FNN100_Fall2023_Week7.pptx

Module 6 Bone Building Nutrients Module 6, Part 1 Bioavailability • rate and extent to which a nutrient is absorbed Factors affecting bioavailability: • Digestive efficiency (including transit time) • Individual’s nutritional status • Concurrent intake of inhibitors/promoters • Food preparation methods • Nutrient source (synthetic versus whole food source) Provitamins • • • inactive forms of some vitamins found in foods also referred to as precursors converted to active forms in vivo • E.g., tryptophan is a precursor of niacin • E.g. beta carotene is a precursor of vitamin A Also note: In vitro = “in glass” In vivo = “in the living body” Bones Types of bone: Trabecular bone (spongy); Cortical bone (compact) • 95-98% is non-living material; 2-5% cellular (living cells) • “osteoid” is the non-living mineral coated protein matrix • Matrix consists of 90% collagen; 10% mixed proteins • Mineral coating (mostly a Ca-P mix): • 40% calcium • 54% phosphate • 6% carbonate + sodium, potassium, magnesium, citrate & other extra-cellular fluid (ECF) ions that get trapped as mineral and are deposited in bone • 99% of the calcium in the body is found in the skeleton (bones) Figure 11.8 Bone Cells & Functions 4 main types of cells (recall: only 2-5% of bone) 1. Lining: • Cells that cover free bone surfaces 2. Osteoblasts: • Cells that create a matrix and conditions for mineralization 3. Osteoclasts: • Cells that resorb (dissolve) bone (cells attach to the surface of bone, secrete acid and enzymes to dissolve mineral and digest the protein matrix); this cellular process releases products to ECF and leaves “pits” that osteoblasts fill in 4. Osteocytes: • Osteoblasts that become embedded in bone Bone Cell Function and Age • Bone cell action is under the control of hormones and other bone cells • Hormones involved in bone cell action include: • Parathyroid hormone (PTH) • Calcitriol (also known as 1,25-dihydroxyvitamin D) • Glucocorticoids • Growth factors • Calcitonin • PTH stimulates bone resorption (dissolving of bone); calcitonin stimulates ossification (mineralization/depositing of minerals) Bone Cell Function and Age (cont.) Bone development: • Humans are born with cartilage • Cartilage is replaced by bone in childhood (cartilaginous cells are replaced) • An active growth phase occurs from birth to approximately age 20 • Peak bone mass development occurs between 12 and 30 (formation exceeds resorption) • Final phase of bone development occurs when bone resorption (dissolve) exceeds bone formation (begins between ages 30-40) and continues • Ossification (osteogenesis)/mineralization stopped by puberty hormones Bone Cell Function and Age (cont.) Bone Modeling (Remodeling) • Continual resorption and replacement of bone (except teeth) • Resorption precedes formation; occurs in many small areas at once • Purpose is to replace damaged bones and to revise the shape of bones during growth • Controlled by PTH (parathyroid hormone) Functions of Bone Consider both the living (2-5%) & non-living material of bone (95-98%): • Provide mechanical rigidity to resist gravity • Protect organs • Permit ambulation • Homeostatic buffer (maintains blood calcium and phosphorus levels) • Storage form (storage that also provides a function as a reserve) Module 6, Part 2 Nutrients and Bone (cont.) • • • • • • Protein matrix Calcium Phosphorus Vitamin D Magnesium Fluoride Calcium (Ca) Roles: • Bone formation • Most common intracellular messenger • Protein (enzyme) co-factor*, activates by binding: muscle contraction, calcium storage, glucose breakdown • Involved in: blood clotting; hormone regulation; nerve impulse transmission • Involved in blood pressure (BP) regulation: • Activates (binds) calmodulin (cell messenger that reduces BP) Calcium (cont.) • Requirement for calcium increases with age; intake tends also to decline with age  deplete stores • Calcium intake is directly related to bone ossification and remodeling • 99% is in bones and teeth as ‘hydroxyapatite’; or the more stable form ‘fluoroapatite’ • Pure hydroxyapatite Ca10(PO4)6(OH)2; Fluoroapatite or calcium fluorophosphate) – Ca5(PO4)3F • Carbonate, sodium, etc may be attached to calcium Blood Calcium Level • In blood, 2.25 to 2.5 mmol of calcium; mostly free, a lot is protein bound; very tightly regulated! • Falling blood calcium signals the parathyroid glands to release PTH (Hypocalcemia) • PTH released from parathyroid glands (embedded in the thyroid) • Increases renal phosphate clearance (hydroxyapatite & fluoroapatite have PO 4) • Increases renal reabsorption of calcium (absorp Ca from kidneys) • Activates bone resorption (dissolve) (stimulate release of Ca from bone to blood) • Activates vitamin D to increase intestinal Ca absorption • Rising blood calcium levels inhibit PTH secretion Blood Calcium Level (cont.) Hypercalcemia: “high blood calcium” • Rising blood calcium signals the thyroid gland to secrete calcitonin • Calcitonin released by thyroid gland • Limits intestinal Ca absorption • Prevents renal calcium reabsorption • Inhibits vitamin D activation • Inhibits bone resorption (osteoclasts are inhibited from breaking down bone) • Stimulates renal Ca excretion (excretion of Ca from the kidneys) • Lower blood calcium levels inhibit calcitonin secretion Calcium Absorption • Calcium is released from food by digestion • Digestion releases Ca ions and low molecular weight Ca complexes (calcium carbonate, etc) • Absolute absorption increases with intake (although efficiency of absorption decreases) • People have different pre-set absorptive efficiencies • As intake of calcium decreases, absorptive efficiency increases…But not enough to counter ongoing/long-term insufficient intake Calcium Absorption (cont.) 2 ways in which calcium is absorbed: 1. Active transfer (active transport) requiring a protein carrier • Vitamin D turns on the synthesis of Ca transport proteins • Calcium transport proteins shuttle Ca across the mucosal cell • A Ca pump that requires energy moves Ca from mucosal cells to bloodstream 2. Passive diffusion Locations of calcium absorption: • Small intestine: duodenum, jejunum, ileum (mostly here); also to a lesser extent in the colon (small amount) Calcium Absorption (cont.) Factors Influencing Absorption: • Vitamin D status • Intestinal transit time • Life cycle stage (breastfed infants absorb by passive diffusion) • Age • Differing intestinal absorptive efficiencies that decline with age • Decreased stomach acid (achlorhydria) impairs Ca absorption (to a lesser degree with Ca consumed with meals) Calcium Excretion • Calcium is lost in urine, feces, sweat, skin sloughing, hair and nails • Total loss of calcium is ~ 60 mg daily Calcium in the Diet • Dairy/plant based alternative products are richest calcium • Plant sources (non-dairy sources) • Brassica genus family: broccoli, kale, bok choy, cabbage, mustard & turnip greens, etc. • Dried seaweed • Almonds • Spinach, rhubarb, swiss hard • Other Ca sources: • Calcium-set tofu • Fish with edible bones (canned sardines) • Blackstrap molasses • Calcium-fortified foods (e.g., orange juice) Dietary Reference Intakes (DRI) for Calcium Estimated Average Requirement (EAR): Children: • • 1 to 3 years: 500 mg/day 4 to 8 years: 800 mg/day Males: • • • 9 to 18 years: 1100 mg/day 19 to 70 years: 800 mg/day 70+ years: 1000 mg/day Females: • • • 9 to 18 years: 1100 mg/day 19 to 50 years: 800 mg/day 50+ years: 1000 mg/day Recommended Dietary Allowance (RDA) Children: • 1 to 3 years: 700 mg/day • 4 to 8 years: 1000 mg/day Males: • 9 to 18 years: 1300 mg/day • 19 to 70 years: 1000 mg/day • 71+ years: 1200 mg/day Females: • 9 to 18 years: 1300 mg/day • 19 to 50 years: 1000 mg/day • 51+ years: 1200 mg/day Dietary Reference Intakes (DRI) for Calcium (cont.) Tolerable Upper Intake Levels (UL): • Indicates a range of safety for Ca consumption • Concerns of hypercalcemia with renal insufficiency at high intakes (also known as milk alkali syndrome) • Increased effect of Ca-nutrient interactions at high intakes Children: • 1 to 8 years: 2500 mg/day Males and Females: • • • 9 to 18 years: 3000 mg/day 19 to 50 years: 2500 mg/day 75+ years: 2000 mg/day Calcium Toxicity Hypercalcemia: due to overconsumption of Ca from supplementation • Can lead to milk alkali syndrome • Symptoms include: • loss of muscle tone • constipation • large urine output • nausea > confusion > coma • Excess dietary Ca does not usually cause kidney stones (stones are more likely due to renal Ca leak that creates high urinary Ca levels; many factors involved in kidney stone formation) Food Sources and Calcium Bioavailability • Dairy products: 30% bioavailable • Supplements: ~30% (depends on the form: carbonate vs citrate) Inhibitors: • Most potent inhibitors: • Oxalic acid (in spinach, rhubarb, dried beans) • Spinach vs milk = 1:10 absorption because of high oxalic acid in spinach • Modest inhibitors: • Phytic acid (storage form of phosphorus in seeds); can be decreased by fermentation • Beans vs milk = 1:2 absorption because of phytic acid in beans Calcium-Nutrient Interactions Factors Influencing Urinary Calcium Excretion: • Sodium intake: shared transport systems (in adult women, each extra 1 g of sodium/day may increase annual rate of bone loss by 1%) • Caffeine intake: postmenopausal women consuming < 750 mg calcium (RDA is 1200 mg/day for 51+ years) with a daily caffeine intake equal to 2-3 cups of coffee had increased bone loss Calcium-Nutrient Interactions (cont.) • Protein intake: doubling protein intake increases renal Ca excretion by 50% • due to acid load of sulfate from sulphur-containing amino acids • Many protein-rich foods contain phosphorus which mitigates loss somewhat. But, increased phosphorus increases fecal Ca loss • In short term studies, protein increases the amount of calcium in urine and the amount absorbed from food (no net loss as first expected)… Calcium and Iron Interactions • There is evidence that non-heme iron absorption is reduced by 50% at meals containing 300 mg Ca (may involve competition for transport) • Iron deficiency is one of the greatest concerns in Canada • Some experts say this effect may disappear within context of whole diet • Health Canada’s statement: • Iron absorption decreases steadily as Ca intake increases • Thus, calcium has an inhibitory effect at all levels of intake Calcium Status • • • • Challenging to assess! Large reserve in skeleton means ECF deficiency is uncommon Skeleton helps to: maintain blood Ca level Skeleton can be considered a “pool” or Ca reserve Assessing Calcium Status: We can estimate the “calcium reserve” size by: • Dual-energy x-ray absorptiometry (DEXA) • Calculating Ca balance • Measuring blood Ca Assessing Calcium Status Dual-energy x-ray absorptiometry (DEXA): • Estimates bone mineral density; but results are hard to interpret due to confounding factors (e.g., inactivity, hormone deficiency…etc.) Calculate Ca Balance: • This is done in hospital or clinical/research setting Measure Blood Ca: • Low level indicates abnormal parathyroid function or other endocrine dysfunction • Low level does not indicate Ca deficiency Calcium Deficiency Chronic • Osteoporosis (in adults – women and men) • Hypertension • Colon cancer Osteopenia: low bone mineral density • Increased fracture risk Osteoporosis Risk factors: • • • • • • • • Postmenopausal (no protection from estrogen) Anorexia nervosa Alcohol abuse Caucasian, East Indian Female Chronic steroid use Thinness Ovaries removed (no protection from estrogen) Protective factors: • African American • Long term estrogen use • High body weight Calcium Deficiency (cont.) • Huge Ca reserve means that low Ca diets deplete reserves very slowly; takes years for bone strength to be reduced enough to increase risk of fractures • 1/2 to 2/3 of broken bones in the US attributed to low Ca intake Calcium Deficiency (cont.) Prevention: • Maximize development of peak bone mass during growth, and minimize loss with age • Peak bone mass (PBM): achieved between age 20-30 years • 60-80% genetically determined • PBM influenced by: • Ca intake (esp. adolescent females) • Activity • Intake of Ca binders • Anorexia nervosa • Substance abuse Bone Loss • Both men and women start losing bone in their 30’s • After PBM has been achieved, “lifestyle” choices can affect the rate of bone loss but the body can no longer “build” bone • Bone loss 5 years after menopause in women = loss in elderly men (indicates differences between men and women) • Low milk intake in childhood is associated with low bone mass and the doubling of hip fractures in post-menopausal women Calcium Supplementation and Forms of Calcium • Supplements are commonly recommended by physicians for adult women showing increased bone loss • Calcium carbonate contains the most elemental calcium by weight (approx. 40%) versus calcium citrate (21%) • Supplements are best taken with meals; and preferably not taken with calcium inhibitors at the same time • E.g., avoid iron supplement at the same time as Ca supplement; avoid high phytate foods at the same time as Ca supplement, etc. Calcium Supplementation (cont.) • The most efficient absorption occurs in doses of 500 mg or less • At a 250 mg dose, the following percentages of elemental Ca is absorbed (varies by type): • Ca citrate – 35% • Ca carbonate – 27% Break 15 mins Module 6, Part 3 Phosphorus (P) Functions: • Plays a key role in all energy production and storage (ATP) • Activates hormones • Phosphorylation (a key molecular event) involved in activating many enzymes • Buffer in acid/base balance • A component of hydroxy- and fluorapatite; phospholipids in cell membranes; nucleic acids (RNA, DNA); and almost all enzymes Phosphorus (P) is recycled; therefore dietary P’s role is: • To support growth (e.g., children, pregnancy) • To replace excretory losses Phosphorus (cont.) Locations of Phosphorus (P) in the body: • 10% found in muscle/soft tissue and blood; 80-85% found in bone Food Sources of Phosphorus: • • • • • • • Protein-rich foods: meat, milk, legumes Cereal grains (high fibre) All animal tissue (especially liver) Sunflower seeds, almonds Processed foods (as phosphate salt additives) Colas and some other soft drinks Spinach, broccoli Phosphorus Absorption • • • • Adults absorb between 55-70% Unlike Ca, no adaptive mechanism for low intake P is absorbed in the small intestine Blood levels of P are loosely regulated and decline with age Mechanism of absorption: • Mostly passive diffusion • Some active transport facilitated by vitamin D • Controlled by vitamin D and phosphate transporters Phosphorus Absorption and Excretion Inhibitors: • Phytic acid, phosphate-binding antacids (aluminum-containing), large doses of calcium carbonate (e.g., from supplements) • Phosphorus absorption is ok at normal Ca intake levels but excess Ca carbonate decreases P absorption Excretion of Phosphorus: • Primarily via the kidneys Phosphorus Bioavailability • From most food sources of P, there is good bioavailability • Some exceptions exists: • All plant seeds (beans, peas, cereals, nuts) due to P contained as phytic acid which bodies can not hydrolyze • Some foods contain phytase (e.g., yeast-raised foods), which helps phosphorus become available Dietary Reference Intakes (DRI) for Phosphorus • EAR, AI (infants), RDA set based on age • Recommended Dietary Allowance (RDA): • 1-3 yrs. – 460 mg/day • 4-8 yrs. – 500 mg/day • 9-18 yrs. – 1250 mg/day • 19+ yrs. - 700 mg/day An Ontario Food Survey (2003) found the average intake among adults aged 1874 yrs was 1504 mg/day (men) and 1124 mg/day (women); similar data from NHANES survey (2015/2016) in US Phosphorus Deficiency “Hypo”phosphatemia • A dietary deficiency is unknown due to recycling of P and widespread availability in foods • Some medications bind P and may lead to deficiency • Clinicians also need to watch for phosphorus depletion in re-feeding of starved individuals; seen with alcoholism and diabetes ketoacidosis • Symptoms of hypophosphatemia include: • Muscle weakness • Anorexia, anemia • Bone pain • Rickets (in children) • Osteomalacia (in adults) Phosphorus Toxicity Tolerable Upper Intake Level (UL): • 4 g/day for people aged 9-70 yrs. “Hyper”phosphatemia: • Affects Ca balance (lowers Ca level in blood) • Calcification in kidney • Reduced Ca absorption • May interfere with iron, copper, zinc absorption • With end stage renal disease, can lead to vitamin D intoxification Magnesium (Mg) Functions: • Bone mineralization • Enzyme cofactors (nucleotide synthesis, Na & K transport) • Used in anaerobic and aerobic energy generation, glycolysis • Ca channel blocker in cells • Needed for ATP metabolism, protein and fat synthesis • Blood clotting (Mg inhibits; Ca promotes) • Helps regulate blood pressure (with Ca) • Supports immune function Magnesium (cont.) Locations of Mg in the body: • 53% in bone; 27% in muscle; 20% in soft tissue • Must abundant divalent cation in cells • Very small amounts lost in sweat compared to other cations (Na, Cl) Food Sources of Magnesium: • Legumes, seeds, nuts, green leafy vegetables • Milk, cereal, halibut, meat, eggs • Hard water Magnesium (cont.) Bioavailability: • About 50% bioavailability from food sources • Inhibitors of Mg absorption include: high fibre in fruit; vegetables; grains (contain phytate); high phosphate diets; high zinc intake Mg Absorption: • Absorbed quickly • Intestinal absorption inversely proportional to the amount ingested • with an average intake, 50-60% absorbed • with a high intake, 15-35% absorbed • Location: small & large intestine, mostly jejunum & ileum Magnesium (cont.) Transport: • (1) Carrier-mediated; and (2) passive diffusion • Under hormonal control, including activated vitamin D Dietary Reference Intakes (DRI) and Magnesium • EAR, RDA, AI (infants) by age & gender • Recommended Dietary Allowance (RDA) Males/(Females): • • • • • • 1-3 years: 80 mg/day 4-8 years: 130 mg/day 9-13 years: 240 mg/day 14-18 years: 410 mg/day (360 mg/day) 19-30 years: 400 mg/day (310 mg/day) 30+ years: 420 mg/day (320 mg/day) Magnesium Deficiency & Toxicity Magnesium Deficiency: • Dietary deficiency is rare; seen largely with protein energy malnutrition • Associated with: GI disorders; malabsorption syndromes (Crohn’s, Celiac); diabetes; alcoholism; excess diuretic use Magnesium Toxicity: • UL set at 350 mg/day over age 9 (related to Mg supplements only) • Associated with excess intake from supplements (hard to do with foods) and disease (severe constipation, renal insufficiency) • Symptoms: diarrhea, hypotension, nausea, vomiting, flushing, personality change, cardiac complications, coma, death Break 15 mins 54 Module 6, Part 4 Fluoride (F) Background: • Found in the body as fluoride ion; 99% of fluoride is found as fluoroapatite – the stabilized form of hydroapatite (the Ca-P mineral component of bone) Functions: • Protects against demineralization of bone & teeth • Cariostatic (prevents dental caries): both inhibits and reverses • Children living in areas with non-fluoridated water are likely to have trouble meeting AI • Evidence of reduction in dental carries varies from 18% ---25%---60% between communities with, and without, fluoride in the water Fluoride (cont.) Metabolism: • 50-90% of F is absorbed quickly – most through stomach, also small intestine • <20% is excreted in feces; 50% of F absorbed is excreted via kidneys • Fluoride is absorbed through passive diffusion Inhibitors: • Antacids (aluminum hydroxide) severely inhibits absorption (fluoride is absorbed in stomach in its acid form); (increased fecal F) Fluoride (cont.) Food Sources: in almost all plants and animals • Water supply (fluoridated in many communities in Ontario, and Canada) • Fish with bones • Tea (leaves take F from water; more so in decaf vs. regular) • Toothpaste and other dental products (encouraged not to swallow) Bioavailability: • Generally high, depends on food/drink ingested at the same time (e.g., 100% in water; 75% in milk and other high Ca foods) • Toothpaste: 100% Dietary Reference Intakes (DRI) for Fluoride AI is set by age and gender: Males: • 19+ years: 4 mg/day Females: • 19+ years: 3 mg/day See values for younger individuals in DRI manual Fluoride Deficiency and Toxicity • Fluoride deficiency is unknown in humans • Dental caries continue to be a major public health problem; most effectively prevented with fluoride Toxicity: • UL for individuals 9+ years: 10 mg/day (see values for younger individuals) • Excess intake can result in ‘enamel fluorosis’ (mottled tooth enamel) • Chronic excess intake can lead to crippling skeletal fluorosis and osteoporosis • Acute F excess can result in nausea, vomiting, diarrhea, abdominal insufficiency, convulsions, sensory disturbances, coma, death (at 5 mg/kg body weight) Vitamin D • Active form of vitamin D: ‘calciferol’ or ‘calcitriol’ – 1,25 dihydroxycholecalciferol or 1,25 dihydroxy vitamin D3 • Photosynthesized in the skin of vertebrates by the actions of solar ultraviolet B radiation (UVB rays) • Many forms of vitamin D: found in very few foods • Vitamin D2 (ergocalciferol) from yeast and is a plant sterol • Vitamin D3 is from a precursor in skin synthesis • “Vitamin D” can mean D2 or D3 or both – biological similar Vitamin D (cont.) Functions: • Maintains blood Ca and P levels within normal range (by enhancing absorption by small intestine); plays a role in bone growth • Enhances intestinal P absorption • With low Ca intake, stimulates osteoclasts to remodel bone and inhibits renal excretion of Ca and Mg • Active vitamin D receptors in other cells hint at some unknown roles Vitamin D (cont.) Functions (cont.): • Anti-proliferation and prodifferentiation hormone action – not fully understood • Inhibits inflammatory response – may play a role in autoimmune diseases including multiple sclerosis, rheumatoid arthritis, Type 1 diabetes • Sufficient vitamin D intake linked to lower all-cause mortality, especially cancer (colorectal) and CVD • Evidence continues to emerge; need for more research Vitamin D (cont.) Food Sources: • Fish liver oils, flesh of fatty fish, liver and fat from aquatic mammals (seals, polar bears) • Fortified milk (and alternatives); cereal • Units: international units (IU) or micrograms (µg) 1 microgram (µg) vitamin D = 40 IU 1 IU = 0.025 micrograms (µg) Vitamin D (cont.) Sources of Vitamin D (cont.)… Sunshine • In sun, UVB photons of a specific energy range absorbed by vitamin D precursor (7-dehydrocholesterol) in skin to form previtamin D3 (not active) • Previtamin D3 synthesis is limited by excess sun (degraded to prevent intoxication) Vitamin D Absorption Absorption is influenced by: • Sunscreen use/level of Sun Protection Factor (SPF) • Skin pigmentation • Latitude • Time of day • Season Factors Affecting Vitamin D Absorption Latitude: • Above and below 40° North latitude and 40° South latitude, vitamin D synthesis from sun does not occur in 3-4 months (up to 6 months in far north) • Toronto is located at 43° N • E.g., Edmonton, Alberta (52° N) – insufficient sun from October to March for vitamin D production Vitamin D Absorption (cont.) • Sun is a major source of Vitamin D for humans • 10 minutes of summer sun on hands and face will produce 400 IU (10 µg) of vitamin D • 5-15 minutes of sunlight 2-3 times/week on hands, face and arms is recommended to provide most people with vitamin D requirements Vitamin D Metabolism • UVB action on 7-dehydrocholesterol (a precursor made in the liver from cholesterol) to form previtamin D3 in the skin • Enters circulation (via chylomicrons, lymph, thoracic duct): can be stored as fat or go to the liver • In liver, inactive form of vitamin D3 is hydroxylated to 25-hydroxy- vitamin D3 (inactive) – circulation to kidney • In kidney, hydroxylated to 1,25 dihydroxycholecalciferol/dihydroxy vitamin D3 (active hormone) • Active vitamin D production is tightly regulated by PTH in response to blood Ca and P levels 70 Dietary Reference Intakes (DRI) for Vitamin D AI: for infants up to 1 year: 10 µg/day (400 IU) Recommended Dietary Allowance (RDA): Males and Females: 1 -70 years: 15 µg/day (600 IU) 70+ years: 20 µg/day (800 IU) Tolerable Upper Intake Level (UL): Children: 1 to 3 years: 63 µg/day (2500 IU) 4-8 years: 75 µg/day (3000 IU) Males and Females: 9+ years: 100 µg/day (4000 IU) Health Canada Recommends: • 400 IU (10 mcg)/day supplement for breastfed babies up to 1 year/age • 400 IU (10 mcg)/day supplement for adults over the age of 50 Vitamin D Deficiency • Malabsorption disorders: Crohn’s disease, liver failure, tropical sprue (diarrheal disease) etc. impair absorption of vitamin D (secondary deficiency) • With age… • Reduced ability to make previtamin D3 in the skin • Lower intake of milk (fortified) • Less daily sunlight exposure • Can result in secondary hyperparathyroidism which accelerates osteoporosis • Vitamin D Deficiency (cont.) • Causes a decrease in blood Ca which causes an increase in PTH (causes bone resorption) • Association between vitamin D deficiency and colon, breast and prostate cancer risk among people living at higher latitudes • Children: rickets is a condition associated with inadequate bone mineralization (appearance of bowed legs and chest) • Adults: osteomalacia is a condition associated with softening of bone and most often seen in multiparous women with low Ca intake and low sun exposure Vitamin D Toxicity Hypervitaminosis D: • Affects kidney, bone, digestive and central nervous systems, heart • Causes increased blood Ca and P • From supplements, not from sun exposure (production of active vitamin D from sun exposure is limited)

FNN100_Fall2023_Week7.pptx

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