Module 8

• Vitamins


  First defined in 1912, complex organic compounds that regulate certain metabolic processes
• Vitamins


  • Organic (carbon containing)
  • Not a source of energy
  • Play crucial roles in reactions that extract energy from macronutrients (coenzymes!)
• Sources of vitamins


  • Plants
  • Animals
  • Fungi
  • Bacteria
• Bioavailability


  Amount of a vitamin actually available for use by the body
• Vitamin absorption


  • Small intestine is the primary site
  • Doesn't absorb 100%, typically increases when the body needs more

  
• Fat-soluble vitamins


  • Chemically similar to lipids, found in fatty portions of food
  • Fat digestion facilitates absorption
  • Absorbed into lymph system, stored in liver and fatty tissues

  
• Water-soluble vitamins


  • Absorbed directly into bloodstream
  • Not stored in appreciable amounts, needed regularly from diet
  • Excess excreted in urine

  
• Diseases affecting the GI tract can reduce vitamin absorption and lead to deficiencies
• Enrichment


  Adding back vitamins that were taken out during refinement
• Fortification


  Adding vitamins that weren't originally there
• Vitamin toxicity can occur when cells are saturated and can't accept additional amounts
• Vitamin deficiencies usually result from inadequate diets or conditions that increase the body's requirement for vitamins
• Water-soluble vitamins


  • B vitamins (8 of them)
  • Vitamin C
• 5 B-complex vitamins


  • Thiamin (B1)
  • Riboflavin (B2)
  • Niacin (B3)
  • Pantothenic acid (B5)
  • Biotin (B7)

  
• Thiamin (B1)


  Part of coenzyme TPP, necessary for breakdown of carbohydrates to release energy

  
• Thiamin (B1)


  • Also needed for synthesis of neurotransmitters
  • Thiamin needs related to energy requirements and carbohydrate intake, slightly higher for men vs women
  • Found in small amounts in many foods, generally enough if diet supplies adequate energy

  
• Thiamin deficiency can lead to beriberi, a very weak and poor muscular coordination condition

  
• Thiamin deficiency can also lead to Wernicke-Korsakoff syndrome, a degenerative brain disorder primarily associated with alcohol-induced malnutrition

  
• Riboflavin (B2)


  Forms active coenzyme FAD, important for breakdown of fatty acids and amino acids, involved in converting other vitamins into active forms
• Light can destroy riboflavin, so milk and milk products should be stored in opaque containers to protect it
• Overt riboflavin deficiency (ariboflavinosis) is rare, but can lead to fatigue, inflammation of mucous membranes, glossitis, chapped lips, and skin disorders
• Niacin (B3)


  Forms active coenzymes NAD and NADP, involved in over 200 reactions including glycolysis, citric acid cycle, and electron transport chain

  
• Niacin can be synthesized from the amino acid tryptophan, but this only provides about half of the body's niacin needs

  
• Niacin deficiency can lead to pellagra, a condition characterized by dermatitis, diarrhea, dementia, and eventually death if left untreated
• Riboflavin (B2)


  • Fatigue
  • Inflammation of mucous membranes that line mouth and throat
  • Glossitis (swollen and sore tongue)
  • Chapped lips
  • Cheilosis (scaling/cracking skin around corners of mouth)
  • Dermatitis (inflammation of skin)
  • Eye disorders
• Niacin (B3)


  • Forms active coenzymes NAD, NADP; involved in ~200 reactions, including glycolysis, citric acid cycle, electron transport chain
  • Also needed to break down fatty acids and some amino acids
  • Unique among B vitamins; body can synthesize it from amino acid tryptophan (but need other nutrients as well [iron, riboflavin, vitamin B6])
  • Precursor tryptophan supplies ~1/2 niacin intake
  • RDA is expressed as niacin equivalents (NEs), 1 NE = 1 mg of niacin or 60 mg of tryptophan

  
• Niacin (B3) Deficiency (Pellagra)

  • People at risk: alcoholism, anorexia nervosa, rare disorders that disrupt tryptophan metabolism
  • Early signs/symptoms: poor appetite, weight loss, weakness
  • Later symptoms (pellagra) include 4 D's: Dermatitis ("rough skin"), Diarrhea, Dementia, Death
  • Since other nutrients (iron, riboflavin, vitamin B6) needed to convert tryptophan to niacin, deficiency in them contributes to damage

  
• Niacin (B3) Toxicity


  • Megadoses of niacin may be prescribed to reduce LDLc and increase HDLc
  • Side effects: flushing of skin, tingling sensation in hands/feet, GI upset, nausea / vomiting, liver damage, high blood sugar levels, blurred vision
  • Using statin along with niacin [to treat elevated LDLc] not shown to reduce death from CVD
  • April 2016 FDA withdrew approval of medications that combine niacin with statin
  • DRI UL: 35mg/day from fortified foods, supplements, or medications
  • No evidence of toxicity from dietary sources

  
• Pantothenic Acid (B5)


  • Component of CoA [required to make Acetyl CoA]
  • Important for breakdown of carbohydrates, fatty acids, amino acids
  • Easily damaged: freezing, canning will decrease content
  • Processing and refining grains destroys ~40-75%
  • Cooking destroys up to 50% in meat and up to 80% in vegetables
• Pantothenic Acid (B5) Deficiency


  • Virtually nonexistent in general population
  • In research settings: irritability and restlessness, fatigue, digestive disturbance, sleep disturbance, numbness and tingling, muscle cramps, staggered gait, low blood glucose levels

  
• Biotin (B7)


  • In coenzyme form biotin participates in chemical reaction that adds CO2 to other compounds
  • Promotes synthesis of glucose and fatty acids
  • Breakdown of certain amino acids
  • Essential for regenerating oxaloacetate in citric acid cycle
  • No RDA (difficult to estimate because some biotin is produced by bacteria in GI tract & absorbed)
  • AI based on extrapolation from amount of biotin in human milk (most major nutrition surveys do not report biotin intake)

  
• Biotin (B7) Deficiency


  • Signs of biotin deficiency conclusively demonstrated in individuals consuming raw egg whites over long periods of time, and in patients receiving total parenteral nutrition (TPN) solutions that do not contain biotin
  • Symptoms: Dermatitis (often appearing as red scaly rash around eyes, nose, mouth), CNS abnormalities (depression, lethargy, hallucinations, paresthesia of extremities)
  • Infants with biotin deficiency experience developmental delays
• Thiamin (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), and biotin (B7) are widespread in the food supply, and overt deficiencies are rare in North America. They are all incorporated into coenzymes that metabolize carbohydrates, proteins, fats. High doses of thiamin and riboflavin appear to be harmless, but megadoses of niacin should be taken only under medical supervision (no RDA, EAR, UL for pantothenic acid or biotin).

  
• Water-Soluble Vitamins


  • The B Vitamins (eight of them!)
  • Vitamin C - Antioxidant, works with fat-soluble antioxidant vitamin E (E quenches free radical and becomes a free radical; C can stabilize it)
• Vitamin B6, Folate (B9), Vitamin B12


  Function in close cooperation with each other to help control homocysteine levels and support red blood cell synthesis

  
• Vitamin B6


  • Family of 3 compounds: pyridoxine, pyridoxal, pyridoxamine
  • Convert vitamin forms to primary B6 coenzyme pyridoxal phosphate (PLP)
  • PLP facilitates reactions involved in amino acid metabolism (including conversion tryptophan to niacin); transamination reactions that form nonessential amino acids
  • PLP participates in production of heme (iron-containing portion of hemoglobin – protein in red blood cells that transport oxygen)
  • PLP converts a potentially toxic amino acid homocysteine to cysteine (a nonessential amino acid)

  
• Vitamin B6 Deficiency


  • Without adequate B6, all amino acids become essential
  • Neurotransmitter synthesis affected (depression, headaches, confusion, numbness and tingling in extremities, seizures)
  • Low B6 causes deficiency in hemoglobin synthesis (red blood cells are small and pale, oxygen binding capacity is decreased)
  • Build up of homocysteine leads to inflammation and atherosclerosis, more prone to endothelial cell injury

  
• Vitamin B6 Toxicity


  • Megadoses of B6 are toxic (2-6g/day), causing severe sensory nerve damage (peripheral neuropathy)
  • Signs and symptoms: walking difficulties, numbness of hands and feet (nerve damage resolves when megadose is stopped)
  • DRI UL: 100mg/day from fortified foods and/or supplements
  • Difficult to take in amounts for toxicity from food sources
  • UL based on amount that will not cause nerve damage in the majority of healthy people

  
• Folate (B9)


  • Before folate can be absorbed, all but one glutamate needs to be removed (by enzymes in brush border of small intestine)
  • Found in foods (50% bioavailable)
  • Found in supplements (100% bioavailable)
  • More glutamates = more work for your body to break down
  • 1 DFE = 1 μg folate = 0.6 μg folic acid
  • Named for its best natural source – green leafy vegetables (foliage)
  • Folate refers to group of related compounds that includes folic acid
  • Folic acid refers specifically to synthetic form of vitamin found in supplements (and added to fortified foods)
  • Currently nutrient databases and nutrition labels do not express the folate content of food in DFEs, which take into account different bioavailabilities of folate sources
  • Cells convert folate to group of folate-containing coenzymes tetrahydrofolate (THF)
  • THF accepts single-carbon group (e.g., CH3) from one compound and transfers it to another
  • THF participates in many chemical reactions involved in DNA synthesis and amino acid metabolism
  • As cells prepare to divide, they need THF to make DNA

  
• Folate (B9) Functions


  • Essential for healthy embryotic development
  • THF needed to make DNA as cells divide (e.g., red blood cells)
  • THF can transfer CH3 group to vitamin B12, that then transfers CH3 group to homocysteine, forming methionine (this process recycles methionine)
  • When B12 is not available, folate can't be used