New Ferritin Guidelines: Why 15 Was Never Normal

Is low ferritin a microbiome issue? I think partly, yes. In 2026 hematologists moved the iron deficiency cutoff from 15 to 30, so many people told their iron was fine were already running low. When iron will not come up, the problem may not be how much you take but the gate it has to pass through: a gut lining inflamed without symptoms, a hormone called hepcidin that locks iron away, gut bacteria whose chemistry decides how many iron doors get built, and fungi competing for the same atom. A depleted gut ecosystem pushes on all of them at once. Here is what the research shows in people, what so far is only in mice, and what to do with your next lab report.

Learn Something with Thaena · Episode 37 · 2026 · 22 min read

Ferritin got a new floor. What changed?

My ferritin came back at 22 and I was told my iron was fine. The lab report said fifteen and above was normal, 22 cleared it, and my fatigue was filed under something else. So many of my friends have the same story: tired, hair in the shower drain, cold hands, a report that said fine, or a system that never ran the test at all.

Ferritin is the protein your cells use to store iron, and the amount circulating in blood is the closest thing we have to a reading on your iron savings account. In August 2026 the American Society of Hematology published its first guideline on diagnosing iron deficiency, and it moved the line (Powers 2026).

The trade press has reported the four numbers. Nobody on the first page of search results explains where fifteen came from, why a lab can still print it, or what to do when you take iron and the number will not move. The first half of this article is the 101: what changed and why it matters to you. The second half is the 205: why iron sometimes cannot get in, and what your microbes have to do with it.

Where did the old cutoff of 15 come from?

One study, and it was built to answer a different question.

In 1968 and 1969, researchers in Gothenburg, Sweden drew blood from 203 randomly selected women, every one of them 38 years old, and took a bone marrow sample from each. The marrow was stained for iron. The question was not "at what ferritin does a person start running low." It was "at what ferritin is the marrow completely empty." The answer, published in 1993 after the stored serum was re-assayed, was a ferritin under 16. That cutoff caught the women with empty marrow with almost no false alarms, a specificity of 98%, and missed one in four of them, a sensitivity of 75% (Hallberg 1993). The same paper reported that signs of iron-deficient red cell production were already showing up at ferritins of 25 to 40.

In 1998 the Centers for Disease Control and Prevention defined iron deficiency as absent marrow iron, cited that Swedish study as the basis for a ferritin of 15 or below, and applied the number to everyone over six months old (CDC 1998). A 2024 analysis from the CDC's own nutrition group states the origin: the threshold was "based on a single small study of adult, nonpregnant women" (Mei 2024). The same paper notes that the World Health Organization used the same criterion, absent marrow iron, which it describes as confirming "established" iron deficiency.

So fifteen was never the point where you start running low. It was the point where the tank was already dry.

A 2021 Cochrane review pooled every study that had used bone marrow as the reference. At a threshold of 30, ferritin found 79% of the people with empty marrow and cleared 98% of those without, with low certainty in the estimate, and the thresholds proposed across those studies ranged from 12 to 200 (Garcia-Casal 2021). There was never one number, only one question, and the question was "empty," not "enough."

Why does my lab report still say 15 is normal?

Because a lab's printed reference range is not built from bone marrow at all. It is built from a crowd.

The usual method takes a large group of people who look healthy, lines up their ferritin values, and calls the middle 95% the normal range. That works if the crowd is healthy on the measure you care about. If a large share of apparently healthy women are already short on iron, and they are, the bottom of normal gets pulled down to meet them. You grade on a curve, and the whole class is short on iron.

A 2025 paper from the Cleveland Clinic ran this test on its own laboratory data. Built the usual way, the lower limit for females came out at 16.9 ng/mL. Then the authors asked at what ferritin iron deficiency shows up, using transferrin saturation and hemoglobin as the yardstick. The best cutoff for females was 45, and moving the line up improved the test's ability to find iron deficiency in females by 44% (Troike 2025).

Two separate errors, stacked. The guideline number came from marrow that was already empty. The lab number came from a population that was already low. Neither was ever a measure of where you feel well.

Is a ferritin of 30 enough?

It depends on what you are asking the number to tell you. I like to think about three ferritin numbers that answer three different questions.

The middle row is the one I find most useful, because it comes from physiology, not from a committee. When a cell is short on iron, it puts more iron receptors on its surface, the way you put up more antennas when the signal is weak, and some of those receptors break off into the blood as soluble transferrin receptor. Mei and colleagues tracked that signal alongside hemoglobin in 1,288 US pregnant women and found the point where both began to move. A threshold of 15 would have missed about one in ten women who already had physiological evidence of deficiency (Mei 2024).

The bottom row matters to anyone planning a pregnancy, and an earlier Danish cohort put the no-deficiency line even higher, at 70 (Milman 2006). I read all of this as: 30 is where you stop being deficient, and somewhere between 50 and 70 is where you have a cushion.

How common is iron deficiency without anemia?

Common enough that it should not be called a rare finding. A 2025 review in JAMA estimated that about 38% of nonpregnant women of reproductive age in high-income countries have iron deficiency without anemia, and listed celiac disease among the absorption-related causes (Auerbach 2025). More than one in three.

You can be deficient with a normal blood count because red blood cells get first claim on iron. Your body will pull iron from muscle, from the brain, from hair follicles, to keep hemoglobin in range. So hemoglobin is the last thing to fall, and a normal blood count tells you about the one compartment the body defends hardest. Non-anemic iron deficiency in otherwise healthy women has been associated with fatigue, poorer physical performance and lower work productivity (Mei 2024). An association in a group does not tell any one person what is causing her fatigue. But it is the pattern the old cutoff was built to miss.

Why can a normal ferritin still hide iron deficiency?

Because ferritin has a second job. It is an acute-phase protein: when the immune system senses a threat, ferritin rises as part of the alarm (Garcia-Casal 2021). At the same time the liver makes a hormone called hepcidin that locks iron away. It is an old defense. Bacteria need iron to grow, so during infection or inflammation the body hides iron where invaders cannot reach it. The catch is that a ferritin of 60 in someone with ongoing inflammation can be a deficiency in disguise, which is why the ASH guideline sets a different line for people with inflammation: under 100, or a transferrin saturation under 20% (Powers 2026).

The cool thing is that this defense runs locally in the gut too. In mice with colitis, immune cells called dendritic cells make their own hepcidin right in the gut wall and use it to pull iron away from the microbes nearby, and mice that could not make it healed their lining more slowly (Bessman 2020). Hold onto that. The body hiding iron from microbes is a theme that comes back.

So a low number means low. A normal number does not always mean normal. That finishes the 101.

The 205: how does iron get from food into blood?

Here is where it gets personal for me again. Lots of women eat iron, take iron, and their ferritin still will not come up. The conversation usually stops at "you must be bleeding too much" or "you must not be taking it." Sometimes that is true. But I like to think about iron as having to get through a gate, and sometimes the gate is the problem.

The gate is your gut lining. Most iron in food is in the ferric form, and it has to be converted to ferrous iron at the surface of the cells lining the upper small intestine by an enzyme called Dcytb. Then it is pulled into the cell through a door called DMT1. Then it is pushed out the back of the cell through a second door, ferroportin, into the blood, and hepcidin can shut that back door (Stoffel 2020). The lining cells themselves live only a few days. Iron that gets stuck inside one of them is shed into the stool when the cell is.

Each door is built on demand. Germ-free mice carry about ten times more DMT1 and eight times more Dcytb in their gut lining than mice with a normal microbiome (Deschemin 2016). That is the first hint that the microbes have a hand on the gate. First, though, the lining itself.

When the lining is the gate: celiac disease you cannot see on a blood test

Back in Episode 34 I wrote about celiac disease and fiber, and I said then that nobody had measured whether fixing the gut chemistry helped anyone absorb more iron. This time iron is the measurement.

A 2026 study from Spain enrolled 1,134 people, found that 538 of them, 47%, had a ferritin under 50, and fully evaluated 86 of those with a duodenal biopsy, celiac antibodies and genetic testing. None had a celiac diagnosis. Ninety-three percent were women, the median age was 41, three quarters had a ferritin under 30, and fewer than a quarter were anemic (Tarancón-Díez 2026).

Look at that last line. Low ferritin, low hepcidin, normal inflammation markers. That combination says the body wanted iron, had the back door open, and still could not get it in. That is an absorption problem, and in this cohort it mostly came without the digestive complaints that would send someone for a biopsy.

Does the lining recover? For most, yes. In a Finnish study of adults whose celiac disease was found through screening, the median ferritin roughly doubled on a gluten-free diet, from 41.5 to 86. But 21% were still under 30, and that had nothing to do with how well they stuck to the diet (Repo 2022). The lining is not the only thing standing at the gate.

When the microbes are the gate: the bacterial brake

A 2020 paper in Cell Metabolism did something simple. The researchers put two groups of mice on a diet with less than 5 parts per million of iron. One group was germ-free. The other had a normal microbiome. The mice with microbes became more anemic (Das 2020).

Then they found out how. Gut bacteria pump out small molecules all the time, and two of them, reuterin and 1,3-diaminopropane, reach into the lining cells and jam a switch called HIF-2 alpha. That switch is the master builder of the iron doors: it turns on the genes for Dcytb and DMT1 when the body needs more iron. It works only as a pair, docked to a partner protein, and the two bacterial molecules keep the halves from joining. Fewer doors get built. More iron stays locked in ferritin inside the lining cell and leaves with it when the cell is shed.

Reuterin comes from Limosilactobacillus reuteri, until recently called Lactobacillus reuteri, which you can buy in a capsule. That is the series lesson again. There are no good bugs or bad bugs. Ask what they make, and in what situation.

The situation is everything. A 2024 study tracked mice and their microbes through changing iron supply: when iron is plentiful, host and microbes cooperate, and when it is scarce, they compete (Noordine 2024). And here is the kicker from the Das paper. The same two molecules, given by mouth to mice with hemochromatosis, a genetic condition in which the body absorbs too much iron, reduced the iron overload (Das 2020).

So I do not want anyone walking away thinking their microbes are stealing their iron. The same switch that starves one mouse protects another. It looks like a safety brake. The trouble comes when the brake is stuck on in someone who is already low.

Three parties at the gate: the fungal competitor

Our gut is not only bacteria. Fungi live there too, including yeasts like Candida albicans, and they want the same atom everything else does.

Candida carries a surface protein called Als3 that helps the yeast stick to tissue and also works as a receptor for ferritin. It docks onto our own storage protein and takes the iron off it, and when the yeast is starved of iron, the amount of Als3 on its surface rises sharply, so it hunts harder (Sorgo 2013). In mice that cannot make hepcidin, Candida grew unchecked, formed more invasive filaments and did more kidney damage, and a drug that mimics hepcidin reversed it (Arekar 2025). And young mice fed a diet short on several micronutrients, iron among them, carried more fungal pathogens (Littlejohn 2023).

I like to think about this as the reason the body hides iron when it senses a threat. Three parties stand at the gate, our cells, the bacteria and the fungi, all reaching for the same atom. And all of that is mice.

Has any of this been shown in people?

Partly. The cleanest mechanism, bacteria switching off iron transporters, is in mice. In people, the pieces are arriving from several directions: the gut lining, the bacteria, and the dose.

A Spanish study of 1,030 adults that sequenced the gut metagenome and measured blood metabolites found that Klebsiella, Escherichia and a bacterial metabolite called phenylacetylglutamine tracked inversely with ferritin: more of them, lower iron stores (Rosell-Díaz 2023). A small Korean study compared 15 women with iron deficiency anemia against 16 controls, found differences in community structure, and found those differences shrank after iron treatment (Seo 2023). Neither can say which direction the arrow points. And I can find no published data in human women on whether a disrupted microbiome drives low ferritin in women who are not anemic. We may have missed a study, or it may exist only in a language I do not read. But I think it is a real question, and as far as I can tell nobody has answered it yet.

What happens to the iron you do not absorb?

It keeps going. Most of the iron in a typical supplement is never absorbed; estimates run from 80 to 90% for nonheme iron (Huey 2026). The rest lands in the colon, where the microbes get it, and iron is a growth factor for a lot of them.

The clearest experiment is in infants. In Kenya, 155 infants were randomized for four months to a micronutrient powder with no iron, 5 mg of iron, or 5 mg of iron plus 7.5 g of a prebiotic called galacto-oligosaccharides, or GOS. Anemia fell by about half in both iron groups. But the iron-alone group ended up with fewer of the bacteria the authors tracked as beneficial, more virulence and toxin genes, a higher marker of gut lining damage, and more treated respiratory infections. The group that got the prebiotic alongside the iron showed none of those differences (Paganini 2017). Other infant trials are more mixed (Baldi 2024; Huey 2026), and adding a probiotic did not help: a 2026 trial gave 307 newborns in Dhaka a Lactiplantibacillus plantarum strain, and it did nothing to fecal iron or ferritin (Khan 2026).

All of this is infants. I could not find the Kenyan design repeated in adult women. I read it as the strongest evidence we have that how iron arrives in the colon matters to the community living there.

How to take iron so more of it gets through: what the trials show

My favorite finding in the whole stack comes from Zurich.

When you take a dose of 60 mg of iron or more, your hepcidin rises and stays up for about 24 hours, then subsides by 48 (Stoffel 2020). So the next morning's pill hits a closed back door. Tuesday's pill shows up and the door is still locked from Monday.

The group tested this in women. In a 2017 trial, iron-depleted women took 60 mg doses either on consecutive days or on alternate days. The alternate-day schedule absorbed a higher fraction, 21.8% against 16.3%, and their hepcidin stayed lower (Stoffel 2017). A 2020 follow-up in 19 women who were already anemic found the same shape: absorption on the second consecutive day was 40 to 50% lower than on the days around it (Stoffel 2020).

The newest trial asked about dose size instead: thirty iron-deficient, non-anemic premenopausal women took four weeks of either 6 mg of iron twice daily on an empty stomach or 100 mg once daily with food. Gastrointestinal side effects were reported by 87% of the high-dose group and 7% of the low-dose group, and the microbiome shifted with dose (Schubert 2026). It was small and open-label, but it points the same direction: less unabsorbed iron reaching the colon.

Less iron sitting in the colon is better for the microbes, and a schedule can change how much gets through. The dose and the schedule are decisions to make with whoever is prescribing your iron, not with a blog post. Bring this to them.

Feeding the colon while you refill the tank

The Kenyan trial is the only one I know of that gave a prebiotic alongside iron and watched the microbiome, and the prebiotic was GOS. No trial has tested partially hydrolyzed guar gum, acacia, or any other fiber alongside iron supplements.

What I can tell you is why the idea is worth thinking about. Fiber is what the colon community ferments, and a community with something to ferment is a different community from one living on leftover iron. Thaena carries a fiber from our partner Dhara Therapeutics, the Gentle Prebiotic Fiber, formulated for people whose guts do not tolerate the usual high-fermentation fibers. It is partially hydrolyzed guar gum, acacia fiber and pomegranate peel extract, with no inulin, FOS, GOS, psyllium or chicory, and it is meant to be started at a quarter scoop and built up slowly. If you have read my piece on why fiber can fail, this is the kind of fiber I was pointing toward, and the pomegranate peel is the ellagitannin source from Episode 36.

It is a fiber. It is one tool in the toolbox for feeding the colon while the gate does its work, and whether it changes what happens to unabsorbed iron is an open question.

The gate is an ecosystem

Iron deficiency has been treated as simple math. Iron in, iron out. If the number is low, add iron. If it stays low, you must be losing it or not taking it.

What the papers above describe is a gate in the middle, and the gate is an ecosystem. So here is my answer to the title question. I think low ferritin is, in part, a microbiome issue. Not because one bad bacterium steals your iron, but because the same pressures that have been thinning out our gut ecosystems for generations push on every side of the gate at once.

A thinner community. People eating traditional diets carry far more microbial diversity than most of us do, as I wrote in the Canary essay linked below, and the job of a diverse community is to keep any one group from taking over. In mice, cutting iron lowered diversity and turned cooperation between host and microbes into competition (Noordine 2024). A depleted gut and a depleted iron supply can feed each other.

Lost jobs, not just lost names. Bacteria matter for what they make. In mice, two bacterial metabolites decide how many iron doors the gut lining builds (Das 2020). Which chemistry your community produces shapes how much iron gets through.

The wrong winners. Escherichia and Klebsiella are oxygen-tolerant groups that thrive in a disturbed gut. In 1,030 adults, more of them tracked with lower ferritin (Rosell-Díaz 2023). Iron you do not absorb feeds them in the colon (Paganini 2017), and fungi like Candida reach for the same atom, especially in a gut short on many nutrients at once (Littlejohn 2023).

An inflamed lining. A lining inflamed for reasons no blood test shows absorbs less, and inflammation tells the body to hide iron through hepcidin.

None of these alone explains a ferritin of 22. Together they describe a gut that is less able to pull nutrients out of food, which is the argument I made in The Canary Is Still Singing: a deficiency not of fruit, but of the ecosystem that turns food into what we need. Iron is one of the places it shows up on a lab report. The mechanisms are mostly in mice, and the human data are associations. But the pattern points the same way.

It is the lesson that runs through this whole series. The precursor is the easy part. What matters is the environment it lands in.

The honest limitations

• The microbial brake is a mouse finding. Das, Deschemin, Noordine, Bessman, Arekar and Littlejohn are all animal work. I could find no study showing that bacterial metabolites lower iron absorption in a person, and the human microbiome data are associations that cannot say which way the arrow points.
• The Spanish celiac cohort is small and selected. Eighty-six fully evaluated people, chosen for low ferritin, and the largest group is an operational category the authors call hypothesis-generating.
• The GOS trial is in infants, and the dosing trials are small. I could not find the Kenyan design repeated in adult women; I found no trial of the fiber above alongside iron; and the alternate-day finding rests on trials of nineteen and thirty women.
• I have not read the ASH guideline's full text. The thresholds come from the society's announcement and the published abstract. The strength of each recommendation and the certainty behind it are in the full paper, and I have not quoted them. The WHO statements likewise come through Mei 2024, because I could not retrieve the 2020 WHO guideline itself.

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Frequently asked questions

What is the new ferritin cutoff for iron deficiency?

The 2026 American Society of Hematology guideline sets ferritin at or below 30 ng/mL as iron deficiency for most adults, including people who menstruate and people who are pregnant, with a higher line of 50 for heavy menstrual bleeding or pregnancy with anemia and a line under 100 when inflammation is present (Powers 2026). It suggests against the older cutoff of 15.

Can you be iron deficient with a normal hemoglobin?

Yes. Red blood cells get first claim on iron, so hemoglobin is the last measure to fall. Iron deficiency without anemia is common in women of reproductive age, and cells elsewhere in the body show signs of shortage well before the blood count moves (Auerbach 2025; Mei 2024).

Why is my ferritin not going up even though I take iron?

Several reasons have been studied. Daily doses raise hepcidin, which closes the door that lets iron out of the gut lining into blood (Stoffel 2017). The lining itself can be inflamed in ways a blood test does not show; in one cohort of people with low ferritin, biopsy found celiac disease in one in seven, most without digestive symptoms (Tarancón-Díez 2026). And inflammation anywhere in the body raises hepcidin. These are questions for whoever is prescribing your iron.

Is it better to take iron every other day?

In trials from Zurich, iron-depleted women absorbed a larger fraction of each dose on an alternate-day schedule than on consecutive days, because hepcidin had time to fall between doses (Stoffel 2017). Whether that schedule is right for you depends on your situation, and it is a decision to make with your prescriber.

Do gut bacteria affect iron absorption?

Partly. In mice, metabolites made by gut bacteria block the switch that builds iron transporters in the gut lining, and mice with a microbiome became more anemic on a low-iron diet than germ-free mice (Das 2020). In people the evidence so far is association, and it runs in both directions. In 1,030 adults, some gut bacteria tracked with lower ferritin (Rosell-Díaz 2023). The microbiome of women with iron deficiency anemia looked different and shifted back after treatment (Seo 2023). And in iron-deficient women who were not anemic, the size of the iron dose changed the microbiome (Schubert 2026). What I could not find is a study testing whether the microbiome itself drives low iron stores in those women.

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The bottom line

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References

1. Powers JM, Lim MY, Achebe MO, et al. (2026). American Society of Hematology 2026 guidelines for diagnosis of iron deficiency. Blood Advances. https://doi.org/10.1182/bloodadvances.2025015950 · FREE FULL TEXT
2. Hallberg L, Bengtsson C, Lapidus L, et al. (1993). Screening for iron deficiency: an analysis based on bone‐marrow examinations and serum ferritin determinations in a population sample of women. British Journal of Haematology, 85(4):787-798. https://doi.org/10.1111/j.1365-2141.1993.tb03225.x
3. Mei Z, Addo OY, Jefferds MED, et al. (2024). Physiologically based trimester-specific serum ferritin thresholds for iron deficiency in US pregnant women. Blood Advances, 8(14):3745-3753. https://doi.org/10.1182/bloodadvances.2024013460 · FREE FULL TEXT
4. Milman N (2023). Effects of iron supplementation to iron depleted and iron replete pregnant Danish women: Defining criteria for identification of women who can manage without supplements: A randomized, placebo-controlled study. Journal of Neonatal-Perinatal Medicine, 16(3):547-562. https://doi.org/10.3233/NPM-231210 · FREE FULL TEXT
5. Das NK, Schwartz AJ, Barthel G, et al. (2020). Microbial Metabolite Signaling Is Required for Systemic Iron Homeostasis. Cell Metabolism, 31(1):115-130.e6. https://doi.org/10.1016/j.cmet.2019.10.005 · FREE FULL TEXT
6. Garcia-Casal MN, Pasricha SR, Martinez RX, et al. (2021). Serum or plasma ferritin concentration as an index of iron deficiency and overload. Cochrane Database of Systematic Reviews, 2021(5). https://doi.org/10.1002/14651858.CD011817.pub2 · FREE FULL TEXT
7. Troike KM, McShane AJ (2025). Re-evaluating ferritin thresholds to diagnose iron deficiency. Clinical Biochemistry, 140:111020. https://doi.org/10.1016/j.clinbiochem.2025.111020 · FREE FULL TEXT
8. Milman N, Byg KE, Bergholt T, et al. (2006). Body iron and individual iron prophylaxis in pregnancy: should the iron dose be adjusted according to serum ferritin?. Annals of Hematology, 85(9):567-573. https://doi.org/10.1007/s00277-006-0141-1
9. Auerbach M, DeLoughery TG, Tirnauer JS (2025). Iron Deficiency in Adults. JAMA, 333(20):1813. https://doi.org/10.1001/jama.2025.0452
10. Bessman NJ, Mathieu JRR, Renassia C, et al. (2020). Dendritic cell-derived hepcidin sequesters iron from the microbiota to promote mucosal healing. Science, 368(6487):186-189. https://doi.org/10.1126/science.aau6481 · FREE FULL TEXT
11. Stoffel NU, von Siebenthal HK, Moretti D, et al. (2020). Oral iron supplementation in iron-deficient women: How much and how often?. Molecular Aspects of Medicine, 75:100865. https://doi.org/10.1016/j.mam.2020.100865 · FREE FULL TEXT
12. Deschemin J, Noordine M, Remot A, et al. (2015). The microbiota shifts the iron sensing of intestinal cells. The FASEB Journal, 30(1):252-261. https://doi.org/10.1096/fj.15-276840
13. Tarancon-Diez L, Perez-Cabeza G, Sanchez-Mingo P, et al. (2026). The hidden link between iron deficiency and celiac disease: a clinical perspective. Frontiers in Immunology, 17. https://doi.org/10.3389/fimmu.2026.1744005 · FREE FULL TEXT
14. Repo M, Kurppa K, Huhtala H, et al. (2022). Significance of low ferritin without anaemia in screen‐detected, adult coeliac disease patients. Journal of Internal Medicine, 292(6):904-914. https://doi.org/10.1111/joim.13548 · FREE FULL TEXT
15. Noordine ML, Seyoum Y, Bruneau A, et al. (2024). The microbiota and the host organism switch between cooperation and competition based on dietary iron levels. Gut Microbes, 16(1). https://doi.org/10.1080/19490976.2024.2361660 · FREE FULL TEXT
16. Sorgo AG, Brul S, de Koster CG, et al. (2013). Iron restriction-induced adaptations in the wall proteome of Candida albicans. Microbiology, 159(Pt_8):1673-1682. https://doi.org/10.1099/mic.0.065599-0
17. Arekar T, Katikaneni D, Kasem S, et al. (2025). Essential role of hepcidin in host resistance to disseminated candidiasis. Cell Reports, 44(5):115649. https://doi.org/10.1016/j.celrep.2025.115649 · FREE FULL TEXT
18. Littlejohn PT, Metcalfe-Roach A, Cardenas Poire E, et al. (2023). Multiple micronutrient deficiencies in early life cause multi-kingdom alterations in the gut microbiome and intrinsic antibiotic resistance genes in mice. Nature Microbiology, 8(12):2392-2405. https://doi.org/10.1038/s41564-023-01519-3 · FREE FULL TEXT
19. Rosell-Díaz M, Santos-González E, Motger-Albertí A, et al. (2023). Gut microbiota links to serum ferritin and cognition. Gut Microbes, 15(2). https://doi.org/10.1080/19490976.2023.2290318 · FREE FULL TEXT
20. Seo H, Yoon SY, ul-Haq A, et al. (2023). The Effects of Iron Deficiency on the Gut Microbiota in Women of Childbearing Age. Nutrients, 15(3):691. https://doi.org/10.3390/nu15030691 · FREE FULL TEXT
21. Huey SL, Cole NL, Pagani I, et al. (2026). Effect of a complementary feeding intervention based on iron- and zinc-biofortified pearl millet on the gut microbiota in 12-18-month-old children: a randomized trial. Nature Communications, 17(1). https://doi.org/10.1038/s41467-026-75674-6 · FREE FULL TEXT
22. Paganini D, Uyoga MA, Kortman GAM, et al. (2017). Prebiotic galacto-oligosaccharides mitigate the adverse effects of iron fortification on the gut microbiome: a randomised controlled study in Kenyan infants. Gut, 66(11):1956-1967. https://doi.org/10.1136/gutjnl-2017-314418 · FREE FULL TEXT
23. Baldi A, Braat S, Hasan MI, et al. (2024). Effects of iron supplements and iron-containing micronutrient powders on the gut microbiome in Bangladeshi infants: a randomized controlled trial. Nature Communications, 15(1). https://doi.org/10.1038/s41467-024-53013-x · FREE FULL TEXT
24. Khan AZ, Roy AK, Qamar H, et al. (2026). Fecal iron quantification in a randomized controlled trial of Lactiplantibacillus plantarum ATCC 202195 in newborns in Dhaka, Bangladesh. Nutrition, 149:113221. https://doi.org/10.1016/j.nut.2026.113221 · FREE FULL TEXT
25. Stoffel NU, Cercamondi CI, Brittenham G, et al. (2017). Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: two open-label, randomised controlled trials. The Lancet Haematology, 4(11):e524-e533. https://doi.org/10.1016/S2352-3026(17)30182-5 · FREE FULL TEXT
26. Stoffel NU, Zeder C, Brittenham GM, et al. (2019). Iron absorption from supplements is greater with alternate day than with consecutive day dosing in iron-deficient anemic women. Haematologica, 105(5):1232-1239. https://doi.org/10.3324/haematol.2019.220830 · FREE FULL TEXT
27. Schubert MG, Dentand A, Karczewski M, et al. (2026). Dose-Dependent Alterations of the Human Gut Microbiome During Oral Iron Supplementation: A Randomized Study in Iron-Deficient Non-Anaemic Women. Nutrients, 18(9):1399. https://doi.org/10.3390/nu18091399 · FREE FULL TEXT