This is a quick reference of the water and fat soluble vitamins that was compliled in preparation for the National Boards in 1997. This information is based on class notes and the bible of physiology, Guyton. I hope I have noted the references appropriately. If there are have been any revalations in the field of vitamin biochemistry in the last ten years, I ask you to e-mail me with the information and reference. Accuracy in the public record is important to me.
The B Complex:
Thiamine: B1, thiamine hydrochloride. Thiamine pyrophosphate (TPP) is the active form of B1, is a coenzyme and has an AKA of cocarboxylase. Essential for the metabolism of carbohydrates and some amino acids. If no B1---pyruvate does not get converted to Acetyl CoA (in the pyruvate dehydrogenase complex) , which means no carbohydrate fuel for the Krebb's cycle causing significantly decreased ATP production and an impaired pentose phosphate pathway. Thiamine deficiency results in decreased metabolism of carbohydrates and an increased utilization of fats. The central nervous system (CNS) normally gets all its energy from carbohydrate metabolism. (class notes, Guyton p. 783)
Daily requirement: 0.5mg per 1000 kcals of food intake (RDA: 1.5 mg). Sources: Best: dry yeast and wheat germ. Also found in seeds, nuts, legumes, most vegetables, and some meats (pork, livers, hearts, kidneys, muscle, eggs). B1 is heat stabile.
Deficiencies: (decr. energy ATP) Wet and Dry beriberi is the name given to the manifestations of chronic B1 deficiency. Moderate deficiency will detrimentally affect the functioning of most of the major organ systems (nervous, GI, circulatory, endocrine…). Wet beriberi is characterized by the effects of heart failure (decr. ATP, the heart doesn't have the "fuel" to sustain itself; thiamine deficiency also causes peripheral vasodilation thus increasing venous return to the heart, making the heart work harder). Symptoms include lung edema due to left sided heart failure and pitting edema of the lower extremities and ascites (serous fluid build up in the abdominal/peritoneal cavity) due to right sided heart failure. Dry beriberi is characterized by polyneuritis (pain radiating on one or more peripheral nerves, caused by the demyelination of the nerve(s)), weakness, nystagmus (LR6), ataxia, Wernickes Encephalopathy, paralysis of the legs, loss of appetite, irritability, and muscle tenderness, constipation, .
Riboflavin: B2. FAD is the coenzyme and is oxidized to FADH2 (reduced). Each FADH2 yields 2 ATP's. FMN is required in the conversion of Pyridoxine (B6) to pyridoxyl phosphate (PLP), the active coenzyme form of B6.
Requirements: RDA: 1.8 mg. Sources: Liver, whole grains, poultry. Heat stabile.
Deficiencies: AKA riboflavinosis. Signs and Symptoms: Note: manifestations are usually mild. Dermatitis, angular stomatitis, cheilosis (reddened fissures at the corners of the mouth), digestive problems, forgetfulness, headaches (H/A).
Niacin: B3. "anti-pellagra vitamin"*. AKA nicotinic acid. Nicotinamide adenine dinucleotide (NAD)(+) is the coenzyme and is reduced to NADH which will yield 3 ATP molecules (intramitochondrial, extramitochondrial NADH yields only 2 ATP's). Niacin (NAD+) is required for glycolysis, pentose phosphate pathway, the pyruvate dehydrogenase complex (PDH), Krebbs cycle, and oxidative phosphorylation. Niacin is often used to treat hypercholesterolemia, which should NOT be done without doctor supervision. The immediate release form is not hepatotoxic, while the sustained release niacin is. Sustained release niacin should not be used to treat hypercholesterolemia. (class notes; Taber's; Guyton p. 783, 784; Modern Medicine, vol. 62, Sept. 1994, p. 56).
The amino acid Tryptophan is converted to niacin at a rate of 60:1. Niacin is important in glycogen (storage form of glucose) synthesis and is prescribed for increased serum cholesterol. Caution is necessary however, because B3 can have toxic effects when taken in excess, i.e., hyperglycemia, dry skin, and abnormal liver function tests. Must also warn patients of the Niacin Flush (blushing/vasodilation).
Requirements: RDA: 20 mg. Sources: meats, beans, bread, dairy. Also synthesized by intestinal bacteria.
Deficiencies: Pellagra* Early: muscle weakness and poor glandular secretion. In severe deficiencies death of tissues can occur; pathological lesions can appear in many parts of the CNS and permanent dementia/psychoses may result. Skin may become cracked, there may be pigmented scaly areas that are exposed to mechanical irritation or UV radiation (dermatitis). Deficiency also causes irritation and inflammation to the mucous membranes of the mouth and GI tract (diarrhea). Can also have widespread GI hemorrhaging. Pellagra is exacerbated in people on corn diets; corn is very low in the amino acid (aa) tryptophan, which can be converted in limited quantities into niacin. In dogs deficiency causes Black Tongue.
*Pellagra: 3-D's: 1. Diarrhea, 2. Dermatitis, 3. Dementia
Pantothenic Acid: B5. Panto = "widespread", therefore there is little to no deficiency of this vitamin. It functions as part of Coenzyme A (CoA) in the Pyruvate Dehydrogenase (PDH) complex and gluconeogenesis. Good sources would be eggs, liver, salmon. Synthesized by the body in small amounts (intestinal bacteria?). RDA: unknown (Guyton p. 782).
Pyridoxine: B6. Key role in protein metabolism. Involved in 3 main types of reactions: 1. Transamination, 2. Deamination 3. Decarboxylation. Pyridoxyl phosphate (PLP) is the active coenzyme. PLP is stored in muscle and is transported by albumin. The following reactions all require PLP as a coenzyme: A. Histidine--->Histamine, B. Tryptophan->Niacin (5-hydroxy tryptophan), C. Tryptophan->Serotonin (5-hydroxy tryptamine). 30-50% is lost on freezing of the food. B6 requires B2 for proper function.
Requirements: (RDA) Adult males: 2.0 mg. Female adult: 1.6 mg. Lactating and pregnant females 2.2 mg. Children: 1.0 to 1.5 mg. Sources: lean meat, wheatgerm, poultry, fish, soy, legumes, peanuts. Moderate sources are many breads, cereals, fruits and vegetables.
Deficiencies: Decreased absorption and low blood and liver levels of B12. Low blood levels of vitamin C. Rarely in children pyridoxine deficiency can cause convulsions, dermatitis, gastrointestinal (GI) problems such as nausea and vomiting (N/V) (Guyton, p. 785).
Toxicities: B6 presents neurological problems doses greater than 2,000 mg/day. Symptoms include tingling sensations in the neck and feet, lack of muscle coordination, a stumbling gait, and degeneration of nerve tissue. Lower doses can be toxic at 200 mg if taken over a period of years.
(Class notes, The Essential Guide to Vitamins and Minerals, p. 52, 53., Guyton p. 785)
Biotin: B7. A component of the B vitamin complex, contains sulfur. Essential for the metabolism of carbohydrates and fats (CO2 fixation, decarboxylation (required by pyruvate decarboxylase), and deamination of amino acids. Good sources: liver, milk, egg yolk, yeast, peanuts, intestinal bacteria, fruits and veggies. Deficiency is rare, can occur if the diet contains a large amount of egg white due to the fact the white contains avidin, a biotin antagonist. Children with this deficiency may suffer mental and physical retardation, alopecia (hair loss), impaired immunity and anemia. Heat labile. (class notes, Taber's)
Folate: B9. Folic acid, folacin. Functions in the coenzyme THF (tetrahydrofolic acid). Sources: green vegetables ("foliage"), fish, breads, pastas and intestinal bacteria. Involved in the transport of single carbon units such as methyl groups. Most important use is in the synthesis of purines and thymine which is required for deoxyribonucleic acid (DNA) synthesis and is therefore essential for cellular replication. Folate even greater growth promoter than B12; folate has different but equally important role in RBC formation and maturation. Folate can mask Pernicious anemia. (Class notes, Taber's, Guyton p. 784)
RDA: 0.4 mg.
A folate deficiency will lead to a macrocytic anemia that is almost identical to Pernicious anemia (B12). A decrease in folate during pregnancy is associated with an increase in neural tube defects (spina bifidas), anencephalopathy, premature births and decreased birth weight.
Test: Serum: Serum Folate (also do serum B12); urine: FIGLU excretion (forminoglutamic acid) (*see below for pathway). Methyl Trap: 5methyl-THF is the coenzyme used in the conversion of homocysteine to methionine (amino acids). The enzyme involved is methyl-cobalamine (B12). If no folate or B12, the methyl group is "trapped" and can't get transferred to the homocysteine so that it may become methionine. Until the THF is freed from the methyl group, it cannot go on to be used in RBC production.
*Histidine-------------------->Glutamic acid. This occurs in the presence of the following enzyme and coenzymes: formiminotransferase, Tetrahydrafolate (THF) and folate. If folate is not present, Formiminoglutamic acid ("for Mimi no glutamic acid") is the result (FIGLU)
Cobalamine: AKA B12, methyl cobalamine, cyanocobalamine, hydroxycobalamine (the latter 2 are the most active forms). The prosthetic group contains cobalt, which has binding properties similar to that of the iron (Fe) in the hemoglobin molecule (reversible binding). 2-3 year storage in the liver (other sources as much as 5 years). Comes from animal sources only, i.e., meats, cheese and milk. B12 requires Intrinsic Factor (produced by the parietal cells of the gastric glands (stomach), they also make HCl) for absorption in the ileum.
2 major functions of B12:
1. Promote growth
2. To promote red blood cell (RBC) development and maturation.
RDA: 3 micrograms
Examples: transfer of a methyl group in the conversion of homocysteine to methionine ("methyl trap" see folate), conversion of Methylmalonyl CoA to Succinyl CoA (Krebb's cycle).
Deficiency: Pernicious anemia (PA) (a macrocytic anemia. note: all dietary deficiency anemia's, with the exception of iron, cause macrocytic, large cell, anemia's) and demeylination of nerve fibers. Guyton: The posterior columns (sensory) of the spinal cord are especially affected; symptoms include the loss of sensation in the extremities and in severe cases become paralyzed.
Tests: Schilling test (dx. PA), Serum B12, Methylmalonic acid assay (urine, if suspect decr. B12 when serum B12 is in normal range). Pathway is as follows: Methylmalonyl coenzyme A (CoA)----->Succinyl coenzyme A. Enzymes and coenzymes required are: methylmalonyl-CoA mutase, adenosylcobalamin, cobalamin. If cobalamin (B12) is not present then Methylmalonic acid is the result. (Guyton p. 784, class notes)
Vitamin C:
Required for collagen synthesis.
Sources: Concentration from high to low: Kiwi fruit (100 mg / serving), broccoli, brussel sprouts, oranges (and juice), green peppers, grapefruit, strawberries, melons, cabbage, tomatoes, spinach, banana, lemon, berries (15-20 mg / serving)
Deficiency: Bleeding gums, easy bruising, scurvy.
RDA: 60 mg / day