Class 18- Trace minerals, nutritional anemia

Trace mineral content in food varies with..

Trace mineral content in food varies with SOIL and WATER composition and food processing

key info about blood

• continually moving

• delivers pr circulate oxygen and nutrients

• removal of waste

• only fluid tissue in body

Key nutrients:

iron, vit k, folate, b12

what are Nutritional anemias

• Nutritional anemias are a group of anemias caused by inadequate intake, absorption, or utilization of nutrients that are essential for red blood cell (RBC) production and hemoglobin synthesis.

• result in decreased oxygen delivery to tissues, leading to fatigue, weakness, pallor, and poor concentration.

• Anemia is a condition where the blood has a reduced capacity to carry oxygen to the body’s tissues.
  This happens when there is:

  1. Too few red blood cells (RBCs),

  2. Too little hemoglobin (the oxygen-carrying protein inside RBCs),
     or

  3. Abnormal RBCs that can’t function properly.

• Particularly concerning in women of reproductive age, pregnant women, infants, and vegetarians/vegans.

3 main types of nutritional anemias

iron deficiency—> hypo chromic or microcytic anemia

Folat or B12 deficiency—> Megaloblastic or

Pernicious Anemia

iron forms, function

FORMS= Ferrous (Fe++), Ferric forms(Fe+++)

FUNCTIONS=

1) Oxidation-reduction reactions

o Part of electron transport chain to make ATP

o Cofactor to many enzymes such as peroxidase, myeloperoxidase, catalase

2) To transfer oxygen: part of Heme group

in a protein

 Hemoglobin for transport of oxygen to tissues

 Myoglobin for muscle storage of oxygen

Heme vs nonheme iron

• Heme iron → animal-based, more bioavailable.

• Non-heme iron → plant-based, less efficiently absorbed, but absorption can be improved by combining with vitamin C–rich foods (like citrus, bell peppers, tomatoes).

what are some iron enhancers vs inhibitors

Enhancers

• Meat factor protein (MFP)

• Vitamin C

• From iron cookware; ↑ acidity of food and cook time = ↑ iron

Inhibitors

• Phytates

• Vegetable proteins

• Calcium

• Polyphenols (e.g., tannic acid)

heme vs nonheme iron sources, what are vegetarian needs for iron

Mixed diets: 18% dietary iron

Vegetarian: 10%, so need 1.8 X RDA

what ia iron absorption process

Iron transport and storage, what delivers iron to things? what is it totes as and where? what form is it found? 

overview of iron metabolism, what are total daily iron losses and where do they occur in body? 

Total:

1.0 mg (men)

1.4 mg (premenopausal women)

 GI losses:

• GI blood (Hgb 0.35 mg)

• GI mucosal (ferritin 0.10 mg)

• Bile (0.20 mg)

 Desquamated skin cells and sweat (0.2-0.3 mg)

 Urinary losses (<0.1 mg)

 Menstrual losses (0.5 mg)

how is iron recycled in the body?

what hormone regulates iron balance? where does it come from?

HEPCIDIN produces  from liver inhibits Fe absorption in mucosa if too much iron

what are some adaptations to increase Fe availability during a deficiency? 

Increase efficiency of absorption and

release from intestinal epithelial cells

 Increase transferrin synthesis and

transferrin receptors

 Decrease ferritin synthesis

how can iron status be assessed? what are test at each point in deficiency ? 

what does normal red blood cell look like vs when there’s iron deficiency? 

what are 3 stages before full on iron deficiency anemia?

1. Stage 1: Depletion of iron stores

dec. serum ferritin blood levels

2. Stage 2: Changes in iron transport

• inc. absorption efficiency, inc. transferrin receptors

• inc. transferrin iron binding capacity

• dec. transferrin saturation %, dec. serum ferritin in Blood

3. Stage 3: Defective erythropoiesis

• dec serum iron

• inc. Erythrocyte protoporphyrin, can’t make Hgb/Hct so it dec.

4. Iron Deficiency Anemia: Microcytic hypochromic erythrocytes

 Associated behavioral signs get worse

 Reduced stores: Blood: dec. Hgb/Hct, dec .MCV

what are iron deficiency anemia symptoms? what are the Hgb lvls for men vs women? 

- Tired and pale

-  work performance & mental productivity

-  childhood development-psychomotor and

intellectual

- Pica- unusual food cravings

- lead poisoning susceptibility

 Men: Hgb < 140 g/L

 Women: Hgb < 120 g/L

what are 4 common causes of iron deficiency ?

1. Decreased dietary iron

 Less iron absorbed

 Vegetarian diets lack heme

2. Inhibition of absorption

 Mineral Interactions: Calcium, zinc

supplements can dec. iron absorption

 Absorption inhibitors

3. Increased red cell mass

 Pregnancy, growth

4. Increased losses

 GI bleeding (occult)

 Heavy menstrual losses

 Blood donation

what are Iron DRIs? what is treatment and prevention 

Treatment=

• diet, supplementation

BUT supps—> Less well absorbed than food

• Best forms: ferrous sulphate

or iron chelate, eat between meals or on empty

stomach with liquids

• note Vitamin C has no effect on absorption

Prevention=

• improve diet quality, fortify foods

are there iron toxicity?

-there can be acue toxicity or poisoning!!

Megadoses of Vitamin C – Pro-oxidant (increases oxidative species -ROS)

• the can reduce ferric iron bound to transferrin to free ferrous iron

• free iron is a powerful oxidant: Fenton reaction=>BAD

what is Hemochromatosis? what can it lead to? symptoms? treatment?

= accumulation of iron in organs, joints… Can be fatal

• Autosomal recessive, most common genetic disorder in US

• More common in men than iron deficiency

- Can lead to Hemosiderosis (deposits of excess Fe)

 Unneeded iron is absorbed (hepcidin)

Hemosiderosis = iron build-up
Hemochromatosis = iron overload disease

Symptoms: apathy, lethargy, and fatigue

 Causes tissue damage (free radicals), infections

treatment= phlebotomy, chelation therapy, low iron diet…Vit.

what is microcytic vs macrocytic anemia?

• Micro = small → iron issue (hemoglobin problem)

• Macro = large → folate/B12 issue (DNA problem)

what is macrocytic anemia? what vit. deficiency is it linked with? 

= when  red blood cells (RBCs) are larger than normal (“macro” = large) and often fewer in number.
- Even though they’re big, they don’t function properly because they’re immature — they didn’t divide enough during development.

Cause	How it affects RBCs
Folate (vitamin B9) deficiency	Needed for DNA synthesis → fewer, larger RBCs
Vitamin B12 deficiency	Same mechanism (also causes neurological symptoms)
Alcoholism or liver disease	Interferes with RBC production
Certain drugs (e.g. chemotherapy)	Inhibit DNA synthesis

is megaloblastic anemia the same ad macrocytic?

Term	Meaning	Relationship
Macrocytic anemia	General term for anemia where red blood cells (RBCs) are larger than normal (↑ MCV)	Broad category — describes size only
Megaloblastic anemia	Specific type of macrocytic anemia caused by impaired DNA synthesis, usually due to vitamin B12 or folate deficiency	Subtype of macrocytic anemia

Why Megaloblastic Happens

• Folate or B12 deficiency → DNA synthesis slows down

• RBC precursors in bone marrow keep growing but don’t divide normally

• Result: large, immature “megaloblasts” in marrow and large RBCs in blood

megaloblastic VS pernicious anemia? which one is primary vs secondary?

MEGA:

• a primary deficiency, lack of dietary folate OR b12—> impairs DNA synthesis 

• very large mega RBCs

• not common, slow development 

PERNI:

• a secondary deficiency, also causes large immature RBS

• has a neurological component 

• CAUSE= intrinsic factor OR atrophic gastritis

• ppl over 50 @ risk

what is Vit. B12 relationship to pernicious anemia?

Pernicious anemia is a type of megaloblastic anemia caused by a vitamin B₁₂ deficiency, not because of poor intake — but because the body can’t absorb B₁₂ properly, so caused by b12 secondary deficiency

• B₁₂ absorption requires “intrinsic factor” (IF) — a protein made by parietal cells in the stomach.

• In pernicious anemia, the immune system destroys these parietal cells or produces antibodies against intrinsic factor.

• Without intrinsic factor → B₁₂ can’t bind and be absorbed in the ileum (small intestine).

• This leads to B₁₂ deficiency, which → impaired DNA synthesis → megaloblastic anemia.

what are zinc functions?

works with proteins in every organ!!

 Stabilizes cell membranes and DNA

 Synthesis, storage, and release of insulin

 Taste perception

 Blood clotting, RBC synthesis

 Thyroid hormone function

 Immune function, wound healing

• release of vitamin A from stores

• Growth and development, reproduction – sperm development

• influences behavior and learning performance

explain zinc absorption and enteropancreatic circulation 

what are some zinc absorption enhancers vs inhibitors? 

ENHANCERS= acids, amino acids

INHIBITORS= phytates, oxalate, polyphenols, insoluble fibers, folate

what are stages of zinc deficiency? info on zincdeficiency, who’s most vulnerable?

Difficult to diagnose

 No sensitive and specific test

 affects Thyroid and Pancreatic function, GI function,infections

Children most vulnerable!!

 Compromised growth and development

- stunting

 Poor appetite, diarrhea

 Poor cognitive and motor development

 Impaired immunity

 Poor wound healing

 Widespread in developing world

zinc toxicity symptoms, what could Zn interfere with? 

Rare!

UL= 40 mg Zn

Zn excess interferes with copper(Cu) and Fe metabolism

Symptoms:

 Acute toxicity: Nausea, vomiting, diarrhea

Chronic Zn Toxicity:

 causes Cu deficiency, alter Fe function and conversion Fe2+ to Fe 3+

 Increased intestinal metallothionein

 Copper not released into blood, lost in shed mucosal cells

 Reduced immunity, urinary problems

 May decrease HDL (“good”) cholesterol in the blood

chromium info, what does it work with? what are some food sources?

 Works with insulin to regulate and release energy from glucose

Food sources:

 Unrefined foods, whole grains, liver, nuts, cheese

copper info, what doe sit help form?

 Helps form hemoglobin and collagen and defense against oxidation, in many enzymes: E.g., ferrous to ferric iron

Food sources:

 Organ meats, seafood, nuts, seeds

 Genetic disorders that affect copper status

 Menkes disease

 Wilson’s disease

how does inc. iron affect zinc? how does inc zinc affect copper? how does dec protein affect zinc?

Iodine vs iodide, what hormones is it a part of? important for? 

Iodine = found in foods,  GI tract converts iodine in food to iodide

Iodide = the form found in the body Dietary, readily absorbed by the body

• Needed in miniscule amounts

 Part of thyroid hormones (i.e., thyroxine)

Important for:

 Regulate body temperature

 Regulate metabolic rate

 Control rate at which cells use oxygen

 Nerve and muscle function and brain development

what does iodine deficiency look like?

• goiter, enlarged thyroid gland bc Increases uptake of iodide causing goiter

Other signs include mental impairment and brain

damage, irreversible if not treated

 During pregnancy, leads to cretinism

Goiter—> Continued deficiency

 Cretinism—> Severe deficiency in pregnancy, Irreversible physical and mental retardation

iodine toxicity, what does it interfere w and what does it look like 

-UL= 1100 ug

 Interferes with thyroid function: Enlarges thyroid gland, just like with deficiency

 Pregnancy: exposure to high intakes

from supplements, foods, meds

dangerous: goiter formation

 Goiter in an infant exposed to toxic

amounts – blocks airways - death

what are trace mineral in low quantities in body?

• no DRI values

 Nickel: a cofactor for enzymes

 Silicon and vanadium: important in bone

health

 Cobalt: part of vitamin B12

 Boron: important in bone health, brain

activity, and immunity

are all trace mineral beneficial? what are ‘bad’ ones

Contaminant minerals!

 Interfere with nutrient functions; diminishes health

 Heavy metals—> Enter food supply via soil, water, and air pollution

lead:

 Indestructible, chemistry remains unchanged

 Displaces iron, calcium, and zinc

 Children with iron deficiency especially vulnerable

Mercury

Cadmium