You can eat plenty of iron and absorb almost none of it. You can also be anaemic without being short of iron at all.

The advice given to an anaemic patient in India is almost always the same: eat more iron-rich food. Green leafy vegetables, jaggery, dates, pomegranate. The advice is well meant and it is incomplete in three separate ways, each of which is interesting on its own.

The first is chemical: iron in food comes in two forms and the body treats them very differently. The second is physiological: the body regulates iron at the point of absorption, and inflammation can shut that door regardless of diet. The third is methodological, and it has recently changed the national headline figure — because how much anaemia India has depends partly on how the blood was drawn.

Two kinds of iron, and only one of them is easy

Iron in food is either haem or non-haem, and the distinction matters more than the total quantity on the label.

Haem iron comes from haemoglobin and myoglobin — so from meat, fish and poultry. It is already held inside a porphyrin ring, it is absorbed through its own pathway, and it is taken up efficiently and fairly consistently: roughly a fifth to a third of what is eaten, largely unaffected by the rest of the meal.

Non-haem iron is everything else: pulses, grains, leafy vegetables, jaggery, fortified foods, and iron tablets. It is absorbed through a different route, it must first be reduced from ferric to ferrous form, and its uptake is enormously variable — anywhere from a couple of per cent to around twenty, depending almost entirely on what else is in the stomach at the same time.

That variability is the crux. In a predominantly vegetarian diet, nearly all dietary iron is the form whose absorption is most easily blocked.

What is on the plate decides how much gets in

The modifiers are well characterised and several of them are everyday habits.

Phytate is the main inhibitor. It is the storage form of phosphorus in seeds, so it is abundant in whole grains, legumes, nuts and seeds — precisely the foods often recommended for iron. It binds iron in the gut and makes it unavailable, and it does so at low concentrations.

Polyphenols and tannins inhibit strongly. Tea is the significant one in Indian practice: a cup with or soon after a meal can cut non-haem iron absorption substantially. Coffee does the same. This is one of the few genuinely actionable pieces of advice in the whole subject — not "stop drinking tea", but "leave an hour or two between tea and the meal that is supposed to be supplying your iron".

Calcium interferes with both forms, which is why iron and calcium supplements taken together work against each other, and why a large glass of milk alongside a meal is not a neutral addition.

On the other side, vitamin C is a powerful enhancer. Ascorbate reduces ferric iron to the absorbable ferrous form and keeps it soluble, and it can multiply non-haem absorption several-fold from the same meal. A lemon squeezed over dal, a tomato in the sabzi, amla, guava or citrus eaten alongside does more measurable good than switching to a slightly more iron-dense vegetable. A small amount of meat or fish also enhances absorption of the non-haem iron eaten with it.

Preparation matters too, and traditional methods turn out to be doing chemistry. Soaking, sprouting, fermenting and leavening all activate or introduce phytase, which degrades phytate — which is part of why idli, dosa and dhokla batters, sprouted moong and properly soaked pulses are better iron sources than the same ingredients cooked straight. Cooking in iron vessels adds some iron to food, with real but variable effect.

Food labels report how much iron is in the food. The body only ever gets what it absorbs, and that figure is set by the rest of the meal rather than by the iron itself.

The body controls the door, not the exit

Here is a piece of physiology that explains a great deal, including why iron supplements can be harmful as well as helpful.

Humans have no regulated mechanism for excreting iron. Small amounts are lost through shed cells, sweat and bleeding, and that is all. Since the body cannot dispose of a surplus, the only place it can regulate iron is at the point of entry — absorption is the control valve.

That valve is operated by a hormone called hepcidin. When iron stores are adequate, hepcidin rises and absorption falls. When stores are low, hepcidin falls and the gut takes up more.

The complication is that hepcidin also rises during inflammation and infection, as an evolved defence — bacteria need iron, so the body withholds it. The consequence is clinically enormous: a person with chronic infection, inflammation or chronic disease develops anaemia while having perfectly adequate iron stores, because the iron is locked away and absorption is suppressed. Giving such a patient iron tablets does not correct the anaemia, may cause gastrointestinal side effects, and in some infectious settings is actively unhelpful.

This is why anaemia is a symptom requiring a diagnosis rather than a diagnosis in itself — and why chronic infection, poor sanitation and hookworm burden are anaemia issues just as much as diet is.

Not all anaemia is iron deficiency

The assumption that anaemia means iron shortage is the most consequential simplification in this whole area, and in India it is often wrong.

Vitamin B12 and folate deficiency produce anaemia and are common, particularly with largely vegetarian diets, since B12 occurs naturally almost only in animal foods. Inherited haemoglobin disorders — sickle cell disease and trait, and the thalassaemias — are present at significant frequency in several Indian populations, and cause anaemia that iron cannot treat and that iron overload can worsen. Hookworm infection causes chronic blood loss from the gut. Malaria destroys red cells. Chronic kidney disease reduces erythropoietin. And in menstruating women, heavy menstrual bleeding is a frequent and frequently unexamined cause.

Treating all of these as one problem with one answer is why a great deal of iron supplementation produces less benefit than expected.

The number itself moved

There is a final twist that deserves to be better known.

India's headline anaemia statistics come from the National Family Health Survey, which has reported very high prevalence — on the order of half of women of reproductive age and around two-thirds of young children in the most recent round. Those measurements are made on capillary blood, a finger-prick sample read on a portable device, which is what makes a survey of that scale feasible.

Capillary sampling is known to read differently from venous blood drawn from the arm, which is the clinical standard. When an Indian national nutrition survey measured haemoglobin from venous samples, it reported substantially lower anaemia prevalence than the finger-prick-based surveys had — a gap large enough to change what the problem looks like, and the government has since indicated that future survey rounds will move to venous sampling.

This is not a reason to conclude that anaemia in India is imaginary; the burden is real and serious by any measure. It is a reason to be careful about which number is being quoted, and a clean illustration of a general principle: a prevalence figure is a property of the measurement protocol as much as of the population. Programmes, budgets and targets are built on these numbers, and a change in sampling method can move a national statistic more than a decade of intervention does.

Why it matters for students and researchers

Nutrition is a field where the biochemistry is well understood and the population-level outcomes stubbornly refuse to follow, and India is where that gap is widest and most consequential. The country runs some of the largest nutrition interventions in the world — iron and folic acid supplementation, the Anaemia Mukt Bharat programme, and large-scale staple fortification including fortified rice through the public distribution system — and the evidence on what each contributes in real conditions is thinner than the scale of the spending warrants.

The open questions are practical. How much of the anaemia in a given district is actually iron deficiency, as opposed to B12 deficiency, haemoglobinopathy or inflammation, which determines whether an iron programme can work there at all. What the real bioavailability of iron is from Indian diets as actually eaten, rather than as modelled. Whether simple, culturally acceptable changes — timing of tea, routine inclusion of a vitamin C source, wider use of fermentation and sprouting — produce measurable haemoglobin change at population scale. And how fortification performs where the underlying cause is not dietary iron shortage.

That interdisciplinary scope — nutrition alongside biochemistry, epidemiology, public health and medicine — is precisely what the International Journal of Nutritions (ISSN 3048-5576), a peer-reviewed journal launched in 2024, sets out to cover. For students of nutrition, medicine and public health, iron is a good first lesson in a rule that applies across the field: what a person eats and what a person absorbs are different quantities, and almost every interesting question lives in the gap between them.

Frequently asked questions

Why does eating iron-rich food not always correct anaemia?

Because most plant iron is non-haem iron, whose absorption varies from a couple of per cent to around twenty depending on the rest of the meal. Phytate, tea and coffee polyphenols and calcium suppress it, while vitamin C substantially enhances it.

What is the difference between haem and non-haem iron?

Haem iron comes from meat, fish and poultry and is absorbed efficiently through its own pathway, largely unaffected by the rest of the meal. Non-haem iron, from plants, pulses, fortified food and supplements, is absorbed through a different route and is heavily modified by other food components.

Does drinking tea with meals affect iron?

Yes. Tea polyphenols substantially reduce absorption of non-haem iron when taken with or soon after a meal. Leaving an hour or two between the meal and the tea is a practical way to avoid the effect.

How can someone be anaemic without being iron deficient?

Inflammation and infection raise the hormone hepcidin, which suppresses iron absorption and locks iron away from red cell production as a defence against bacteria. Anaemia can also result from B12 or folate deficiency, inherited haemoglobin disorders, hookworm, malaria or kidney disease.

Are iron supplements always helpful?

No. The body has no way to excrete surplus iron, so absorption is the only control point. Where anaemia is caused by inflammation or by an inherited haemoglobin disorder, iron supplementation does not correct it and may cause harm, which is why anaemia should be diagnosed rather than assumed.

Why have India's anaemia figures been debated?

Because the large national surveys measure haemoglobin from finger-prick capillary blood, while the clinical standard is venous blood from the arm, and the two read differently. An Indian survey using venous sampling reported substantially lower prevalence, and future rounds are expected to move to venous measurement.