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NFS284 Chapter 8-9 Review Notes

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University of Toronto St. George
Nutritional Science
Tom Wolever

Nutrition: Science and Applications Water-soluble vitamins  B1, B2, B3, B6, B12, folate, C Chapter 8 – The water-soluble vitamins Fat-soluble vitamins  A, D, E, K Chapter 9 – The fat-soluble vitamins Thiamine (Vitamin B1) (energy metabolism) - Beriberi o Thiamine deficiency disease due to unenriched white rice Fortified foods - Foods to which nutrients have been added o Symptoms = weakness, nerve tingling, poor coordination, o To replace nutrients lost during processing (e.g., iron, thiamin, paralysis, death riboflavin, niacin are lost when making white flour) - Wenicke-Korsakoff syndrome o To increase the amount of a nutrient in the food supply (e.g., o Thiamine depletion disease due to alcohol folate is added to grain products) Riboflavin (Vitamin B2) (energy metabolism) - Must be listed in the nutrition facts table - Found in milk Vitamins in the digestive tract - Destroyed by light - Mouth  chewing releases the vitamins from food Niacin (Vitamin B3) (energy metabolism) - Stomach  digestion releases the vitamins from food  some niacin - Pellagra absorption o Niacin deficiency disease due to diets high in corn  niacin is bound to protein  not bioavailable - Gall bladder  bile absorbs fat-soluble vitamins - Pancreas  digestive enzymes releases the vitamins from food o Symptoms = dermatitis, diarrhea, dementia, death - Small intestine o Southern US  serious public health issue in the early 1900’s o South America  corn treated with lime  releases bound niacin o Fat-soluble vitamins (micelles)  brush border  mucosal cells (chylomicrons)  lymph  blood  bioavailable o Water-soluble vitamins  blood - Synthesized from tryptophan - Large intestine  bacteria synthesize small amounts of vitamins - Used in the treatment of cardiovascular disease - Bioavailability  how much a nutrient can be absorbed and used in the o Dose = 50 mg  lower LDL cholesterol, raise HDL cholesterol, body lower serum triglycerides Storage and excretion of vitamins o UL = 35 mg  side effects of 50 mg = flushing, burning, tingling - Water-soluble vitamins sensation of the skin (e.g., face, chest) o No storage Vitamin B6, vitamin B12, and folate function together o Excess excreted in urine - Homocysteine hypothesis o Depleted more quickly than fat-soluble vitamins o Homocysteine is toxic to blood vessels  Derived from the metabolism of methionine o Vitamin B12 stays in the body for several years (EXCEPTION) - Fat-soluble vitamins o ↑ homocysteine = ↑ risk of cardiovascular disease o Stored in the liver and the adipose tissue o ↑ vitamin B6, vitamin B12, and folate = ↓ serum homocysteine = ↓ risk of cardiovascular disease Vitamins function as co-enzymes - Vitamin + chemical group = functional coenzyme  Most concerned with the intake of folate (e.g., hardest to - Incomplete enzyme + functional coenzyme = active enzyme obtain) - Molecule + active enzyme = enzyme reaction - Vitamin B6  converts homocysteine into cysteine - Enzyme reaction = to form one or more new molecules o Folate + vitamin B6  methyl folate Understanding vitamin functions - Vitamin B12 and folate  converts homocysteine into methionine - Energy metabolism o Methyl folate + vitamin B12  folate + methyl B12 o Thiamin, riboflavin, niacin, pantothenic acid, biotin  Transfer of methyl group from methyl folate to vitamin - Single carbon metabolism  transfer of methyl groups B12  methyl B12 o Vitamin B6, vitamin B12, folate o Methyl B12 + homocysteine  vitamin B12 + methionine - Antioxidants  protection from oxidative damage or oxidative stress  Transfer of methyl group from methyl B12 to homocysteine  methionine o Vitamin C, vitamin E Vitamin B6 (amino acid metabolism) - Folate intake - Transamination for the synthesis of non-essential amino acids o Folate in red blood cells - Deamination for the production of ATP and glucose  Folate deficiency cut-off = 0% of the population - Decarboxylation for the synthesis of neurotransmitters  Optimal folate level to prevent neural tube defects = 22% Folate (single carbon metabolism)  High folate concentration cut-off = 60% - Folate, homocysteine, and cardiovascular disease o Folate in food o ↑ folate = ↑ cardiovascular disease  Women  high prevalence of inadequate folate intake  Confirmed by observational studies  Men  low prevalence of inadequate folate intake o ↑ folate = ↓ serum homocysteine o Additional research revealed that food processes are over-  Confirmed by intervention trials fortifying o ↓ serum homocysteine = ↓ cardiovascular disease - Human observational trials  Confirmed by observational studies o ↑ folate = ↓ risk of colon cancer  Not confirmed by intervention trials - Animal studies - Folate (food) or folic acid (supplement) o Absence of pre-existing cancer = ↑ folate = ↓ risk of cancer o Folate monoglutamate (folic acid) o Presence of pre-existing cancer = ↑ folate = ↑ risk of cancer  Found in fortified food (e.g., synthetic compound)  Folate is required for DNA synthesis  More stable than folate  Cancer cells require folate to make enough DNA to o Folate polyglutamate (folate) proliferate  Found naturally in food Vitamin B12 (single carbon metabolism) - Folate function in the body - Biosynthesized by micro-organisms o Folate  DNA synthesis  red blood cell formation - Concentrated in animal tissue  Synthesis of the components of DNA - Required for proper myelin sheath and red blood cell formation  DNA methylation controls gene expression (e.g., number - Neurological symptoms (myelin sheath) = tingling, loss of balance and type of genes expressed) - Megaloblastic anemia (red blood cells) o Due to secondary folate deficiency (e.g., can’t convert methyl  Megaloblastic anemia folate into folate)  Inhibition of DNA synthesis during red blood cell - Pernicious anemia (red blood cells) formation o Autoimmune disease  destroys the cells that produce IF   Cells are unable to divide (megaloblast) inability to absorb sufficient vitamin B12  Vitamin B12 is covalently bound to food (B12–food)  Large immature and dysfunctional red blood cells (macrocyte)  Stomach  acid and pepsin releases vitamin B12 from o Folate  methionine derivative  DNA methylation  neural food  Stomach  cells in the stomach lining releases intrinsic tube formation  brain and spine  Fortification of food supply with folate (e.g., white flour, factor (IF) cornmeal, pasta)  Small intestine (duodenum)  IF binds to vitamin B12  Reduced neural tube defects by 50% (B12–IF)  Reduced childhood cancers  Small intestine (ileum)  B12–IF complex can be absorbed and enter the blood stream  Multivitamin should contain at least 400 μg of folate  Neural tube defec
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