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Place · Level 3
两种形式 · 红血球的核心 · 储存有名片 · 不该乱补
synergy · 3
Reverse of C → Fe; classic same-meal pairing for plant-iron uptake.
B2 (as FAD) cofactors the ferroportin/hephaestin oxidation step that releases dietary iron into blood. B2 deficiency worsens iron-deficiency anemia; combined repletion outperforms iron alone in B2-deficient populations.
Both are required inputs to red-cell production, but their deficiencies pull opposite ways: iron shortage makes cells small, folate/B12 shortage stalls DNA synthesis and makes them large. Lack both and MCV lands back in the 'normal' band, hiding both problems at once.
cofactor · 8
Copper enzymes help iron oxidation and transport; deficiency can impair iron mobilization.
Vitamin C reduces Fe³⁺→Fe²⁺ and forms soluble complexes, boosting plant-iron uptake 2–3×.
Thyroid peroxidase (TPO) is a Fe-heme enzyme. With adequate iodine, iron deficiency still impairs TPO → low T4 synthesis. Iron-deficient pregnancy with adequate iodine can still show borderline thyroid status — fetal neurodev risk.
Vitamin C eaten in the same meal reduces plant Fe³⁺ to Fe²⁺, so produce does not merely contain iron — it sets how much of the non-heme iron alongside it is absorbed.
About two thirds of your iron sits at the heme centre of haemoglobin — that's the atom that grabs oxygen in the lung and lets go in the tissue. Short on iron, the marrow builds red cells that are small and pale, and oxygen delivery drops. Ferritin empties first; haemoglobin falls last.
Lungs load and tissues unload thanks to haemoglobin's cooperative binding curve plus the Bohr effect — and at the centre of every haemoglobin sits an iron atom. Short on iron, the lung is fine; the carriers are missing.
↔Zinc
Zinc occupies backup sites on ALA-D + ferrochelatase under lead exposure, preventing lead-for-iron substitution (zinc-protoporphyrin ZPP is the classic pediatric lead-exposure marker). A second Zn↔Fe interaction beyond gut absorption competition.
Red meat delivers heme iron through HCP1 rather than DMT1, so phytate, tannins and calcium do not blunt it. High bioavailability is the upside; the same pathway catalysing oxidation in the gut lumen is the downside.
antagonism · 4
Calcium competes with non-heme iron at the gut; high-calcium meals lower iron absorption.
↮Zinc
High-dose zinc inhibits iron absorption (and vice versa) — don't megadose together.
Mn and Fe share the DMT1 transporter — iron deficiency upregulates DMT1 → Mn uptake increases compensatorily → manganese toxicity risk rises under environmental exposure. Iron-deficient children in high-Mn well-water regions are silent victims.
What blocks non-heme iron is the polyphenols in tea and coffee, not caffeine itself — a strong cup with a meal can wipe out most of that meal's non-heme iron absorption. Moving tea and coffee between meals is enough.
depletes · 2
Blood carries about 0.5 mg of iron per mL, and a period typically loses 30-40 mL — so 15-20 mg of iron leaves with it. That once-a-month exit is the main reason a menstruating woman's iron requirement is nearly double a man's (the recommendation is set near the heavy end of the range, not the average). Above 80 mL is heavy menstrual bleeding, and the iron ledger more than doubles.
Why the ledger does not balance itself
The debit side is simple: 15-20 mg of iron leaves with each period. The credit side is the hard one — iron is not 'you get what you eat'; it is throttled by **absorption**. Plant-source non-heme iron absorbs at only 2-20%, and swings hard with the meal (tannins in tea and coffee cut roughly 60%; calcium and phytate each take a share). Animal-source heme iron holds steady at 15-35%. That is why the RDA is **18 mg/day** for women against 8 mg for men — the near-doubling exists to cover that monthly exit. And note: that figure is set **near the heavy end of the range, not at the average**.
The warehouse empties before the blood does
The body does not wait for haemoglobin to fall before it feels this. The monthly exit draws first on the **ferritin warehouse** — about 60% in the liver, 25% in bone marrow. Clinically, serum ferritin is the most sensitive read on stored iron: **below 15 µg/L is absolute deficiency (an empty warehouse)**, 15-30 is borderline. Which means someone with a perfectly normal blood count can already be scraping the bottom — fatigue, hair shedding and dropping endurance often arrive before anaemia does. So checking iron cannot mean checking haemoglobin alone.
When this stops being a nutrition problem
Losing more than **80 mL** meets the definition of heavy menstrual bleeding, and the iron ledger more than doubles — at that scale, diet cannot catch up. The practical trouble is that nobody can measure 80 mL at home. Usable proxies: needing to change a pad or tampon every one to two hours, having to get up at night to change, passing large clots, or bleeding longer than seven days. When those show up, the question to ask is **why is the bleeding this heavy**, not **how much iron should I take** — the latter is topping up a tap nobody turned off. This is education, not care; see a clinician for diagnosis.
Blood volume expands by about 50%, and the fetus and placenta build their own blood on top of that — pushing the iron recommendation from 18 mg/day to 27. That isn't 'a bit more', it's a different balance sheet.
regulates · 2
Pregnancy raises blood volume and iron demand together, while how much the gut can absorb is set by hepcidin — which is why pregnancy iron deficiency rarely yields to 'just eat more' and needs a real supplementation plan.
Hair follicles are among the fastest-proliferating tissues in the body, so they are demoted first when iron runs low. The telogen effluvium of low ferritin regrows once iron is restored — check ferritin before buying shampoo.