During drug de-addiction, it is vital importance to provide adequate nutrition. Malnutrition during drug addiction treatment may hamper proper treatment and it may cause failure or it may take much longer time for drug de-addiction than with proper, adequate and balanced nutrition.

If you are resident of Indiana, you may be aware that drug addiction is pretty common (more common than many other States of US) in Indiana due to easy access of the State for the drug traffickers. Due to high drug addiction, the Drug Rehab in Indiana is also better than many States. There are many Indiana Drug Rehab or Indiana Drug Rehabilitation centers in the State which provide good drug de-addiction treatment and also provide rehabilitation after successful treatment of drug addiction.

There are many Indiana Drug Rehab centers which look after all aspects of successful treatment of drug addiction. If you are a resident of Indiana, you can get all the information about drug addiction treatment online. Most of the Indiana Drug Rehabilitation centers provide treatment for all types of addiction such as treatment of cocaine, heroine, marijuana, alcohol and many more.

Pellagra is traditionally a disease of maize eating regions, where maize is the staple diet and it occurs among poor people as they eat mainly maize and very little else and do not get enough niacin from other food sources (as they consume very little of other foods). That is why pellagra is still prevalent in many maize eating areas of the world where poverty is still predominant.

Although pellagra is predominantly a disease of maize eating regions in some parts of India (like in some segment of Telangana area of Andhra Pradesh State of India) pellagra is reported. In a study it was found that the pellagra in that area is due to consumption of Sorghum vulgare (locally known as jowar) as staple diet and traditionally people are pure vegetarians in the area and do not consume milk or foods of other animal origin. In the study it was found that there is excess of an amino acid leucin in Sorghum vulgare or jowar, which cause imbalance in amino acids and excess leucin interfere with conversion of tryptophan to niacin, thereby causing deficiency of niacin and consequently pellagra results.

What are the symptoms of pellagra?

Pellagra is characterized by Diarrhea, Dermatitis and Dementia (loss of memory or unable to remember), classically known as three D’s. Other symptoms of pellagra includes glossitis (inflammation of the tongue and the tongue becomes enlarged), stomatitis (inflammation of the lips which also becomes enlarged) etc. The dermatitis of pellagra occurs only in those areas or parts of the skin which is exposed to sunlight and generally is symmetrical. The common areas where dermatitis occurs in pellagra are face, hands, legs and the back. Along with dementia, other mental changes like irritability, delirium, depression etc. can occur in pellagra.

Niacin or nicotinic acid belongs to B-complex group of vitamins and is essential vitamin for maintaining optimal health. Niacin is required for metabolism of the major constituents of food namely proteins, fats and carbohydrates. Niacin is also essential for smooth functioning of nervous system, GIT (gastrointestinal system) and also for maintaining normal texture of skin or maintaining skin health.

In which way niacin differs from other B-complex group of vitamins?

Niacin differs from other B-complex group of vitamins in that it is produced from an essential amino acid “tryptophan” which serves as a precursor of niacin (in other words a single chemical step of tryptophan produces niacin). Another way niacin differ from other B-complex group of vitamins is that niacin is not excreted in the urine as such (as niacin), unlike other B-complex group of vitamins which are excreted in urine without undergoing any change. Niacin is excreted in the urine as in two of its major metabolites namely N-methyl-nicotinamide and N-methyl-pyridone.

What are the food sources of niacin?

As mentioned earlier, niacin is produced from essential amino acid tryptophan, so any food source which is rich in tryptophan is a good source of niacin. Food sources which are rich in niacin are liver, meat, kidney, fish, poultry, and legumes, peanuts etc. many of the foods are poor in niacin but are rich in tryptophan and can act as good source of niacin e.g. milk, as milk proteins are rich in niacin. Many cereals and grains (e.g. maize) have niacin in “bound form” and niacin is not available for use and can not act as source despite having good quantity of niacin in bound form.

Niacin is formed from tryptophan with just single chemical step. To produce 1 mg of niacin, approximately 60 mgs of tryptophan is required.

The daily recommended requirement of riboflavin is 0.6 mg per 1000 Kcal of energy intake. If a person is consuming 3000 Kcal of energy per day he/she will require approximately 1.8 mg of riboflavin per day. There is no body store of riboflavin and it has to be consumed daily to prevent deficiency disorders of riboflavin. Vitamin-health is incomplete without recommended intake of riboflavin every day.

Deficiency of riboflavin:

The deficiency of riboflavin is known as “ariboflavinosis”. Deficiency of riboflavin is common in many areas of the world. It is more common, especially in the developing countries where rice is the staple food. The reason is, riboflavin is destroyed during cooking of rice as riboflavin is a water soluble vitamin. Ariboflavinosis is sometimes used as an index of malnutrition (state of nutrition) during clinical survey of malnutrition.

The most common symptom associated with riboflavin deficiency is angular stomatitis (inflammation of angle of the mouth) and this occurs frequently among malnourished children (so used as index of malnutrition in malnutrition surveys). Other clinical signs of riboflavin deficiency are glossitis, nasolabial deformity etc. But these are not specific signs of riboflavin deficiency, unlike angular stomatitis.

In many under developed countries the sub-clinical deficiency of riboflavin (hypo riboflavinosis) is present in as many as 80% of the children among lower income groups. Sub clinical riboflavin deficiency is determined by a test known as “erythrocyte glutathione reductase activation test”. Hyporiboflavinosis do not incapacitate the child even if it is very severe, but it can cause many problems of function, especially neurological functions like impaired neuromotor function, impaired wound healing and increased susceptibility to develop cataract (possibly).

Deficiency of riboflavin generally occurs along with deficiency of other B-complex group of vitamins and presents as a part of multiple vitamin deficiency syndrome. But fortunately deficiency of riboflavin is becoming uncommon even in developing countries due to diversification of diet.

Riboflavin is the second among B complex group of vitamins to be identified and so named as vitamin B₂. The main use of riboflavin is in cellular oxidation. Riboflavin also plays a very important role in maintaining the structural integrity of the mucosal layers of the body. In the energy metabolism Riboflavin plays as a co-factor with many enzymes and is essential in maintaining vitamin-health of individuals.

Richest food sources of Riboflavin:

Among plant and animal foods the richest sources of Riboflavin are green leafy vegetables, eggs, liver, milk and kidneys.

Plant sources of Riboflavin:

Riboflavin is widely distributed in the plant kingdom. But some of the plant foods are particularly rich in Riboflavin like green leafy vegetables. Other plant sources of Riboflavin are different cereals (whole as well as milled, unlike thiamin which is present mainly in whole cereals and very less in milled cereals). Pulses are not very rich source, but it can be important source if consumed in larger quantity, as is seen in countries like India and other south Asian countries. The Riboflavin contents of pulses can be increased significantly by germination. For germination pulses (with husk) are soaked in water for approximately 24 hours and cooked after that. Excess cooking can cause loss of riboflavin in the foods.

Animal (meat) sources of Riboflavin:

Many animal foods are rich in Riboflavin. Examples of rich animal sources of Riboflavin are all type of meat, eggs (especially hens egg), liver (especially sheep liver), milk (especially cow’s milk) etc.

Thiamin (vitamin B₁) deficiency is more common among rice eating population, where highly polished rice is eaten. The most of the thiamin in rice is present in the outermost layer of rice, which is removed during milling of rice and large portion of the vitamin is also lost during cooking (because thiamin is water soluble vitamin and destroyed during heating).

Thiamin (vitamin B₁) deficiency mainly causes two types of deficiency disorders beriberi and Wernick’s encephalopathy. Beriberi mainly occurs in three forms namely dry beriberi, wet beriberi and infantile beriberi.

Dry beriberi:

The manifestations of dry beriberi are mainly of nerve involvement like peripheral neuritis. Nutritional replacement of thiamin can solve the problem of peripheral neuritis.

Wet beriberi:

The manifestations of wet beriberi are mainly of cardiac type and it is also known as cardiac beriberi.

Infantile beriberi:

Infantile beriberi is mainly seen in infants of 2-4 months of age. The baby who suffers from infantile beriberi is generally fed by thiamin deficient mother. The mother generally shows signs of peripheral neuropathy (neuritis).

Wernick’s encephalopathy:

This is most commonly seen in chronic alcoholics who have many other nutritional deficiencies. The characteristics of Wernick’s encephalopathy are mental deterioration, polyneuritis, ophthalmoplegia, and ataxia. Wernick’s encephalopathy can also occurs in persons on fasting.

]]> http://nutritionnhealth.net/deficiency-disorders-of-thiamin/feed/ http://nutritionnhealth.net/prevention-of-thiamin-b1-deficiency/ http://nutritionnhealth.net/prevention-of-thiamin-b1-deficiency/#comments Tue, 18 Aug 2009 12:28:32 +0000 drjupitor http://nutritionnhealth.net/?p=187 Deficiency of vitamin B₁ (thiamin) can cause two major deficiency disorders in humans, beriberi and Wernick’s encephalopathy. That is why it is very important to prevent deficiency of thiamin and prevent the deficiency disorders. The prevention of deficiency of thiamin is not difficult, it can be done by educating people about the deficiency disorders and how to prevent them.

Recommended daily allowance of thiamin:

The requirement of thiamin is not fixed like many other vitamins. The requirement of thiamin is based on the number of calorie intake per day and it is approximately 0.5 mg per thousand kilo calorie (Kcal) of food intake per day (if a person is consuming 2000 Kcal per day he/she need 1 mg of thiamin in diet). The body storage of thiamin is approximately 30 mg and if more thiamin is consumed, it is lost in the urine (as thiamin is a water soluble vitamin).

Prevention of thiamin deficiency:

Thiamin deficiency disorders (beriberi and Wernick’s encephalopathy) can be eliminated by educating people (wherever it is prevalent) to take balanced, mixed diet with rich thiamin foods. In rice eating regions rice should be undermilled and preferably parboiled (undermilling and parboiling prevents loss of thiamin from rice). Alcohol consumption should be stopped (reduced). Food rich in thiamin are fresh vegetables, gram, yeast, legumes, pulses etc. and should be consumed in liberal amounts.

Direct thiamin supplementation to particular groups like pregnant and lactating women is another approach to prevent thiamin deficiency. In general thiamin deficiency disappears if economic condition improves due to intake of variety of foods.

Special cases like patients on dialysis should be given thiamin on routine basis and also it should be given to persons who are on fast for long duration, suffering from persistent vomiting and are on prolonged gastric aspiration for some medical condition.

In most of the developed western countries the causes of deficiency of thiamin are alcoholism and chronic illness like cancer. Alcohol directly interferes with the absorption of thiamin and also with formation of thiamin pyrophosphate. Thiamin should always be replenished when re-feeding a patient with alcoholism. Carbohydrate repletion in a patient with alcoholism without adequate thiamine can precipitate acute thiamine deficiency (because the thiamin present will be utilized for metabolism of carbohydrate). Pregnant women with prolonged hyperemesis gravidarum (excess vomiting during pregnancy) and anorexia can also develop thiamin deficiency. Patients with an overall poor nutritional status (parenteral glucose), and patients on chronic diuretic therapy due to increased urinary thiamine losses are at risk of developing of thiamin deficiency. Maternal thiamine deficiency can lead to infantile deficiency (infantile beriberi) in breastfed children. Thiamine deficiency should also be considered in the setting of motor vehicle accidents associated with head injury.

In areas where rice is staple food there may be thiamin deficiency (thiamin is lost during milling, washing and cooking, as thiamin is a water soluble vitamin). This is the reason for advising people to eat under-milled rice and also eat parboiled rice (parboiling of rice is a process to preserve B-complex group of vitamins in rice, where paddy is heated in a big container at controlled manner and allowing the B-complex vitamins to penetrate to inner side of the rice as the B-complex vitamins are present in the outer aspect of rice, which is lost during milling it).

Thiamin is also lost from fruits during prolonged storage and also during toasting and if baking soda is used during preparing food. So the local custom and tradition of food habit is an important factor in the causation of deficiency of thiamin.

Thiamin is the first among B complex group of vitamins to be identified and so named as vitamin B₁. All the B complex vitamins are water soluble vitamins including thiamin. Thiamin is essential in the metabolism and utilization of carbohydrates. It functions in the decarboxylation of alpha-ketoacids, like pyruvate alpha-ketoglutarate, and branched chain amino acids and is a source of energy generation. Thiamine pyrophosphate (TPP) acts as a coenzyme of carboxylase enzyme that causes activation of transketolase that mediates the conversion of hexose (like glucose with six carbon) and pentose (five carbon carbohydrates) phosphates. In thiamin deficiency there is accumulation of lactic acid and pyruvic acid in tissues and also in body fluids. Thiamin has also been postulated to play a role in peripheral nerve conduction, although the exact chemical reactions underlying this function are unknown.

Food Sources of Thiamin:

Thiamin is present in many food sources (both plant and animal sources) in nature in abundance. The vegetable or plant food sources of thiamin are whole grain cereals (wheat, maize, rice etc. although milling of rice removes considerable quantity of thiamin and other B complex vitamins from rice and can be commonest cause of thiamin deficiency in predominantly rice eating cultures), gram, yeast, legumes, pulses, nuts and oilseeds (groundnut or peanut), and many different fruits though fruits contains comparatively lesser quantity of thiamin. The animal food sources of thiamin are pork, beef, organ meat, fish, eggs, milk etc. Milk is an important source of thiamin in infants if the mother’s thiamin level in blood is satisfactory. In poor and underdeveloped countries the main source of thiamin is generally the cereal or whole grain (rice, wheat or maize, depending on the dietary habit).

Coffee, both regular and decaffeinated; tea, raw fish, shellfish, contain thiaminases an enzyme which can destroy thiamin and theoretically can cause thiamin deficiency or deplete thiamin stores in heavy tea or coffee drinkers.

Deficiency of vitamin K:

Deficiency of vitamin K is mostly seen in infants. In adults the deficiency of vitamin K is not common. The causes of vitamin K deficiency in infants and adults are different.

In adults the deficiency of vitamin K is mainly due to chronic small intestinal disease like celiac disease, Crohn’s disease, in patients with obstruction of biliary tract or due to resection of small intestine. Treatment with broad spectrum antibiotics like tetracycline, chloramphenicol etc. can lead to aggravation of vitamin K deficiency by reducing the intestinal flora which synthesize menaquinones, and by inhibiting the metabolism of vitamin K. In patients with warfarin (an anti coagulant) therapy, the hypoloipidemic drug Orlistat can lead to INR (international normalized ratio) changes due to vitamin K mal absorption.

The diagnosis of vitamin K deficiency is usually made on the basis of an increased prothrombin time, reduced clotting factors and also by directly measuring vitamin K level in blood.

Treatment of vitamin K deficiency:

Vitamin K deficiency is treated by administering 10 mg of vitamin K parenteral dose. Patients of chronic mal absorption should receive oral dose of 1–2 mg/day of vitamin K or 1-2 mg parenteral dose of vitamin K every week. Patients with liver disease may have an elevated prothrombin time because of liver cell destruction as well as vitamin K deficiency. So if an elevated prothrombin time does not improve on vitamin K therapy, it can be said that it is not due to vitamin K deficiency.

In infants the deficiency of vitamin K is usually due to loss of blood, low fat stores and liver immaturity (both are stores of vitamin K); low breast milk levels (15 mcg/liter) of vitamin K, sterility of the infantile intestinal tract and no or very small number of intestinal flora which synthesize menaquinones, and poor placental transport.

Deficiency of vitamin K in infants can lead to intracranial bleeding, gastrointestinal bleeding and skin bleeding in 1–7 days after birth. To prevent these problems infants should be administered vitamin K (1 mg IM) prophylaxis at the time of delivery.

Toxicity of vitamin K:

Vitamin K toxicity is not seen due to excess dietary consumption of vitamin K (phylloquinones and menaquinones). But high doses of vitamin K can impair the actions of oral anticoagulants like warfarin.