Good Nutrition Nutrition and Nutrients

Nutrition Notes

B Vitamins

The B vitamins are coenzymes - molecules that combine with an inactive protein to make it an active enzyme. The B vitamins work help release energy from the three energy nutrients: carbohydrate, fat, and protein. B vitamins help to manufacture red blood cells, which carry oxygen to the tissues requiring it for the release of energy. Unlike the fat-soluble vitamins, the water-soluble ones are generally absorbed directly from the intestine into the blood. Because they are water soluble, they are easily excreted in the urine.

Vitamin B1 Thiamin

Thiamin acts as a coenzyme in the pathways that release energy from carbohydrate.Deficiency Disease- Beriberi. RDA 0.40 mg/1000 kcal (0.48 mg/5000 kJ. Supplement Recommendation 2 - 50 mg per day.

Symptoms: nausea, exhaustion, loss of appetite, tenderness in the calf muscles, leading to emaciation, loss of control of the limbs, and abnormal heart action; first observed in the Far East when polishing rice became common - thiamin was present in the rice husk but not the kernel. Locally, deficiency is most often associated with alcoholism. During starvation or semi-starvation, tissue stores of thiamin are rapidly depleted. The requirement for thiamin was found to be proportional to the intake of energy. The mean daily intake for adults should not go below 0.8 mg per day, even if energy intake falls below 2000 kcal (8400 kJ) per day.

Thiamin deficiency may contribute to the development of delirium, heart failure and peripheral neuropathy in elderly patients; according to one study thiamin deficiency is common in elderly patients admitted to hospital and may contribute to the development of delirium.

Thornalley et al studied thiamine levels in 26 type 1 diabetics, 48 type 2 diabetics, and 20 healthy controls. Thiamine concentration was decreased 76% in type 1 diabetics and 75% in type 2 diabetics. Renal clearance of thiamine was increased 24 times in type 1 diabetics and 16 times in type 2 diabetics. Thornalley suggested a link between thiamine deficiency and the vascular complications of diabetes. In another study, type 2 diabetics were given 300 milligrams of vitamin B1 (thiamine) each day for three months. The vitamin supplement reduced the rate of albumin excretion by 41%; 35% of patients with microalbuminuria returned to normal after being treated with the vitamin. Increasing thiamine intake is a safe and prudent precaution.

Thiamin deficiency may occur in long-term alcohol users as a consequence of both inadequate ingestion and malabsorption of the vitamin. With severe deficiency, major brain disturbances and an alcoholic psychosis emerge (Wernicke-Korsakoff syndrome). The brain dysfunction is global, with disordered thinking, feeling, remembering, and disturbed motor coordination. Thiamin replacement corrects the grosser dysfunctions of the brain and it has been proposed that alcoholic beverages be fortified with thiamin as a means of preventing this syndrome.

Vitamin B2 Riboflavin

Deficiency Disease- Mouth-tongue syndrome

RDA - 0.5 mg/1000 kcal (0.6 mg/5000 kJ

Supplement Recommendation 0.5 to 10 mg/day

Riboflavin acts as a coenzyme in energy-releasing reactions in tissue respiration and oxidation and helps prepare fatty acids and amino acids for breakdown. A deficiency of riboflavin is characterized by a variety of symptoms including soreness of the tongue and lips, painful cracks at the corners of the mouth, a red swollen tongue, and teary or bloodshot eyes.

Signs of riboflavin deficiency have been recorded in adults on diets providing 0.5 mg or less of riboflavin daily. Urinary riboflavin excretion increases sharply if riboflavin intakes rise above 1.1 to 1.2 mg. In pregnant and lactating women, it is suggested that an intake of at least 0.9 mg of riboflavin daily is required. Riboflavin is unevenly distributed among the food groups. Meat and generous servings of dark-green leafy vegetables provide some riboflavin. Riboflavin is light sensitive and can be destroyed by the ultraviolet rays of the sun or by fluorescent light.

Vitamin B3 Niacin

Deficiency Disease - Pellagra.

RDA 7.2 NE/1000 kcal (8.6 NE/5000 kJ).

Supplement Recommendation 25 - 100 mg niacinamide

Daily Dose 25 mg niacinamide 1-4 times/day

Overdose: >4000 mg/day

Niacin is the generic term for nicotinic acid - related forms of niacin include nicotinamide and niacinamide. Pellagra is characterized by disturbances of body tissues most dependent on glucose for energy. Symptoms include weakness of muscles, loss of appetite, lethargy, and digestive upsets such as diarrhea. In later stages, dark blotches appears on parts of the body exposed to the sun, and mental confusion develops, including loss of memory. These symptoms are the "three D's" of pellagra: diarrhea, dermatitis, and dementia. Pellagra, or niacin deficiency, is common in chronic alcoholics.

Trytophan is converted to niacin in the body. About 3% of ingested tryptophan is converted; 60 mg of tryptophan provides 1 mg of niacin: one niacin equivalent equals 1 mg of niacin or 60 mg of tryptophan. The recommended intake in adults is based on the average amount of niacin required to produce an increase in the urinary excretion of niacin metabolites.

Nicotinic acid (niacin) has been used for almost 50 years as a lipid-lowering drug using higher doses than are provided by diet.Niacin decreases lipolysis in adipose tissue by inhibiting hormone-sensitive triglyceride lipase. The use of megadoses of niacin (More than 4000 mg/day) may produce toxic effects such as liver damage with jaundice, skin rashes, peptic ulcers, and elevated serum levels of glucose, uric acid and liver enzymes.

The main sources of niacin in the diet are meat, legumes, peanuts, beans and peas, and whole grain or enriched cereals or bread.

Vitamin B6; Pyridoxine

Deficiency Diseases- Seizures, Mouth-Tongue Syndrome, Impaired Immunity, AnemiaRDA 2.0 mgSupplement Recommendation 10 to 100 mg per day Overdose: >500 mg

Vitamin B6 has three forms - pyridoxine, pyridoxal, and pyridoxamine As pyridoxal phosphate and pyridoxamine phosphate, vitamin B6 acts as a cofactor for over 60 enzymes that catalyze many biochemical pathways involving amino acids, especially the synthesis of nonessential amino acids. Vitamin B6 helps remove amine groups from amino acids to be used for energy. As a coenzyme, it aids in the conversion of the amino acid tryptophan to the vitamin niacin. It also helps convert the essential fatty acid, linoleic acid to other fatty acids. It plays a role in the synthesis of hemoglobin and the secretions of the adrenal glands. It is also part of the enzyme that releases glucose from stored glycogen and is therefore important for maintaining blood glucose levels.Vitamin B6 is widely distributed in small amounts throughout nature. Pyridoxal phosphate and pyridoxamine phosphate are found in animal products, while pyridoxine is found mainly in plant foods. Vitamin B6 is absorbed better from animal than from plant sources. Cooking may reduce B6 content by 25% to 30%. Some drugs interfere with B6 metabolism (isoniazid, clycloserine, penicillamine) Pyridoxine metabolism is disturbed in alcoholics.

B6 deficiency symptoms included lesions around the eyes, nose and mouth, cheilosis (fissuring and scaling at the angle of the mouth), glossitis (inflammation of the tongue), and stomatitis (inflammation of the oral mucosa), weight loss, apathy, increased irritability, impaired antibody response, and hypochromic microcytic anemia, a result of decreased hemoglobin biosynthesis. Deficiency symptoms clear rapidly after pyridoxine is administered. Prolonged excessive intake of vitamin B6 at 500 mg to 6000 mg/day causes a sensory neuropathy with loss of sensation in the extremities and impairment of position and vibration sense. Impaired memory has also been noted at intakes greater than 100 mg/day. The requirement for vitamin B6 is related to the dietary intake of protein. For adults, it is suggested that a ratio of 0.015 mg/g dietary protein should be sufficient. High protein intake is usually derived from animal sources, which are also rich in vitamin B6.

Vitamin B12 - Cobalamin

Deficiency Disease- Pernicious Anemia, Subacute Combined Degeneration RDA2 ug/day:Supplement Recommendation 1-400 ug/day orally. Treatment of deficiency: 1000 ug/day by mouth

Vitamin B12 is not available in plant foods and must be supplemented to complete a strict vegetarian diet. Deficiency results from low intake levels and malabsorption that becomes increasingly common with age. High doses of Vitamin C (>500 mg per day) can interfere with B12 absorption. Absorption requires a carrier protein, intrinsic factor, which is produced in the stomach. Vitamin B12 deficiency syndrome is characterized by five stages, the fifth of which results in irreversible damage to the brain and spinal cord. Earlier signs of deficiency disease involve nervous system symptoms: numbness and tingling in arms and legs and loss of coordination. Decline of cognitive function, especially in the elderly, should always suggest B12 deficiency. The end-stage disease of B12 deficiency is pernicious anemia with disabling and permanent degeneration of sensory circuits in the spinal cord.

According to Savage et al: Neuropsychiatric syndromes occur in about 40% of B12-deficient patients and are characterized by progressive and variable damage to the spinal cord, peripheral nerves and cerebrum. The first abnormality is usually sensory impairment, most often presenting as distal and symmetrical paraesthesiae of the lower limbs and frequently associated with ataxia. Almost all patients demonstrate loss of vibratory sensation, often in association with diminished proprioception and cutaneous sensation and a Romberg sign. Corticospinal tract involvement is common in more advanced cases, with abnormal reflexes, motor impairment and, ultimately, spastic paraparesis. Patients can exhibit mental or psychiatric disturbances or autonomic signs. Diagnosis of Cbl neuropathy can usually be made in the presence of the typical neuropsychiatric abnormalities, a low serum Cbl level and evidence of megaloblastic haemopoiesis.”

Blood values of the vitamin should be above 200 pg/ml. When there is doubt about the adequacy of B12 levels, measurement of metabolites can be helpful; urine levels of methylmalonic acid and homocysteine rise significantly when the functional level of B12 is inadequate. Vitamin B12 deficiency may be underestimated: high-risk groups include the elderly, vegetarians, alcoholics, patients on ulcer therapy or who have had stomach or small bowel resection and patients with dementia.

Deficiency is easily treated with monthly injections, large doses of daily oral supplements or an intranasal gel, which is better absorbed than oral supplements. The response to treatment may be slow in patients with neurological damage. Some improvement usually occurs within the first 3 months, and further improvement may occur over the next year. Patients with advanced disease may be left with residual disability. Folic acid prevents and reverse the anemia of B12 deficiency but does not prevent neurological damage.