Chapter 7 – Vitamins Vocabulary

Classification of Vitamins

• Two broad categories
• Fat-soluble (A, D, E, K)
• Water-soluble (C and all B-complex)
• Shared characteristics
• Fat-soluble: dissolve in lipid, require bile for absorption, travel via lymph, stored in liver/adipose, toxicity more likely with supplements
• Water-soluble: dissolve in water, absorbed directly into blood, minimal storage, excess excreted in urine, toxicity rare
• Practical implication → Fat-soluble vitamins behave much like dietary lipids; anything that impairs fat absorption (e.g.
pancreatic insufficiency, xenical/orlistat) may precipitate deficiency.

Vitamin A (Retinol, Retinal, Retinoic Acid)

• Chemical forms & precursor
• Active forms: retinol ↔ retinal → retinoic acid
• Precursor: \beta-carotene (plant pigment); need approx. 6 \times as much carotene to yield the same amount of retinol.
• Physiological roles
• Gene expression → controls synthesis of >100 proteins
• Vision: part of retinal pigment; night-vision & prevention of xerophthalmia (Fig 7-1)
• Maintains epithelial integrity (skin, mucous membranes)
• Immune defence (T-cell differentiation)
• Bone & tooth growth
• Reproduction (spermatogenesis, embryonic development)
• DRI (RDA)
• 700\text{–}900\,\mathrm{\mu g\, RAE/day} (RAE = retinol activity equivalents)
• Major food sources
• Animal: beef liver, fish oil, fortified milk
• Plant (as \beta-carotene): deep-orange & dark-green F&V (carrots, sweet potato, spinach, kale, mango)
• Deficiency (common in developing countries)
• Night blindness → total blindness; xerosis → keratomalacia
• Keratinisation of skin (frog-skin bumps, Fig 7-2)
• Impaired bone growth / decaying teeth
• Compromised immunity → ↑ infection risk
• Public-health responses: high-dose capsules; biofortified “Golden Rice”.
• Toxicity
• UL =3000\,\mathrm{\mu g/d}
• Early signs: headache, fatigue, muscle & bone pain, loss of appetite, skin rashes
• Chronic: liver damage, enlarged spleen, teratogenicity (esp. isotretinoin/Accutane, topical Retin-A)
• \beta-carotene excess → harmless yellowing of skin (carotenemia).

Vitamin D (Cholecalciferol)

• Unique dual origin
• Synthesised in skin from 7-dehydrocholesterol under UV-B
• Obtained from diet (fortified milk/margarine, eggs, fatty fish)
• Core functions
• Hormone that regulates \text{Ca}^{2+} & \text{P}^{3-} homeostasis → bone mineralisation
• Impacts brain, heart, pancreas, immune maturation
• RDA =15\,\mathrm{\mu g} (600 IU) adults 19–70 y
• Sun factors
• Light skin: ~15 min sun to face/hands 3–7×/week
• Dark skin: up to 3 h for equivalent synthesis
• At 49^{\circ} N (Manitoba) cut-off ≈ Oct–Apr → rely on liver stores/diet
• Sunscreen (SPF ≥8) blocks ≥95 % UV-B
• Deficiency syndromes
• Children: rickets (bowed legs; Fig 7-5)
• Adults: osteomalacia
• Emerging links: hypertension, autoimmune disorders, MS, IBD, RA, certain cancers; risk rises with age (↓ skin synthesis, ↓ renal activation).
• Toxicity
• Highest toxicity potential of all vitamins; UL =100\,\mathrm{\mu g} (4 000 IU)
• Symptoms: anorexia, nausea, polyuria, depression
• Chronic → calcium deposits in heart, lungs, kidneys → death.

Vitamin E (Tocopherols & Tocotrienols)

• Primary role = lipid-phase antioxidant protecting PUFA in cell membranes (Fig 7-7)
• DRI (RDA) =15\,\mathrm{mg \;\alpha\text{-}tocopherol/day}
• Sources (Snapshot 7-3)
• Vegetable oils & products (margarine, dressings)
• Nuts, seeds, whole grains, green leafy vegetables
• Easily destroyed by heat & oxygen (Fig 7-8)
• Deficiency (rare)
• Premature infants → erythrocyte hemolysis
• Adults with fat-malabsorption → neuropathy, muscle weakness
• Toxicity (UL =1000\,\mathrm{mg})
• Nausea, GI distress, blurred vision
• >400 IU/d with anticoagulants ↑ bleeding & all-cause mortality.

Vitamin K

• Functions
• Coenzyme for \gamma-carboxylation of glutamate residues → activates clotting factors (II, VII, IX, X)
• Synthesises osteocalcin → bone mineralisation
• DRI: males 120\,\mathrm{\mu g/d}; females 90\,\mathrm{\mu g/d}
• Sources
• Intestinal bacteria (~½ needs)
• Green leafy veg (kale, broccoli), cabbage, liver, eggs, milk, legumes (Snapshot 7-4)
• Antibiotics ↓ bacterial production.
• Deficiency conditions
• Newborns (sterile gut) → prophylactic injection
• Fat-malabsorption, long-term antibiotics → easy bruising, hemorrhage
• Toxicity (rare)
• High-dose supplements in infants/pregnancy → hemolytic jaundice (bilirubin release).

Water-Soluble Vitamins – General Traits

• Dissolve freely in water → direct absorption to portal blood
• Limited storage → require frequent intake
• Excess excreted; toxicity uncommon
• Act mainly as coenzymes in energy or protein metabolism.

Vitamin C (Ascorbic Acid)

• Physiological roles
• Collagen synthesis (wound healing, bones, teeth)
• Antioxidant; regenerates vitamin E
• ↑ non-heme iron absorption (reduces \text{Fe}^{3+} \to \text{Fe}^{2+})
• Supports immune cells (neutrophil oxidative burst)
• Cold prevention: research inconclusive; placebo effect possible.
• DRI: males 90\,\mathrm{mg/d}; females 75\,\mathrm{mg/d}; smokers +35\,\mathrm{mg}
• UL =2000\,\mathrm{mg/d}
• Sources (Snapshot 7-5) = citrus, berries, peppers, broccoli; heat & O_2 destroy vit C.
• Deficiency = Scurvy (Fig 7-9) → bleeding gums, petechiae, loosened teeth, anemia, fatigue.
• Toxicity (>2 g) → GI upset, rebound scurvy, altered insulin response; avoid in hemochromatosis; interferes with anticoagulants.

The B-Complex Vitamins – Overview

• All serve as coenzymes (Fig 7-11) facilitating reactions that release energy from CHO, fat, protein (Fig 7-12).
• Memory aid: “T R N P P B F C”
• Thiamin (B1), Riboflavin (B2), Niacin (B3), Pantothenic (B5), Pyridoxine (B6), Biotin (B7), Folate (B9), Cobalamin (B12).

Thiamin (B1)

• Functions = decarboxylation in CHO metabolism; nerve conduction.
• RDA: males 1.2 mg; females 1.1 mg.
• Sources: pork, legumes, seeds, whole-grain/fortified cereals (Snapshot 7-6).
• Deficiency: Beriberi
• Wet = edema; Dry = neuropathy, muscle wasting (Fig 7-13)
• Alcohol abuse → Wernicke-Korsakoff (confusion, ataxia).
• No known toxicity.

Riboflavin (B2)

• Functions: FAD/FMN coenzymes; skin & vision support.
• RDA: males 1.3 mg; females 1.1 mg.
• Sources: milk products, enriched grains, eggs, meat, greens (Snapshot 7-7).
• Deficiency = Ariboflavinosis → cheilosis, magenta tongue, dermatitis; often with other B-deficits.
• Stable to heat but destroyed by light → opaque milk cartons.
• No toxicity.

Niacin (B3)

• Functions: NAD/NADP → redox reactions.
• RDA: males 16 mg NE; females 14 mg NE; UL =35 mg.
• Tryptophan (60 mg) → 1 mg niacin equivalent.
• Sources: protein foods, whole/enriched grains, mushrooms, greens (Snapshot 7-8).
• Deficiency = Pellagra (4 D’s: dermatitis, diarrhea, dementia, death) – historical corn diets.
• Toxicity (supplements) → skin flushing, tingling, liver injury; pharmacological doses prescribed to lower LDL/raise HDL but require monitoring.

Folate (B9)

• Synthetic = folic acid (better bioavailability).
• Functions: carbon transfers for DNA/RNA synthesis; critical in rapid cell division & early neural tube closure.
• RDA =400\,\mathrm{\mu g} DFE; UL =1000\,\mathrm{\mu g}.
• Pregnancy: +200 µg food + supplement.
• Sources: leafy greens, legumes, seeds, liver (Snapshot 7-15); fortification of flour since 1998 → ↓ neural tube defects.
• Deficiency → megaloblastic (macrocytic) anemia, smooth tongue, depression, NTDs (spina bifida; Fig 7-15); 1 in 1000 births (Canada).
• Low status → ↑ homocysteine (CVD risk), some cancers.
• Toxicity masks B12 deficiency.

Cobalamin (B12)

• Functions: regenerates folate coenzyme; maintains myelin sheath.
• RDA =2.4\,\mathrm{\mu g/d}.
• Requires intrinsic factor (IF) for absorption in ileum; elderly ↓ IF.
• Sources: animal products, fortified plant beverages, fermented foods.
• Deficiency → pernicious anemia, neuropathy, paralysis; vegans, malabsorption, breast-fed infants of vegan mothers at risk; treat with injections or high-dose oral.
• Nontoxic.

Pyridoxine (B6)

• PLP coenzyme → amino-acid transamination, heme & neurotransmitter synthesis, tryptophan→niacin conversion.
• RDA =1.3 mg; UL =100 mg.
• Sources: meats, fish, poultry, whole grains, legumes, leafy greens (Snapshot 7-11).
• Deficiency → microcytic anemia, dermatitis, convulsions.
• Toxicity (supplements) → reversible neuropathy; B6 touted for PMS/carpal tunnel but evidence weak.

Biotin (B7)

• Function: cofactor for carboxylase enzymes in FA synthesis & gluconeogenesis.
• RDA =30\,\mathrm{\mu g}.
• Raw egg whites (avidin) bind biotin → rare deficiency (dermatitis, alopecia).
• Sources: widespread, intestinal bacteria.

Pantothenic Acid (B5)

• Part of Coenzyme-A → essential for acetyl-CoA formation.
• RDA =5 mg.
• Deficiency & toxicity = rare; sources ubiquitous.

Controversy 7 – Vitamin Supplements

• Who may benefit?
• People with documented deficiencies
• Increased needs (pregnancy, elderly, chronic disease, strict vegans)
• Malabsorption disorders
• Individuals on restricted caloric intake (<1200 kcal) • Table C7-1 lists valid indications. • Regulation (Canada) • Classified as Natural Health Products (NHP); must carry NPN or DIN-HM; available OTC. • Research outcomes • Antioxidant hypothesis largely unproven; vitamin E trials show no CVD benefit. • \beta-carotene supplements ↑ lung cancer in smokers (ATBC, CARET trials). • High vitamin A intake (>10\,000\,\mu g/d) linked to hip fractures & hepatotoxicity.
• Reasons to think twice (Table C7-4)
• Toxicity risk, cost, false security → may displace healthy eating patterns.
• Bottom line → Aim for nutrient-dense diet first; supplement only when evidence-based need exists.

Practical & Ethical Considerations

• Biofortification (Golden Rice) raises debates on GMOs vs. public-health urgency to prevent blindness.
• Sun-exposure for vitamin D must balance rickets prevention with melanoma risk → public-health messaging tailored by latitude & skin type.
• Over-supplementation culture → self-prescribing mega-doses can harm (vit D, niacin, vit A).
• Healthcare providers need to assess drug–nutrient interactions (e.g.
warfarin & vitamin K; vitamin E & anticoagulants).
• Social determinants: developing countries face deficiencies (A, folate), while affluent societies risk toxicities.