Micronutrients (Fe, Zn, I) Flashcards
describe the body’s abosorption rate when deficient
absorbs nutrients that are deficient faster
excess of vit can lead to…
potential toxicity ie. gummy bears
metabolic interactions:
vitamins can compete w/ binding sites
what are metalloenzymes?
Enzymes that contain one or more minerals as part of their structures.
common in redox rxns because metal ions can exist in multiple states
ie. catalase has Fe in it. Can’t function without Fe
what are approx amounts of major minerals in a 60kg person?
- Ca 1150g
- Phosphorus 600g
- Potassium 210g
- Sulphur 150g
- Sodium 90g
- Chloride 90g
- Magnesium 30g
what are the fat soluble or water soluble vits?
fat soluble: DEAK
water soluble: Bs and C
define a vitamin
essential organic nutrients required in small amounts (mg or ug) for specific functions that promote growth, reproduction ,maintenance of health/life.
generally function as coenzymes
what is a vitamer
different forms of a vitamin can have diff functions.
conversion between forms, and from precursors
factors that affect bioavailability of vitamins
- efficiency of digestion
- other foods consumed at the same time
- method of food prep
- source of nutrient
- previous nutrient intake and nutrition status
what are the 9 B vitamins?
thiamin riboflavin niacin biotin pantothenic acid vit B6 folate vit B12
how does the solubility of fat or water soluble vitamins affect metabolism?
water soluble vit:
- found in watery compartments of food
- moves directly into blood when absorbed
- travels freely in blood
- excess is removed in urine
- possible to reach toxic levels if consumed from supplements
- needed in more frequent doses (every 1-3 days)
fat soluble vits:
- must first enter the lymph and then the blood
- need protein carriers for transport in the blood
- less readily excreted (tends to remain in fat storage sites)
- likely to reach toxic levels from supplements
- needed in less frequent doses: (weeks of months)
are vitamins easily degraded?
yes. ie by light or o2
describe process of co enzyme use with enzymes
enzyme is inactive without enzyme because substrate can’t bind
enzyme is activated by adding coenzyme
example of hormonal function of vitamins?
vit A as retinoic acid in cell differentiation
vit D as calcitriol in calcium availability
What type of anemia does a Fe deficiency lead to?
hypochromic microcytic anemia
what type of anemia does folate or vit B12 deficiency lead to?
megaloblasitic or pernicious anemia
functions of Fe
To transfer oxygen
part of a heme group in 2 types of protein
- hemoglobin (in RBC) for transport of o2 to tissues. hemoglobin accounts for 80% of body’s iron
- myoglobin: oxygen holding protein in muscle cells
- transport of electrons through resp chain (cytochromes)
- enzymes such as peroxidase, catalase, etc
what are the two ionic states of iron?
ferrous iron: Fe2+ (reduced)
ferric iron: Fe3+ (oxidized)
can easily be reduced or oxidized between the forms. Thus Fe is a good cofactor to REDOX enzymes
what is ferritin
the iron storage protein
what is transferrin
iron transport protein
what is heme
iron holding part of the hemoglobin and myglobin proteins. Found only in animal protein products (40%). Nonheme Fe (60%) is found in plant and animal sources
What are vulnerable stages of life that are high risk for FE deficiency?
women in reproductive years (repeated blood loss from menstruation)
pregnant women (needs extra Fe to support added blood volume for growth of fetus and blood loss during childbirth)
infants and young children( need extra Fe to support fast growth)
teens
What is an iron deficiency anemia
microcytic hypochromic anemia
severe depletion of iron stores that results in less hemoglobin and small and pale RBC
signs and symptoms of Fe deficiency anemia?
tiredness
low work performance
low childhood development (psychomotor and intellectual)
high lead poisoning susceptibility
stages of iron deficiency
- Fe stores diminish: serium ferritin (in the blood) reflect iron stores
- decrease in transport iron: serium iron falls and transferrin (iron-carrying protein) increases. as the severity of the deficiency increases: more transferring and less iron
- hemoglobin production declines: lack of iron limits hemoglobin production. Hemoglobin precursor (erythrocyte protoporphyrin) accumulates
describe RBC without anemia (healthy)
normochromic and normocytic cells (dark and bigger compared to anemic cells)
hemoglobin count of iron deficiency anemia for men and women?
HGB < 140g/L
Hgb < 120 g/L
what is usually tested for when evaluating iron status? How is this limiting?
hemoglobin level.
lower hemoglobin levels = lower ability to carry o2
limiting because it only tests for 3rd step of deficiency (shows only advance Fe deficiency, not earlier stages where problems begin)
what is hematocrit?
measurement of the volume of RBC in a specific volume of blood
difference between iron deficieny and anemia?
people can be deficient wihtout being anemic
iron def: depleted body iron stores without presence of anemia
iron def anemia:
- hemoglobin synthesis decreases. Results in low hemoglobin and small, pale RBC (hyprochronic and microcytic cells).
- These cells can’t carry enough O2 from lungs to the tissues (results in lower energy metabolism. Ie. fatigue, weakness, headache)
- impared neurotransmitter synthesis results in slower work performance and productivity. Can begin in the 1st stage of iron deficiency, even when no outward symptoms are showing. Can be easily mistaken for behaviour problems
why are women more at risk of IDA?
women have higher EAR because of menstruation
high percent of women are under EAR
describe iron metabolism
- Fe2+ binds to Fe3+ (ferritin) and crosses membrane to transferring (needs to be bound in ferric state)
- transferrin brings iron to bone marrow where stem cells become RBC. Involves Fe2+ and protoporphyrin (precursor)
- Heme is made. Becomes hemoglobin in RBC. Circulates for approx 120 days in the blood
- RBC is taken up by the liver where it is broken down
- Heme is converted to billirubin (toxic compound) and goes out into bile and excreted in feces (billirubin makes it brown). Some is excreted in urine (makes it yellow. higher billirubin = higher dehydration)
- Fe is recycled back into transferrin
sources of heme and nonheme iron in foods?
absorption of these sources?
animal sources: contain heme and nonheme iron. (heme iron)
plant sources: only nonheme iron (elemental iron)
heme iron is 25% absorbed
Nonheme iron is 17% absorbed
heme iron is 10% of average daily iron intake.
non heme is 90%.
how is iron recycled in the body?
- RBC lives approx 4 months before the spleen and liver removes it from the blood
- RBC are taken apart and parts are prepared for excretion/recycling
- iron is salvaged and attached to transferrin (protein that carries iron in blood) which transports it back to bone marrow to be reused for making new RBC
only small amounts of iron are lost in urin, sweat and shed skin
why do vegetarians/vegans need more Fe in diet?
lower absorption in nonheme iron sources (approx 10% absorption)
don’t have MFP peptide to enhance absorption (only found in animal products)
what are factors that inhibit or enhance nonheme iron absorption?
enhance: MFP factor ( a peptide in Meat, Fish, Poultry). Vit C
inhibits: phytates (legumes and grains), veg proteins, calcium, phosphate, tannic acid and polyphenols (in tea and coffee)
where does RBC synthesis occur?
in bone marrow (stem cells become RBC)
difference between EAR and how much iron you absorb?
EAR is the amount that you need. How much iron you actually absorb is less.
Must take into account the bioavailability of the iron source to see if there is adequate iron in the diet
ie. spinach is very high high in iron, but also high in oxalates. The oxalates bind to Fe and lowers bioavilability of the Fe source. Thus spinach is not a good source of Fe
primary vs secondary deficiency?
primary: caused by inadequate intake of that nutrient
secondary: caused by other problems inside the body that affect absorption/metabolism of that nutrient
both results in declining nutrient stores which results in symptoms of deficiency
What changes in Fe transport occurs when deficient in Fe?
- iron is drawn from ferritin stores
- plasma ferritin decreases
- efficiency of transporting Fe increases
- transferrin production increases
- absorption efficiency increases (transferrin binding capacity and # of receptors increases)
- intestinal epithelial cells absorb Fe better when Fe is present
- defective erythropoiesis (no production of RBC). Not enough iron for protoporphyrin (precursor). Results in hemoglobin being made without Fe.
- RBC doesn’t function properly without hemoglobin. Results in hypochromic and microcytic cells (IDA)
ie. when someone is deficient or requires more Fe, they absorb more and faster (higher efficiency)
Describe causes of iron deficiency
- Decreased dietary iron (less iron absorbed or from vegetarian diet which lacks heme)
- inhibition of absorption. From mineral interactions where Ca and zinc supplements decrease absorption or other absorption inhibitors (ie. phytates and oxalates)
- increased red cell mass (pregnancy and growth)
- increased losses (hemolysis, GI bleeding, heavy menstrual losses)
Name of iron overload disorder (toxicity)
hemochromatosis: caused by a genetic failure to prevent unneeded iron in diet from being absorbed
characterized by:
- tissue and liver damage
- infections are likely because bacteria thrive on iron-rich blood
too much vit C can reduce transferrin to free ferrous iron. results in potential toxicity
calculate EAR for iron for healthy individuals
how much is the assumed percent of ingested iron that is absorbed?
1.5mg (iron needed) / 0.18 (% iron absorbed) = 8mg of iron (EAR)
assumed that 18% of ingested iron is absorbed
RDA for healthy women in reproductive years?
RDA for healthy men?
18mg/day (loses iron through menstruation)
men: 8mg/d
RDA for vegetarian men and women?
to calculate RDA for vegetarians: multiply by 1.8
veg men: 8mg x 1.8 = 14mg/d
veg women: 18mg x 1.8 = 32mg/day
supplements for IDA treatment?
ferrous sulphate (Fe2+) because higher solubility and absorption than dietary ferric (Fe3+)
why do vegetarians need more iron?
to make up for low bioavailability of their diets
only nonheme sources are found in plants, which have a lower absorption rate
how to treat a widespread deficiency across a population?
fortify food supply
ie. Fe sulphate in wheat flour
but need to be careful of toxicity for some population groups (because men have much lower EAR and UL)
where is iron stored?
mostly in the liver. Also in bone marrow and spleen
Most is circulating RBC
UL of iron for adults?
45mg/d
how does a deficiency of copper affect iron absorption?
copper is needed for iron to be absorbed.
deficiency of copper results in secondary Fe deficiency
Not very common to occur because we receive copper from water pipes
functions of zinc?
- required as a cofactor for many enzyme metabolic reactions to occur (ie. gene regulation)
- important for immune system, growth and development, synthesis and storage of hormones, activation of vit A, taste perception
zinc deficiency impairs many normal body functions. but zinc deficiency is hard to diagnose and easily seen as a general protein deficiency
what does saturation of transferring indicate about iron levels?
low saturation of transferrin indicates deficiency of iron
high saturation indicates over-supply of iron
the number of transferrin receptors is highly regulated (there is more transferrin when there is more Fe)
basal daily iron losses?
men: 1.0mg
premenopausal women: 1.4mg
loss from:
-GI blood, GI mucose, bile, skin cells and sweat, unire, menstrual losses
total Iron DRIs of all categories?
men: 8mg/d (14mg if vegan)
women: 18mg/d
27mg if pregnant
33mg if vegan
RDA of women and men?
UL?
men: 11mg/d
women: 8mg/d
UL: 40mg/d
good sources of zinc
beef: 5mg
eggs: 1mg
seafood: more than 5mg
legumes/nuts: 1.5mg
whole grains and foritifed cereals
describe zinc absorption
- if more zinc is needed, more is absorbed (higher absorption if deficient)
- approx 33% absorption efficiency
- primarily absorbed in small intestine (carrier mediated process)
- bioavailability is affected by consuming with other foods (ie. phytates bind with zinc and decrease bioavailability)
- 2 options of absorption:
1. involves itself in the metabolic functions of the cell
2. retained in the cell by metallothionein (binds and transports metals. Regulates zinc absorption by storing the zinc until the body needs it. Zinc is released into the blood stream where it is transported around the body)
what are factors that enhance/inhibits zinc absorption?
enhance: acids, AA
inhibits: phytate, oxalate, polyphenols, fibre, folate
describe zinc deficiency and the results of it
- difficult to diagnose. Usually misdiagnosed as general protein deficiency deficieincy
- no specific test because zinc has so many roles
- children are most vulnerable (immune system dysfunction compromised growth, poor appetite)
- also vulnerable to pregnant women, elderly and the poor
results of chronic zinc deficiency:
- growth retardation and slow sexual development
- slow digestion and absorption
- worsens malnutrition
- impairs immune response (infections are likely)
- damages central nervous system and brain
- impairs vit A metabolism
what is parakeratosis?
skin rash resulting from zinc deficiency
describe enteropancreatic circulation of zinc
refer to diagram
why do children have high zinc needs
growing rapidly and synthesizing many zinc containing proteins
what factors control homeostatic regulation of zinc?
zinc content is controlled between:
- absorption efficiency of dietary zinc
- endogenous secretions in pancreatic fluid (ie. fecal losses)
describe steps in dietary zinc deficiency
- increased absorption and decreased losses
- tissue zinc conservation
- mobilization of zinc from exchangeable pool
- general tissue dysfunction
describe zinc recycling in enteropancreatic circulation
intestine receives two doses of zinc with each meal:
- one from dietary zinc from food
- from zinc-rich pancreatic secretions
zinc can be excreted in shed intestinal cells or absorbed into the body when circulating in the blood
describe symptoms of acute zinc toxicity?
chronic toxicity?
acute: nausea, vomiting, diarrhea
chronic toxicity:
- increase of metallothionein in intestine
- induces absorption
- copper is not released in blood
- copper is lost in shed mucosal cells
copper deficiency has similar symptoms to iron deficiency
why is it hard to diagnose copper deficiency?
it has similar symptoms to an iron deficiency
What are the roles of iodide in the body?
-thyroid hormones (T3 and T4) that regulate body temp, metabolism, reproduction, growth, RBC production, brain development, nerve and muscle function
describe iodine deficiency
without dietary iodine:
- thyroid hormone (T3 and T4) production declines
- body responds by secreting more TSH to accelerate iodide uptake by the thyroid gland
- if deficiency persists, thyroid gland cells enlarge to trap as much iodide as possible (one of the causes of goiter)
Refer to diagram fo full
What is the average intake of iodide?
sources of iodine?
9g/d
sources: iodized salt
what is cretinism
mental and physical retardation caused by maternal iodine deficiency during pregnancy
affects approx 6 million people worldwide
describe how increase of iron affects zinc (mineral interactions)
increase Fe = Fe occupies all transferrin binding sites = lower Zn absorption and transport
how does increasing zinc affect copper (mineral interactions_
increase zinc = high metallothionein = Cu binds more strongly = Cu not released from mucosal cell
how does decreasing protein affect zinc
decrease protein = decrease albumin = decrease Zn release from mucosal cell = more growth failure = immune dysfunction
