10. Water Soluble Vitamins Flashcards

1
Q

Which B vitamins are no longer considered vitamins?

A
  • Other substances once thought to be vitamins were given numbers in the B- vitamin numbering scheme, but were subsequently discovered to be either not essential for life or manufactured by the body, thus not meeting the two essential qualifiers for a vitamin.
  • Vitamin B4: can refer to the distinct chemicals choline, adenine, or carnitine.
  • Vitamin B8: refers to adenosine monophosphate (AMP), or to inositol.
  • Vitamin B10: para-aminobenzoic acid (PABA), a chemical component of the folate molecule produced by some plants and bacteria.
  • Vitamin B11: pteryl-hepta-glutamic acid.
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2
Q

What are vitamins?

A
  • Necessary compounds for growth and cellular metabolism
  • Only necessary in trace amounts
  • Organic compounds
  • Some can be made in vivo in small amounts.
  • eg. Niacin, Vitamin D, Vitamin K and Vitamin B12 (but not absorbed)
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3
Q
A
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4
Q

What are the 8 B group vitamins?

A
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5
Q

What is the function of vitamin B1 thiamine?

A
  • Main function is in energy metabolism as an integral part of the coenzyme TPP (thiamin pyrophosphate) involved in the conversion of pyruvate to acetyl CoA.
  • TPP facilitates the removal of a carbon group from pyruvate to yield acetyl- CoA (2 carbons) and a carbon dioxide. TPP is also involved in a later step in the TCA cycle in which a carbon group is removed from a 5C compound.
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6
Q

What happens in the beriberi form of thiamine deficiency?

A
  • Thiamin deficiency leads to nerve tissue damage, paralysis, oedema and muscle wasting (wet beriberi).
  • The common term for thiamine deficiency is Beriberi. Common in populations consuming high white rice diets with little other food types, as the thiamine containing germ portion of the rice grain is removed in the milling process.
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7
Q

What happens in the alcohol induced form of thiamine deficiency?

A
  • There is also an alcohol induced form of thiamine deficiency called Wernicke-Korsakoff syndrome common in alcoholics (dry beriberi).
  • Alcohol displaces food from the diet and lowers thiamine intake and increases urinary excretion of thiamine.
  • Both forms of deficiency can be treated with thiamine supplements.
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8
Q

What is dry beriberi?

A
  • Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves. It is characterized by:
  • Difficulty in walking
  • Tingling or loss of sensation (numbness) in hands and feet
  • Loss of tendon reflexes
  • Loss of muscle function or paralysis of the lower legs
  • Mental confusion/speech difficulties
  • Pain
  • Involuntary eye movements
  • Vomiting
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9
Q

What is wet beriberi?

A
  • Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart
  • failure and weakening of the capillary walls. Wet beriberi is characterized by:
  • Increased heart rate
  • Vasodilation
  • Dyspnea (shortness of breath) on exertion
  • Peripheral edema (swelling of lower legs)
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10
Q

Are dry and wet beriberi considered different types of deficiencies?

A
  • Beriberi – two stages of the same deficiency:
  • In dry beriberi, the peripheral neuropathy and brain damage are seriously symptomatic before the congestive heart failure begins.
  • In wet beriberi, the heart starts to fail before the nerve and brain damage are obvious. Beriberi mainly seen in famine, people on binge drinks, abuse of children or the disabled, or extreme goofy diets.
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11
Q

What are the food sources of thiamine?

A
  • Thiamin is found in many foods such as whole grains, meat and fish, but is particularly rich in ham, pork, sunflower seeds, watermelon, fortified cornflakes and soy milk.
  • Thiamine is lost from grains in milling (removal of germ of grain) and is easily destroyed by prolonged heating in food processing and leached from foods when cooked in water.
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12
Q

What is the function of riboflavin vitamin B2?

A
  • This vitamin is a tricyclic ring structure composed of C,H,O,N.
  • One of its most important functions is as the coenzyme Flavin adenine dinucleotide (FAD), involved in numerous reactions including the movement of Hydrogen atoms and their high energy electrons from the TCA cycle to the ETC.
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13
Q

What are the food sources of riboflavin?

A

Primary sources are dairy products, meat, leafy green vegetables, cereals, eggs, liver and fortified cornflakes.

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14
Q

What are the deficiency and toxicity symptoms of vitamin B2 riboflavin?

A
  • Deficiency symptoms
    • Inflamed eyelids, sensititivity to light, sore throat, cracks and redness at corners of mouth, painful, smooth, purple tongue, general skin inflammation with greasy scales.
  • Toxicity symptoms
    • None known.
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15
Q

What is the structure of vitamin B3 niacin?

A
  • A single ring structure composed of C, H, O, N
  • Exists in two molecular forms: nicotinic acid and nicotinamide which are easily inter-converted.
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16
Q

What amino acid can niacin be made from?

A
  • Some niacin can be made in the body from the amino acid tryptophan, though the conversion rate is poor (1:60), ie 1 mg niacin results from 60 mg ingested tryptophan.
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17
Q

How does niacin give rise to the coenzyme NAD?

A
  • Niacin has two coenzyme forms in the body:
  • Nicotinamide adenine dinucleotide (NAD) and its phosphate form NADP
  • Both participate in many energy transfer reactions and carry Hydrogens and their high energy electrons from the TCA cycle to the ETC in a similar manner to riboflavin coenzymes.
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18
Q

Where is the hydrogen atom carried on NAD?

A
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19
Q

What happens when there is niacin deficiency?

A
  • Termed pellagra, symptoms include diarrhea, dermatitis, dementia (ddd) and eventual death
  • In the dermatitis of pellagra, the skin darkens and flakes away as if it were sunburned.
  • The dermatitis is symmetrical and occurs only on parts of the body exposed to the sunlight.
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20
Q

What are the food sources of niacin?

A
  • Good sources include liver, meats, fish, mushrooms and fortified breakfast cereal
  • Niacin can also be made in vivo from the amino acid tryptophan
  • Dietary protein contributes to niacin supply, therefore protein rich diets are never deficient in niacin. However it takes 60 mg of tryptophan to make 1 mg of niacin.
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21
Q

What are the symptoms of niacin toxicity?

A
  • Painful skin flush, hives and rash, excessive sweating, blurred vision, liver damage, impaired glucose tolerance.
  • Large doses of niacin have a pharmacological effect on the nervous system, blood lipids and blood glucose.
  • Large doses have been used in lowering blood cholesterol levels
  • In the nicotinic acid form large doses can dilate capillaries in the skin causing a hot tingling flush.
  • Diarrhoea, nausea, ulcers, vomiting, dizziness, fainting, liver damage and low blood pressure can result from
  • high doses.
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22
Q

What is the function of vitamin B5 pantothenic acid?

A
  • Pantothenic acid is involved in over 100 metabolic steps, mostly in its coenzyme form (coenzyme A)
    • Energy metabolism
    • Lipid synthesis
    • Neurotransmitter synthesis
    • Steroid hormone synthesis
    • Haemoglobin synthesis
  • In energy metabolism pantothenic acid is critical as a component of acetyl-CoA, as the cross-roads compound leading into energy release from the TCA cycle and electron transport chain or to fat production .
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23
Q

What is the common form pantothenic acid is found in?

A
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24
Q

What are the symptoms of pantothenic acid deficiency and toxicity?

A
  • Pantothenic acid deficiency
    • Deficiency is rare but results in general failure of bodily systems, with nervous system faults often being early signs (insomnia/fatigue), followed by nausea and vomiting.
  • Toxicity symptoms
    • None known
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25
Q

What are the three forms of vitamin B6 pyridoxine?

A
  • Exists in 3 forms.
  • All can be converted to the active coenzyme forms: PLP (pyridoxal phosphate) and PMP (pyridoxamine phosphate).
  • The three forms consumed in our diet are:
    • pyridoxal
    • pyridoxine
    • pyridoxamine
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26
Q

What is the function of pyridoxine vitamin B6?

A
  • PLP (pyridoxal phosphate) coenzyme useful in amino acid metabolism as it has the ability to transfer amino groups from one amino acid to other compounds such as keto acids, therefore helping to synthesise non-essential amino acids.
  • Also involved in protein and urea metabolism
  • Involved in conversion of the amino acid tryptophan to niacin and the neurotransmitter serotonin
  • Involved in synthesis of haem protein, nucleic acids and lecithin
  • Influences cognitive development, immune function and steroid hormone activity
  • Different to other water soluble vitamins because it can be stored in muscle tissue.
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27
Q

What are the two coenzyme forms of vitamin B6?

A
28
Q

Which drugs interact with vitamin B6 pyridoxine?

A
  • Many drugs interact with vitamin B6:
    • eg; INH (isonicotinic acid hydrazide), a drug which inhibits tuberculosis bacterium, but inactivates vitamin B6 by binding to it and leading to a deficiency.
  • Alcohol interacts seriously with vitamin B6:
    • Acetaldehyde from alcohol oxidation interferes with PLP coenzyme.
    • PLP is separated from its enzyme and is excreted, therefore alcohol is responsible for vit B6 deficiency
29
Q

What are the symptoms and toxicity of vitamin B6 pyridoxine?

A
  • Vitamin B6 deficiency
    • Deficiency can lead to: weakness, kidney stones, irritability, insomnia, anemia, dermatitis, depression
    • Eventually this can result in: growth failure, impaired motor function, convulsions, impaired immune function
  • Vitamin B6 toxicity
    • Difficult to reach toxicity from normal food intake. Some women using concentrated supplements for PMS have suffered from nerve damage, bloating, depression, fatigue and headaches.
30
Q

What are the food sources of vitamin B6 pyridoxine?

A

Main sources include meat, fish, poultry, vegetables and fruit. There is a lower bioavailability from plant derived foods and it can be lost through heating food.

31
Q

What is the structure of biotin vitamin B6?

A
  • Biotin has an unusual ring structure containing C,H,O,N and S attached to a short chain fatty acid
  • Forms a coenzyme which is involved in several important metabolic pathways
  • The most critical function of biotin in energy metabolism is in facilitating the reaction of CO2 with pyruvate to yield oxaloacetate (critical for TCA cycle continuity).
32
Q

What is the role of biotin in metabolism?

A
  • Biotin acts as a coenzyme in this critical energy metabolism pathway. Assisting the enzyme Pyruvate carboxylase to add a carbon dioxide to the 3C pyruvate molecule to produce oxaloacetate (4C).
  • In this way the TCA Cycle is kept functioning. Without added oxaloacetate the acetyl CoA entering the TCA Cycle would have insufficient oxaloacetate to react with to continue the cycle.
33
Q

What are the symptoms of biotin deficiency and toxicity?

A
  • Deficiency is extremely rare due to the small amount required and its availability in many foods.
  • Deficiency can be induced by massive consumption of raw egg whites (contains the binding protein avidin, which prevents absorption of biotin).
  • General symptoms being nausea, loss of appetite, depression, fatigue, dry skin.
  • Toxicity symptoms are not known
34
Q

What is the structure of vitamin B9 folate?

A
  • Triple ring structured complex made up of C,H,O,N and is often referred to as folic acid or folacin, depending on its exact molecular structure.
  • The various forms are easily inter-converted and have the same biological function
  • Chemical name for folate is pteroylglutamic acid (PGA)
  • Folate contained in our food consists of the ring structures with multiple glutamic acids (an amino acid) attached.
  • The supplemental form of folate has only one glutamic acid unit attached.
35
Q

What are the coenzyme forms of folate?

A
  • Folate forms the coenzymes: dihydrofolate (DHF) and tetrahydrofolate (THF).
  • The latter (THF) being important in the metabolism of 1 carbon compounds. That is in adding or removing methyl (CH3) groups during metabolic processes.
36
Q

How does folate act as a methyl group donor?

A
  • Folate and vitamin B12 interact substantially and are important in cell division and multiplication and a number of other metabolic steps where transfer of a methyl group is critical.
  • ie Vitamin B12 acts as the transfer agent, transferring a methyl group from folate to the compound requiring a methyl group.
37
Q

How is folate processed in the body for its digestion, transport and storage?

A
  • Folate in food has a chain of glutamates (amino acid) attached (thus folate is said to be in a bound form). Intestinal cell wall enzymes remove all but one glutamate (free form) then attach a methyl group. This form of folate (methyl-THF) is inactive.
  • Absorption into blood follows, then storage in cells occurs as the inactive methyl-THF form. Excess folate is secreted by the liver into the gall bladder with bile. The intestines reabsorb some of this folate and return it to the liver (enterohepatic circulation), any excess transits the GI tract and removed in faeces.
38
Q

How is folate activated?

A
  • The folate is absorbed with only one glutamic acid attached.
  • A methyl group is then attached to the remaining glutamic acid end.
  • Once formed the methyl-THF is inactive and is stored in this form until needed.
  • Activation occurs by removal of the methyl group by vitamin B12.
  • The THF now becomes active and the vitamin B12 now with a methyl group is activated also. Thus the two vitamins work in unison
39
Q

What happens in folate deficiency?

A
  • Folate deficiency impairs cell division and protein synthesis. Red blood cells, DNA and GI tract mucosal cells are effected the most noticeably.
  • GI tract injury can impair folate reabsorption leading to greater folate deficiency and further GI tract injury.
  • High alcohol intake initiates GI tract injury leading to folate deficiency which again lowers absorption of other nutrients.
  • Visual evidence of folate deficiency are large immature RBC termed macrocytic or megablastic anemia.
  • Factors leading to deficiency include lack of fruit and vegetable intake, and goats milk formulas in young children and some drugs in adults
40
Q

How does folate deficiency change morphology of red blood cells?

A
41
Q

How does folate deficiency affect red blood cell production?

A
42
Q

How can folate deficiency cause neural tube defects?

A
  • Cause is uncertain, but women consuming excess levels of folate have a lower probability of having a baby with a neural tube defect.
  • Neural tube is embryonic tissue of the central nervous system (CNS).
  • Defects in formation of this tissue lead to spina bifida and anencephaly (portion of brain, skull and scalp does not form).
43
Q

How have folate supplements during pregnancy helped foetal development?

A
  • Extra folate during pregnancy, particularly the first trimester has resulted in decreased cases of Spina Bifida, and neural tube defects in general.
  • Most countries now fortify foods with folate for the benefit of growing children and pregnant women.
  • Also pregnant women are usually advised by doctors to take supplemental folate during pregnancy, particularly the first trimester, which appears to be a “window of opportunity” (critical period) for neural development that cannot be fully recovered from later.
44
Q

What are the food sources of folate?

A
  • Best sources are liver, legumes and vegetables and folate fortified foods. Dairy products are a poor source, and folate is destroyed easily by cooking.
  • Folate is the most vulnerable B group vitamin in terms of interactions with drugs, leading to deficiency.
  • In Australia, from 13 September 2009, mandatory folic acid fortification began requiring the addition of folic acid to all wheat flour for bread making, with the exception of organic bread.
45
Q

What are the symptoms of folate toxicity?

A

None known, however excess dietary folate (supplementation) can mask a vitamin B12 deficiency.

46
Q

What are the different forms of vitamin B12?

A
  • A cobalt containing organic molecule also known as cobalamin
  • Cyanocobalamin (shown*) is a synthetic form of vitamin B12 found only in supplements, while methylcobalamin (CH3-B12) is a naturally occurring form that you can get through either food sources or supplements.
  • When cyanocobalamin enters your body, it’s converted into either methylcobalamin or adenosylcobalamin, which are the two active forms of vitamin B12 in humans
47
Q

What is the function of cobalamin vitamin b12 in the body?

A
  • Works in conjunction with folate. The cobalamin removing a methyl group from the folate and in doing so activating both the folate and cobalamin
  • Vitamin B12 is indirectly necessary for DNA and RNA synthesis and cell multiplication as it converts the inactive methyl-THF to the active THF form of folate to support these functions
  • Vitamin B12 itself also maintains the myelin sheath around nerve fibres. Nerve cell damage results from B12 deficiency. Bone cell activity and metabolism are also B12 dependent.
  • Viatamin B12 is only available from animal foods. It is made by bacteria in the GI tract of many animals, including us. But we cannot absorb this B12 as it is made in the lower part of the GI tract.
48
Q

How is vitamin B12 processed in the body?

A
  • Vitamin B12 is attached to proteins in food and must be removed by HCl and pepsin (stomach enzyme) during digestion.
  • An intrinsic factor (glycoprotein carrier) is attached to vitamin B12 in the stomach, which is essential to allow absorption into bloodstream from the small intestine.
49
Q

How does vitamin B12 deficiency occur?

A
  • Deficiency is rare due to poor diet but if it does occur, it is most likely in vegans
  • Deficiency is usually due to poor absorption rather than inadequate intake. Major reasons being low stomach HCl levels (atrophic gastritis) or lack of intrinsic factor (pernicious anaemia).
  • Pernicious anaemia is characterised by large red blood cells (megablastic anemia) as in folate deficiency, weakness and nerve dysfunction. All have a slow onset.
  • Low B12 also leads to folate deficiency. Although the diet may have adequate folate, it is trapped as the inactive form (methyl-THF) due to absence of sufficient B12 to activate it.
  • Vitamin B12 deficiency has been often misinterpreted as folate deficiency and treated with folate supplements resulting in disability or death from the underlying, untreated Vitamin B12 deficiency.
50
Q

What are the food sources of vitamin B12?

A
  • Found exclusively in foods from animals such as meat, milk, cheese, eggs.
  • Vegans need to consume fortified soy milk, fortified TVP (textured vegetable protein, soy based) or take supplements
  • Miso (soybean paste) spirulina, yeast and mushrooms do not contain Vitamin B12 even though many non scientific references suggest they do. These are not active B12 molecules but “analogues” that do not have B12 functionality in humans.
  • Mushrooms may have some Vitamin B12 on them from contamination by fecal matter from the growing medium
  • Vitamin B12 is produced by bacteria in the GI tract of animals (even humans) so is rich in fecal material
51
Q

Which b group vitamins are seen in coenzymes?

A
52
Q

What is the structure of vitamin C?

A
  • Only non B group vitamin that is water soluble.
  • It is a 6 carbon compound, structurally similar to glucose.
53
Q

What are the two forms of vitamin C?

A
  • Has 2 active but interchangeable forms, the reduced form (ascorbic acid) and the oxidised form (dehydroascorbic acid).
  • Two hydrogen atoms with their electrons are lost when ascorbic acid is oxidised and gained when it is reduced again.
54
Q

What is the role of vitamin C as an antioxidant?

A
  • Vitamin C is oxidised in preference to other substances and therefore protects them.
  • As an antioxidant it is often added to processed foods as a preservative.
  • In the body it is involved in vitamin E regeneration when it (Vit E) has been oxidised.
  • Vitamin E complements vitamin C as a fat soluble antioxidant in cell membranes, while Vitamin C protects compounds and structures in the fluid environment within cells and around them.
55
Q

How does vitamin C assist in collagen formation?

A
  • Vitamin C assists in the formation of the structural protein collagen, which is a fundamental component of connective tissue (cartilage, bones, blood vessels etc).
  • Collagen contains many proline and lysine groups, which must be hydroxylated prior to their addition to the peptide chain.
  • This reaction requires the enzyme hydroxylase which requires iron as a cofactor.
  • Iron in turn requires vitamin C to maintain it in the correct oxidative state.
56
Q

What are the symptoms of vitamin C deficiency?

A
  • Helps maintain blood vessel integrity through collagen formation. Therefore depleted vitamin C leads to bleeding gums and subcutaneous bleeding followed by failure to make collagen.
  • This leads to internal hemorrhaging, muscle degeneration, rough dry skin, bone degeneration, infections, hysteria, depression and death.
  • Early symptoms known as scurvy involve bleeding gums.
  • Symptoms are cleared within 5 days by simple Vitamin C supplementation of 100 mg per day.
57
Q

What is the role of vitamin C in stress?

A
  • Vitamin C is required in higher amounts in stress situations, mainly wound healing and infection.
  • This is due to increased immune system activity which uses oxygen, producing dangerous oxidants (vitamin C inhibits their formation).
58
Q

How does vitamin C affect hormones?

A
  • Norepinepherine (noradrenaline a hormone and neurotransmitter responsible for mobilizing the brain and body for action) and thyroxin (T4 – involved in regulation of metabolism) require vitamin C in metabolism of amino acids prior to their formation.
  • The hormone producing adrenal glands are extremely rich in vitamin C. During stress the vitamin is released into the blood
59
Q

What are the symptoms of vitamin C toxicity?

A
  • Excess intake (>1-2 grams/ day) can lead to nausea, diarrhoea and abdominal cramps.
  • Can interfere with anticoagulants such as warfarin and heparin although the method is unclear.
  • In metabolic abnormalities can form kidney stones if intake is high.
  • High vitamin C intake can lead to increased iron absorption and release from body tissue leading to iron overload in the blood
  • High vitamin C intake and excretion can give false positive urinary diabetes tests as vitamin C can be falsely identified as glucose due to their similar structure.
60
Q

How does the body adapt to high vitamin C intake?

A
  • The body adapts to high Vitamin C intake by up-regulating efficiency of excretion.
  • A sudden drop in intake to normal RDI levels may cause a deficiency (with-drawl reaction) as the body is still excreting large amounts and takes time to adjust.
61
Q

What are the food sources of vitamin C?

A

The main dietary sources of vitamin C are fruits and vegetables, in particular citrus, berries, cabbage type vegetables, dark green vegetables, strawberries, watermelon, peppers, kiwi fruit, tomatoes etc.

62
Q

What is choline as a water soluble vitamin consideration?

A
  • Important part of phospholipids in cell membranes and can be made in vivo from the amino acid methionine (meat, milk, liver, eggs, peanuts)
  • Synthesis alone cannot produce enough choline at all stages of life, so it must be obtained from foods (lecithin and any membrane material in the diet) at certain times
  • It is therefore termed conditionally essential
63
Q

What are inositol and carnitine as water soluble vitamin considerations?

A
  • The situation with these two compounds is less clear and it seems the body can synthesise the amount required. No intake levels have been set.
  • Inositol like choline is a component of phospholipids in cell membranes
  • Carnitine is needed to as part of carnitine tranferase enzyme, to move fatty acids from the cytoplasm to the mitochondria for metabolism into energy.
  • The body can make carnitine and does so locally where needed in the cytoplasm.
  • There is controversy still over whether dietary/supplemental carnitine actually gets to the cell cytoplasm where needed.
64
Q

Why is PADA not required in the human body?

A
  • Vitamin imposters
  • In other cases of supposed new vitamins, the body makes its own supply or does not require the compound at all (eg para-amino benzoic acid : PABA).
  • PABA is an intermediate in the bacterial synthesis of folate. It has been referred to as Vitamin Bx. Humans lack the enzymes to convert PABA to folate, and thus require a dietary supply of folate.
65
Q

What are the six predominant vitamin imposters?

A
  • Hesperiden (vit P)
  • Pyroloquinoline quinone: (insufficient information is available so far to state that PQQ is a vitamin for mammals, although PQQ may be an important biological factor)
  • Orotic acid: (once believed to be part of the vitamin B complex and called vitamin B13, but it is now known that it is not a vitamin but is manufactured in the body by intestinal flora)
  • Lipoic acid: (Humans biosynthesize lipoic acid and it is not a required vitamin)
  • Vitamin O (oxygenated sea water)
  • Pangamic acid (vit B 15): (it is not a true vitamin, has no nutritional value, has no known use in the treatment of any disease and has been called a “quack remedy”)