Minerals - Cu, Se, Cr, I, Mn Flashcards

1
Q

Do acidic mediums increase or decrease copper absorption?

A

INCREASE - Gastric acid seems to enhance Cu absorption.

Hark, p. 76

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2
Q

Copper plays an essential role in the production of ___, ___ and ___ pigment (melanin).

A

Skin, hair and eye pigment

Hark, p. 76

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3
Q

Copper absorption is decreased by:

a. calcium
b. phytates
c. fiber
d. zinc
e. a and d
f. all of the above

A

e. all of the above

Hark, p. 76

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4
Q

Copper has 2 main forms: _____ (Cu²⁺) and _____ (Cu⁺). Copper’s ability to switch between these oxidation states make it important for redox reactions + scavenging free radicals by readily accepting and donating free radicals.

a. cupric and cuprous
b. ceruloic and cerulous
c. copric anc coprous

A

a. Cupric (Cu²⁺ = mostly found in the body) and cuprous (Cu⁺)

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5
Q

A key function of copper is protecting cells from from oxygen damage - it does this as a component of antioxidant enzymes such as ______ _______, an antioxidant that makes radicals less reactive by converting O₂⁻ > H₂O₂.

a. superoxide dismutase
b. glutathione
c. pycnogenol
d. coenzyme Q-10

A

a. superoxide dismutase (SOD)

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6
Q

Copper’s role in the synthesis of _____ tissue is critical for the development of healthy bones, teeth and vascular structures.

a. connective
b. epithelial
c. muscle
d. nervous

A

Connective tissue

Hark, p. 76

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7
Q

Copper is necessary for maintenance of the ____ ____ surrounding nerve fibers.

A

Myelin sheath

Hark, p. 76

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8
Q

Most copper is excreted in ____, and a small amount is excreted in _____.

a. urine; bile
b. bile; urine
c. urine; sweat
d. sweat; urine

A

b. bile; urine

https: //ods.od.nih.gov/factsheets/Copper-HealthProfessional/

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9
Q

Copper levels in the body are tightly regulated via copper absorption from the _____ ______ and copper release by the _____ into bile to provide protection from copper deficiency and toxicity.

A

Small intestine (mostly duodenum); liver.

High copper intake = copper is sequestered in metallothionein (metal-binding proteins) within enterocytes & increased excretion via bile

Low copper intake = intestinal absorption increases

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10
Q

Only small amounts of copper are typically stored in the body - of this, almost two-thirds of the body’s copper is located in:

a. skeleton and muscle
b. liver
c. enterocytes
d. red blood cells

A

a. skeleton and muscle

https: //ods.od.nih.gov/factsheets/Copper-HealthProfessional/

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11
Q

Copper is a cofactor for several enzymes, known as ________ involved in energy production, iron metabolism, neuropeptide activation, connective tissue synthesis, neurotransmitter synthesis and regulation of gene expression.

A

cuproenzymes

Energy production - copper needed for the electron transport chain

Iron metabolism - oxidizes Fe²⁺ to Fe³⁺ (req. for transport via transferrin) & involved in heme synthesis

Connective tissue synthesis – req. to cross-link collagen + elastin; involved in bone mineralization

CNS function – involved in neurotransmitter synthesis + metabolism; req. for synthesis + maintenance of myelin

Regulation of gene expression – Cu-dependent transcription factors (regulates transcription of certain genes)

https://ods.od.nih.gov/factsheets/Copper-HealthProfessional/

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12
Q

One abundant cuproenzyme is ________, which plays a role in iron metabolism and carries more than 95% of the total copper in healthy human plasma.

a. transferrin
b. hephaestin
c. hepcidin
d. ceruloplasmin

A

d. ceruloplasmin - the major copper-binding protein synthesized by the liver.
https: //ods.od.nih.gov/factsheets/Copper-HealthProfessional/

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13
Q

Copper is needed for the metabolism of ______ required in the functioning of the nervous system

a. catecholamines
b. acetylcholine
c. peptides
d. purines

A

a. catecholamines

Hark, p. 76

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14
Q

Although rare, copper deficiency can be acquired or inherited, and can occur in:

a. malnourished infants
b. premature infants
c. malabsorption syndromes (i.e. celiac disease)
d. Menke’s syndrome
e. excessive zinc intake
f. all of the above

A

f. all of the above

Other conditions/individuals with increased risk of Cu deficiency = prolonged diarrhea (infants), parenteral nutrition, cystic firbrosis.

High supplemental zinc intakes of 50 mg/day or more for extended periods of time may result in copper deficiency.

Menke’s syndrome = a rare, X-linked (more common in men), recessive disorder of copper homeostasis resulting in poor distribution of copper to the body’s cells. Primarily affects male infants. Copper accumulates in some tissues, such as the small intestine and kidneys, while the brain and other tissues have unusually low levels of copper. Symptoms = failure to thrive, impaired cognitive development, aortic aneurysms, seizures, poor muscle tone, weak bones and unusually kinky and/or colorless/steel-colored hair. Most individuals with Menkes disease die by age 3 years if untreated (Daily copper injections may improve outcome if given within days after birth; but since newborn screening for this disorder is not available, and early detection is infrequent because clinical signs are subtle in the beginning, the disease is rarely treated early enough to make a significant difference).

Hark, p. 76-77

https: //my.clevelandclinic.org/health/articles/6068-menkes-disease
https: //lpi.oregonstate.edu/mic/minerals/copper

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15
Q

The RDA for copper in adults 19+ is:

a. 500 mcg
b. 600 mcg
c. 800 mcg
d. 900 mcg

A

d. 900 mcg

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16
Q

Symptoms of copper deficiency include:

a. anemia
b. neutropenia (low white blood cell count)
c. loss of pigmentation in skin/hair
d. connective tissue damage
e. neurological symptoms
f. a and c
g. all of the above

A

f. all of the above

Other symptoms include: impaired growth and bone lesions/osteoporosis. Damage to connective tissues can result in lung damage or excessive bleeding.

Hark. p. 77

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17
Q

Top food sources of copper include:

a. organ meats, shellfish, nuts, seeds, whole grains, chocolate
b. milk, cheese, yogurt, beef, chicken, turkey
c. peppers, sweet potato, broccoli, Brussel sprouts, beans, legumes

A

a. organ meats, shellfish, nuts, seeds, whole grains, chocolate

Copper can also be high in hard water / houses with copper pipes. Running tap water for several seconds before using the water can reduce copper concentrations.

Kraus, p. 574

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18
Q

The TUL for copper in adults 19+ is:

a. 2,000 mcg/day
b. 5,000 mcg/day
c. 10,000 mcg/day
d. 15,000 mcg/day

A

c. 10,000 mcg/day

Hark, p. 77

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19
Q

True or false: Excessive copper intake or poisoning may occur with consumption of acidic beverages stored in containers made with copper.

A

True

Symptoms of copper toxicity include nausea, diarrhea, vomiting, abdominal pain, anemia, anuria, and, in extreme cases, liver damage, kidney failure, coma & death.

Hark, p. 77

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20
Q

Which genetic condition is most associated with copper toxicity?

a. Menke’s syndrome
b. Bartter syndrome
c. Paget’s disease
d. Wilson’s disease

A

d. Wilson’s disease. Copper toxicity is rare and usually associated with Wilson’s disease - an autosomal-recessive disorder associated with impaired biliary copper excretion, leading to copper overload via accumulation in various tissues (especially the liver, but also the brain, cornea and kidneys). Untreated, it can result in nervous system and liver damage. Low serum ceruloplasmin levels, elevated copper concentration in a liver biopsy, and high urinary copper excretion confirm the diagnosis. Patients can present with acute, fulminant (occurring suddenly with great severity), or chronic active hepatitis and neuropsychiatric symptoms. Copper chelating agents (to release copper from organs where it can be filtered out of the blood and excreted in urine) and zinc supplementation (to inhibit intestinal copper absorption and binding in the liver) is used to treat Wilson’s disease once it is diagnosed. Ongoing copper chelation is required to prevent relapses and liver failure; transplantation is needed corrects the metabolic defect (if Wilson’s disease isn’t dx until onset of liver failure, transplant is needed to survive). A low copper diet is no longer required, but may be helpful in initial treatment.

NFPE - Kayser-Fleischer rings in the eyes (dark yellowish ring encircling the iris, due to copper deposits in the cornea) are one sign of Wilson’s disease.

Kraus, p. 567

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21
Q

True or false? High dose zinc supplementation can deplete copper, and zinc supplements should be taken with copper to prevent copper depletion.

A

True (although for best absorption, separate supplementation).

Kraus, p. 202

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22
Q

To optimize absorption of copper supplementation, it’s best to supplement away from:

a. iron
b. alpha lipoic acid
c. vitamin C
d. zinc
e. a and d
f. all of the above

A

f. all of the above

Iron - competes for intestinal absorption; Cu req. for normal Fe metabolism + transport to bone marrow for erythropoiesis

ALA - can chelate Cu + incr. Cu urinary excretion

Vit C - can inhibit Cu absorption if supplementing with high doses (500-600mg/day+), administer separately

Zinc - high dose Zn can lead to Cu deficiency; high Zn also increases level of metallothionein, which has affinity for Cu (leads to decreased Cu absorption)

Molybdenum: high doses of Cu may lead to Mo deficiency + vice versa

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23
Q

Which drugs can interfere with copper absorption?

a. antacids
b. penicillamine
c. oral contraceptives
d. a & b
e. all of the above

A

d. a & b

High doses of antacids may interfere w/ absorption (gastric acid aids Cu absorption)

Penicillamine (used in chelation) binds to Cu and increases its elimination in Wilson disease – if taking this + no Wilson disease, may be increased need for Cu

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24
Q

True of false? Copper supplements may improve the effectiveness of vitamin D and calcium in improving bone density in post-menopausal women.

A

True

Hark, p. 77

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25
Q

Selenium is absorbed in the GI tract in the range of:

a. 10-20%
b. 30-45%
c. 50-100%

A

*Selenium absorption is efficient and is not regulated. Selenium in the form of selenocysteine and selenomethionine in the diet is absorved in the GI tract in the range of c. 50-100%.

Hark, pg. 79

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26
Q

Selenium leaves the body via:

a. urine
b. feces
c. skin
d. pulmonary metabolites that are exhaled
e. all of the above

A

e. all of the above

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27
Q

Selenium is an essential component of the enzyme_________ which protects cells from the damaging effects of free radicals (such as H202, by reducing it to water, and lipid peroxide).

a. beta-galactosidase
b. glutathione peroxidase
c. citrate synthase

A

b. glutathione peroxidase.
* For example - LDL oxidation is reduces by selenium

Hark, pg 79

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28
Q

Selenium is essential for normal functioning of the __________ (select any/all that apply)

a. immune system
b. kidneys
c. lungs
d. thyroid gland

A

a. immune system - lowers oxidative stress thereby reducing inflammation
d. thyroid gland - removes free radicals generated by the production of thyroid hormone.

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29
Q

Though selenium deficiency is not common in the U.S and seldom causes illness when it occurs in isolation, it has been seen in people

a. on total parenteral nutrition (TPN)
b. with gastrointestinal problems
c. who have kwashiorkor (a severe form of malnutrition observed in developing regions where people do not get enough protein).
d. all of the above

A

d. all of the above.
* Children and babies most commonly have kwashiorkor due to protein deficiency and other essential nutrients, including selenium, as selenium is only absorbed in amino acid form (selenomethionine and selenocysteine).

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30
Q

Selenium deficiency observed in livestock is otherwise known as:

a. Bloat
b. Hardware disease
c. White muscle disease
d. Foot rot

A

c. White muscle disease.
* Signs of selenium deficiency are seen in countries where the selenium content in the soil is very low and therefore the selenium intake of domestic animals is poor. Includes: China, New Zealand, and Venezuela.
* People in China, New Zealand, and Venezuela may develop an enlarged heart with poor cardiac function as a result of selenium deficiency.

Hark, pg. 79

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31
Q

Lower selenium levels have been observed in both men and women with _____.

a. goiters
b. adrenal dysfunction
c. low cortisol
d. heart palpitations

A

a. goiters.
* Note - selenium supplementation did not improve thyroid hormone levels (per this reference).

Hark, pg 79.

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32
Q

High blood levels of selenium (selenosis) leads to symptoms including:

a. GI upset
b. joint pain
c. hair loss and nail discoloration
d. fatigue
e. all of the above

A

e. all of the above.
* Selenium toxicity is rare in the U.S. The few reported accidents were from manufacturing error leading to high dose in supplement form.
* Acute toxicity can lead to respiratory distress syndrome, myocardial infarction, and renal failure.

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33
Q

The TUL for selenium is:

a. 200 micrograms daily
b. 300 micrograms daily
c. 400 micrograms daily
d. 500 micrograms daily

A

c. 400 micrograms daily.

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34
Q

Most cases of selenium deficiency occur as a consequence of ____________________.

a. inadequate intake
b. gastroenterological disturbance
c. both a and b

A

b. gastroenterological disturbance (such as Crohn’s disease)

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35
Q

Promising research is emerging on the role of selenium in ____________.

a. autoimmune thyroiditis
b. lupus
c. prostate cancer prevention
d. a and c

A

a. autoimmune thyroiditis
*
Selenium supplementation in people with Hashimoto’s thyroiditis might reduce antibody levels and result in a decreased dosage of levothyroxine (LT4) and may provide other beneficial effects (e.g. on mood and health-related quality of life).

source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005265/
c. prostate cancer prevention
* While research is mixed, the Nutritional Prevention of Cancer study reports selenium supplementation to be associated with reduced risk of colorectal cancer and adenomas in subjects with low baseline selenium levels.

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36
Q

The RDA of selenium for ages 14+ is:

a. 35 micrograms daily
b. 55 micrograms daily
c. 100 micrograms daily

A

b. 55 micrograms daily for men and women, increased to 60 micrograms for pregnant women and 70 micrograms for breastfeeding women.

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37
Q

Sources of selenium in food include:

a. Brazil nuts
b. seafood
c. organ meats
d. all of the above

A

d. all of the above

* Muscle meats, cereals and other grains, and dairy contain selenium as well.

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38
Q

Selenium content in foods is determined by _____________.

A

The soil.

  • Soil pH, amount of organic matter in the soil, and whether the selenium is in a form that is amenable to plant uptake. This also depends on the plants the animals eat.
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39
Q

True or False?

Selenium deficiency is associated with mood states such as major depressive disorder.

A

True.

*This may be due to selenium’s function as an antioxidant, and as a constituent of selenoproteins that are important in redox homeostasis reducing depression risk.

40
Q

Selenium may decrease the clearance and excretion of ___________.

a. antibiotics
b. barbiturates
c. PPI’s

A

b. barbiturates

41
Q

Medications selenium may moderately interact with include:

a. anticoagulants (aspirin, Plavix, Coumadin)
b. cholesterol lowering drugs (Lipitor, lovastatin).
c. both a and b

A

c. both a and b.

42
Q

Which mineral is known as a glucose tolerance factor?

a. selenium
b. chromium
c. copper
d. manganese

A

b. chromium - chromium is thought to potentiate the action of insulin and thus has been identified as a glucose tolerance factor.

Hark, p. 81

43
Q

Generally the efficiency of chromium absorption is:

a. high
b. medium
c. low

A

c. low - Chromium absorption depends on the form and physiochemical reactions in the intestinal lumen, but generally the efficiency of absorption is low (<3 percent). A Cr deficient diet results in higher fractional absorption rates.

Hark, p. 81

44
Q

How is chromium thought to support blood sugar balance?

a. by facilitating insulin binding to its receptor
b. by increasing insulin production
c. by decreasing glucagon production

A

a. by facilitating insulin binding to its receptor - Chromium is hypothesized to potentiate the action of insulin via an oligopeptide that has been named “chromodulin,” which binds to the insulin receptor stimulating its tyrosine kinase activity.

Hark, p. 81

45
Q

Through which of the below mechanisms do chromium and iron interact?

a. iron inhibits absorption of chromium
b. chromium competes with iron for binding sites on transferrin
c. iron increases absorption of chromium
d. chromium is needed for iron to bind to transferrin

A

b. chromium competes for binding sites on transferrin (but not enough clinical research to support that Cr supplementation adversely affects Fe status)

46
Q

Chromium is primarily regulated by excretion via:

a. urine
b. bile
c. skin
d. a and b

A

a. urine - While some chromium is lost via skin, most is excreted via urine.

47
Q

Which of the below result in decreases chromium status?

a. phytates
b. fiber
c. refined carbohydrates/sugars
d. zinc
e. vitamin C
f. a-c
g. all of the above

A

f. a-c. Phytates and fiber decrease chromium absorption, and diets high in refined carbs/sugars promote urinary secretion of chromium.

Hark. p. 81

48
Q

Which of the below may increase chromium absorption?

a. vitamin C
b. vitamin B6
c. vitamin D
d. vitamin B12
e. all of the above

A

a. vitamin C

49
Q

True or false: The best way to measure chromium levels is via urine testing.

A

False - There is currently no reliable way to measure chromium levels, so deficiency is generally diagnosed from a food diary, clinical history, and/or response to therapeutic trial of chromium supplementation.

50
Q

What is the TUL for chromium?

a. 10 mcg
b. 20 mcg
c. 30 mcg
d. no TUL has been established

A

d. no TUL has been established - As no adverse effects have been observed from excess chromium intake from food, no TUL has been established.

(Hark, p. 81)

51
Q

What is the predominant form of chromium in food and supplements, and thus the form thought to be most important for human health?

a. trivalent chromium (Cr+3)
b. quadvalent chromium (Cr+4)
c. pentavalent chromium (Cr+5)
d. hexavalent chromium (Cr+6)

A

a. Trivalent chromium - Trivalent chromium is the most stable form of chromium that is found in food and supplements and is not toxic. Hexavalent chromium is found with industrial pollution and is toxic and carcinogenic when inhaled.

BACKGROUND: Hexavalent chromium at high levels in drinking water in a Chinese province is believed to be responsible for increased mortality from stomach cancer, creating concerns about the overuse of chromium sup- plements. A meta-analysis reported that hexavalent chromium was only weakly linked to lung cancer and not to any other cancers.

(Hark, p. 81)

52
Q

True or false: The best way to measure chromium levels is via urine testing.

A

False - There is currently no reliable way to measure chromium levels, so deficiency is generally diagnosed from a food diary, clinical history, and/or response to therapeutic trial of chromium supplementation.

53
Q

Which of the below best represent the top food sources of chromium?

a. whole grains, eggs, brewer’s yeast, lentils, molasses, chicken, broccoli
b. eggs, yogurt, milk, beef, turkey, chicken, pork, organ meats
c. leafy greens, brussel sprouts, broccoli, cauliflower, beans, lentils

A

a. whole grains, eggs, brewer’s yeast, lentils, molasses, chicken, broccoli

However, 40-60% of chromium is lost in refining grains. Chromium can also be obtained via stainless steel cookware.

54
Q

Which of the following clients (if any) need to be cautious with chromium supplementation?

a. those w/ pre-existing liver or kidney disease
b. those w/ cardiovascular disease
c. those w/ thyroid dysregulation
d. all of the above
e. none of the above

A

a. those w/ pre-existing liver or kidney disease

55
Q

Which drug class increases urinary excretion of chromium?

a. Glucocorticoids
b. SSRIs
c. Antibiotics
d. Benzodiazepines

A

a. Glucocorticoids

56
Q

Symptoms of chromium deficiency include:

a. glucose intolerance
b. weight loss
c. peripheral neuropathy
d. confusion
e. negative nitrogen balance
f. a and e
g. all of the above

A

g. all of the above

57
Q

What usage instructions are recommended with chromium supplementation?

a. with meals, in divided doses, in the evening
b. between meals, in divided doses, in the morning
c. with meals, in the morning
d. between meals, in the evening

A

b. between meals, in divided doses, in the morning

Morning supplementation is preferred, since some research shows that chromium supplementation increases dream activity and development of insomnia. Chromium supplementation is usually reco’d between meals and in divided doses

58
Q

Chromium is used clinical for the prevention/treatment of each of the following conditions EXCEPT:

a. Impaired glucose intolerance
b. Type II diabetes
c. Cardiovascular disease
d. Thyroid disease

A

d. all EXCEPT thyroid disease

PREVENTION of impaired glucose intolerance, Type 2 diabetes mellitus and CVD (used to improve glucose utilization and blood lipid profiles - dosages typically 200ug/d for 2-3months).

TREATMENT of Type 2 diabetes (chromium picolinate improves glycemic control).

59
Q

What is the AI for chromium in adults 19-50 yo?

a. males 35 mcg, females 25 mcg
b. males 45 mcg, females 35 mcg
c. males 55 mcg, females 45 mcg
d. males 75 mcg, females 65mcg

A

a. males 35 mcg, females 25 mcg

60
Q
\_\_\_\_\_\_\_\_\_\_\_\_ can inhibit the absorption of iron. The inverse is also true, so co-supplementation is often advised.
A. Copper
B. Vitamin E
C. Manganese
D. Vitamin A
A

C. Manganese

61
Q

True or False. Metabolically active tissues containing mitochondria and pigmented tissues will typically have increased manganese.

A

True.

62
Q

There is about 10-20mg of manganese in the body, of which 25-40%
is found in the ________?

A

Bone

63
Q
Manganese is an essential cofactor for a number of enzymes and functions/plays a role in:
A. Metabolism
B. Wound healing
C. Antioxidant actions
D. Bone development
E. A & C
F. All of the above
A

F. All of the above

Antioxidant actions: MnSOD (Manganese Superoxide Dismutase) is the main antioxidant in the mitochondria.

Metabolism: required for activation of enzymes which are involved in the metabolism of amino acids, cholesterol and carbohydrates. Examples of these
enzymes include pyruvate carboxylase (involved in gluconeogenesis), arginase (required for the urea cycle to detoxify ammonia,converts the excitatory neurotransmitter glutamate to glutamine.

Bone development: Manganese is a cofactor needed for forming cartilage and bone.

Wound healing: Manganese is needed to activate the enzyme needed for the formation of collagen.

64
Q

There is _______ absorption with increased manganese intakes.
A. Lower
B. Higher

A

A. Lower

65
Q
Manganese absorption is increased in?
A. Hemochromatosis
B. Iron deficiency
C. A & B
D. None of the above
A

C. Both hemochromatosis and iron deficiency

**After absorption, manganese is bound to transferrin (also transports iron)

66
Q

True or False. Manganese can cross the blood brain barrier.

A

True. by carrier mediated transport. Zinc transporters may also be involved in manganese uptake.

67
Q

True or False. Manganese deficiency has only been well documented in animals.

A

True.

Human deficiency is not well documented.

In animals, manganese deficiency can present as impaired growth, skeletal abnormalities, impaired glucose tolerance, and altered metabolism of carbohydrates and lipids.

68
Q

Manganese toxicity in this form can lead to neurological issues because it passes the blood brain barrier and doe snot go through the liver for detoxification.
A. Ingested
B. Inhaled
C. Both A & B

A

B. Inhaled.

This can be a hazard for welders and smelters.

Severe toxicity can manifest as an irreversible Parkinsonian like syndrome with tremors, difficulty walking and spasms of the facial muscles, known as manganism.

Psychiatric symptoms can precede neurological symptoms and include
aggressiveness, irritability and hallucinations. Exposure to manganese can also lead to inflammation in the lungs (cough, acute bronchitis and decreased lung function.

High level of manganese in kids can lead to cognitive and behavioral deficits and increased rates of hyperactivity disorders.

69
Q

True or False. Manganese in water may be more bioavailable than in food.

A

True.

With high levels in drinking water, one can see neurological symptoms similar to Parkinson’s disease.

Toxicity has not been reported from dietary sources.

70
Q

True or False. Manganese is rich in omnivorous nutritional approaches.

A

False.

Manganese is rich in vegetarian diets and can be found in whole grains, nuts, leafy vegetables, soy, beans and seeds.

Levels of manganese in the diet may be significantly lower in modern diets as refined grains have 86% less manganese than their whole, unrefined, counterpart and the manganese content of soil is lowered by some modern agricultural practices.

71
Q
\_\_\_\_\_\_\_, \_\_\_\_\_\_\_, and \_\_\_\_\_\_\_\_\_\_ limit the retention of manganese.
A. Iron, calcium, phosphorus
B. Iron, vitamin D, magnesium
C. Magnesium, calcium phosphorus
D. None of the above
A

A. Iron, calcium, phosphorus

72
Q

Cabbage, spinach, sweet potatoes, and chard all contain _______, which inhibit absorption of manganese.

A

oxalates.

73
Q

The bioavailability of manganese is ______ in breast milk than in infant formula.
A. Lower
B. Higher

A

B. Higher

74
Q
\_\_\_\_\_\_\_\_\_\_\_ can decrease bioavailability of manganese, and \_\_\_\_\_\_\_\_\_\_\_ has the ability to decrease absorption.
A. Magnesium, vitamin D
B. Magnesium, calcium
C. Calcium, vitamin D
D. None of the above
A

B. Magnesium, calcium

Particularly when in the form of calcium carbonate or a calcium phosphate supplement.

75
Q
The RDA for manganese is:
A. 1mg/day
B. 2mg/day
C. 5mg/day
D. 6mg/day
A

B. 2mg/day

Manganese supplementation beyond 100% of the RDA (2 mg/d) is not recommended.

76
Q
Manganese deficiency can present clinically in:
A. Osteoporosis
B. Seizure disorders
C. Diabetes
D. All of the above
A

D. All of the above

Women with osteoporosis have decreased plasma/serum manganese levels and exhibit a greater plasma response to oral manganese supplementation.

Humans with epilepsy have lower whole blood manganese than non-epileptic
controls.

Manganese deficiency manifests in a glucose intolerance similar to diabetes
mellitus.

77
Q

Supplementation of manganese __(form)__ with glucosamine hydrochloride and chondroitin sulfate has been shown to be helpful in relieving pain in mild to moderate cases of osteoarthritis.
A. ascorbate
B. gluconate
C. sulfate

A

A. ascorbate

78
Q

AI for manganese in 0-12 month old infants is:
A. 0.003-0.6mg/day
B. 0.6-0.8mg/day
C. 1.2mg/day

A

A. 0.003-0.06mg/day

79
Q

AI of manganese for children, ages 1-3, is:
A. 0.6mg/day
B. 1.0mg/day
C. 1.2mg/day

A

C. 1.2mg/day

80
Q

AI of manganese for adults, 19yo and older is:
A. 1.2mg/day females, 1.6mg/day males
B. 1.8mg/day females, 2.3mg/day males
C. 1.8mg/day, there is no difference among male versus female

A

B. 1.8mg/day females, 2.3mg/day males

81
Q

True or False. Manganese may lead to decreased absorption of magnesium containing antacids or laxatives and also to tetracycline and fluoroquinolone antibiotics (ciprofloxacin, norfloxacin).

A

True.

82
Q

True or False. Neuroleptics may chelate manganese – leading to decreased manganese and/or a deficiency.

A

True.

83
Q

Iodine is essential for humans as a component of _____________.

a. thyroxine (T4)
b. ACTH
c. cortisol
d. all of the above

A

a. thyroxine

Hark, pg. 80

84
Q

Natures number one source of iodine is ____ (list food)

A

salt.
* While salt contains iodine, it doesn’t contain enough to meet the RDA, therefore it is often iodized.

Iodine is a trace element present in the earth. Distributed variably around the world due to the effects of the ice age, iodine has accumulated primarily in coastal areas. The most common dietary sources of iodine are seaweed, fish and dairy products. Inland areas have fewer natural sources of iodine. In the U.S., areas where iodine deficiency was common in the early 1900s —the Great Lakes, Appalachians and Northwest — were known as the “goiter belt.”

source:https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-q-and-a-sea-salt-and-sufficient-iodine-intake/

85
Q

Approximately ____% of the body’s iodine is store in the thyroid gland.

a. 15%
b. 25%
c. 40%
d. 60%

A

c. 40%

Hark, p. 80

86
Q

If there is not enough iodine in the body, there is a decrease in the production of the thyroid hormones T3 and T4. To compensate for this lack of production the thyroid gland hypertrophies, causing ________.

a. hypothyroidism
b. a goiter
c. congenital goiter

A

b. a goiter

*A goiter that’s present at birth is called a congenital goiter. These can be caused by:
1. a genetic disease that prevents the baby from producing thyroid hormone properly
2. thyroid issues in the mother during pregnancy
an expectant mother taking medicines or other substances that affect the baby’s thyroid
3. the child being born without half of the thyroid, causing the remaining half to get bigger.

A goiter that develops later is called an acquired goiter.

87
Q

Symptoms of iodine deficiency include:

a. Lethargy
b. dry skin
c. thick lips,
d. enlarged tongue
e. reduced muscle and skeletal growth
f. cretinism
g. all of the above

A

g. all of the above

88
Q

Currently (Hark, 2014) ___% of the world’s population is felt to be at risk for iodine deficiency.

a. 20%
b. 40%
c. 60%

A

b. 40%

* The lowest prevalence is found in the Americas while the highest prevalence is found in Europe.

89
Q

Risk factors for iodine deficiency (aside from inadequate intake include:

a. pregnancy and oral contraceptives
b. smoking and alcohol consumption
c. excessive calcium intake or selenium deficiency
d. exposure to radiation, perchlorates, or thiocyanates.
e. all of the above

A

e. all of the above

Perchlorates occur naturally in potash ore, nitrate fertilizer, and in the atmosphere. Unnatural sources include: rocket propellant, explosives, fireworks, and road flares.

Human exposure to high dosages of perchlorate can interfere with iodide uptake into the thyroid gland, disrupting the functions of the thyroid and potentially leading to a reduction in the production of thyroid hormone. In fact, perchlorate has been used as a drug to treat hyperthyroidism (excess thyroid hormone production) and to diagnose disorders related to thyroid or iodine metabolism.

source:https://www.fda.gov/food/chemical-contaminants-food/perchlorate-questions-and-answers

90
Q

The TUL for iodine has been established at:

a. 100 micrograms/day
b. 500 micrograms/day
c. 1100 micrograms/day

A

c. 1100 micrograms/day

* Iodized salt contains 45 micrograms of iodine per gram of table salt. 1 g = 1/6 tsp.

91
Q

_______ has been reported to occur at a rate of one out of every 4000 children and early treatment with iodine is necessary to avoid mental retardation.

a. Congenital hypothyroidism
b. Adrenal insufficiency
c. Hashimotos thyroiditis

A

a. congenital hypothyroidism

92
Q

True or false? Supplementation with iodine has been shown to be effective in reducing the risk of an iodine-deficient child developing thyroid cancer after exposure to radiation from an accidental contamination or from medical procedures.

A

True.

93
Q

True or false? Many people are interested in potassium iodide supplements to prevent radioactive iodine uptake in the event of a nuclear accident or after exposure to medical radiation?

A

True

  • The thyroid gland cannot tell the difference between stable and radioactive iodine and will absorb both. KI works by blocking radioactive iodine from entering the thyroid. When a person takes KI, the stable iodine in the medicine gets absorbed by the thyroid. There is so much stable iodine in the KI that the thyroid gland becomes “full” and cannot absorb any more iodine—either stable or radioactive—for the next 24 hours.

Source: https://www.cdc.gov/nceh/radiation/emergencies/japan/ki.htm#:~:text=KI%20works%20by%20blocking%20radioactive,for%20the%20next%2024%20hours.

94
Q

True or false? Iodine is absorbed in the GI tract in the ionized form (I-).

A

True.

*Extra iodine in the body is excreted via the urine.

95
Q

What is the RDA for Iodine (for both men and women)?

a. 150 micrograms
b. 300 micrograms
c. 400 micrograms

A

a. 150 micrograms