Lecture 3; Folate, Vitamin B12, Iron

Iron primary biological role

Enables oxygen transport and energy metabolism as a component of hemoglobin and myoglobin.

Why iron deficiency is the most common micronutrient deficiency worldwide

Iron requirements are high and absorption is relatively low.

Main function of hemoglobin

Transport oxygen from the lungs to body tissues.

Main function of myoglobin

Store and facilitate oxygen use in muscle tissue.

Two major dietary forms of iron

Heme iron from animal sources and non-heme iron from plant sources.

Which form of iron is better absorbed

Heme iron is more efficiently absorbed than non-heme iron.

Why non-heme iron absorption is variable

Its absorption is strongly influenced by dietary enhancers and inhibitors.

Major enhancers of non-heme iron absorption

Vitamin C and meat, fish, or poultry consumed with the meal.

Major inhibitors of non-heme iron absorption

Phytates, polyphenols (tea and coffee), calcium, and oxalates.

Why vitamin C improves iron absorption

It reduces ferric iron (Fe3+) to ferrous iron (Fe2+) and keeps iron soluble.

Why iron requirements are higher in pregnancy

Expanded maternal blood volume and fetal iron needs increase demand.

Primary clinical outcome of iron deficiency

Iron deficiency anemia characterized by reduced oxygen-carrying capacity.

Early indicator of depleted iron stores

Low serum ferritin levels.

Why iron deficiency leads to fatigue and weakness

Reduced hemoglobin limits oxygen delivery to tissues.

Why infants and young children are at risk of iron deficiency

Rapid growth increases iron requirements.

Key public health concern related to iron deficiency

Impaired physical performance, cognition, and increased maternal mortality risk.

Folate core biological role

Supports DNA synthesis and cell division through one-carbon transfer reactions.

Why rapidly dividing tissues are sensitive to folate deficiency

DNA replication fails when folate is insufficient, impairing cell division.

Why early pregnancy has high folate demand

Neural tube formation involves rapid cell division during weeks 3–4 of gestation.

Main consequence of folate deficiency in early pregnancy

Increased risk of neural tube defects such as spina bifida and anencephaly.

Why neural tube defects occur before many pregnancies are recognized

The neural tube closes before most individuals know they are pregnant.

Primary public health rationale for folic acid fortification

To reduce neural tube defects in the general population, including unplanned pregnancies.

Why folic acid is used instead of natural food folate for fortification

Folic acid is more stable, inexpensive, and more bioavailable.

Main form of folate circulating in blood

5-methyltetrahydrofolate (5-methyl-THF).

Functional relationship between folate and vitamin B12

Vitamin B12 is required for folate to participate in DNA synthesis reactions.

What happens to folate metabolism when vitamin B12 is deficient

Folate becomes trapped as 5-methyl-THF and cannot support DNA synthesis.

Definition of the methyl-folate trap

Accumulation of 5-methyl-THF during B12 deficiency, leading to functional folate deficiency.

Why high folic acid intake can mask vitamin B12 deficiency

Anemia improves while neurological damage from B12 deficiency progresses.

Primary hematologic outcome of folate deficiency

Megaloblastic anemia due to impaired DNA synthesis.

Why vitamin B12 deficiency causes neurological symptoms

Vitamin B12 is required for myelin maintenance and nervous system function.

Key reason the UL for folic acid was established

To prevent masking of vitamin B12 deficiency.

Main population groups targeted by folate recommendations

Women of childbearing age, pregnant individuals, and infants.

Why folate status improved more from fortification than diet alone

Synthetic folic acid has higher bioavailability than food folate.