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Clinical Nutrition 1 > Microminerals > Flashcards

Microminerals Flashcards

1
Q

iron distribution in the body

A

65% as part of hemoglobin
10% in myoglobin
1-5% as part of enzymes
20% in storage

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2
Q

two categories of sources for iron

A

heme iron

non-heme iron

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3
Q

sources of heme iron

A

heme iron is contained within a porphryin structure and is derived from hemoglobin and myoglobin so is only find in animal products
meat, fish, poultry, oysters, clams

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4
Q

sources of non-heme iron

A

meat
beans, dark green leafy veggies, dried fruits
blackstrap molasses
enriched foods fortified with iron

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5
Q

which minerals are microminerals?

A 
iron
copper
zinc
selenium
chromium
iodine
manganese
molybdenum (Mo)
fluoride
boron
silicon
vanadium (V)
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6
Q

chemical forms of iron in the body

A

2 stable forms are:

ferric (Fe3+) and ferrous (Fe2+) iron

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7
Q

digestion of heme iron

A

heme iron is hydrolyzed from hemoglobin or myoglobin by proteases in the stomach and SI

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8
Q

digestion of non-heme iron

A
  • non-heme iron is hyrolyzed from food components by HCl and proteases in the stomach releasing iron in the Fe3+ form
  • some of it is reduced to Fe2+ by low pH of the stomach but it may complex to FeOH3 in the alkaline environment of the SI an and be poorly absorbed
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9
Q

duodenal cytochrome b

A

acts as a ferric reductase

reduces Fe3+ to Fe2+ in the duodenum and improves solubility and absorption

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10
Q

what is needed as a cofactor for duodenal cytochrome b/ferric reductase?

A

vitamin C is required for it so it can help absorption of non-heme iron

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11
Q

absorption of heme iron

A
  • absorbed throughout the SI but absorbed most in the duodenum by the carrier protein HCP1 (heme carrier protein 1)
  • then, once absorbed heme is hydrolyzed by heme oxygenase to give inorganic Fe2+ and a porphyrin ring
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12
Q

what percentage of heme iron is absorbed?

what percentage of non-heme e iron is absorbed?

A

15-35% of heme iron is absorbed

2-20% of non-heme iron is absorbed

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13
Q

absorption of non-heme iron

A

any Fe2+ is absorbed via the DMT1 (divalent mineral transporter 1), stimulated by low iron stores
iron present in the Fe3+ form is reduced to Fe2+

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14
Q

factors that enhance absorption of non-heme iron

A
  • vitamin C
  • other organic acids (malic, citric, tartaric, lactic acids)
  • meat, fish, poultry
  • low iron status
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15
Q

factors that inhibit iron absorption

A 
phytic acids (phytases)
polyphenols
oxalates
phosvitin (found in egg yolks)
other minerals (calcium, zinc, copper, manganese)
soy, wheat, egg, whey, casein protein
herbal teas: peppermint, green tea, linden flower and chamomile
rapid transit time
decreased stomach acidity
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16
Q

what does hepcidin do?

A

when iron stores are high or adequate, hepcidin is released from the liver which promotes the degradation of ferroportin which decreases the transport of iron across the membrane of the enterocyte
- also, low levels of hepcidin cause increased ferroportin levels

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17
Q

actions of mobilferrin, ferroportin, and transferrin

A
  • mobilferrin transports iron through enterocytes
  • ferroportin is required to transport iron across the basolateral membrane
  • transferrin transports iron in the blood while in the Fe3+ form
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18
Q

how is Fe2+ iron converted into Fe3+ iron before it enters the bloodstream?

A

with either of:

  • hephaestin
  • ceruloplasmin
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19
Q

where is iron stored in the body?

A

60% stored in lover

also stores in bone marrow and spleen

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20
Q

storage proteins for iron?

A
  • ferritin - primary storage protein for iron

- hemosiderin - a degradation product of ferritin

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21
Q

when do levels of hemosiderin increase?

A

during iron overload

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22
Q

why is iron turnover so high?

A

because the dietary intake cannot meet the daily needs of the body so iron is constantly recycling its stores from degradation of ferritin, hemoglobin, and hemosiderin

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23
Q

functions of iron in the body

A
  • oxygen transport and storage
  • electron transport and energy metabolism
  • some iron-dependant enzymes
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24
Q

what are some examples of iron-dependant enzymes?

A
  • peroxidases (catalyse, myeloperosidase, thyroperosidase)
  • ribonucleotide reductase
  • tyrosine hyroxylase
  • monooxygenases
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25
Q

3 levels of iron deficiency

A
  1. storage iron depletion
  2. early functional iron deficiency
  3. iron-deficiency anemia
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26
Q

symptoms of iron deficiency

A

most result from associated anemia (fatigue, tachycardia, arrhythmias, dyspnea on exertion)
other symptoms:
- cold intolerance
- poor concentration, mood disturbances
- angular stomatitis and atrophic glossitis
- alopecia and brittle and spoon shaped nails

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27
Q

who is at increased risk of iron deficiency?

A 
infants, young children, adolescents
menstruating females
pregnancy
chronic blood loss
parasitic infections
hypochlorhydria
gastric bypass surgery and faster GI transit time
celiac disease
vegetarians, vegans
regular intense exercise
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28
Q

clinical indications for iron

A

restless leg syndrome

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29
Q

adverse effects of iron supplementation

A 
constipation or occasionally diarrhea
dark tarry stools
nausea and vomiting
epigastric pain
generally they are tolerated better when taken in smaller doses divided with food
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30
Q

who has higher risk of chronic iron toxicity?

A

hemochromatosis - increased absorption in the intestines caused by a genetic mutation
thalassemia or sideroblastic anemia
alcoholic cirrhosis

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31
Q

nutrient interactions of iron

A
  • vitamin C - enhances absorption of non-heme iron
  • copper - both hephaestin and ceruloplasmin are copper-dependent enzymes and required to mobilize iron from tissues
  • calcium, zinc, copper, manganese - non-heme iron and these divalent minerals compete for a common absorptive pathway
  • lead - iron deficiency increases led absorption which inhibits incorporation of iron into heme
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32
Q

what oxidation states of copper are found in the body?

A

Cu1+

Cu2+

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33
Q

sources of copper

A 
organ meats
shellfish
whole grains
nuts and seeds
it's in a wide variety of foods
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34
Q

how is copper released from its organic components during digestion?

A

HCl and pepsin in the stomach

proteolytic enzymes in the SI

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35
Q

absorption of copper in the body

- what enzyme is involved

A

most Cu2+ is reduced to Cu1+ by the enzyme copper reductase

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36
Q

what methods are used in copper absorption?

A
  • active carrier mediated transport by CTR1 (copper transporter 1) and DMT1 (divalent mineral transporter) in low concentrations of copper
  • nonsaturable passive diffusion in high concentrations of copper
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37
Q

factors that enhance copper absorption

A 
amino acids (especially histidine and methionine)
organic acids (HCl, citric, lactic, malic, acetic)
low copper status
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38
Q

factors that inhibit copper absorption

A

phytates
vitamin C and cystiene
other minerals (zinc, iron, molybdenum, calcium, phosphorous)
hypochlorhydria or excessive use of antacids

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39
Q

transport of copper in the body

A
  • enters circulation from enterocytes via transport protein ATP7A
  • bound primarily to albumin in hepatic portal circulation
  • in liver, binds to ceruloplasmin to be transported to other tissues as needed
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40
Q

where is copper stored in the body?

A

liver, brain, kidneys

bound to various proteins (thionine, forming metallothionine)

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41
Q

function of copper in the body

A

as a cofactor for various copper-dependent enzymes

also angiogenesis and production of neutrophils

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42
Q

what enzymes use copper as a cofactor?

A
  • feroxidases (ceruloplasmin and hephaestin)
  • copper-zinc SOD
  • cytochrome C oxidase
  • lysys oxidase
  • dopamine monoxygenase (aka dopamine beta-hydroxylase)
  • tyrosinase
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43
Q

when is there increased risk of copper deficiency?

A
  • high supplemental zinc intakes (50mg/day for extended period of time)
  • Menkes disease - recessive genetic disorder that results in mutations of the copper transport gene ATP7A
  • frequent use of antacids
  • infants fed exclusively cow’s milk based formula
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44
Q

signs and symptoms of copper deficiency

A
  • microcytic, hypochromic anemia not responsive to iron supplementation
  • neutropenia and subsequent impaired immune function
  • deterioration of the neurological system
  • hypopigmentation of skin and hair, kinky hair
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45
Q

clinical indications for copper supplementation

A

only for treating or preventing a copper deficiency

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46
Q

which form of copper should not be used as a supplement?

A

cupric oxide - has shown to be unavailable for absorption through the digestive tract

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47
Q

symptoms of copper toxicity
general
acute
chronic toxicity

A

N & V
constipation
for doses of 2mg or more (supplemental)
acute toxicity (much higher dose needed): abdominal pain, diarrhea, N&V
chronic toxicity: causes liver and kidney damage and eventually death

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48
Q

what is Wilson’s disease?

A

a genetic disorder of copper metabolism resulting in defective biliary copper excretion and so copper accumulates in the liver, brain, kidneys, cornea, spleen

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49
Q

nutrient interactions of copper

A
  • iron
  • zinc
  • molybdenum
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50
Q

how does copper affect iron levels in the body?

A
  • prolonged copper deficiency can cause secondary/functional iron deficiency anemia
  • Fe2+ must be converted into Fe3+ by a copper containing enzyme before it can be used
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51
Q

how does zinc affect copper levels in the body?

A
  • high supplemental zinc intake of 50mg/day can lead to a copper deficiency
  • zinc stimulates the synthesis of thionine which has higher binding affinity for copper than zinc so causes copper to be trapped in the enterocyte and will cause it to be sloughed off with old intestinal cells so additional copper must be taken when supplementing high doses of zinc for extended periods
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52
Q

how does copper interact with molybdenum?

A

copper forms an insoluble complex with molybdenum in the digestive tract preventing the absorption of either mineral

53
Q

distribution of zinc in the body

A

zinc is widely distributed - found in all tissues and fluids

54
Q

sources of zinc

A

shellfish
beef and other red meats
nuts and legumes are relatively good plant sources of zinc

55
Q

bioavailability of zinc in meat vs plant sources

A
  • zinc is more bioavailable in meat, eggs, and seafood because the compounds that inhibit zinc absorption are not present and these are sulfur-containing AAs that improve zinc absorption
  • zinc is less bioavailable in plant products because of the high content of phytic acid which inhibits zinc absorption
56
Q

how do maillard reaction products affect zinc absorption?

A

they decrease zinc absorption

57
Q

digestion of zinc

A

first needs to be hydrolyzed from AAs and nucleic acids in the stomach and SI by HCl, proteases and nucleases before it can be asbrobed

58
Q

absorption of zinc in the body
how many pathways?
what are they pathways?

A

3 pathways:
carrier mediated processes are more efficient with low zinc intake:
-1. ZRT and IRT-like proteins 4 (ZIP4)
-2. divalent mineral transporter 1 (DMT1) plays a minor role
when zinc intake is high:
-3. passive paracellular diffusion

59
Q

factors that enhance zinc absorption

A

organic acids (citric acid, picolinic acid)
low pH
amino acids, glutathione
low zinc status

60
Q

factors that inhibit zinc absorption

A

phytates
oxalates
polyphenols
folate and other minerals (iron, calcium, magnesium)

61
Q

transport of zinc in the body

A
  • CRIP (cystiene rich intestinal protein) transport zinc within the cytoplasm of a cell
  • ZnT1 (zinc transporter 1) transports zinc across the basolateral membrane of the enterocyte
  • bound to proteins in the blood like albumin
62
Q

storage of zinc in the body

  • what organs?
  • storage form?
A

all organs of the body

  • especially the liver, kidneys, muscles, bones, skin
  • is usually stored bound to thionein as metothionein which also binds copper
63
Q

main functional roles of zinc in the body?

A
  • catalytic role - zinc used as a cofactor for enzymes
  • structural role in the proteins of cell membranes
  • regulatory role (gene expression, spermatogenesis in men, immune system function)
64
Q

what is a zinc finger motif?

A

a finger like structure that stabilizes the structure of several proteins in the body and also regulate gene expression by acting as transcription factors

65
Q

which viruses does zinc possess direct antiviral activity against?

A
  • rhinovirus

- herpes simplex virus (HSV)

66
Q

symptoms of severe zinc deficiency

A
  • growth retardation and skeletal anomalies
  • delayed sexual maturation
  • dermatitis, especially around orifices, impaired wound healing
  • diarrhea
  • impaired immune function
  • dysgeusia - impaired sense of taste
  • night blindness
  • hair loss
  • white spots on finger nails
67
Q

who is at risk for severe zinc deficiency?

A

severe burns
prolonged diarrhea
chronic alcohol abuse
genetic disorder affecting zinc metabolism

68
Q

who is at risk for MILD zinc deficiencies?

A

premature or low birth weight infants and older breast fed infants and toddlers with inadequate intake of zinc-rich foods
adolescents
pregnant and lactating women
elderly people
inflammatory bowel disease or severe prolonged diarrhea
strict vegetarians

69
Q

clinical indications of zinc supplementation

A

the common cold

  • reducing duration
  • free ionized zinc may directly interfere with viral replication processes
70
Q

of the different forms of zinc, which ones are: less bioavailable; not well tolerated; better absorbed; preferred for lozenges/colds

zinc acetate, zinc gluconate, zinc sulfate, zinc oxide, zinc picolinate

A

less bioavailable: zinc sulfate, zinc oxide

not well tolerated: zinc sulfate

more bioavailable: zinc picolinate - debated

lozenges: zinc acetate and zinc gluconate

71
Q

what is the main consequence of zinc toxicity?

A

copper deficiency

72
Q

signs and symptoms of acute zinc toxicity

A 
metallic taste
headache
N&V
abdominal cramps
bloody diarrhea
73
Q

nutrient interactions of zinc

A
  • copper - high zinc intake can lead to copper deficiency
  • vitamin A - zinc is required for conversion of retinol to retinal AND deficiency of zinc could result in decrease in mobilization of retinol from liver stores
  • calcium, magnesium and iron may decrease zinc absorption and vice versa
74
Q

sources of selenium

A

meats - especially organ meats and seafood

selenium content of plants is extremely variable but brazil nuts, whole grains, legumes are good sources

75
Q

bioavailability of selenium

A

fish contains substantial amounts of selenium but can have low bioavailability due to the mercury content which forms an insoluble complex with selenium

76
Q

location of absorption of selenium

A

small intestine - mainly duodenum

77
Q

what inhibits selenium absorption

A

phytates

heavy metals - especially mercury

78
Q

what are the main forms of selenium that are absorbed in the body?
why?

A

selenimethionine
selinocystiene

due to its structural similarity to sulfur

79
Q

transport of selenium in the body

A

bound to proteins to travel in the blood like:

  • VLDL
  • LDL
  • selenoprotein P
80
Q

what organs store selenium in the body?

A 
thyroid gland
kidney
liver
heart
pancreas
muscle
81
Q

functions of selenium in the body

A

a cofactor in selenium-dependent enzymes
enhances immune function
may have direct antiviral activity

82
Q

selenium and iodothyronine deiodinases (IDI)

A

the IDI enzyme converts T4 -> T3 which selenium is required for
ie. selenium maintains normal growth, metabolism, and development because of its role in regulating thyroid hormones

83
Q

selenium and glutathione peroxidase (GPX)

A

GPX is an important antioxidant enzyme that reduces potentially damaging ROS (like hydrogen peroxide and lipid hydrogen peroxides) to harmless produces like water and alcohols

84
Q

what is the function of selenoprotein P (SEL P)

A

SEL P functions primarily as a transport protein for selenium
it also acts as an antioxidant that protects endothelial damage by reactive nitrogen species

85
Q

excretion of selenium

  • primary
  • what regulates homeostasis
  • how is it excreted as dimethylselenide?
A

primarily via urine and feces
homeostasis is maintained by the kidneys
can also be excreted by the lungs as dimethylselenide with high intakes

86
Q

results of selenium deficiency?

A
  • decreased activity of glutathione peroxidases and thyroid deiodinases
  • if severe: muscle weakness, muscle wasting, cardiomyopathy
87
Q

selenium deficiency related diseases?

A

Keshan disease

Kashin-Beck disease

88
Q

what is Keshan disease?

what causes it?

A

a cardiomyopathy that affects young women and children in a selenium-deficient region of China
thought to be caused by oxidative stress (due to selenium deficiency) that causes malignant changes to the Coxackie virus that invades and damages the heart

89
Q

does selenium supplementation help Keshan disease?

A

prevents/protects people from developing Keshan dsiease but CANNOT reverse heart damage once it occurs

90
Q

what is Kashin-Beck disease?

what causes it?

A

degeneration of articular cartilage between joints

associated with poor selenium status in areas of northern Chia, North Korea, eastern Siberia

91
Q

who is affected by Kashin-Beck diasese?

A

affects children ages 5-13

mostly in northern Chia, North Korea, eastern Siberia

92
Q

clinical indications of selenium supplementation

A

Hashimoto’s thyroiditis

HIV/AIDS

93
Q

is the organic or inorganic form of selenium better absorbed and metabolized by the body?

A

neither seems to be consistently shown as better than the other

94
Q

what is the difference in absorption between:
selenate
selenite
selenomethionine

A
  • selenate - almost completely absorbed but most of it is excreted before being used
  • selenite - about 50% is absorbed but is better retained
  • selenomethionine - is 90% absorbed, occurs naturally in foods
95
Q

what is selenosis?

what are the early warning signs?

A

selenium toxicity

early warning signs: brittle nails, hair loss, dermatitis

96
Q

symptoms of chronic selenosis

A 
hair and nail brittleness and loss
diarrhea, N&V
skin rashes
a garlic breath odor
fatigue, irritability
nervous system abnormalities
97
Q

nutrient interactions of selenium

A

iodine - selenium deficiency can trigger or worsen hypothyroidism in those with severe iodine deficiency

98
Q

sources of chromium

A

brewer’s yeast contains GTF - a biologically active, organically complexed form of chromium
meats, whole grains, green beans, slices like cinnamon, cloves, bay leaves, turmeric

99
Q

absorption of chromium

  • location
  • mechanism
A

in small intestine

through diffusion or a carrier mediated transporter

100
Q

factors that enhance chromium absorption

A

picolinate

vitamin C

101
Q

factors that inhibit chromium absorption

A

phytates

antacids

102
Q

transport of chromium in the body

A

bound to transferrin but if transferrin sites are unavailable chromium will bind to albumin for transport in the blood

103
Q

storage sites of chromium in the body

A 
kidneys
liver
muscle
spleen
heart
pancreas
bone

is thought to be stored along with iron

104
Q

function of chromium in the body and mechanism

A

potentiates the action of insulin via

  • glucose tolerance factor (GTF) which enhances insulin activity
  • acts as part of the protein chromodulin which attaches to insulin receptors to enhance their activity
105
Q

symptoms of chromium deficiency

A

weight loss
impaired glucose tolerance and insulin resistance
peripheral neuropathy

106
Q

who has increased risk of chromium deficiency

A

regular exercise at high intensity

insulin resistance, metabolic syndrome, diabetes mellitus

107
Q

clinical indications of chromium supplementation

A

type 2 diabetes

108
Q

symptoms of chromium toxicity

A

enhanced dreaming and psychomotor agitation due to high-dose chromium supplementation

109
Q

food sources of iodine

A
  • fish, seafood, kelp, other seaweeds
  • dairy products
  • meat, eggs, beans
  • iodized salt
110
Q

what forms of iodine are absorbed?

A

free iodine and iodate are absorbed as they are
iodine bound to AAs must first be hydrolyzed to release free iodine (except for thyroid hormones which are absorbed unchanged)

111
Q

what percentage of dietary iodine is absorbed?

A

100%

112
Q

where is iodine absorbed in the body

A

stomach and SI

113
Q

transport of iodine in the body

A

transport freely as iodide in the blood

114
Q

where is iodine stored in the body?

does it require any special transport system?

A

70-80% in thyroid gland which requires a Na-dependent active transport system with a Na/I symporter

115
Q

functions of iodine

A
  • essential in the formation of thyroid hormones and thyroid function
  • has direct antimicrobial activity
116
Q

iodine excretion

is there a mechanism to conserve iodide?

A

excreted freely through the kidneys

there is NO mechanism in kidneys to conserve idodide

117
Q

who has increased risk of iodine deficiency?

A
  • vegans, vegetarians but not if they regularly consume seaweeds
  • infants of mothers who smoke
  • exposure to high amounts of goiterogens
118
Q

what are goiterogens?

A

substances that interfere with iodine metabolism and inhibit thyroid hormone production

119
Q

examples of goiterogens

A
  • halide ions (bromide), thiocyanate, perchlorates
  • edible plants have some amounts of thiocyanates ang goiterin (brassica vegetables, soy, millet, cassava)
  • perchlorates interfere with organification of iodide required for thyroid hormone synthesis
  • polycyclic hydrocarbonds and some phenol compounds interfere with iodine metabolism in the body also
120
Q

how is goiter related to iodine deficiency

A

thyroid enlargement (goiter) is one of the earliest signs of an iodine deficiency

121
Q

who is most negatively affected by iodine deficiency? why?

A

it is most damaging to the developing brain
- can cause cretenism: a condition caused by severe congenital hypothyroidism and results in irreversible mental retardation

122
Q

what are the 2 forms of cretenism?

A

neurological cretenism

myxedematous cretenism

123
Q

clinical indications of iodine supplementaiton

A

prevent radiation induced thyroid cancer

fibrocystic breast changes

124
Q

what are the preparations of iodine available?

A
  • potassium iodide
  • Lugol’s solution - a combination of molecular iodine and potassium iodide
  • kelp and other seaweed extracts - are much less concentrated
125
Q

signs and symptoms of acute iodine toxicity

A 
burning of the mouth, throat and stomach
increased salivation and swelling of thyroid glands
metallic taste
N&V, diarrhea
severe headache
126
Q

signs and symptoms of chronic iodine toxicity

A
  • in iodine deficiency: can see iodine induced hyperthryoidism in iodine supplementation
  • in iodine sufficiency: see hypothyroidism, goiter
127
Q

nutrient interactions of iodine

A
  • selenium deficiency can exacerbate the effects of iodine deficiency
  • high doses of vitamin A have been associated with decreased iodine uptake by the thyroid gland
128
Q

sources of manganese

A

whole grains, legumes, nuts and seeds
leafy green vegetables
tea

Clinical Nutrition 1 (2 decks)

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