1. B-VITAMINS Working individually and in concert 1

2. Relationship with Energy Metabolism Vitamins do not provide the body with fuel for energy However, they can work as coenzymes Assist enzymes with release of energy Without coenzyme, an enzyme cannot function B-vitamins assist enzymes that unlock energy from our energy- yielding nutrients 2

3. Function of a Coenzyme 3

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5. Thiamin Part of coenzyme thiamin pyrophosphate (TPP) Energy metabolism Conversion of pyruvate to acetyl CoA in glucose metabolism Participates in citric acid cycle in mitochondria Essential for nerve activity and muscle activity 5

6. Thiamin Deficiency – Malnourished and alcoholics – Beriberi Dry – nervous system Wet – cardiovascular system Toxicity – No adverse effects No UL Prolonged cooking destroys thiamin Leaches into water when boiling or blanching foods 6

7. Food Sources of Thiamin 7

8. Riboflavin Serves as coenzyme in energy metabolism – Flavin mononucleotide (FMN) – Flavin adenine dinucleotide (FAD) Carries hydrogen atoms and their electrons to electron transport chain Each time it does this, 2 molecules of ATP are generated Deficiency – Inflammation of membranes Toxicity – No UL Destruction of riboflavin – Ultraviolet light (thus the opaque containers for milk) – Irradiation – Not destroyed by cooking 8

9. Food Sources of Riboflavin 9

10. Niacin Two chemical structures Nicotinic acid Nicotinamide Major form of niacin in blood Two coenzyme forms participate in metabolic reactions Nicotinamide adenine dinucleotide (NAD) Carries hydrogen atoms and their electrons to electron transport chain 10

11. Niacin Deficiency Pellagra Symptoms: 3 Ds Diarrhea Dermatitis Dementia  Toxicity  Naturally occurring: no harm  Supplements or drugs  “Niacin flush”  Nausea, vomiting, liver damage, glucose intolerance  Potential health benefits of large doses of nicotinic acid: may lower LDL cholesterol 11

12. Food Sources of Niacin Niacin is tolerant to heat but can be lost in cooking water 12

13. Biotin  Coenzyme critical in citric acid cycle  Facilitates first step in cycle (entry point for acetyl-CoA  Participates in breakdown of fatty acids and amino acids  Participates in gluconeogenesis and fatty acid synthesis  Deficiency is very rare, no known toxicity  Widely distributed in foods, needed in small amounts (30 mcg/day)  Raw egg white consumption  Deficiency symptoms: hair loss, rash, neurological impairment 13

14. Pantothenic Acid  Part of chemical structure of coenzyme A  Entry point into many metabolic pathways  Involved in >100 different steps in synthesis of lipids, hormones, neurotransmitters, and hemoglobin  Deficiency is rare, no known toxicity  Symptoms: failure of all body systems, fatigue, GI distress, neurological disturbances  Food sources  Widely available in meats, whole grains, potatoes, egg yolks, broccoli  Easily destroyed in food processing: freezing, canning, refining 14

15. Vitamin B6  Three forms  Pyridoxal, pyridoxine, and pyridoxamine  All converted to coenzyme pyridoxal phosphate (PLP)  Amino acid metabolism  Urea metabolism  Conversion of tryptophan to niacin or serotonin  Synthesis of heme, nucleic acids, & lecithin  Influences cognitive performance, hormone activity, and immune function  Stored extensively in muscle tissue  Large doses do not enhance muscle performance! 15

16. Vitamin B6  Deficiency  Impacts amino acid metabolism  Abnormal compounds made from tryptophan accumulate in brain  Early signs: depression, confusion  Advanced symptoms: abnormal brain wave patterns, convulsions  Alcohol: increases breakdown and excretion of PLP  Isoniazid (anti-tuberculosis med): B6 antagonist  Toxicity: only from supplements  Can cause irreversible nerve degeneration  In food  Small amounts in lots of foods  Lost when food is heated 16

17. Food Sources of B6 17

18. Folate  Known as folacin or folic acid  Primary coenzyme form – THF (tetrahydrofolate)  Transfers single-carbon compounds during metabolism (methlyation)  Converts vitamin B 12 to coenzyme form  Involved in DNA synthesis  Needed for cell division  Helps process amino acid homocysteine 18

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20. Folate  Folate disposal from body  Secretion by liver into bile  Can be recycled via enterohepatic circulation  Vulnerable to GI tract injuries  Depletion occurs rapidly with alcohol abuse  Leads to greater tissue damage, greater losses (and impaired absorption of other nutrients, too)  Bioavailability  Synthetic form (folic acid) 1.7x more bioavailable than natural form (folate) 20

21. Folate Status and Birth Defects Needs rise during pregnancy Closure of neural tube, from which brain and spinal cord develop, occurs during first few weeks Low folate status in mother can cause brain and spinal cord disorders, and even death of infant/fetus Rate of neural tube defects has declined since folate fortification began in 1996 Adequate folate status may also prevent cleft lip or palate Supplementation or careful monitoring of dietary folate adequacy recommended for all women of childbearing age To get 400 mcg/d, at least 5 servings of fruits and vegetables recommended 21

22. Folate  Deficiency  Impairs cell division and protein synthesis  Red blood cells and GI tract cells falter  Anemia  GI tract deterioration  Primary deficiencies: due to inadequate intake or increased need  Secondary deficiencies: drugs  Anti-cancer meds (folate antagonists)  Heavy use of aspirin or antacids  Oral contraceptives  Smoking  Toxicity  Can occur from natural or supplemental/fortified sources  Primary concern: can mask B12 deficiency, since early signs of B12 deficiency are usually due to impaired folate activity  Food sources  Heat and oxidation destroy folate 22

23. Food Sources of Folate 23

24. Vitamin B12  Vitamin B 12 and folate depend on each other for activation  Very important for DNA synthesis, cell replication  Individual roles of vitamin B 12  Maintains myelin sheath, promotes normal growth of nerve cells  Involved in bone cell metabolism/activity 24

25. Vitamin B12  Digestion and absorption  Stomach  HCl acid and proteases release B12 from dietary protein  Secretes intrinsic factor  Small intestine  Intrinsic factor binds to B12, absorbed as complex  Enterohepatic pathway continuously recycles B12  In healthy individuals, deficiency is rare, since it is constantly reabsorbed 25

26. Vitamin B12  Deficiency  Inadequate absorption or intake  Lack of hydrochloric acid or intrinsic factor  Lack of animal foods  Individuals at risk  Older adults: atrophic gastritis  Vegans  Those with anemia of folate deficiency  Symptoms of vitamin B 12 deficiency  Moderate: cognitive impairment  Severe: creeping paralysis  Toxicity unknown 26

27. Anemia of B12 or Folate Deficiency 27

28. Choline  Manufactured from amino acid methionine in body  When insufficient in diet, body alone cannot meet needs  Used to make neurotransmitter acetylcholine  Supports neural tube closure and nervous system development in fetus  Common sources: milk, eggs, peanuts  Deficiencies are rare 28

29. B-Vitamins In Concert  Each B-vitamin coenzyme is involved in energy metabolism  Some vitamins are necessary to activate others  B12 and folate  Riboflavin and B6  Riboflavin, B6, and Niacin (synthesis from tryptophan)  Deficiencies  Single B-vitamin deficiencies seldom show up in isolation  Frank deficiency is rare in US, but suboptimal intake is more common 29

30. B-Vitamins in Concert 30