The doctor explains

You're taking iron but your ferritin stays low? What if the problem is coming from your stomach?

Written and reviewed by Doctor Florian A. Vallecillo Cabrera· Published: 15 April 2026· Last medical review: 26 August 2026
You're taking iron but your ferritin stays low? What if the problem is coming from your stomach?
Unsplash

Why I'm telling you this

You were told you were iron-deficient. You started taking iron tablets. A few weeks or months later, you had another blood test done. And your ferritin is still low. Or it goes up a little… then drops back down.

So the iron dose gets increased. The formulation gets changed. Sometimes you're told you probably aren't eating enough meat. But there is one question that is sometimes forgotten: why are you iron-deficient in the first place?

I am Dr Florian A. Vallecillo Cabrera, and today I want to talk to you about a cause that is still not widely enough known to the general public: Helicobacter pylori. This small bacterium that lives in the stomach can, in some people, contribute to iron deficiency, or even to true iron-deficiency anaemia. And what is particularly interesting is that this can sometimes happen without significant stomach pain and without any dramatic digestive symptoms.

First of all: what is iron for?

Iron is essential to our body. We need it in particular to produce haemoglobin, the protein found in red blood cells that carries oxygen throughout the body.

When we are lacking in iron, several things can appear: fatigue, reduced physical performance, faster breathlessness during exertion, palpitations, difficulty concentrating, headaches, brittle nails, sometimes hair loss and, when the deficiency becomes significant enough, a true anaemia.

But there is a very important nuance: you can be lacking in iron even before becoming anaemic. This is where ferritin comes in, in particular.

Low ferritin does not necessarily mean anaemia

Ferritin represents, in simplified terms, our iron reserves. Imagine that your body has a small warehouse in which it stores iron so that it can use it when needed. Ferritin gives us an idea of the quantity available in that warehouse.

It is therefore possible to have low ferritin — iron reserves that are declining — but a still-normal haemoglobin level. At this stage, you do not necessarily have anaemia. But your body is already beginning to run low on reserves.

If the situation continues, haemoglobin can then decrease and anaemia can appear. This is why, when I see a low ferritin level, I never look at ferritin alone. I want to understand why it is low.

And this is where Helicobacter pylori comes into play

Helicobacter pylori, often simply called H. pylori, is a bacterium capable of living in the gastric mucosa. It is extremely common worldwide. Many infected individuals, moreover, present no symptoms at all.

But in some people, it causes chronic inflammation of the stomach: gastritis. It can also promote gastric or duodenal ulcers and is a recognised risk factor for certain long-term gastric diseases.

But its influence does not stop at the stomach. It can also play a role in iron metabolism. And this occurs through several mechanisms.

First mechanism: your stomach plays a part in iron absorption

We often imagine that the stomach serves only to receive and digest food. In reality, its acidic environment also plays a role in preparing certain nutrients before they are absorbed.

Dietary iron — particularly non-haem iron found notably in many plant-based foods — must be converted into a form that the intestine can more readily absorb. Gastric acidity contributes to this process.

Now, a chronic H. pylori infection can alter the functioning of the gastric mucosa. In some people, particularly when the gastritis becomes significant or atrophic, acid production can decrease.

Result: iron may become less readily available for absorption. You may therefore be consuming iron… but not necessarily absorbing as much as expected.

Second mechanism: the bacterium also needs iron

And here is another fascinating part of the story. Iron is essential to human beings. But it is also necessary for many micro-organisms. H. pylori therefore has its own mechanisms for using the iron available in its environment.

It can be explained very simply like this: you and the bacterium are partly drawing on the same resource.

This obviously does not mean that the bacterium 'eats all your iron'. The physiology is far more complex than that. But in some people, particularly when reserves are already borderline, this competition can contribute to the problem.

Third mechanism: inflammation changes the way our body manages iron

This is probably the mechanism least known to the general public. When our body is faced with inflammation, it deliberately alters the circulation of iron.

Why? Because iron is also useful to bacteria. Our body therefore has a defence system consisting of making iron less available when it detects an infection or inflammation.

A hormone called hepcidin plays a central role in this phenomenon. I will avoid giving you a biochemistry lecture. Simply remember this: when certain inflammatory pathways are activated, our body may tend to sequester more iron in its stores and reduce its availability.

This is a useful short-term strategy when fighting an infection. But when inflammation becomes chronic, this strategy can become problematic. Iron is present somewhere in the body… but it circulates and is used less efficiently. This is one of the reasons why inflammation and iron metabolism are intimately linked.

Fourth mechanism: sometimes, there can also be small amounts of blood loss

An H. pylori infection can be associated with gastritis or ulcers. And a digestive lesion can sometimes cause blood loss, occasionally small enough to go unnoticed.

You do not necessarily see blood. You do not necessarily feel any pain. But if these losses recur over time, they can contribute to a gradual depletion of iron stores.

This is an additional reason why unexplained iron deficiency should never be reduced to: 'Take an iron supplement and we'll see.'

Can you have H. pylori without having stomach pain?

Absolutely. And this is probably one of the most important messages in this article.

Many people associate H. pylori with stomach pain, heartburn, reflux, bloating, or difficult digestion. But some infected individuals experience virtually no digestive symptoms.

The discovery may then come about through an entirely different problem: an iron deficiency, anaemia, an endoscopy performed for another reason, or a family or medical investigation. The absence of pain therefore absolutely does not rule out infection.

But be careful: low ferritin does not mean H. pylori

And here I really want to emphasise this. Because in medicine, when an interesting explanation is discovered, the danger is wanting to use it to explain every case. Iron deficiency has many possible causes.

In a woman with heavy periods, gynaecological losses are obviously an important cause to consider. In an adult man or a woman after menopause, unexplained iron deficiency may require investigation for digestive blood loss.

Depending on the context, one must also consider a diet insufficiently rich in iron, repeated blood donations, coeliac disease, certain intestinal conditions, absorption disorders, certain digestive surgical procedures, chronic bleeding, certain medications, or indeed certain inflammatory diseases. And sometimes several factors exist simultaneously.

H. pylori is one possible piece of the puzzle. It is not automatically the whole explanation.

So, when should H. pylori be considered?

It becomes particularly worth considering when a person presents with unexplained iron deficiency. Or when they are taking iron correctly but their reserves are slow to recover. Or when the deficiency recurs as soon as treatment is stopped.

Or when there are simultaneously digestive symptoms, a history of ulcer, gastritis, relevant family history, or other elements that raise suspicion of a gastric infection.

International guidelines now recognise this association sufficiently for H. pylori testing to be part of the evaluation of certain cases of unexplained iron-deficiency anaemia. This does not mean that every person with slightly low ferritin should immediately be tested for H. pylori. It means that, in the right clinical context, it should not be forgotten.

How is Helicobacter pylori detected?

Several methods exist. Two non-invasive tests are particularly widely used.

The urea breath test: you are asked to swallow a substance containing a specific urea. If H. pylori is present in your stomach, the bacterium transforms this substance and we can detect the result in your breath. It is a very useful test when performed under the right conditions.

The stool antigen test: this allows direct detection of elements from the bacterium in a stool sample. It is also very widely used, particularly to diagnose an active infection or to confirm that a treatment has worked.

There is also the biopsy performed during a gastroscopy when an endoscopy is indicated.

And the blood test?

Antibodies against H. pylori can be detected in the blood. But this raises a problem: antibodies can remain positive for a long time after the infection has cleared.

In other words, a positive serology can tell you: 'This person has been in contact with H. pylori.' But it does not always allow us to reliably determine: 'Is this bacterium still present today?'

This is why, when we want to know whether an active infection exists, the breath test or the stool antigen test are often more useful.

Beware of medications before the test

This is a very important detail because it can lead to false-negative results. Certain medications that strongly reduce gastric acidity, particularly proton pump inhibitors, can interfere with some tests. Antibiotics and bismuth can also distort results for a certain period of time.

This is why tests must be properly scheduled in consultation with your doctor. Obviously, do not stop a prescribed treatment on your own initiative simply to undergo a test. Your doctor will advise you on when and how to carry it out.

If H. pylori is found, should it be treated?

When an active infection is diagnosed, the current principle is to eradicate it. Why? Because we are not only looking to treat a possible iron deficiency. H. pylori is also responsible for chronic gastritis, is a major cause of peptic ulcer disease, and increases the long-term risk of gastric cancer in certain individuals.

Treatment generally combines several medications over a defined period of time. And here, a very important message: treatments have evolved. Bacterial resistance to certain antibiotics has increased considerably. This is particularly the case with clarithromycin in many regions.

We must therefore no longer assume that an old antibiotic combination used for years is automatically the best treatment for everyone. The choice depends in particular on the region, bacterial resistance patterns, previously received treatments, allergies, and the patient's profile. Treatment must therefore be prescribed in an individualised manner.

Treating is not enough: the disappearance of the bacterium must be confirmed

This is another extremely important point. You complete your treatment. Your symptoms improve. And you think: 'It's over.' Not necessarily.

Current guidelines emphasise the need to confirm eradication after treatment. Why? Because an improvement in symptoms does not guarantee that the bacterium has truly disappeared.

A breath test or a stool antigen test is generally performed several weeks after the end of treatment, under the appropriate conditions, as notably highlighted by the American College of Gastroenterology. This is essential.

And what about ferritin after eradication?

This is where things become particularly interesting. In certain patients who have both an H. pylori infection and an iron deficiency, eradicating the bacteria can help improve the response to iron treatment.

Some data show an improvement in haemoglobin levels and iron status after eradication, even though the magnitude of the benefit varies depending on the populations studied. The European Maastricht consensus considers this association significant enough to recommend eradication when H. pylori is found in certain cases of unexplained iron-deficiency anaemia.

But a word of caution: we do not treat H. pylori 'instead of' treating an iron deficiency. If reserves are very low, it may be necessary to correct the deficit simultaneously. We therefore act on both levels: replacing what is missing and correcting the cause once it has been identified. And that distinction is fundamental.

Why taking iron without looking for the cause can be a mistake

Imagine a leaking bucket. You keep pouring water into it. The level rises momentarily. Then it drops again. You might conclude: 'We simply need to add more water.' Or you might ask yourself: 'Where is the hole?'

Iron deficiency sometimes works in this way. Oral or intravenous iron can replenish reserves. But if you continue to lose blood, to absorb iron poorly, or if another mechanism persists, the problem can return.

This is why a low ferritin level is not simply a number to correct. It is sometimes a signal that needs to be understood.

And what about hair loss?

This is an aspect that will be of particular interest to many of my patients. Iron deficiency can be associated with certain forms of hair loss, especially when reserves are genuinely low.

But here again: not every case of hair loss is caused by low ferritin, and not every case of low ferritin is caused by H. pylori.

If we discover an unexplained iron deficiency and hair loss at the same time, our job is to look for the cause of the deficit rather than simply prescribing iron indefinitely. And in some patients, the stomach can indeed be part of the explanation.

A stomach bacterium can have consequences well beyond the stomach

This is probably what I find most interesting about this subject. Our body is not made up of independent systems. The stomach influences the absorption of nutrients. Nutrients influence the blood. Blood carries oxygen. Iron is involved in many enzymatic systems.

A chronic digestive inflammation can therefore end up manifesting as symptoms that seem, at first glance, completely unrelated to the stomach: fatigue, reduced performance, anaemia, and sometimes hair loss. And the person may spend months treating the consequence without having yet identified the mechanism.

Key takeaways

If your ferritin is low, don't immediately assume you aren't eating enough iron. And if you've been taking iron supplements for months without satisfactory improvement, the question doesn't necessarily have to be: "What additional dose should I take?" The right question may be: "Why am I deficient in iron?"

Helicobacter pylori is one possible cause. The bacterium can promote chronic gastritis, alter the gastric environment, disrupt iron availability, and in certain situations, contribute to iron-deficiency anemia. Medical guidelines now recognize this association.

But the essential message is not that every iron deficiency originates in the stomach. The message is far more important than that: a deficiency is a result. Its cause still needs to be identified.

I am Doctor Florian A. Vallecillo Cabrera. And if I were to leave you with just one idea today, it would be this: when your body is lacking something, simply replacing it isn't always enough. Sometimes you need to understand why you are losing it, or why you are no longer absorbing it properly.

Because in medicine, correcting a number is useful. Understanding why that number is abnormal can change the entire course of care.

What to remember

  • A low ferritin is not just a number to correct: it is a signal that should prompt a search for the underlying cause of the iron deficiency.
  • Helicobacter pylori, a common stomach bacterium, can contribute to iron deficiency, sometimes without any digestive pain whatsoever.
  • Several mechanisms coexist: reduced gastric acidity (decreased absorption), competition for iron, chronic inflammation (hepcidin) and minor blood losses.
  • For an active infection, the urea breath test or stool antigen test is preferable to serology, which cannot distinguish a current infection from a past one.
  • If H. pylori is found, it is eradicated (individualised treatment, with rising resistance rates) and eradication is then confirmed, while correcting iron levels if reserves are very low.
  • Not every case of iron deficiency originates in the stomach, and not every instance of hair loss is due to low ferritin: each situation must be individualised and the underlying mechanism identified.
Doctor Florian A. Vallecillo Cabrera

Doctor Florian A. Vallecillo Cabrera

The doctor explains

Informational content, written and reviewed by Doctor Florian A. Vallecillo Cabrera. It does not replace an in-person consultation or an individual diagnosis.

Would you like a medical assessment?

Request a consultation
CallWhatsAppBook

We use cookies to improve your experience and for analytics.

+