NEP ch15

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54 Terms

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calcium

absorption occurs primarily in upper part of the small intestine. Depends on active vitamin D (vit D induces synth of calbindin)

20-60% absorption depending on stage of life (pregany also)

absorb enhanced by: lactose, oligosaccharides, PTH, estrogen

absorb limited by: phytic acid, oxalic acid, excess Phosphorus, dietary fibers?, vit D def, fatty “soaps”, low HCI

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calcium regulation and balance

bone, small intestine, kidney

hormones: vitamin D (calcitriol), parathyroid hormone (PTH), calcitonin

calcitonin when clacium is high

PTH when calcium is low

normal range 10.8 mg to 8.5 mg

2% lost as sweat, 85% lost as feces, 14% lsot as urine, skeletal calcium 500 to 700 mg is readily exchangeable

calcium rigor = too much calcium in the blood, heart muscle cant relax

calcium tetany = too low of calcium in the blood, uncontrolled skeletal contraction

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functions of clacium

bone development and mineralization: 99% body calcium in skeleton. 2 roles: structure, support and to act as a calcium bank (too low ca in diet → body will take ca from bones)

hydroxyapatite = ca-containing matrix that makes up bones and teeth Ca5(PO4)3(OH)

other 1% of calcium is in body fluids and cellular compartments. Involved in intercellular signalling as secondary messenger (calmodulin), blood clotting, transmittion of nerve impulses, muscle contraction

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bone types

trabecular(spongy) - ends of bones, vertebrae, most metabolically active, absorbs shock

cortical (hard)

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bone cells

osteoblasts = build

osteoclasts = resorption, clasts = chew

osteocytes =

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bone growth

determines bone size, begins in the womb, continues until early adulthood

more formation than resorption

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bone modeling

determines bone shape, begins in the womb, continues until early adulthood

more formation than resorption

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bone remodeling

maintains integrity of bone, replaces old bone with new bone to maintain mineral balance, involves bone resorption and formation, occurs predominantly during adulthood

healthy: formation happens at same rate as resorption

some life stages resorption happens more than formation (loss of bone)

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calcium in foods

dairy products (myplate reccomends 2-3 servings which is around 900 mg of calcium)

many leafy greens have it, but some have limited absorbtion

fortified foods

canned fish (bones)

some tofu; corn tortillas; almonds; sesame seeds

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calcium supplement

calcium carbonate is highest concentration of calcium by wt. followed by calcium citrate and then calcium phosphate.

calcium citrate maleate = greatest absorbability, proprietary blend, expensive

500 mg 2x daily is safe, safer to space doses apart

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calcium reccomendations

DV = 1300

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calcium deficiency

since bones are calcium banks, chronic deficiency leads to

osteopenia = low bone mass

osteoperosis = bones so weak they may fracture with daily activities. common in post-menopausal women (estrogen is protective against thsi) exacerbated by smoking, excessiv EtOH, inactivty, early onset of menopause or ovariectomy

dowagers hump

avoided by building peak bone density before age 30

identified by blood tests or DEXA

tx: hormone replacement therapy, dietary phytoestrogens (isoflavones, coumestans, lignans), ca supplement w/ vitamin D, phys activity (resistance), drugs to increase bone formation and lower resorption

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calcium toxicity

rare, GI responds by lowering absorption, may occur with Ca supplements

UL = 2500 mg; 2000 mg for 50+ (bc shitty kidneys)

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phosphorus

up to 70% of dietary intake absorbed

absorption enhanced by vitamin D

primary mechanism is passive absorption, based on phosphorus concentration in lumen, some active transport

excretion happens via kidneys

fibroblast growth factor 23 (FGF23) = boen derived hormone suppressing phosphate reabsorption and vitamin D activation in kidney

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phosphorus functions

80-85% in bones and teeth as hydroxyapatite

15% in cells, some in extracellular fluid as phosphate (HPO42)

component of: enzyme systems (regulation through phosphorus)

ATP DNA, RNA, phospholipids, lipoprotines

acid-base balance

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phosphorus in foods

dairy, bakery products and meats

20-30% from food additivies (as much as 1000 mg of P added to diet)

soft drinks add some (around 40 mg per can) as phosphoric acid

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phosphorus reccomendations

RDA = 700 mg

DV = 1250 mg

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phosphorus deficieincy

highly unlikely in healthy adults

can contribute to bone loss, decreased growth, poor tooth development

sx: anorexia, wt loss, weakness, irritability, stiff joints, bone pain

at risk: preterm infants, alcoholics, elderly, aluminum-containing antacids, early TPN formulations

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phosphorus toxicity

problems if certain kidney disease present (bc then you cant excrete it in urine)

can contribute to bone loss by competing with calcium

UL = 3-4 g

soft drinks increase consumption of phosphorus which lowers bone density. Acidic properties and high P content can increase calcium loss from bone as it goes to neutralize acid. Caffiene increases calcium loss through urine

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magnesium

40-60% absorbed from diet

passive and active absorption in small intestine

kidneys regulate blood concentration

stored in bones, some tissues

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magnesium functions

required in over 300 enzyme-catalyzed reactions —> stabilize ATP by binding to phosphate groups

DNA, RNA synthesis

bone structure

nerve and heart function

insulin action

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magnesium in foods

plant products are best, seeds and nuts

animal products supply some

hard tap water (MgOH2)

high zn doses interfere with mg absorb and balance

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magnesium reccomendations

RDA male - 400-420 mg; female - 310-320 mg

DV = 420 mg

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magnesium deficiency

hypomagnesemia

sx: increase heart rate, weakness, muscle spasm, disorientation, naseua, vomit, dizzy

at risk: diuretic users, heavy persiration; increased vomiting and diarrhea, alcoholics, diabetics (increase urinary loss with high blood glucose)

50 % of US intakes below EAR

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magnesium toxicitiy

rare

UL = 350 mg (only for pharmacologic agent)

excessive intakes of nondietary mg (antacids)

seen in kidney failure

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vit D

2 prohormone forms: 7-dehydrocholesterol (pro D3) skin and ergosterol (pro D2) plant and fungi sources

Vitamin D forms: ergocalciferol, cholecalciferol

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Vit D formation in skin

7-dehydrocholesterol located in skin

UVB light on skin opens ring turning it into vit D3

D3 bound to protein and transported to liver

north of 37 degrees, very little if any vit D synthesize din skin from November thru february

sunscreen/SPF blocks vit d synthesis

melanin blocks it

clothing blocks it

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Absorb and formation of Vit D from Food

after consumption of food with vit D, 80% of it is incorporated into micelles in small intestine, absorbed and transported to liver by chylomicrons (CM)

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vit D activation

to be active hormone, has to undergo 2 hydroxylation rxns: liver: adds OH on C25 making calcidiol (the kind measured clinically to assess vit D status)

kidney: adds OH on C1 to make calcitriol (PTH regulates production)

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vit D excretion

occurs in bile and a small amount of vit D metabolites thru urine

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vit D functions

is a homrmone

acts thru a nuclear receptor on cells

vit D receptors (VDR) on many cell types

main target tissues: GI, bone, kidney

major role in Ca regulation and bone health

in bone: promote normal mineralization by making Ca (and P) available in blood that bathes bone. Raises blood calcium concentration in 3 ways:

  • increases calcium absorption from GI (CaBP - calcium binding protein)

  • release of Ca from bone (with PTH)

  • retention of Ca from kidney (with PTH)

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Vit D foods

very few natural foods contain vit D

most nutrient dense sources: fish (tilapia), egg yolks, fortified milk, other fortified products, shitake mushrooms

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vitamin D deficiency

rickets in children: skeleton fails to mineralize properly. malformed bones, abnormal rib formation, tetany

osteomalacia in adulthood - signs include bone fracture and bone/muscle pain

vitamin D resistance - lack of synthesis of 1,25(OH2-D in kidneys, inability of 1,25(OH)2-D to bind to VDR in body

at risk: breastfed infants, elderly, darker skin pigment, living in northern latitudes, sun avoidance (sunscreen, cover), low outdoor time (ex. nursing homes, prisons), no milk intake, excess adiposity

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Vit D reccomendations

Holick formula for safe sun: expose 25% of your body’s surface area to 25% of 1 MED dose 2-3 times a week. (MED= amount of sun needed to nake skin a little bit pink)

dietary supplement form is D3

Rx form is D2

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Vit D pharmacologic Use

vit D analogs used as a safe effective treatment in psoriasis and others

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Vitamin D toxicity

UL = 100 mcg (but probably too low)

breastfed infants most susceptible

symptoms: hypercalcemia and calcification of soft tissues

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fluoride

absorbed thru out GI tract by passive difusion

80-90% absorbed

transported in ionic form

excreted in kidneys as urine

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fluoride function

increases resistance of tooth enamel to dental caries

protects against demineralization of bone - F substitutes for the OH in hydoxyapatite creating a denser and harder surface = hydroxyfluorapatite

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fluoride in foods

fluoridated water

toothpaste, dental treatments

tea, seaweed, seafood

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fluoride reccommendations

AI male 3.8 mg; female 3.1 mg

based on resistance to dental carries without causing mottling (brown spots on teeth, but strong)

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fluoride toxicity

sx: pulmonary distrub, convulsions, paralysis, excess salivation and tearing, cardiac weakness, sensory problems, coma

mottling of teeth during development

skeletal fluorosis (bones are too hard, not bendy enough)

UL = 10 mg

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Vit A and carotenoid organization

carotenoid = precursors to vit A (beta carotene and zeaxanthin)

retinoids = prefromed vita A (retinol, retinal, retinoic acid)

retinol and retinal interconvert in both directions

retinal can become retinoic acid

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Vit A (retinoids)

hydrolysis of retinyl esters (retinol plus fatty acid) yields retinol

bile, pancreatic lipase, and retinyl ester hydrolase

transported via CM

sotred in liver (90%) and other (adipose, kidney, lungs)

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carotenoids

released from food proteins, absorbed intact via passive diffusion (5 to 60%)

enterocyte cleaves yielding retinal which turns into retinol for body usage

may enter bloodstream directly, traveling on LP (CM)

storage: liver, fat pads

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Vit A excretion

not readily excreted; kidney disease raises risk of toxicity

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cellular retinoid-binding protien

retinoids are bound to specific retinoid-binding proteins as they are transported thru blood (eg. RBP, transthyretin) and within cells (CRABP)

binding proteins also protect from breakdown

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nuclear-retinoid receptors

two main families: retinoic acid receptor, retinoid X receptor

receptors interact with retinoic acid and bind with specific sites on DNA, which regulates gene expression (allows for cell differentiation and other cellular responses)

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functions of vit A

retinol and retinal: vision, sexual reproduction, bone health, immune function

retinoic acid: cell differentiation, bone health, immune function

not strongly established as an antioxidant

vision fx: forms part of rhodopsin (11-cis retinal and opsin), FOUND WITHIN RODS visual cycles, rods = dim light, cones = bright light

iodopsin is inside cone cells

cellular growth and differentaion

gene expression (via RXR/RAR) - directs cell differentiation. growth and development of embryo, prod, strx, fxn of epithelial cells (lining of eyes, lungs, trachea, skin, GI, etc) differentiation of cells of retina, cornea

immunity: deficiency is associated with lower resistance to infection. contributes to several immune processes, directly and indirecly (eg. maintiaing epithelial lining, barrier fxn)

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Vit A in foods

preformed: eggs, liver

carotenoids: carrots, liver, greens, sweet potatoes, winter squash, broccoli

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vit A reccomendations

measured as RAEs = retinol activity equivalents

1 RAE = 1 mcg of retinol

RDA female 700 mcg RAE; male 900 mcg RAE

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vit A deficiency

infectious diseases, night blindness, xerophthalmia, xerosis, keratomalcia, follicular hyperkeratosis (skin, GI, lungs)

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vit A toxicity

Acute

chronic

teratogenic - accutane

UL = 3000 mcg RAE

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carotenoid functions

weak antioxidant, effective against lipid oxidation in cell membrane, enhance immune system, protect skin from UV light damage, protect eyes from damage, preventing or delaying age-related vision impairment

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carotenoid recommendations

no DRIs

advises against supplementation

large consumption not toxic

carotenosis or carotendodermia is harmless and reversible (skin discoloration-- me as a baby)