L11 & 12 - Vitamins Flashcards
What are vitamins?
Vitamins is a complex organic substance which is required in diet in small amounts. Absence of vitamins causes deficiency diseases.
How are vitamins categorised?
Fat soluble Vitamins: A, D, E, K
- stored - not needed regularly (less likely to get deficiency)
- not absorbed or excreted easily
- excess amounts is toxic (A, D)
Water soluble Vitamins: B group (co-factors of metabolic pathways), C
- not stored
- required regularly - more prone to getting deficiencies
- excess amounts is not toxic (B, C, E)
THIAMIN (B1):
What is thiamin? And which individuals are more susceptible to this?
DRV?
Source?
Foodstuff deficient in thiamin?
Role?
Thiamin deficiencies:
Wernicke Encephalopathy/ Korsakoff Psychosis:
How does alcohol causes thiamin deficiency?
Why do alcoholics suffer from Vit B deficiencies:
Thiamin is an anti Beri-Beri factor. Individuals whose staple food is white rice and raw fish (thiaminase) tend to be thiamin deficient.
DRV: 1mg/day (more is required in those who primarily have carb rich diet)
Source: Vegetables, Dairy, Fish and poultry, Whole grain
Foodstuff deficient in thiamin: Raw fish (Thiaminase), processed foods and white rice, tea and coffee (anti thiamin factor)
Role: Thiamin pyrophosphate (TPP) found in pyruvate dehydrogenase and allows conversion of pyruvate to acetyl CoA. If no thiamin = no TPP. No conversion of pyruvate to acetyl CoA —> instead converted to lactate. Causes fatigue.
Thiamin Deficiencies:
1) Infantile Beri-Beri = mother is thiamin deficient so no thiamin in milk and none in baby. Causes cardiovascular symptoms.
2) Acute cardiac Beri-Beri (wet Beri-Beri) = Congestive/sudden heart failure, enlarged heart and liver, engorged neck veins, OEDEMA.
3) Chronic Dry Beri-Beri = Symmetrical ascending peripheral neuropathy (causes weakness, numbness and painful extremities).
Wernicke Encephalopathy/ Korsakoff Psychosis:
- commonly seen in alcoholics (3rd most common cause of dementia)
Wernicke’s (WE) = confusion, ataxia, polyneuropathy, disorientation in time and space. (Reversible)
Korsakoff = memory loss of recent events. (Irreversible, occurs if WE is untreated and prolonged thiamin deficiency).
Alcohol causes:
- anorexia
- inhibits thiamin absorption
- inhibits enzyme which converts thiamin to TPP
Why do alcoholics suffer from Vit B deficiencies:
- impairs nutrient absorption
- alcohol is empty calories so reduces intake of vitamins and nutrients
- liver cirrhosis can impair transport, storage and metabolism of fat-soluble vitamins (esp Vit A)
RIBOFLAVIN (B2):
Source?
Function?
Deficiency?
Source:
- milk (UV-sensitive)
- proteins (bound to proteins)
Function:
- FAD and FMN in redox reactions
Deficiency:
- rare unless alcoholic, elderly, school children
- mild symptoms: Cheliosis, Stomatitis and Cataracts
If have adequate protein intake, then riboflavin intake is adequate.
NIACIN (Vit B3):
Functions?
Source?
Deficiency?
Functions:
- NAD and NADP in redox reactions
Source:
- found in cereal (low bioavailability)
- produced from Trp (if lack niacin, you usually tend to lack Tryptophan too)
Deficiency: PELLAGRA
- diarrhoea
- dementia
- dermatitis (casal’s necklace)
PYRIDOXINE (Vit B6):
Function?
Deficiency?
Function:
- active form: pyridoxal phosphate
- needed in amino acid metabolism (transamination and deamination) and haem synthesis
Deficiency:
- commonest: 2˚ deficiency (caused by antagonistics)
- iatrogenic deficiency (doctor-induced) - isoniazid (treats TB) combines with PP causing it to be unavailable so patients are usually given Vit B6 supplements.
Therapeutic use of excess Vit B:
Treat seizures, autism, PMS, and down’s syndrome.
FOLATE (Vit B9) and VITAMIN B12 (COBALAMINE):
Function of Vit B12:
Function of Folate:
What is the active form of folate and how is this maintained?
Sources and DRV of folate and B12:
What is the purpose of the intrinsic factor and what happens if no IF is present?
Homocysteine to Methionine:
Deficiencies:
1) megaloblastosis anaemia
2) inadequate myelin synthesis
3) NEURAL TUBE DEFECTS
4) CVD
5) BRAIN ATROPHY/SHRINKAGE
Causes of Deficiency in Folate and B12:
Function of Vit B12:
- carries methyl groups
- conversion of homocysteine + MeTHF → THF (folate) + Methionine (involved in a.a metabolism)
- purine and pyrimidine synthesis
Function of Folate:
- a carrier of 1-C unit
- purine and pyrimidine synthesis
- needed for a.a. metabolism (conversion of homocysteine + MeTHF → THF (folate) + Methionine)
Active form of folate: THF (tetrahydrofolate) this is maintained by DHF reuctase (dihydrofolate reductase).
Sources of folate:
- vegetables and in liver (plant origin)
- DRV: 50μg/day
Sources of B12:
- animal origin (vegan have no B12)
- DRV: 1μg/day
What is the purpose of the intrinsic factor and what happens if no IF is present?
- Allows absorption and transport of Vit B12
- if no IF is present = pernicious anaemia
Homocysteine to Methionine:
Vit B12 catalyses conversion of homocysteine + MeTHF → THF (folate) + Methionine. This allows production of folate (THF).
∴ deficiency in Vit B12 causes deficiency in Folate.
Deficiencies:
- megaloblastosis anaemia - if no Vit B12 → no conversion of MeTHF to THF so no folate → no purine and pyrimidine synthesis - no DNA synthesis.
Haematopoietic cells die in bone marrow as can’t complete cell cycle.
- inadequate myelin synthesis (B12 DEFICIENCY ONLY NOT FOLATE)
Symptoms: Numbness of fingers, hand and forearm, tingling of hands and feet, loss of position, sense, time and space, and confusion, ataxia, depression, etc, SC, brain lesions. - folate deficiency causes NEURAL TUBE DEFECTS (by giving supplements you can prevent this).
- Lack of B12 (hyperhomocysteinaemia - no conversion of MeTHF to THF) can cause CVD. Supplements can lower risk of CVD.
- Folate, Vit B12 and B6 supplements can also reduce rate of BRAIN ATROPHY/SHRINKAGE - prevents memory loss.
Causes of Deficiency in Folate and B12:
B12:
- lack of IF/ defective IF
- Gastrectomy/ gastric atrophy
- crohn’s disease or coeliac disease
Folate:
- Malabsorption
- Drugs
- Oral contraceptives
PANTOTHENIC ACID (Vit B5):
Source:
Function:
Deficiency:
Source:
- ubiquitous (present in all foods)
Function:
- component of CoA (needed in glucose and fat metabolism)
Deficiency:
- Very Rare
BIOTIN (Vit B7):
Source:
Function:
Deficiency:
Source:
- widely distributed (chocolate, peanuts, egg yolk)
- adequate amounts are produced by intestinal bacteria
Function:
- prosthetic group for carboxylation reactions
Acetyl CoA → Malonyl CoA (FA synthesis)
Pyruvate → Oxaloacetate
Deficiency:
- rare
- long-term antibiotic therapy can lead to deficiencies (sterilising the gut of bacteria - Vit K and Biotin deficiencies)
VITAMIN C:
Source:
Function:
Deficiency:
Status in UK:
Benefits and Risks of Megadoses of Vit C:
Source:
- citrus fruits
- tomatoes
- berries
- potatoes
Function:
- ANTI-OXIDANT (with Vit A and E)
- Reduces Fe3+ to Fe2+ in proline/lysine hydroxylase. This is needed for the hydroxylation of lysine and proline for collagen formation.
- Reduces Fe in stomach to allow absorption
Deficiency:
- Scurvy (impaired would healing, haemorrhages and anaemia)
Status in UK:
- low status in elderly, in alcoholics, and in adolescents (who primarily have junk food)
- smokers need twice the amount (due to fast Vit C turnover)
Benefits and Risks of Megadoses of Vit C:
BENEFITS:
- supplements can improve cold symptoms
- improve risk of heart disease, cancer, eye disease
- improve cholesterol turnover, immune function, male fertility etc.
RISKS:
- oxalate kidney stones
- diarrhoea
- too much Vit C, causes requirements to be higher; so the ideal amount in normal people would be insufficient in individuals who have megadoses.
What are the causes of deficiency of fat-soluble vitamins:
Primary:
- dietary deficiency
- low fat diet (by choice in developed countries)
- fat malabsorption
VITAMIN A:
Source:
Absorption:
Active Forms:
Functions:
Transport and Storage:
Deficiencies:
- prevalence in which type of countries
- what is it usually associated with?
- types of deficiencies (2)
Toxicity/Teratogenicity (birth defects):
Source:
- it has both plant and animal origin
- exist in animals as retinol: animal liver, fish liver oils, milk and egg yolk
- exist in plants as β-carotene: green, yellow and orange fruit and veg
Absorption:
- Carotenoids can be cleaved to 2 retinol (more potent)
- Conversion is inefficient
- Instead, 6 carotene is needed to produce 1 retinol
Active Forms:
- retinoic acid - acts as a hormone
- retinal - vision
- β-carotene - antioxidant
Functions:
- Retinoic acid can bind to intracellular receptor in cytosol and can then bind to chromatin i.e. DNA sequence. This regulates gene transcription of proteins involved in cell growth and differentiation.
- allows scotopic vision - enables vision in low light intensity (conversion of light energy to impulses in optic nerve)
Transport and Storage:
- Taken from Gut to Liver via chylomicrons
- Stored temporarily in liver
- Taken from Liver to Tissues via retinol binding protein (its secretion depends on [retinol])
Deficiencies:
- commonly seen in developing countries
- rare in developed countries
- usually associated with protein deficiencies
1) Effects synthesis and secretion of RBP
2) Night blindness
No Vit A leads to keratinisation (xerophthalmia) and then softening of cornea (keratomalacia). This then leads to permanent blindness.
Development of night blindness represents the role of Vit A in regulating cell growth and differentiation of epithelial cells.
Toxicity/Teratogenicity (birth defects):
- Dermatitis
- Thinning of Hair
- Mucous membrane defects
- Hepatic Dysfunction
- Thinning and fracturing of long bones
Pregnant women should not take supplements or eat liver regularly ~3.3mg/day.
RNI: 0.7mg/day
VITAMIN E:
Source:
- where is it found and not found
- what is a form of Vit E which is associated to fertility
- main function (with A, C, E)
- safe levels?
Function:
Deficiency:
Source:
- found in vegetable oils, nuts, and green vegetables
- not found in frozen or canned foods
- α-tocopherol is a form of Vit E → associated with fertility
- antioxidant
- safe levels: 1g/day (we need more if have high PUFA Intake)
Function:
- prevents oxidation of PUFA in cell membrane and in circulating lipoproteins
- PUFA can be oxidised by free radicals - forming PUFA radicals → attacks other PUFAs.
- affect membrane structure and cell integrity and also PG metabolism (some PUFA are precursors of prostaglandins)
(Vit A, C, E acts as antioxidants - Vit E can become a radical but this is reduced by Vit C)
- protect against CVD and cancer?
- Protects FAs and Apo B in LDL from oxidative damage and hence prevents atherosclerosis
Deficiency:
- sterility
- muscular dystrophy
- human deficiencies are very rare
- premature, low birth weight babies tend to have deficiency as Vit E can’t cross placenta and no Vit E in human milk
- can lead to haemolytic anaemia if you get oxidation and fragility of RBC membrane
VITAMIN D:
A group of similar compounds
Cholecalciferol (Vit D3):
Vit D2 (Ergocalciferol):
Sources:
Function:
Deficiency:
- rickets + symptoms
- osteomalacia + symptoms
- how do these differ from osteoporosis
- which groups are most susceptible
Toxicity:
- Symptoms
- RNI
Cholecalciferol (Vit D3):
- naturally occurring in animals
- functions by binding to intracellular receptors and subsequently binding to DNA (acts like steroid hormones)
- derived from cholesterol
Cholesterol → Dihydrocholesterol → Vit D3 (needs UV)
Vit D2 (Ergocalciferol): - Found in plants, fungi and mould as ergosterol
Sources: - milk and dairy products, margarine, eggs - Both need UV light to form Dihydrocholesterol ― UV → Vit D3 Ergosterol ― UV → Vit D2
Function:
- needed to allow Ca absorption
- maintain levels of Ca and phosphate in blood → bone mineralisation.
Deficiency:
- RICKETS in children
- OSTEOMALACIA in adults
In these two conditions, mineral (Ca): matrix (collagen) ratio is reduced.
This differs from osteoporosis where mineral:matrix ratio is normal but has reduced bone mass.
In rickets, bending of long bones occurs and kyphosis (bending of spine). Tooth eruption is delayed.
In osteomalacia, muscle weakness, bone pain and fractures, decalcification of long bones is seen.
This is usually due to Vit D deficiency rather than calcium deficiency.
More prevalent in elderly, in Asian children with dark skin, etc.
Toxicity: If have excess Vit D, it is toxic. - causes hypercalcaemia - GI tract distrubances - calcification of heart, lungs, and kidneys (soft tissues) Fatal when severe.
RNI: 10μg (10 times of this is toxic)
