It can occur (rarely) after any type of protracted vomiting state. Cases have been reported in which severe vomiting was associated with post-cholecystectomy and suspected Crohn's disease.[ 9 ][ 10 ] Hypermetabolic states also predispose to deficiency and this includes fever , pregnancy, postoperative state, total parenteral nutrition and renal dialysis.[ 11 ] A loop diuretic can also increase the risk.[ 12 ] Presentation Anorexia, nausea, vomiting, abdominal pain.

Later features Paraesthesia, peripheral neuropathy, depressed tendon reflexes, loss of vibration sense. Tender leg muscles and muscle cramps. Congestive heart failure with dyspnoea, orthopnoea and oedema. In infancy, beriberi can present as acute fulminating, acute cardiac, aphonic and pseudomeningitic. In the aphonic form there is hoarseness and a weak cry due to paralysis of the laryngeal nerve. In the pseudomeningitic variety there there are symptoms of nystagmus, vomiting and convulsions but normal cerebrospinal fluid (CSF). Examination Beriberi is often classified as 'dry beriberi' when features are neurological and muscular and 'wet beriberi' when there is predominantly heart failure. Physical findings include: Pallor and waxy skin. Tachycardia, hepatomegaly, cardiomegaly and peripheral oedema. Paraesthesia and peripheral neuropathy, including depressed tendon reflexes. Two conditions caused by thiamine deficiency that are usually related to alcohol abuse in western societies are Wernicke's encephalopathy and Korsakoff's syndrome.

See separate article Wernicke-Korsakoff Syndrome . Diagnosis A high index of suspicion should be maintained for patients with chronic alcohol abuse, special diets and malnutrition. Congestive heart failure may need to be excluded as may other vitamin deficiencies (vitamin B12, niacin) if neurological symptoms are present. Investigations Probably the best diagnostic test is a good clinical response to administration of intravenous thiamine. Another test (performed occasionally as it is expensive) is a thiamine loading test. This involves administering a test dose of thiamine.

In deficient patients the urine excretion of thiamine and thiamine pyrophosphate is lower than normal.[ 13 ] Pre-loading and post-loading whole blood or erythrocyte transketolase activity is also sometimes assessed.[ 14 ] Other tests include blood thiamine level, pyruvate, lactate, alphaketoglutarate and glycosylate.[ 15 ] Thiamine concentration in whole blood can now be measured using high-performance liquid chromatography.[ 16 ] In Wernicke's encephalopathy, the CSF is normal or protein is slightly elevated but, if left untreated, blood pyruvate and blood transketolase will rise.[ 17 ] MRI scan and, to a lesser extent CT, have been used to detect brain changes in Wernicke's encephalopathy.[ 18 ] The electroencephalogram (EEG) may show diffuse slowing.[ 19 ] Echocardiogram should be used to assess heart failure. Management There is often a deficiency of more than one vitamin and so the patient must be carefully monitored as treatment starts.

Thiamine is available in both oral and parenteral form and the latter may be employed at first, with transfer to oral preparations later. However, the Medicines and Healthcare products Regulatory Agency (MHRA) advises that potentially serious allergic adverse reactions may occur during, or shortly after, parenteral administration. They recommend that:[ 20 ] Use be restricted to patients in whom parenteral treatment is essential. Intravenous injections should be administered slowly over 10 minutes. Facilities for treating anaphylaxis should be available. 25-100 mg daily by mouth are recommended for chronic mild deficiency and 200-300 mg daily for more severe deficiency.[ 21 ] Vitamin B deficiency, other than vitamin B12 deficiency, is rare in the UK and should be treated with preparations containing thiamine (B1), riboflavin (B2) and nicotinamide.

Parenteral administration followed by oral treatment are recommended for Wernicke's encephalopathy and Korsakoff's syndrome.[ 21 ] There is usually no need for the usual diuretics and angiotensin-converting enzyme (ACE) inhibitors for heart failure as there is often improvement in 6 to 24 hours and marked improvement in a few days.[ 22 ] However, some patients can go into standard cardiac failure and require input from a cardiologist.[ 23 ] If alcoholism is the underlying problem, a 3-stage approach is required: If alcohol is suddenly stopped, a withdrawal syndrome of delirium tremens may result. A reducing dose of benzodiazepine, usually chlordiazepoxide, should therefore be started during the withdrawal process, the starting dose being dependent upon the level of alcohol consumption. The next stage is to get the patient to admit that there is a problem of alcohol abuse. The final stage is to get the patient to enter into long-term management of the problem. For more information, see separate article Alcoholism and Alcohol Abuse - Management .

Complications The heart failure of beriberi, if untreated, can be fatal.[ 24 ] Anaphalaxis can result from parenteral treatment.[ 20 ] Thiamine deficiency may occur with deficiencies of other B group vitamins which may need treatment in their own right.[ 25 ] Korsakoff's syndrome is considered more fully elsewhere. The essential features are anterograde and retrograde amnesia, often with disorientation and confabulation. The last usually makes the patient delightful but any check of the authenticity of stories will reveal them as confabulation. Wernicke's encephalopathy is also covered elsewhere. Patients are often apathetic and confused. There is ataxia and nystagmus and even coma may result. Prognosis Mortality is rare and is usually associated with the wet form due to cardiac failure.[ 26 ] Morbidity is also rare and usually presents in the dry form with neurological symptoms. In both situations, recognition of the condition and early replacement with thiamine rapidly reverse organ dysfunction.

Korsakoff's syndrome may, however, only be reversible to a small degree.[ 27 ] Prevention[ 28 ] Adults or the families of children need education about the cause of the disease and how to prevent recurrence. In third world countries the child may be discharged back to the same environment. Good dietary sources of thiamine are whole grains, lean pork and legumes. Thiamine is not present in fats, oils and refined sugars and is destroyed by heat, pasteurisation and ionising radiation. Freezing does not affect thiamin content of foods. In developed countries the problem is usually one of the very difficult management of alcohol abuse. If there are other reasons, such as after bariatric surgery, supplements can be continued. History The disease was described by the Chinese around 2700 BC but the cause was unknown. In the 19th century it was realised that the diet needed protein, fat and most of the calories from carbohydrate but it was not until the late 19th and early 20th centuries that the need for other nutrients was appreciated.

Christiaan Eijkman studied prisoners in the Dutch East Indies who were fed a diet of polished rice and he noted a high incidence of neurological disorders.[ 29 ] He also found that either feeding prisoners the whole rice or adding the husk would reverse the disorder. In 1911 Funk confirmed such findings in birds and postulated substances called vital amines, later abbreviated to vitamins.[ 30 ] Beriberi was not uncommon on long naval voyages and was thought to have much in common with scurvy. In 1753 Royal Navy Surgeon James Lind demonstrated that the consumption of fresh lemons and oranges cured scurvy.[ 31 ] He divided twelve sailors into four groups of three to try three treatments and a control group in what was almost the first randomised controlled trial on record. There was a similar naval controlled trial in the early 1880s. A young Japanese medical officer, Kanehiro Takaki, arranged that two ships left Japan on similar voyages but with different diets. The first ship served the usual fare of rice, with some vegetables and fish. The second also served the crew wheat and milk, in addition to more meat than was served on the first ship.

The results were impressive with 25 deaths from beriberi on the first ship and none on the other. The Japanese Admiralty adopted the new diet for the entire navy. In 1926 two biochemists, called Jansen and Donath, isolated a tiny amount of a substance they called aneurin but there was too little to be of much value.[ 32 ] Commercial production did not start until 1937 but it achieved great importance in the 1950s with the demand for the fortification of food. Beriberi Beriberi is a disease in which the body does not have enough thiamine -LRB- vitamin B1 -RRB- . The disease does cause the body to be more sensitive to viruses because of the lack of immune system.

Overview Symptoms of dry beriberi include : Difficulty walkingLoss of feeling -LRB- sensation -RRB- in hands and feetLoss of muscle function or paralysis of the lower legsMental confusion / speech difficultiesPainStrange eye movements -LRB- nystagmus -RRB- TinglingVomitingSymptoms of wet beriberi include : Awakening at night short of breathIncreased heart rateShortness of breath with activitySwelling of the lower legs Can dry eye syndrome cause blepharitis because tear works as antibiotics, but dry eye sufferers lack that tear? Symptoms The goal of treatment is to replace the thiamine your body is lacking . This is done with thiamine supplements . Thiamine supplements are given through a shot -LRB- injection -RRB- or taken by mouth.Other types of vitamins may also be recommended.Blood tests may be done after you are given thiamine supplements to see how well you are responding to the medicine .

Treatment There are two major types of beriberi : Wet beriberi affects the cardiovascular system.Dry beriberi and Wernicke - Korsakoff syndrome affect the nervous system.Beriberi is rare in the United States because most foods are now vitamin - enriched . If you eat a normal , healthy diet you should get enough thiamine . I have low blood counts due to lack of ability to process B-12 and to absorb iron through the normal process of eating food. Today , beriberi occurs mostly in patients who abuse alcohol . Drinking heavily can lead to poor nutrition , and excess alcohol makes it harder for the body to absorb and store thiamine.A rare condition known as genetic beriberi is inherited -LRB- passed down through families -RRB- . People with genetic beriberi lose the ability to absorb thiamine from foods . This can happen slowly over time and symptoms occur when the person is an adult . However , because doctors may not consider beriberi in non - alcoholics , this diagnosis is often missed.Beriberi can occur in breast - fed infants when the mother 's body is lacking in thiamine .

The condition can also affect infants who are fed unusual formulas that do n't have enough thiamine.Getting dialysis and taking high doses of diuretics raise your risk of beriberi . Causes A physical examination may show signs of congestive heart failure , including : Difficulty breathing with neck veins that stick outEnlarged heartFluid in the lungsRapid heartbeatSwelling in both lower legsA person with late - stage beriberi may be confused or have memory loss and delusions . Can anyone suggest any type of vitamins for memory loss or lack of concentration? The person may be less able to sense vibrations.A neurological exam may show signs of : Changes in the walkCoordination problemsDecreased reflexesDrooping of the eyelidsThe following tests may be done : Blood tests to measure the amount of thiamine in the bloodUrine tests to see if thiamine is passing through the urine Tests & diagnosis Untreated , beriberi is often deadly . With treatment , symptoms usually improve quickly.Heart damage is usually reversible , and a full recovery is expected . However , if acute heart failure has already occurred , the outlook is poor.Nervous system damage is also reversible , if caught early .

If it is not caught early , some symptoms -LRB- such as memory loss -RRB- may remain even with treatment.If a patient with Wernicke 's encephalopathy receives thiamine replacement , language problems , unusual eye movements , and walking difficulties may go away . However , Korsakoff syndrome -LRB- or Korsakoff psychosis -RRB- tends to develop as Wernicke 's symptoms go away . Prognosis Eating a proper diet that is rich in thiamine and other vitamins will prevent beriberi . Although present in many foods, the B group vitamins are delicate and easily destroyed, particularly by alcohol and cooking (B vitamins tend to leak into cooking water). but by all means do not take B vitamins individually without taking a good B complex, or a multivitamin with an adaquate amount of the B's, because a B vitamin taken alone can create a deficiency in one of the other B vitamins Nursing mothers should make sure that their diet contains all vitamins and be sure that infant formulas contain thiamine.People who drink heavily should try to cut down or quit , and take B vitamins to make sure their body is properly absorbing and storing thiamine .

A B-complex will generally contain all the B vitamins, not just vitamins B-6 & B-12. Prevention 4 Diseases Caused by a Lack of Essential Vitamins and Minerals | Mental Floss 4 Diseases Caused by a Lack of Essential Vitamins and Minerals Retronaut.com Like us on Facebook Companies pushing products with added vitamins and minerals can fool people into thinking that they’re eating a “healthy” food when they’re not—but it’s not like those vitamins and minerals are there for no reason. For much of human history, diseases of nutrient deficiency were the norm, and in some parts of the world, they still persist. Even into the 20th century, conditions caused by a lack of certain vitamins or minerals were endemic to North America and Europe. Artificially added nutrients may not make a food “healthy,” but they do stave off several debilitating, and sometimes fatal, diseases of malnutrition. Here are a few of those maladies. 1. Scurvy Courtesy of The Diseases of Infancy and Childhood The disease of pirates: the grey-death.

Scurvy is caused by a lack of vitamin C, whose chemical name, ascorbic acid, is derived from the Latin term for scurvy, scorbutus. Even though the disease was known since ancient times (described by Hippocrates around 400 BCE), it was not a scourge to those who were largely land-bound. Even though its causes were unknown, many cultures realized that eating certain herbs could reverse the symptoms, and as long as there was access to fresh food, it was generally kept under control. Scurvy didn’t become a significant problem until the Age of Discovery (beginning in the 15th century), when people at sea were not able to access that much-needed fresh food for months at a time. Preserved meats and carbohydrates contained no vitamin C, and unlike most animals, the human body is not able to create vitamin C on its own. The early symptoms of scurvy include spongy gums, pain in the joints, and blood spots appearing under the skin.

As the disease progressed, the teeth would become loose, extreme halitosis (bad breath) would develop, the afflicted would become too weak to walk or work, be in too much pain to eat, and would die “mid-sentence,” often from a burst blood vessel. Many of the early explorers lost great numbers of men to scurvy : Vasco de Gama lost 116 out of 170 men in 1499, and in 1520, Magellan lost 208 out of 230. A few deaths were attributable to other causes, but the vast majority were due to scurvy. Courtesy of TaussMarine.com Despite not being able to pinpoint the exact cause of scurvy, in the 18th century, Naval physician James Lind was able to prove , in what’s considered to be the first controlled scientific experiment, that scurvy could be prevented (and cured) by incorporating citrus fruits such as limes and oranges into the diet of sailors.

Although his findings weren’t widely accepted at first, the British Navy eventually began issuing standard rations of lemon juice, and later, limes, to their sailors—which gave rise to the term “limey” in reference to the British. These days, scurvy is an extremely rare condition, almost exclusively caused by someone eating a completely unvaried diet . In most cases, high levels of oral supplementation of vitamin C are enough to reverse the condition in a matter of weeks, and death by scurvy is almost unheard of. 2. Rickets Courtesy of Blatner.com This condition is brought on by a lack of vitamin D, which causes the body to be unable to absorb or deposit calcium. Less commonly, it can also be caused by a lack of calcium or phosphorus, but vitamin D deficiency is by far the most common cause. Unlike vitamin C, the human body is able to produce vitamin D, but only if it has the metabolic precursors available to it. When the skin is exposed to ultraviolet light (such as from the sun), cholesterol in the skin reacts and forms cholecalciferol, which is then processed in the liver and kidneys to create the active form of vitamin D.

Even with a nominally healthy diet, without enough sun exposure, the body can’t produce the vitamin D precursors on its own. This is actually re-emerging as a health concern among some increasingly-indoor groups of people, and is one of the few hypovitaminosis (lack of vitamin) conditions not considered to be a “disease of the past.” Luckily, when the deficiency is recognized, cholecalciferol can be directly taken as a vitamin supplement or acquired from eating organ meats and oils, such as cod liver oil, allowing the body to resume producing vitamin D. Rickets is a condition of children, as the deficiency’s most severe effects are on developing bones; in adults, “bone-softening,” or osteomalacia, can be caused by the same vitamin deficiency. But in adults, it both takes significantly longer to develop and tends to cause tip-off signs that something is wrong before bone warping sets in, such as extreme pain in the bones, and unexplained muscle weakness. In children, especially those that don’t or can’t receive regular check-ups, deformity and debilitation by the deficiency is often only noticed after significant damage has been done to their developing skeletons.

The most telling symptoms of rickets are at the epiphyses (growth plates) of bones: The body is unable to lengthen bones by depositing calcium, and ends up with bones that flare outward in a “cupping” appearance. This leads to costochondral swelling, or what’s known as the “rachitic rosary” along the ribcage of the child, as well as widened wrists and “thick” joints. Before widened wrists or rachitic rosary appears, the softening of the skull bones can lead to “Caput Quadratum”—a square-headed appearance, and often the first sign of skeletal growth problems. If left untreated, rickets also can cause an extremely curved back, stunted growth, and frequent fractures—all of which can lead to permanent and debilitating deformity. 3. Beriberi Courtesy of Wikimedia Commons This condition is largely confined to Asia, especially in countries where boiled rice is a staple.

The Sinhalese term “beri-beri” means, “I cannot, I cannot,” and derives from the inability to perform even the simplest of tasks once the polyneuritis (nerve inflammation) caused by the deficiency of vitamin B1 (thiamine) has permanently damaged the neurons, when the condition has progressed to the end-stage. Although beriberi was known to exist in rice-eating countries several centuries back , its prevalence boomed with the introduction of steam-driven rice-polishing mills from Europe. The superior taste of the milled white rice led many locals to abandon the local (unpolished) brown rice, and in doing so, abandon their primary source of thiamine. From the 1860s to the turn of the 20th century, people whose plant consumption was limited to the polished white rice would often come down with weakness, pain, weight loss, difficulty walking, and emotional disturbances. Beriberi became one of the leading causes of mortality in the region.

In the 1880s, a doctor named Christiaan Eijkman began researching the causes of this epidemic at a laboratory in the Dutch East Indies (now Jakarta, Indonesia), and initially believed that the condition was caused by a bacterial infection. However, after years of study, he came to the conclusion that “white rice is poisonous.” He discovered this by feeding a group of chickens solely white rice, and another group unpolished brown rice. The chickens that ate the white rice came down with beriberi-like symptoms, while the others stayed healthy. Eijkman also discovered that when the chickens fed white rice were subsequently fed brown rice, they recovered from their illness! Later dietary testing on prisoners confirmed his results. Even though he didn’t know the cause of the condition, Eijkman proved that white rice was the culprit, and shared the 1929 Nobel Prize in Medicine for his discovery. Beriberi is occasionally seen in the modern world, but its primary cause is chronic alcoholism —the poor diets of some chronic alcoholics, combined with the decreased absorption of what thiamine is consumed, leads to symptoms that unfortunately are sometimes left undiagnosed until it’s too late.

Recently, beriberi was also seen in Haitian prisons , when the prison system began buying imported polished rice from the United States, and stopped feeding their inmates the local brown rice. 4. Pellagra Courtesy of Open Library What causes blistering of the skin in the sun, pale skin, a craving for raw meat, blood dripping from the mouth, aggression, and insanity? If you answered “vampirism,” you’re close—the myth of the vampire may have its roots in the condition known as “pellagra.” Pellagra is caused by a lack of vitamin B3 (niacin). First identified and commonly diagnosed in the Asturian Empire (now Northern Spain), it was originally called “Asturian leprosy.” However, the condition was seen throughout Europe, the Middle East, and North Africa, wherever a large percentage of food energy was derived from corn, and fresh meat was not available. The area of highest prevalence was Northern Italy, where Francesco Frapoli of Milan called it “pelle agra,” meaning “sour skin.” It was initially believed that either the corn itself, or some insect associated with corn, was causing pellagra.

This belief was reinforced when much of France eliminated corn as a food staple and virtually eradicated the condition. Between the era that corn was introduced to Europe (the early 16th century) and the late 19th century, pellagra was found almost everywhere that poor people subsisted on cornmeal and little else. Around the turn of the 20th century, people began to notice that despite subsisting on just as much corn as poor Europeans, poor Mesoamerican natives didn’t come down with the condition. It was eventually discovered that this was because the traditional processing of corn in the Americas involved “ nixtamalization ,” in which the kernels were soaked in limewater before hulling them. The alkali solution freed up the niacin that was present in the grain, but previously inaccessible. Despite the extensive work of Dr. Joseph Goldberger in the 1910s and 1920s , which proved that pellagra wasn’t caused by a germ but by a dietary deficiency, the condition was occurring in epidemic proportions in the rural Southern US until the 1940s.

Today, pellagra is most common in the poorest regions of the world, especially places that rely upon food aid programmes. Some countries still ship unfortified cornmeal rather than corn masa (nixtamalized corn) or fortified cornmeal to developing countries or to their own impoverished populations. China, parts of Africa, Indonesia, and North Korea all have endemic pellagra among their lowest classes. ******* The discovery of important vitamins and how to produce them has been so significant to human health that many of those who were integral to the discoveries have been awarded the Nobel Prize in Medicine; more than 10 Nobel Prizes have been divided among almost 20 eminent scientists for the discovery or isolation of vitamins A, B1, B12, C, D, E, and K. Over the second half of the 20th century, after the beginning of widespread supplementation to everyday food items, the incidences of the conditions covered here went down dramatically across much of the world. Of course, the minerals essential to the human body play similarly important roles in maintaining health. However, humans have not historically had a widespread significant problem acquiring these nutrients, as most plants absorb many minerals from the soil.

With the increased processing of our food throughout the 20th century, however, some of these minerals have been lost, and have had to be re-added to the average Western diet through supplementation. In the rest of the world, displacement due to war, and unfortified food from aid programmes, has left survivors with enough calories, but not enough nutrients. Supplementation of assistance food and local fortification of salt and flour is beginning to help give displaced people (especially displaced children) a new chance at life without these and other nutritional diseases. In the developed world, you won’t be the healthiest bloke on the block if you eat nothing but breakfast cereal and cartons of juice—but the food industry has ensured that you at least won’t die of malnutrition. Even people with healthy diets benefit from the supplementation of vitamins and minerals in common foodstuffs, and adding the nutrients costs next to nothing. Doctors and nutritionists still agree that the healthiest way to acquire your necessary vitamins and minerals is by eating a balanced diet and spending time outdoors each day, but in the course of modern life, that’s not always possible, and if people are going to eat poorly either way, we may as well keep them from dropping dead of scurvy!

beriberi | disease | Britannica.com Beriberi Alternative Titles: thiamine deficiency, vitamin B1 deficiency Related Topics scurvy Beriberi, nutritional disorder caused by a deficiency of thiamin ( vitamin B1 ) and characterized by impairment of the nerves and heart . General symptoms include loss of appetite and overall lassitude, digestive irregularities, and a feeling of numbness and weakness in the limbs and extremities. (The term beriberi is derived from the Sinhalese word meaning “extreme weakness.”) In the form known as dry beriberi , there is a gradual degeneration of the long nerves, first of the legs and then of the arms, with associated atrophy of muscle and loss of reflexes. In wet beriberi , a more acute form, there is edema (overabundance of fluid in the tissues) resulting largely from cardiac failure and poor circulation. In infants breast-fed by mothers who are deficient in thiamin, beriberi may lead to rapidly progressive heart failure . The cardiac symptoms, in both infants and adults, generally respond promptly and dramatically to the administration of thiamin.

When neurological involvement is present, the response to thiamin is much more gradual; in severe cases, the structural lesions of the nerve cells may be irreversible. Thiamin normally plays an essential role as a coenzyme in the metabolism of carbohydrate s; in its absence, pyruvic acid and lactic acid (products of carbohydrate digestion) accumulate in the tissues, where they are believed to be responsible for most of the neurological and cardiac manifestations . nutritional disease: Thiamin Thiamin occurs widely in food but may be lost in the course of processing, particularly in the milling of grains. In East Asian countries, where polished white rice is a dietary staple, beriberi has been a long-standing problem. The history of the recognition, the cause, and the cure of beriberi is dramatic and is well documented in medical literature. In the 1880s the Japanese navy reported that beriberi had been eradicated among its sailors as a result of adding extra meat, fish, and vegetables to their regular diet. Before that time, almost half of the sailors were likely to develop beriberi, and many died of it.

In 1897 Christiaan Eijkman , working in the Dutch East Indies (now Indonesia), found that a beriberi-like disease could be produced in chickens by feeding them a diet of polished rice. British researchers William Fletcher, Henry Fraser, and A.T. Stanton later confirmed that beriberi in humans was also related to the consumption of polished white rice. In 1912 Casimir Funk demonstrated that beriberi-like symptoms induced in pigeons could be cured by feeding them white rice that was supplemented with a concentrate made from rice polishings. Following this discovery he proposed that this, as well as several other conditions, were due to diets that were deficient in specific factors that he called “vitamines,” later called vitamin s. Similar Topics

Question: The disease beriberi is caused by the deficiency of which vitamin?
Answer: B1