Micronutrient Final

Calcium teen AI

1300 mg/day

Calcium 19-50 yo AI

1000 mg/day

Calcium 50+ yo AI

1200 mg/day

Calcium osteoporosis AI

1500 mg/day

Calcium UL

2500 mg/day

Modeling vs remodeling

Modeling:

- Occurs in children

- Reshapes bones during growth

Remodeling:

- Adults

- Maintains bone mass and repairs damage

- Bone is continually remodeled

Osteoblast function

1. Mineralization and matrix synthesis

2. Bone formation

3. Lays out matrix

Osteoclast function

1. Bone resorption

2. Release a lot of materials

3. Smooths out bone

Osteocytes function

1. Channels out to the environment to send signal about bone health

Bone lining cells function

1. Covers surface

Factors enhancing calcium absorption

1. Acidity

2. Lactose

3. V-D

4. Physiological demand

- Pregnancy

- Deficiency

- Growth

Factors decreasing calcium absorption

1. High Ca intake

2. Oxalate/phytates

3. Fiber

4. Steatorrhea - fatty stool

5. Age - gastric acid secretion

Calcium functions

Typical absorption rate of calcium

20-30% low bioavailability

Short term deficiency of calcium

Tetany --> muscle spasms

Long term deficiency of calcium

Osteoporosis

What does failure of PBM cause?

Osteoporosis

When does bone loss begin?

30 years old

What determines maximum bone density?

Genetics

When is 90% of PBM achieved?

18 years old, grows til 30 years old

Dietary sources of calcium

1. Milk/milk products

2. Yogurt

3. Fortified OJ

4. Cheese

5. Salmon w bones/sardines

6. Broccoli

Osteoporosis

A condition where the bones become fragile and porous

Non-modifiable risk factors of osteoporosis

1. Caucasian/asian

2. Family hx

3. Advanced age

4. Females (E2)

5. Premature menopause (<45)

6. Prolonged time without menstrual periods: eating disorder, low weight

7. Small frame

Modifiable risk factors of osteoporosis

1. Low intake of Ca/VD

2. LBW

3. Inactivity

4. Prolonged immobilization

5. Smoking

6. Alcohol

7. Protein

8. Sodium

9. Caffeine/soft drinks

Cause of osteoporosis

PBM failure

Common fracture sites (osteoporosis)

Dx of osteoporosis

Measurement of osteoporosis

Ca supplement recommendation

500 mg/twice a day split

Highest absorption form of calcium

Calcium citrate

Most prevalent form of calcium

Calcium carbonate

AI for V-D 0-12 months

10 mcg/400 IU

AI for V-D 1-70 years old

15 mcg/600 IU

AI for V-D 70+ years old

20 mcg/800 IU

Functions of V-D

1. Acts as hormone: homeostasis of Ca in bone

2. Bone health: raises calcium levels in the blood to promote calcium deposit on bones

3. Increase in muscle strength

4. Prevention of diseases

What diseases does V-D help prevent?

1. Cancer

2. DM

3. CVD

4. Pain syndrome

5. Infertility

6. AI diseases - senile cataract, glucose intolerance, MS, RA, thyroiditis

Toxicity of V-D level and what occurs?

10x RDA

Increases Ca absorption and increases Ca deposits on soft tissue --> kidney stones

Deficiency of V-D in children + sx

Rickets

Sx: bowed legs because bones not strong enough to sustain growth

Deficiency of V-D adults

Osteomalacia (softening of bone)

V-D deficiency sx

1. Bone pain

2. Chronic pain

3. Restless sleep

4. Muscle weakness

5. HBP

6. Headache/migraine

7. Depression

What occurs if V-D levels are low in relation to Ca?

Ca excretes even if blood Ca is low

Groups at risk for V-D deficiency

1. Exclusively breastfed babies

2. Vegetarians

3. Dark skinned people

4. Older people, older skin

5. Risk factors

- Low intake

- Malabsorption

- Indadequate exposure to sun

Dietary sources of V-D

1. Fish

2. Milk

3. Egg

4. Sun exposure

Iron RDA for men

8 mg/day

Iron RDA for women

18 mg/day

UL for iron

45 mg/day

What does typical western diet provide in iron?

5-7 mg/1000 kal

Ferrous iron, where is it?

Fe2+, in tissues

Ferric iron, where is it?

Fe3+, in blood

How is iron absorbed?

Ferric to ferrous

Iron functions

1. Oxygen transport

- Part of Hbg/myoglobin

2. Cofactor for enzymes

3. Normal brain and immune function

- if not enough iron, O2 carrying capacity decreases then anemia

Enzymes that iron required for

1. Catalase

2. Cytchrome a, b, c

3. P450 (H' synthesis, drug metabolism)

4. Monooxygenases/dioxygenases

5. Peroxidases

What is catalase?

Antioxidant that protects cells by rapidly decomposing H2O2 into H2o2 and O2

Factors affecting iron absorption

1. Dietary iron content

2. Bioavaliablity of dietary iron

3. Amount of storage iron

4. Physical status

Enhancing factors of iron absorption

1. Animal protein (MFP factors)

2. V-C

3. Fructose, sorbitol

4. Cysteine

5. Low iron status

Factors inhibiting iron absorption

1. Calcium/other minerals

2. Oxalate/phytate/fiber

3. Lack of stomach acid/dietary protein

4. Coffee/tea

What is the storage form of iron?

Ferritin

Storage sites of iron

1. Liver

2. Spleen

3. Bone marrow

What is the form of iron that is transported in blood

Transferrin

Why is transferrin important?

It binds to iron to transport because free iron promotes oxidation and can be used by bacteria

Dietary sources of iron

High sources

1. Clams

2. Beef

3. Oysters

4. Fortified cereal

Good sources

1. Lentils

2. Beans

3. Poultry

4. Fish

Iron deficiency without anemia sx

1. Behavioral disturbances

2. Impaired performance in cognitive taks

3. Impairment of learning ability

4. Short attention span

5. Impaired immune system, resistance to infection

When does deficiency without anemia occur?

When there is depletion of bone marrow sites; hemoglobin is still normal

Iron deficiency anemia symptoms

1. Fatigue

2. SOB

3. Lightheadedness

4. Rapid heartbeat

5. Brittle nails

6. Headaches

Histology of iron deficiency anemia

Microytic & hypochromic

Populations at risk for iron deficiency anemia

1. Infants/young children

2. Adolescents

3. Women at childbearing age

4. Pregnant women

5. Chronic blood loss

- Cancer in GI

- Parasitic infestation

Why/when are infants/young children at risk for iron deficiency?

6m-4 years; not before 6 months due to breast milk having more absorbable form (lactoferrin)

Growing requires iron; increase body cells/volume

Why are adolescents at risk for iron deficiency?

1. 2nd growth spurt

2. Females start period

3. Begin competitive activites

What nutrients does iron interact with?

Best indicator of iron

Plasma ferritin

Plasma ferritin level of deficiency

<12 ug

Total iron binding capacity levels (transferrin)

>400 ug/dL

Serum iron levels

>50 ug/dL

Varies per time of day

Hemoglobin/hematocrit levels

Hbg <12-13g/dL

Hct <37-40%

Positive effects of iron supplementation

Treats iron deficiency anemia

Negative effects of iron supplementation

1. People with hemochromatosis toxic levels due to increased iron absorption

2. Can decrease iron, copper, calcium absorption

3. Fatal in young children

Causes of iron toxicity

1. Hemochromatosis (genetic)

2. Accidental overload in young children

What is hemochromatosis ?

Genetic disorder of iron overload due to increased absorption/failure of regulation

What does hemochromatosis cause?

1. Excess deposits in soft tissues

2. Oxidative stress to tissues --> organ failure

Tx of hemochromatosis

1. Phlebotomy

2. Fe-chelators

Tx of acute iron toxicity

1. Whole bowel irrigation

2. Chealator

Iodine AI

150 mcg/day

Iodine UL

1,100 mcg/day

Distribution of iodine in the body

75% thyroid gland

25% mammary gland, gastric mucosa, blood

How much of iodine does iodine normally have?

20-30 mg

Iodine functions

Thyroid H' synthesis

Active form of iodine hormone

T3/triiodothyronine

3 atoms of iodine per molecule

Inactive form of iodine hormone

T4/thyroxine

4 atoms of iodine per molecule

What is T3 and T4 needed for?

Thyroid stimulating H'

Diff between T3, T4, and TSH

T3 and T4 are produced by thyroid galnd

TSH is produced by pituitary gland to regulate them

Dietary sources of iodine

1. Seaweed

2. Foods or marine origin

4. Processed foods, iodized salt

Iodine deficiency

1. Hypothyroidism --> underactive thyroid gland

2. Cretinism --> during pregnancy

3. Goiter --> enlarged thyroid

Causes of hypothyroidism

1. AI disease

2. Iodine deficiency

Sx of hypothyroidism

1. Tingling in extremities

2. Dry hair, brittle nails, dry skin

3. Muscle cramps

4. Headaches

5. Weight gain

6. Tiredness

What does severe iodine def in pregnancy cause?

Cretinism

1. Short stature

2. Protuberant abdomen

3. Swollen features

4. Fetal death

5. Irreversible mental/physical retardation

Why does goiter occur?

Iodine deficiency causes thyroid H level to decrease and the thyroid gland is over stimulated to promote hormone production to overcome low thryoid H in the blood

Over time, the gland increases

Cause of goiter

1. Hypothyroidism

2. Goitrogens (block iodine absorption)

3. Selenium deficiency (needed to convert T4 to T3)

When are goiters usually dx?

After dysphagia and dyspnea appear

(trouble swallowing/breathing)

Usually asymptomatic until these

Iodine toxicity

Rare because humans are tolerant to high iodine intakes

When is iodine toxicity a concern

1 .If someone is iodine deficiency, replention must be done slower because can cause hyperthyroidism

2. In asia with high intakes of seaweed --> paradoxical goiter