Water Soluble Vitamins Midterm #2 Flashcards
1
Q
Generalities: Metabolism and Storage
A
only B12 and folate are stored in the body, in general water soluble vitamins are excreted rapidly and not stored. Depletion is more of a problem than toxicity.
2
Q
Generalities: Toxicity
A
Only niacin and pyridoxine can become toxic at high concentrations. In general there are very few toxicities.
3
Q
Generalities: Measuring body levels
A
water soluble vitamins are coenzymes for various common biochemical reactions and their status can be determined by measuring the appropriate enzyme activities. Typically enzyme activity is measured in the absence and the presence of exogenously added coenzyme and then determined if the patient needs more of the vitamin.
4
Q
Vitamin B1
A
Thiamin
5
Q
Vitamin B1 (thiamin): Structure
A
pyrimidine and thiamin ring. Thiazole is the “business end”. phosphorylation occurs at the alcohol group off the thiamin ring. Addition of one ATP forms TMP (thiamine monophosphoate) and addition of a second ATP forms TPP (Thiamine pyrophosphate).
6
Q
Vitamin B1 (thiamine): Function
A
Metabolism of carbohydrates in glycolysis and TCA cycle. Cofactor for pyruvate dehydrogenase (glycolysis) and alpha-ketoglutarate dehydrogenase (TCA).
7
Q
Vitamin B1 (Thiamine): Reactions
A
Oxidative carboxylation of alpha-keto acids
and transfer of alpha-ketols
8
Q
Vitamin B1 (Thiamine): oxidative decarboxylation of alpha-keto acids enzymes
A
Pyruvate dehydrogenase complex
alpha-ketoglutarate dehydrogenase complex
9
Q
Vitamin B1 (thiamine): pyruvate dehydrogenase reaction
A
Oxidative decarboxylation of alpha-keto reaction.
form acetyl-CoA intermediate for the TCA cycle and NADH
10
Q
Vitamin B1 (Thiamine): alpha-ketoglutarate dehydrogenase reaction
A
Oxidative decarboxylation of alpha-keto acids
form succinyl CoA and NADH in TCA cycle.
11
Q
Vitamin B1 (Thiamine): transfer of alpha-ketos reaction
A
used in the pentose phosphate pathway (pentose shunt in glycolysis).
Provides 5 carbon pentose sugars for DNA and RNA synthesis and also produces NADPH.
Runs both directions.
12
Q
Vitamin B1 (Thiamine): Mechanism
A
All occurs on the thiamin ring. The 2-C loses a hydrogen atom to form a negative charge on the carbon and a positive charge on the nitrogen. The negative charged carbon can attack C=O to form a tetrahedral intermediate. Alpha-hydroxy-ethyl TPP is the intermediate with a two carbon structure attached and is used to move 2 carbon groups around.
13
Q
Vitamin B1 (Thiamin): needs
A
Thiamin needs are proportional to caloric intake.
14
Q
Vitamin B1 (Thiamin): measuring deficiency
A
Measure deficiency using erythrocyte transketolase assay
15
Q
Vitamin B1 (thiamin): deficiency in alcoholics
A
About 40%-50% of chronic alcoholics are deficient. Low intake and alcohol affects the conversion of thiamin to TPP. Also, increased urine flow may cause thiamin washout. This includes fetal alcohol syndrome, which can be helped with supplementing the mother with thiamin.
16
Q
Vitamin B1 (thiamin): Signs of deficiency
A
Early signs: anorexia, nausea, vomiting, fatigue, weight loss, nystagmus, tachycardia.
Late signs: beriberi (polyneuritis). Wet beriberi includes cardiac issues including cardiac edema, and enlargement of heart.
17
Q
Wernicke-Korsakoff syndrome
A
Vitamin B1 (thiamin deficiency)
neurological disorder resulting in impaired mental functioning usually requiring institutionalization. Symptoms include confusion, memory loss, confabulation, psychotic behavior, and maybe irreversible in part. Seen in alcoholics.
18
Q
Vitamin B1 (thiamin): factors causing deficiency
A
Increased carbohydrate intake, i.e. TPN and alcoholics
Decreased absorption, i.e. ulcerative colitis and alcoholics
Decreased intake, i.e. poor diet, geriatrics, breast fed infant from B1 deficient mother
alcoholism
19
Q
Vitamin B1 (thiamin): cellular uptake
A
Thiamin specific receptor in intestinal cells (hTHTR) which only recognizes thiamin, not TPP. Common to ingest thiamin in plants and TPP in meats, this has to be broken down to thiamin for uptake. Have been polymorphisms in the gene encoding hTHTR which may cause thiamin-responsive megaloblastic anemia.
20
Q
Vitamin B1 (Thiamin): Source
A
Present in most tissues as TPP and plants as thiamin.
Rich sources include lean meat, especially pork, cereal grains, eggs, yeast, nuts.
Thiaminase in some raw fish and raw shellfish have an enzyme that can hydrolyze thiamin
In the milling or processing of rice and flour, thiamin is lost. Whole wheat or rice contains 10X the amount of thiamin as white. In the US most white flour, rice, pastas are “enriched” to restore thiamin levels. “Enriched” products also have added riboflavin, niacin, iron and folic acid.
21
Q
Vitamin B1 (thiamin): Stability
A
labile at pH > 4 and when heated.
22
Q
Vitamin B1 (thiamin): diagnosis of deficiency
A
increased pyruvate and lactate in plasma (because can’t form pyruvate) or the transkelotase activity in RBC. You compare the activity of the enzyme in the presence and absence of thiamine. If addition of thiamine increases activity that person is said to be deficient.
23
Q
Vitamin B1 (Thiamin): Uses
A
- deficiency states - alcoholics
- thiamin responsive inborn errors of metabolism
- mosquito repellant - questionable efficacy
- Acute alcoholism - have to give IV or IM because don’t absorb well orally
- Alzheimer’s disease - huge dose, questionable efficacy
24
Q
Vitamin B1 (Thiamine): Responisve inborn errors of metabolism
A
- Wernicke-Korsakoff: transketolase defect
- Maple Syrup urine disease: failure to decarboxylate branched chain amino acids defect
- Thiamin responsive megaloblastic anemia
- Hyperalanemia: unknown defect
- Hyperpyruvate acidurea: pyruvate dehydrogenase defect
25
Vitamin B1 (Thiamin): Toxicity
nontoxic on oral administration. Anaphylaxis have been observed in patients receiving repetitive parenteral doses.
26
Vitamin B1 (Thiamine): Patient Counseling
1. needed to drive carbohydrates to energy
2. rarely used as a single supplement, use a multivitamin
3. special benefit in alcoholics at higher doses, responsive population
27
Vitamin B2
Riboflavin
28
Vitamin B2 (Riboflavin): Structure
1. Oxidized form appears bright-yellow or orange.
2. Riboflavin monophosphate, FMN, is produced from riboflavin in the gut mucosa
3. Flavin adenine dianucleotide, FAD, is produced from FMN in the liver
29
Vitamin B2 (riboflavin): function
1. Redox, tissue respiration, H transfer as flavin containing enzyme
2. Oxidized FMN or FAD accepts two hydrogen ions to form the reduced colorless form FMNH2 or FADH2.
3. Reduced form is used to oxidize double bonded carbons into a single bond
30
Vitamin B2 (riboflavin): Some enzymes that use flavin groups
succinate dehydrogenase, fatty acid acyl CoA dehydrogenase, glutathione reductase
31
Vitamin B2 (riboflavin): Important flavoproteins containing FMN
cytochrome C reductase, NADP cytochrome C reductase, cytochrome P450 reductase, flavin monooxygenase
32
Vitamin B2 (riboflavin): deficiency state
1. Not usually seen in isolation but occurs in combination with other B vitamin deficiencies.
2. Fatigue, cheilosis, glossitis, vascularization of cornea, dermatitis
3. Vegans and teenagers may be low in B2 if dairy intake is low
4. Low B2 intake may be a risk factor for cataract development
5. Alcoholics are at risk due to low intake and low absorption
33
Vitamin B2 (riboflavin): source
milk, meats, leafy vegetables, eggs, yeast, "enriched" products
34
Vitamin B2 (riboflavin): Stability
usually \> 30% destroyed by cooking, labile to light, more stable in acid than alkali in absence of light
35
Vitamin B2 (riboflavin): Use
1. deficiency states: component of most multivitamins
2. May help in migraine headache prevention - new use
3. High intake (3 mg) may be associated with lower risk for cataracts - new use
36
Vitamin B2 (riboflavin): Patient counseling
1. Normal to turn urine bright yellow in higher dose
2. routine single dose supplementation not needed, use a multivitamin to get needed riboflavin
3. Nontoxic
37
Vitamin B6
pyridoxal
38
Vitamin B6 (pyridoxal): Structure
1. 3 vitamers: pyridoxine (P) is inactive, pyridoxal (PL) is active and pyridoxamine (PN) is active.
2. PP is transformed to PLP through FMN and PNP is transformed to PLP through FMN. These are the phosphorylated forms of the three vitamers.
3. Coenzyme form is PLP, pyridoxal-5-phosphate
39
Vitamin B6 (PLP): functions
1. transamination
2. decarboxylation
3. sulfur amino acid metabolism
4. methionine formation
5. tryptophan metabolism to serotonin and niacin
6. glycogen phosphorylase
7. heme biosynthesis
8. nuceic acid biosynthesis through SAM
40
Vitamin B6 (PLP): transamination function
example is glutamate-aspartate transaminase. Formation of external amine.
41
Vitamin B6 (PLP): decarboxylation function
examples include glutamic acid to GABA, 5-hydroxytryptophan to serotonin, histidine to histamine, and DOPA to dopamine
42
Vitamin B6 (PLP): DOPA therapy
DOPA to dopamine: B6 is contraindicated in levo-DOPA therapy because B6 enhances peripheral decarboxylation of levo-DOPA to dopamine which will not cross the blood brain barrier. Larobec contains no pyridoxone and can be used if multivitamin supplementation is desired for patients on levo-DOPA. The anti-Parkinson's drug Sinemet contains levo-DOPA and carbidopa, a DOPA decarboxylase inhibitor and there is no interaction with pyridoxine.
43
Vitamin B6 (PLP): sulfur amino acid metabolism
1. elevated homocysteine is an independent risk factor for cardiovascular disease and birth defects.
2. PLP catalyzes the conversion of homocysteine to cystathionine
3. and the conversion of cystathionine to alpha-ketobutyrate and cysteine
44
Vitamin B6 (PLP): methionine formation
B6 is therefore indirectly involved in methylation, lipid metabolism and nucleic acid formation and immune function
45
Vitamin B6 (PLP): Tryptophan metabolism to serotonin and niacin.
Tryptophan can either be converted to serotonin, PLP mediated or niacin through many steps some of which involve PLP.
46
Vitamin B6 (PLP): internal vs external imine
external imine forms ketone and NH2 on the pyridine ring. The internal imine forms an aldehyde on the ring and a amine. The PLP enzymes control which carbon gets attacked by oxygen by switching between the internal and external imine.
47
Vitamin B6 (PLP): Deficiencies
1. if seen is associated with other vitamin deficiencies
2. symptoms include rash, peripheral neuritis, anemia and possible seizures.
3. Diagnosed by low plasma PLP and low transaminase activities by adding PLP and measuring enzyme activity in the presence and absence of PLP
4. Iatrogenic deficiencies: drug induced
48
Vitamin B6 (PLP): iatrogenic deficiencies
1. isoniazid: antituberculosis drug that forms a Schiff base with B6. Results in neuritis, convulsions. Treat with high levels of B6.
2. 4-Deoxypyridoxine (experimental only): competitive inhibitor, symptoms include skin lesions on face, glossitis, stomatitis, convulsive seizures (possibly due to decreased GABA), anemia (possibly due to decreased heme synthesis)
3. Oral contraceptives: older higher doses of progesterone, but generally not a problem now.
49
Vitamin B6 (PLP): Sources
milk, meats, legumes, tuna, whole grains, beans
50
Vitamin B6 (PLP): Stability
pyridoxine is stable, some loss on cooking especially with meats due to Schiff base formation to proteins
51
Vitamin B6 (PLP): diagnosis of deficiency
measure erythrocyte transaminases in the presence and absence of PLP.
52
Vitamin B6 (PLP): Uses
1. routine in multivitamin products
2. used isoniazid therapy
3. Very rare inborn errors of metabolism
4. PMS: unclear evidence, PLP may bind to steroid receptors
5. Carpal tunnel syndrome: unclear evidence, if it works effects are modest
6. Lowering homocysteine levels which are independent risk factor for cardiovascular disease.
7. N/V in pregnancy: PremesisRx though contraindicated in Fluorouracil because side effects may increase. Premesis no used in the US any longer.
53
Vitamin B6 (PLP): Inborn errors
1. B6-dependent infantile convulsions: defective glutamic acid decarboxylase. causes clonic and tonic seizures
2. B6-responsive anemia: defective hemoglobin synthesis. causes microcytic, hypochromic anemia
3. Xanthurenic acidurea: defective tryptophan metabolism due to faulty kyureninase, xanthurenic acid spills into urine. causes mental retardation
4. Homocystinurea: defective cystathionine synthetase causing mental retardation and early heart disease
5. Cystahionurea: defective cystathionase causes mental retardation.
54
Vitamin B6 (PLP): Toxicity
doses greater than 1-2g/day can cause serious neuropathy by an unknown mechanism. Avoid long term use in doses above 200 mg/day
55
Folic Acid: Function
The folate cycle and methylation
1. Forms purines through N10 formyl THFA
2. Forms folinic acid, N5 formyl THFA, "Leucovoran" (all different names for same thing)
3. Forms pyrimidines. Enzyme is thymidylate synthesis results in pyrimidine and DHFA
4. Regenerates THFA through combination of N10 methyl THFA + homocysteine to get THFA and methionine
56
Folic Acid: Chemistry
Active coenzyme is THFA which is formed from a pteridine ring with PABA by DHFA reductase and NADPH to form DHFA. DHFA reductase and NADPH then convert it to the reduced active form THFA
Folic acid is a pteroyl monoglutamic acid and is fully oxidized and found in supplements but not found naturally
Reduced polyglutamates are found in animal and plant foods.
57
Folic Acid: deficiency
1. Results in megaloblastic anemia. Symptoms include headache, fatigue, weight loss, anemia, nausea, anorexia, diarrhea, insomnia, irritability, forgetfulness.
2. May result in teratogenesis with neural tube defects and orofacial clefts. All women of childbearing age who are capable of becoming pregnant should consume 0.4 mg/day.
3. May result in elevated homocysteine, which is associated with increased risk of coronary disease. May be a defect in the N5N10 methylene THFA reductase enzyme
4. Oral contraceptives and anticonvulsants may increase folate catabolism.
5. Often seen in poor nutrition, alcoholism, pregnancy and lactation.
6. Alcohol decreases enterohepatic circulation of N5 methyl THFA.
58
Folic Acid: B12 deficiency and folate
regeneration of active folate depends on B12. Deficiency in B12 will result in folate deficiency. Results in megabloblastic anemia (due to folate deficiency) and neurological damage due to lack of B12. Hard to distinguish whether it is caused by B12 or folate deficiency but high doses of folate are toxic, so folate is prescription.
59
Folate antagonists (6)
1. Methotrexate: Decreases DHFA reductase and therefore stops all cell in the "S" phase of the cell cycle. Use Leucovoran in combination to allow ordinarily lethal doses to be administered with consequent increased tumor kill
2. Trimethoprim: inhibits bacterial DHFA reductase and combined with sulfamethoxazole which is a PABA antagonist. Very little effect on mammalian DHFA reductase.
3. Alcohol: affects enterohepatic circulation of folate
4. Nitrous oxide: continued frequent inhalation has produced fatal megaloblastic hematopoisis and a neuropathy similar to pernicious anemia. Not clinically relevant
5. Phenytoin: suboptimal levels observed with long term therapy are rare megaloblastic anemia however high doses of folic acid decreases phenytoin levels with cases of seizures reported.
6. Pyrimethamine: used for parasitic infections (malaria, toxoplasma) as a parasite DHFA reductase target. Folic acid supplements reduce effect of drug, leucovorin is okay.
60
Folic Acid: Use
1. deficiency use with oral contraceptives and during pregnancy and lactation
2. Prevent neural tube defects in fetus. Supplement with 0.4 mg folic acid
3. cervical dysplasia, bronchial squamous dysplasia and dysplasia of colonic tissue in ulcerative colitis patients. Elevated risk is associated with low folate
4. Colon cancer: low folate, high alcohol and low methionine intake as well as family history give an elevated risk.
5. Breast cancer: high dietary intake decreases risk?
6. Alzheimer's Disease: preliminary evidence shows low folate levels associated with increased risk ?
7. Coronary heart disease and stroke: Efficacy of B6, B12 and folic acid not shown to lower outcomes but are associated with outcome.
61
Folic acid: source
leafy vegetables, fruit juices, beans, enriched flour. Low levels in meat and fruits.
62
Folic Acid: stability
labile to light, heat, storage. Get from fresh vegetables.
63
Vitamin B12
cyanocobalamin (synthetic)
64
Vitamin B12
- CN, cyano- storage form found in vitamins
- OH, hydroxy- storage form found in vitamins
- CH3, methyl- active form of coenzyme
- CH2-adenosine, deoxyadenosine- active form of coenzyme
65
Vitamin B12: function
1. methyl transfer reaction
2. metabolism of odd chain fatty acids (mutase reaction)
3. Myelin synthesis
66
Vitamin B12: methyl transfer reaction
necessary for recycling of THFA (folic acid). to reform active cobalamin form of Vitamin B12 need convert homocysteine to methionine.
67
Vitamin B12: metabolism of odd chain fatty acids (mutase reaction)
B12 is a cofactor for mutase which converts methyl malonyl CoA into succinyl CoA which can be used in the TCA cycle. You can diagnose B12 deficiency because methyl malonyl CoA is excreted in the urine as methyl malonic acid in deficiency.
5-deoxyadenosyl cobalamin is the coenzyme form of B12 used in this reaction
68
Vitamin B12: Myelin synthesis
mechanism of involvement may relate to the buildup of methyl malonic acid with a resulting decrease in myelin synthesis. B12 deficiency can result in demyelination and neurological damage.
69
Vitamin B12: deficiency
Pernicious anemia. Symptoms are related to inadequate myelin synthesis and megabloblastic anemia due to failure to recycle folate. Numbness, poor coordination, poor memory, confusion, depression. Deficiency takes years to develop and is rarely diet based though vegans are at a risk.
70
Vitamin B12: absorption
Acid in the stomach splits B12 from food and intrinsic factor, which is secreted by stomach mucosa, is required to transport B12 across the ileum wall. Usually deficiency is due to lack of synthesis of intrinsic factor.
71
Vitamin B12: source
meats, especially liver and yeast; microorganisms are the ultimate sources of B12.
72
Vitamin B12: production
by fermentation
73
Vitamin B12: stability
stable at pH = 4-7, labile to light
74
Vitamin B12: diagnosis
Schillings test (older test) most common is to measure methyl malonic acid in plasma.
75
Vitamin B12: Use
1. pernicious anemia: can use IM for methylmalonic acidurea, which is an inborn error of metabolism
2. Maintaining folic acid levels high and homocysteine levels low (cardiovascular implications)
3. Vegans: take supplements
4. Elderly: over 65 take supplement due to decreasing HCL needed for absorption
76
Vitamin B5
Pantothenic Acid
77
Vitamin B5: Chemistry
peptide in diet that gets converted to CoASH (coenzyme CoA). Only the D enantiomer of CoASH has biological activity
78
Vitamin B5 ( Pantothenic acid): function
thioester bond, which is a high energy bond used to transfer acyl groups
79
Vitamin B5 (pantothenic acid): deficiency
rare. Intestinal synthesis is important as well as widespread occurrence in foods. Symptoms include fatigue, numbness in extremities and cramps.
80
Vitamin B5 (pantothenic acid): use
deficiency states or topically for ulcers/sores. Panthoderm. However, Panthoderm MOA is that it is a hydroscopic compound. It is not stereospecific and has no activity as a cofactor.
81
Vitamin B5 (pantothenic acid): source
widespread in foods including liver, meat, eggs and potatoes
82
Vitamin B5 (pantothenic acid): properties
alcohol or calcium salt somewhat more stable and are used in vitamin preparations. Stable at neutral pH but not in acid or alkali.
83
Vitamin B5 (pantothenic acid): RX in Europe
a disulfide dimer called pantethine is used in Europe as a drug to lower cholesterol. Available in the US as a dietary supplement. Same with mild effects on decreasing total cholesterol. Controversial use in treating acne.
84
Biotin: Structure
Bound to enzymes so dietary proteins must be digested to lysine-biotin (biocytin) which is hydrolyzed by biotinase to release biotin. An inborn error with a defect in biotinase is known.
85
Biotin: Function
Carboxylation reactions. Examples are acetyl CoA to malonyl CoA to form lipids; pyruvate carboxylase in gluconeogenesis; propionyl-CoA carboxylase.
Active form is carboxybiotin
86
Biotin: deficiency
rare but symptoms include rash, hair loss, fatty acid deposits on face and depression
87
Biotin and Avidin
Protein found in egg whites that can precipitate deficiency state. Avidin has an incredibly high affinity for biotin and mainly is used in biotechnology. Streptavidin has the same properties of avidin.
88
Biotin: use
rarely used alone. Several biotin responsive inborn errors of metabolism are known, the most common is defective biotinidase. Some use for brittle nails and used together with selenium (Diachrome) for improved glucose tolerance in diabetics
89
Niacin: Chemistry
two active forms, niacin (nicotinic acid) and niacinamide, both are found in the diet. Coenzyme form is NAD (ADP attached) or NADP (ATP form). When you reduce the quartenary Nitrogen you get the reduced forms NADH and NADPH.
90
Niacin: Function
1. Redox and electron transport: know reaction for exam. Take a single C-C bond and form a double C=C bond.
2. Ribosylation of proteins in cell signaling and DNA replication and repair. NAD + protein --\> niacin + ADP-protein
91
Niacin: deficiency state
Pellagra. 4 D's include dermatitis, dementia, diarrhea and death. Common to see a "red tongue" and pigmentation. Occurred frequently in the "corn belt" during the 1900's because the strain of corn being produced contained little to no tryptophan or nicotinic acid.
92
Niacin: biosynthesis
B6 dependent mechanism from tryptophan to produce niacin. 60 mg of tryptophan produces about 1 mg of niacin through this mechanism. Isoniazid therapy can precipitate pellagra by binding up PLP and preventing conversion of tryptophan to niacin.
93
Niacin: source
meat, fish, whole grain cereals and peanuts. Typically is ingested as NAD or NADP and then is hydrolyzed in the intestinal mucosa in order to be absorbed.
94
Niacin: stability
very stable but much is lost if you discard the cooking water.
95
Niacin: uses
1. Improving serum lipids: used in high doses, side effects are a problem and include flushing. Extended release from is Niaspan which is RX only. Mechanism isn't entirely known.
2. Schizophrenia: high doses, unproven efficacy
3. peripheral vasodilator: unknown efficacy, based on side effect of flushing.
4 .diabetes: interest in niacinamide to prevent type 1 diabetes in high risk children and type 2 in adults. May help prevent pancreatic beta cells but results are preliminary so far.
96
Niacin: toxicity
peripheral vasodilation, flushing, GI upset, ulcers, diarrhea, impaired glucose tolerance, liver damage and increased gout. Associated with high doses and incidence decreases with continued use.
97
Vitamin C
ascorbic acid
98
Vitamin C (ascorbic acid): structure
Vitamin C in the reduced form is an active coenzyme only in the L configuration. Addition of 2 electrons forms dehydroascorbic acid which is inactive but acts as a free radical scavenger. Metabolism of dehydroascorbic acid forms oxalic acid which is excreted and may result in kidney stones.
99
Vitamin C (ascorbic acid): function
1. Dopamine --\> norepinephrine through DBH, dopamine beta-hydrolase. Ascorbic acid is the cofactor
2. proline --\> hydroxyproline which is a major mechanism of collagen synthesis and is the reason why signs of scurvy are generally associated with impaired collagen synthesis.
3. lysine hydroxylase --\> collagen
4. Folic acid --\> THFA. Explains the reason we see macrocytic anemia in scurvy.
5 .Involved in the absorption of iron in the gut. Fe has to be in the 2+ form which is catalyzed by ascorbic acid, for absorption. Vitamin C acts as a chemical reductant.
6. General antioxidant/free radical scavenger. Involved in preventing oxidation of LDL, vitamin E regeneration, and prevention of mutagenic compounds in gastric juices.
100
Vitamin C (ascorbic acid): deficiency
1. causes scurvy
2. Symptoms: hemmorhages, lassitude, weight loss, bone weakening, anemia, edema, and tooth loss
3. Biological lesions: impaired collagen synthesis due to lack of hydroxyproline, hydroxylysine and low THFA.
101
Vitamin C (ascorbic acid): Use
1. Surgery and fractures to increase collagen synthesis
2. Common cold prophylaxis: Linus Pauling started initial hypothesis. May reduce reduction in severity of colds but it does not prevent you from getting the cold
3. Cancer: High doses associated with lower cancer risks, including esophagus, stomach, colon and lung but studies that have supplemented with vitamin C have conflicting results
4. Heart disease: low dietary and blood levels are associated with an increased risk but supplements have no clear effect on outcomes.
5. Cataracts: higher intake shows lower risks but there is no proven benefit of intervention with supplements.
102
Vitamin C (ascorbic acid): Storage
present in most tissues at low levels. Threshold of about 200 mg/day and above this excess is excreted.
103
Vitamin C (ascorbic acid): Source
Richest source is green vegetables (uncooked) including broccoli, brussel sprouts and peppers. Citrus products, potatoes and tomatoes have modest/high amounts.
104
Vitamin C (ascorbic acid): Stability
in solution is unstable. Oxidized by air and is photolabile. Most vitamin C is destroyed in cooking foods.
105
Vitamin C (ascorbic acid): toxicity
nontoxic though gram doses may increase oxalate urine concentrations and subsequent increased risk for urinary stones. Can cause false positive sugar urine tests and false negative haemoccult tests
106
Vitamin C (ascorbic acid): bioavailability
the more vitamin C you ingest the lower the bioavailability becomes. Best dose is between 200-500 mg/day
