Guide to Nutrition

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.

There are two natural forms of vitamin K and they are vitamin K₁ and vitamin K₂. Vitamin K₁ is also known as phylloquinone and vitamin K₂ is also known as menaquinone. Phylloquinone can be converted to menaquinone in some organs in humans.

Sources of vitamin K₁:

Vitamin K₁ is found mainly in the dark green leafy vegetables like kale and spinach. Vitamin K is present in vegetable oils also and it is particularly rich in olive, canola, and soybean oils. Margarine and liver also contain good quantity of vitamin K₁. Cow’s milk (60 mcg/liter) is a richer source of Vitamin K than human milk (15 mcg/liter).

Vitamin K₂ is synthesized in the intestines by intestinal flora (bacteria), which can usually supply adequate quantity of vitamin K in humans. Vitamin K is stored in liver and adipose tissues (fat store) in humans. If antibiotics are taken for long term (usually more than a week), it can suppress the normal intestinal flora that are sources of vitamin K₂ and can cause deficiency of vitamin K.

Vitamin K is required to stimulate the production and release of certain blood coagulation factors. Vitamin K is required for the posttranslational carboxylation of glutamic acid, which is must for calcium binding to alpha-carboxylated proteins such as prothrombin (blood coagulation factor II), factors VII, IX, and X. in vitamin K deficiency the prothrombin content of blood is reduced and the blood coagulation time is prolonged considerably.

Recommended daily allowance (RDA) of vitamin K: The recommended daily allowance of vitamin K in humans is approximately 100 mcg (micro gram) per day. This RDA is generally met in humans by combination of dietary sources and microbial synthesis in intestine by intestinal flora.

Infants usually have lower level of vitamin K, due to non establishment of intestinal flora, low breast milk (15 mcg/liter) levels of vitamin K, liver immaturity, poor placental transport and also due to low fat content where vitamin K is stored.

There is no clearly known deficiency disorder of vitamin E. But there is also no doubt that humans need tocopherol or vitamin E in his diet. The deficiency of vitamin E is seen only after resection of small intestine and in prolonged malabsorptive diseases, like celiac disease. There is also a very rare familial form of vitamin E deficiency disease, which is due to defect in  alpha tocopherol transport protein.

Children may develop vitamin E deficiency due to prolonged cholestasis (stasis of bile) or cystic fibrosis of long duration and this is characterized by hemolytic anemia and areflexia. If children suffer from abetalipoproteinemia, they develop vitamin E deficiency very rapidly as they can not absorb or transport vitamin E.

Symptoms of Vitamin E Deficiency:

Vitamin E deficiency causes degeneration of large myelinated axons. Peripheral neuropathy is also a major sign which is characterized by at first areflexia that progresses to ataxic gait and decrease in position and vibration sensation. Pigmented retinopathy, ophthalmoplegia and skeletal myopathy are some other symptoms of vitamin E deficiency. Deficiency of vitamin E increases virulence of viral infection due to increase in viral mutation.

Diagnosis of Vitamin E Deficiency:

Laboratory diagnosis of vitamin E deficiency is done by measuring the blood levels of alpha tocopherols. Vitamin E deficiency is if the level of alpha tocopherol is less than 5µgm/ml or alpha tocopherol is less than 0.8 mg per gram of total lipids.

Vitamin E Toxicity:

High dose of vitamin E (more than 800 mg per day) daily can cause vitamin E toxicity. All forms of vitamin E can cause toxicity. High dose of vitamin E can interfere with vitamin K metabolism and high dose is contraindicated if a patient is taking anticoagulant like warfarin. The symptoms of vitamin E toxicity are diarrhea, nausea, flatulence etc. if the daily intake is more than 1 gram.

Treatment of Vitamin E Deficiency:

Treatment of vitamin E deficiency depends on the severity and type of deficiency. Moderate deficiency with symptoms can be treated with 800-1200 mg of alpha tocopherol per day (RDA is about 15 mg per day). If deficiency is due to abetalipoproteinemia, than as much as 5000-7000 mg per day may be required. Children with symptomatic vitamin E deficiency can be treated with 400 mg/day of water-miscible (which can be mixed with water by adding an emulsifying agent) esters.