When the gut cannot absorb iron

There are people who do everything right. They eat iron-rich food, dutifully take their tablets, and still the stores stay empty. The reason then often lies not on the plate, but in the gut. When the lining is inflamed, the stomach acid is missing or a stretch of bowel has been bypassed, the iron simply does not arrive. This article shows which absorption problems are behind it, how to find them and why an infusion can be a sensible path in this situation.

Iron deficiency essentially has three big paths: the body loses iron, it needs more, or it absorbs too little. The first two paths are described in detail in the article on the causes of iron deficiency. Here it is specifically about the third path, the impaired absorption, and about the conditions that block exactly this path.

Where iron is absorbed, and why that is so easily disturbed

Iron from food is absorbed mainly in the uppermost section of the small bowel, in the duodenum and the upper jejunum. For this to work, several things have to play together. The stomach delivers acid that releases the iron from food and brings it into a more absorbable form. The small bowel lining needs intact villi, the fine projections through which the exchange of substances runs. And the body must not be in a state of constant inflammation that shuts down absorption through the hormone hepcidin.

If only one link in this chain fails, absorption drops. This is exactly where the conditions discussed now come in. Some damage the lining, some take the acid away from the stomach, some inflame the whole gut. The result is the same: the iron sits in the gut and does not reach the blood.

Coeliac disease: the classic of the silent absorption problem

Many people with coeliac disease first think of abdominal pain, diarrhoea and bloating. Yet a considerable share have exactly none of that. In them the condition makes itself known through other channels, and one of the most common is a stubborn iron deficiency. That fits the biology: in coeliac disease the immune system attacks the small bowel lining after contact with gluten. The villi flatten, exactly where iron is absorbed. The absorption surface shrinks, and with it the amount of iron that reaches the blood.

The tricky part: as long as gluten stays in play, every iron tablet can run up against a damaged lining. When the coeliac disease is recognised and a consistent gluten-free diet is followed, the lining often recovers, and iron absorption can improve. That is why the search for coeliac disease here is not only diagnostics, but often already the first step of treatment.

Helicobacter pylori: the lodger in the stomach

Helicobacter pylori is a bacterium that nests in the stomach lining. Very many people carry it, often without knowing. It can sustain a chronic inflammation of the stomach lining and alter acid production. Both interfere with iron absorption. Less usable acid means that non-haem iron is dissolved and absorbed less well. In addition, the bacterium itself consumes iron and the chronic inflammation pushes hepcidin up.

Atrophic gastritis and the underestimated stomach

For iron to be absorbed well, an acidic environment in the stomach helps. But there is a state in which the stomach lining gradually thins out and produces less and less acid, the so-called atrophic gastritis. It can arise as a late consequence of a long-standing Helicobacter infection or as an autoimmune form in which the immune system attacks the acid-producing cells. In both cases the acid sinks, and with it iron absorption.

The autoimmune form is especially interesting because it often occurs together with other autoimmune themes, for example the thyroid. It also affects the absorption of vitamin B12. That is why two deficiency states sometimes appear side by side here, both coming from the same stomach.

Inflammatory bowel disease: three problems at once

In Crohn's disease and ulcerative colitis, iron deficiency comes through several paths at once. First, the inflamed, partly bleeding lining can lose iron. Second, absorption in the affected bowel section can be impaired. And third, the chronic inflammation keeps hepcidin high, so that even existing iron becomes poorly available. This mix of true deficiency and inflammation-driven blockade makes the topic especially knotty here.

Irritable bowel and SIBO: what can hide behind them

Here an honest classification matters. An irritable bowel in the proper sense does not damage the gut lining and is rarely a direct cause of iron deficiency. Still the topic is worthwhile, because behind irritable-bowel-typical complaints such as bloating, changing stool and abdominal pain, something else can hide that very much has to do with iron absorption.

A coeliac disease, for instance, is often misread at first as irritable bowel because the complaints resemble each other. And a small intestinal bacterial overgrowth, in technical jargon called SIBO, can come with irritable-bowel-like symptoms. In SIBO too many bacteria settle in the small bowel and can interfere with the digestion and absorption of nutrients. The evidence on a direct connection between SIBO and iron deficiency is still limited, but the mechanism is plausible.

After stomach and bowel surgery

Some absorption problems are the consequence of a procedure. In bariatric operations for weight reduction, for example a gastric bypass, the stomach is made smaller and part of the upper small bowel is bypassed, exactly the section in which iron is absorbed. In addition, the acidic pre-digestion sinks. Both together make iron deficiency one of the most common long-term consequences of such operations.

Something similar applies after partial removals of the stomach for other reasons. Whenever acid or absorption surface is permanently missing, oral iron absorption is structurally limited. This is no question of good or bad will, but of anatomy.

How to find an absorption problem

The good news: an absorption problem can be narrowed down in a structured way. It is not about random tests, but about an order that begins with the most likely. Which steps make sense depends on history, complaints and previous examinations and belongs in medical hands.

1. Read the iron status correctly. Ferritin for the store, transferrin saturation for the current supply and an inflammation marker such as CRP, because ferritin can rise with inflammation.
2. Coeliac antibodies in the blood. A simple blood test for certain antibodies is often the first step with unexplained iron deficiency, ideally while gluten is still being eaten.
3. Test for Helicobacter pylori. Via breath test, stool test or as part of a gastroscopy, depending on the situation.
4. Consider gastroscopy and colonoscopy. Especially in men and in women after menopause, to assess bleeding sources, coeliac disease, gastritis and inflammation directly.
5. Check for inflammation in the gut. For example calprotectin in the stool as a hint of an inflammatory bowel disease.

Why an infusion here can be a sensible path

When the absorption path in the gut is blocked, oral iron reaches a logical limit. A tablet has to pass through exactly the gut that is the problem. This is precisely where the sober advantage of the infusion lies: it bypasses the gut and brings the iron directly into the bloodstream. With a confirmed absorption problem this is often no luxury, but the path that fits the cause.

What matters is the framing. An infusion is a good path when the indication is right and an iron overload, for example in hereditary haemochromatosis, has been ruled out beforehand. It belongs in a setting with good monitoring during and after the administration and with a modern preparation. The poor reputation that iron infusions still have in some places stems mostly from the era of old, high-molecular preparations with a higher reaction rate. Modern agents are to be classified differently. This is no disparagement of cautious colleagues, but a question of the state of knowledge.

At the ViveCura practice in Berlin we work at the interface of conventional and integrative medicine: in the exhaustion and hormone consultation, in gut and metabolism support, and in the medical guidance of iron therapies. Especially with the topic of absorption problems, these three areas sit close together. A sensible order starts with the basics: first narrow down the cause in the gut, then replenish in a targeted way, then treat the cause alongside.

And now you know why

When you eat enough iron, take your tablets and still make no progress, it is rarely down to you and rarely down to too little iron. Often it is down to the path into the blood being disturbed. Coeliac disease, Helicobacter, an acid-poor stomach, an inflamed bowel lining or a changed anatomy after surgery are the usual suspects. You may ask the question: is my iron arriving at all? This question is often the turning point at which unsuccessful replenishing becomes a treatment that starts at the right place.

Read on in the iron guide