Vitamins Flashcards

1
Q

What is a vitamin?

A

Vitamins are organic compounds that are required for growth, maintenance of normal health and metabolism, reproduction. Cannot be synthesized in the body – with some exceptions.

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2
Q

Which are the vitamins that can be produced in the body?

A

Vitamin D – individuals without suffucuent exposure to UV light require a dietary source of vitamin D.

Niacin – can be found in beans, whole grains, nuts. Can be synthesized from the amino acid tryptophan, at low dietary intakes of tryptophan a dietary niacin source is needed.

Vitamin K – produced by the microbioata in the small intestine. New born infants haw low stores – they are usually given a prophylactic dose of vitamin K

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3
Q

What are come common reasons for vitamin deficiency?

A

Common reasons fro vitamin deficiency
1. Inadequate intake/absorption – poor diet, losses during food preparation (especially with water solubale vitamin), low bioadvailability of vitamins.

  1. Increased requirements – pregnancy and lactation, growth, ageing.
    Other factors: diseases, fat mal-absorption (A, D, E and K), drugs, alcohol and smoking.
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4
Q

Which are the fat soluble vitamins?

A

Fat soluble (A, D, E, K)

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5
Q

Which are the water soluble vitamins?

A

water soluble (B(8 different) and C)

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6
Q

Define vitamers and provitamins

A

Vitamers – members of the same family e.g. tocopherol, belong to the vit E family.

Provitamins – precursors that can be converted to yield a metabolically active form of the vitamin, e.g. 7-dehydrocholestrol -> cholecalciferol (vitamin D)

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7
Q

Where can vitamin A be found?

A

Vitamin A in animal food -> retinol (aldehyde form retinal and retinoic acid) can be found in liver, fish oil, milk, eggs, butter.

Carotenoids (with provitamin A-activity) (beta-carotene, alfa-carotene, beta-cryptoxhantine.

Carotenoids – yellow, orange, green , and red pigments synthesized by plants. Sources: yellow-orange fruits and vegetables and dark green leafy vegetables.

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8
Q

Where is vitamin A digested and absorbed?

A

~70-90% of dietary retinol absorbed in the small intestine (carotenoid uptake is lower).

Transported together with fatty acids.

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9
Q

How is fat soluble vitamins absorbed?

A

Consist of 7 steps.

  1. Release from food matrix.
  2. Solub. in fat, bile, pancr. secr.
  3. Micelle formation
  4. Uptake into mucosa (sv: slemhinna)
  5. Packag. chylomicrones
  6. Transport with the lymph to tissue and the liver.
  7. Storage in the liver.
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10
Q

Describe the overview of the absorption, metabolism and transport of carotenoids.

A

Carotenoids (betaC) are partly metabolized to retinol (RE) within the intestinal cells and incorp. In chylomicrons, stored in the liver or distr. In LDL to various tissues.

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11
Q

Describe bio-availability of carotenoids.

A

The more processed the better bio-availability.

Physicochemical properties: species of carotenoids (LUTEIN* > alfa-, beta-carotene > lycopene. TRANS vs cis isomers. FREE vs esterified vs protein bound.

Food matrix and processing: particle size (PUREE>chopped>leas/whole). Raw vs PROCESSED.

Mechanical and thermal pre-treatments of crushed tomatoes: effects on consistency and in vitro accessibility of lycopene. Higher release of lycopene after longer crushing time combined with high- temp treatment. Both particle size and heat treatment are important factors.

Factors that can improve the uptake of carotenoids from fruit and vegetables.
Heat treatment (denature protein associated with it), homogenization (pureeing, chopping, grating) (When we create samller particles we also make the caratones more assaisable for the enzymes aswell as destroying cellstructures), addition of fat( solubalisation)
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12
Q

What is the function of vitamin A?

A

Vitamin A plays essential roles in: vision, growth and development, cell differentiation, immune functions, reproduction, maintenance of healthy skin, hair and membranes.

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13
Q

What are some symptom of vitamin A deficiency?

A

Night blindness is one of the first signs of vitamin A deficiency. In ancient Egypt, it was known that night blindness could be cured by eating liver. Vitamin A deficiency contributes to blindness by making the cornea very dry and damaging the retina and cornea.

Signs in order of severity:
1. Night blindness – impairment/inability to see in dim light (reversible)

  1. Conjunctival xerosis/bitots spot (dryness and foaming accum. Of the inner eye lids/membranes)
  2. Corneal xerosis (dryness of the cornea)
  3. Xeropthalmia (keratinization and ulceration of the cornea) causes blindness.
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14
Q

What are some groups at risk of Vitamin A deficiency?

A

Premature infants – preterm infants do not have adequate liver stores of vitamin A at birth – increased risk of eye, chronic lung, and gastrointestinal diseases.

Infants and young children in developing countries – in women with vitamin A deficiency, breast milk volume and vitamin A content are suboptimal. The most common and readily recognized symptom of vitamin A deficiency in infants and children is xerophthalmia.

Pregnant and lactating women in developing countries – pregnant women need extra vitamin A for fetal growth and tissue maintenance and for supporting their own metabolism. WHO estimates 9.8 million pregnant women around the world have xerophthalmia as a result of vitamin A deficiency. Other effects – increased maternal and infant morbidity and mortality increased anemia risk and slower infant growth and development.

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15
Q

How is zinc and vitamin A connected?

A

Severe zinc deficiency often accompanies vitamin A deficiency. Zinc is required to make retinol binding-protein(RBP) -> a deficiency in zinc limits the bodys ability to move vitamin A stores from the liver to body tissues.

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16
Q

What are som risk with to high vitamin A intake?

A

Potential and major adverse effects:
1. Tetratogenicity (increases risk of birth defects) – pregnant women are advised not to consume >3mg/d.

  1. Excessively high intakes – accumulation in liver and other tissues (>7-9 mg/d).
  2. Reduced bone mineral density – may result in osteoporosis.
17
Q

How does antioxidant supplement impact cancer incidence?

A

Supplementation with vitamin C, vitamin E or beta-carotene failed to reduce cancer risk. (totally 7,627 women who were at high risk of cardiovascular disease in the study). Additionally, beta-carotene use was associated with a modest excess of lung cancer, which is consistent with previous reports.

However, epidemiological evidence show that high dietary intakes of carotenoids are associated with a low incidence of CVD and some forms of cancer. -> dietary sources (food) of vitamins provide a combination of “phytochemical” nutrients that may have beneficial effects… and at a “natural” level.

18
Q

Where can vitamin D be found?

A

Vitamin D comes in two forms D2 and D3.

We can obtain vitamin D2 from the provitamin ergosterol (in plants, micro-organisms) that becomes D2 – ergocalciferol.

Vitamin D3 from 7-dehydrocholesterol (animal products and formed in the skin) becomes vitamin D3 – cholecalciferol.

Food sources of vitamin D
Fish, milk, egg, mushrooms.

19
Q

How is vitamin D converted in the body?

A

Conversion of 7-dehydrocholestrol in the body. Skin -> liver -> kidney -> target tissues
Enzymatic conversion by enzymes in the liver and the kidney.

20
Q

Describe the metabolism of vitamin D.

A

Vitamin D3 either from food or provitamin D3 (7-DCH) via the skin -> plasma vitamin D3 -> vitamin D3 in the liver -> 25 (OH)D3 by enzymes hydroxylase from the liver to the kidney 25(OH)D3 -> 1,25 (OH)2D3 via enzyme hydroxylase -> plasma 1,25 (OH)2D3. Hydroxylases comes from the PTH (parathyroid hormone).

21
Q

What is the main function of vitamin D in the human metabolic processes?

A

Increased active calcium absorption: maintain normal blood levels of calcium and phosphate, mineralization of bone, muscle contraction, cellular functions, gene transcription -> Ca-transporting and bone matrix proteins.

22
Q

What is the action of calcitriol (“active vitamin D”)?

A

Increases absorption of Ca and P, maintains Ca-homeostatic in interaction with PTH, regulates its own renal production/degradation?, facilitates skeletal mineralisation, stimulates bone resorption (urinary Ca-reabsorption in kidney)

23
Q

What can cause vitamin D deficiency and what are some results of it?

A

Reduced intake/uptake (low fat) or synthesis of cholecalciferol. Disorder associated with abnormal gut function: small bowel disorders, pancreatic insufficiency, bilary obstruction. Reduced synthesis in skin or enhanced degradation 25OHD.

Rickets (children) – poor absorption of calcium -> “soft bones”
Osteomalacia (adults) – inadequate bone mineralization -softening and weakening of bones. Loss of bone mass (low vitamin D- and Ca-status) -> fragile bones.

24
Q

What are some factors that can redige the skin synthesis of vitamin D?

A

Latitude and season – both influence the amount of UV-light reaching the skin. In winter no vit D prod. At latitudes >42 degree N/S.
The ageing process . the thinning of the skin reduces the efficiency of the process. Pigmentation – people with darker skin may need 3-6 times longer exposure. Clothes -religious or culture habits

25
Q

What is the toxicity of vitamin D?

A

Cannot be caused by prolonged exposure of the skin to UV-light. Vitamin D intoxication may occur with excess oral intake through supplementation (> 250 mikrog/day) adults (some infants sensitive to intake of 50 mikrog/day) results in high blood pressure, calcinosis (calcification of tissues in kidney, heart, lungs)

26
Q

Where can vitamin E be found?

A

Found in different oils
Tocopherols and tocotrienols.

High intake (>1.2 mg/d) may impair the ability of thromb to aggregate (vit K metab.)

27
Q

Who can have a risk for deficiency when it comes to water soluble vitamins?

A

small bowel diseases, drug intakes and elderly, alcoholics.

28
Q

What are some consequence of vitamin B1 deficiency?

A

Beriberi: Singhalese, meaning “cannot”, since persons with severe beriberi cannot move easily – affects the peripheral nervous systems. Common in populations with diets in which polished (white or dehulled) rice is the major food. Thiaminases, enzymes in e.g. fermented fish can also lead to deficiency.

29
Q

What are some consequence of niacin (B3) deficiency?

A

Pellagra (from the Italian words: pelle=skin; agra=rough) Characterized by tissue damage, dermatitis – reddish skin rash, especially on face, hand, feet and gastrointestinal tract, nerve. Advance pellagra(the 3D): diarrhoea, depression or dementia

30
Q

What is B-vitamins function?

A

Function – coenzymes in many areas of metabolism some are very important for cell differentiation and growth.

Vitamin B12 helps to maintain healthy nerve cells and red blood cells, it is also needed for DNA.

Thiamine B1, riboflavin B2, Pyridoxin B6, biotin, niacin, pantothenic acid, Cobalamin B12 and folate/folic acid.

31
Q

Where can you find B12?

A

Vitamin B12 cobalamin – primarily in animal products; eggs, milk and meat (can be formed by micro-organism).

Total body pool 2.5 mg, daily losses ~1-2.5 mikrog. An egg or glass of milk contain ~1mikrog. Absorption of B12 – the role of the glycoprotein “intrinsic factor”, gastric acid and pepsin.

32
Q

How is B12 absorbed?

A

Consist of 5 steps.

  1. Hydrolysed form protein in the stomach.
  2. Binding to R-proetin
  3. Released by digestive enzymes binding to IF
  4. Absorption of B12 in the ileum
  5. Transport to the liver.
33
Q

What is the result of vitamin B12 deficiency?

A

Pernicious anaemia. Functional folate deficiency, degeneration of the spinal cord.

34
Q

What is the most common results of vitamin B12 deficiency?

A

The most common results of adult vitamin B12 deficiency. Caused by impaired absorption of vitamin B12 – due to absence of intrinsic factor, and more specifically loss of gastric parietal cells. A form of megaloblastic anemia (due to B12 and/or folate deficiency resulting in inability to produce enough DNA for blood cell synthesis) (characterized by many large immature and dysfunctional red blood cells (megaloblasts) in the bone marrow)

35
Q

What is folate and folic acid?

A

Folate is a group pf water soluble B vitamin with a structure similar to that of folic acid.
Folic acid is the synthetic form of folate (used in supplements)
Food sources of folate: liver, dark green leafy vegetables, broccoli, oranges, berries and legumes

36
Q

Describe folate and folic acid, in terms of stability and bio-availability.

A

Natural food folate are quite unstable during processing – in vegetables >40% per cent of folates can be destroyed by cooking. In grains/cereals >70% can be destroyed by milling and baking, bio-availability vary 30-98% depending on folate form and type of food. Folic acid – more stable during storage and processing – appears to have a bio-availability of close to 100%.

37
Q

What is folates function in the body?

A

Folate has a number of critical functions within the body: production of rede and white blood cells, RNA & DNA, normal development of the foetus in pregnant women. Folate deficiency is associated with an increased risk of: neural tube defects (NTD) e.g. spina bifida, CVD and stroke, certain forms of cancers, Alzheimer’s, dementia, megaloblastic anaemia.

Spina bifida (“split spine”) one of a class of serious birth defects called neural tube defects (NTD). Can happen anywhere along the spine if the neural tube does not close all the way, often results in damage to the spinal cord and nerves (leading to a range of motor and sensory problems, and disturbance of e.g. bowel and bladder functions). Studies have shown that women how get 400 mikrog/day of folic acid prior to conception and during early pregnancy reduce the risk of NTDs by 70%.

38
Q

What is the metabolic role of folate?

A

The metabolic role of folate is as a carrier of one carbon fragments in amino acids metabolism and is very essential for the synthesis of RNA and DNA.

In the diet, folate exist as polyglutamates and needs to be methylated and reduced within the jejunal mucosa in order to be absorbed, a major form is 5-methyl-tetrahydrofolate.

39
Q

How is B12 and folate dependent on each-other?

A

B12 will pick the metyl group from 5-metyl-tetrahydrofolate and tetrahydrofolate is produced. This is used for RNA and DNA synthesis.

B12 with metyl group is the moved on and reacts with homocysteine creating methionine.

Methionine syntethase is a vit. B12 dependent enzymes.

Methionine (essential AA) is produced from 5-metyl-tetrahydrofolate.

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