Zinc Deficiency in Breastfed Infants

Breast milk normally carries enough zinc to cover a baby's needs for about the first six months of life. A small number of exclusively breastfed babies nonetheless develop a striking zinc-deficiency rash, usually in the first months after birth. Doctors call this transient neonatal zinc deficiency (TNZD), or transient symptomatic zinc deficiency. The word "transient" matters: in the cases that come from the milk, the problem lies with the milk and not with the baby's own body, so the baby's zinc supply usually recovers once other foods arrive. This page explains the two ways a breastfed baby can run short of zinc, the gene in the mother that is behind many of the milk cases, how the rash looks, how it differs from the lifelong inherited disease acrodermatitis enteropathica, how the diagnosis is reached, what case reports describe after zinc is given, why later brothers and sisters can be affected, and what researchers still do not know.

The broader picture of zinc-related rashes in children and adults is on the Zinc Deficiency: Skin Rashes and Acne page. This page stays with infants who are breastfed.

Table of Contents

  1. Two Ways a Breastfed Baby Runs Short of Zinc
  2. The Mother's Milk Gene: SLC30A2 and ZnT2
  3. How the Rash Looks and Where It Appears
  4. How It Differs From Acrodermatitis Enteropathica
  5. How the Diagnosis Is Reached
  6. What Case Reports Describe After Zinc Is Given
  7. Later Brothers and Sisters Can Be Affected
  8. How Common It May Be
  9. What Is Not Known
  10. Key Research Papers
  11. Connections
  12. Featured Videos

Two Ways a Breastfed Baby Runs Short of Zinc

Case reports describe two quite different routes to the same rash.

Route one: the milk itself is low in zinc. Here the baby is healthy and absorbs zinc normally, but the mother's milk contains far less zinc than usual. A 2017 review describes this form as caused by loss-of-function changes in the mother's zinc-transporter gene SLC30A2, which lead to poor secretion of zinc into breast milk; babies fed only this milk then develop severe zinc deficiency. In this route the mother herself is usually well. Several reports describe a mother whose blood zinc was normal while her milk zinc was low, for example a 2017 case from Singapore in which a 4-month-old full-term, fully breastfed boy had a low blood zinc, and his mother's milk zinc was low although her own blood zinc was normal.

Route two: the milk is normal, but the baby's needs outrun it. This route is seen mainly in babies born early. In a 2006 case from Portugal, a boy born at 27 weeks and fed breast milk from his second day of life developed the rash from his second month, even though his mother's blood and milk zinc were normal and his milk had at first been fortified with a supplement that contained zinc. The authors write that premature infants have a negative zinc balance, mainly because they are born with small stores and have high requirements. A 2007 Austrian report of a breastfed preterm boy and a 2009 Italian report of a girl born at 29 weeks likewise found normal zinc in the mother's milk. The Italian authors describe this as zinc deficiency caused by increased requirements in breastfed, mainly preterm infants, and expected it to become more frequent as more premature babies are fed breast milk only.

Some reports do not fit neatly into either route. A 2020 case from India described a 2-month-old boy whose mother had low zinc in both her blood and her milk, and both rose after the mother herself took zinc. The authors called this a non-heritable form, in contrast with the genetic form, in which the mother's milk zinc does not improve with zinc supplements. A 2012 study of 750 breastfeeding women in Shanghai also found that mothers with a body mass index above 25 secreted less zinc into their milk, which shows that factors other than genes play a part.

The Mother's Milk Gene: SLC30A2 and ZnT2

The cells that line the milk glands of the breast have to pump large amounts of zinc into milk. A 2013 Japanese paper notes that zinc levels in breast milk are considerably higher than those in the mother's blood, which means an active transport system is at work. The main pump is a protein called ZnT2, made from the gene SLC30A2.

The first family. In 2006, researchers at the University of California, Davis described a family in which two exclusively breastfed infants developed zinc deficiency, and both of their mothers had low milk zinc. Both women carried the same change in SLC30A2, called H54R, and so did several of their siblings. In cells grown in the laboratory, switching off SLC30A2 reduced zinc secretion from milk-gland cells. The authors also noted that this condition is not corrected by giving the mother zinc, which pointed to an inherited cause rather than a poor diet.

One faulty copy is enough. In 2012 an Israeli team described a second change, G87R, in two unrelated mothers whose babies had the condition. In laboratory cells, the faulty G87R pump got stuck inside the cell instead of reaching its proper place, and it also dragged the normal pump down with it, because the two copies pair up. This "dominant negative" effect explains why a mother with one normal and one faulty copy of the gene can still make low-zinc milk. A 2017 review states that this autosomal dominant inheritance is now established.

How low the milk gets. The 2013 Japanese paper reports that mothers carrying one copy of H54R or G87R secrete more than 75% less zinc into their milk. The same paper described a Japanese mother with two different changes, one on each copy of the gene (W152R and S296L), whose milk zinc was more than 90% lower and whose infant developed severe zinc deficiency.

More changes keep turning up. A 2016 study of three Japanese mothers who made low-zinc milk found a different new change in each one; every faulty pump tested was defective and unstable in cells, and of 31 common single-letter variants in the gene that the team evaluated, four caused a significant loss of zinc-transport activity, similar to the disease-causing changes. A 2023 report of three more Japanese mothers found a change in the zinc-binding site of the pump in one mother and, in the other two, multiple changes in the gene's "promoter," the stretch of DNA that controls how much of the pump is made. The authors describe these as the first reported changes in the gene's control region. The 2012 Shanghai study of 750 women linked two common SLC30A2 variants to low milk zinc, but those two variants explained only 3.23% of the differences in milk zinc between women.

How the Rash Looks and Where It Appears

The skin signs in breastfed babies look very much like those of the inherited disease acrodermatitis enteropathica, and many reports describe the two as hard or impossible to tell apart by eye. The rash follows a recognizable map:

The patches tend to be sharply edged, red, scaly or crusted, and in more severe cases eroded and weeping. Not every case looks textbook. A 2018 Canadian report described two full-term brothers and sisters whose rash took an unusual ring-shaped, raised and scaly form, and a 2026 American report described a 5-month-old whose rash looked like eczema and did not respond to the usual eczema treatment. In a 2011 German case of the inherited disease, the rash was first thought to be impetigo, a bacterial skin infection, and it did not respond to antiseptics or antibiotics; the authors note that bacterial and fungal infection on top of zinc-deficient skin is common, which makes the picture harder to read.

Signs beyond the skin. The 2017 review lists the main early signs of this condition as skin inflammation, diarrhea, hair loss and loss of appetite. The 2026 American report lists skin inflammation, hair loss, diarrhea and growth faltering, and its 5-month-old patient was admitted to hospital for growth faltering. The 2017 Singapore boy had poor weight gain and irritability alongside the rash. A 2010 report from India described a nine-month-old full-term breastfed girl with a rash on the face, the area between the legs and the arms and legs, sparse hair and diarrhea.

Timing. Because the problem comes from the milk, the signs appear while the baby is still exclusively breastfed. In the case reports cited on this page, the babies were between 2 months and 9 months old when they were seen. A 2011 Tunisian report notes that the condition has generally been reported in premature babies, but its own patient was a full-term 7-month-old.

How It Differs From Acrodermatitis Enteropathica

Acrodermatitis enteropathica is a rare inherited disease in which the baby's own gut cannot absorb zinc properly. It is caused by changes in a different gene, SLC39A4, which makes the gut zinc transporter ZIP4. The two conditions produce the same kind of rash, but they behave very differently over time. A 2015 review of the two conditions puts it plainly: acrodermatitis enteropathica is fatal if zinc is not supplied to the infant after weaning, whereas in transient neonatal zinc deficiency the defect is the mother's, and the infant usually obtains enough zinc once weaned.

FeatureZinc deficiency from low-zinc breast milkAcrodermatitis enteropathica
Gene involvedSLC30A2, which makes ZnT2, the pump that moves zinc into milkSLC39A4, which makes ZIP4, the pump that takes zinc in from the gut
Whose gene is faultyThe mother'sThe baby's
InheritanceAutosomal dominant: one faulty copy in the mother can be enoughAutosomal recessive: the baby inherits a faulty copy from each parent
When it startsDuring exclusive breastfeedingTypically around weaning, after breast milk stops
After weaningThe baby usually gets enough zinc from other foodsFatal if zinc is not supplied
Length of treatment in reportsWeeks to months, then stoppedLifelong zinc is described as the standard treatment

Why breastfeeding shields babies with the inherited disease. A 2020 Indian report describes acrodermatitis enteropathica as starting after weaning, with breastfeeding during the earlier period being protective. A 2019 German dermatology review likewise states that babies with acrodermatitis enteropathica develop signs shortly after weaning. In the 2011 German case, the first skin lesions appeared one week after weaning, in the fifth week of life, and the baby's blood zinc was 2 micromoles per litre against a normal range of 9.2 to 18.4.

The timing is a clue, not a rule. A 2010 review of 29 Tunisian children with acrodermatitis enteropathica treated between 1981 and 2008 found ages of onset from 15 days to 12 months, with a mean of 6.86 months. That overlaps the age range of breastfed babies with low-zinc milk. A 2024 Chinese report of a premature girl aged 4 months and 23 days notes that the two conditions are often confused because their rashes are so alike, and the authors propose testing the SLC39A4 gene in babies with this kind of rash; in their patient, neither the baby nor the parents carried a change in that gene.

The lines can blur. In the 2011 Tunisian case, a full-term 7-month-old from a family with a history of acrodermatitis enteropathica had low zinc in his blood, and his mother had low zinc in her blood and in her milk. Gene testing found that the baby and his mother each carried one faulty copy of SLC39A4, not two, and the diagnosis was changed from acrodermatitis enteropathica to transient symptomatic zinc deficiency.

Siblings in the inherited disease. In the 2011 German case, the same two gene changes were later found in the patient's newborn brother shortly after birth, so his zinc deficiency could be identified and treated before any signs appeared. The authors state that lifelong zinc substitution is recommended for acrodermatitis enteropathica, and a 2025 report from Bahrain on a 19-month-old girl describes lifelong zinc supplementation as the standard treatment.

How the Diagnosis Is Reached

The rash itself. The 2019 German dermatology review states that, because the lesions around the body's openings and on the hands and feet are so characteristic, dermatologists usually make the diagnosis from the clinical picture.

Blood zinc. Laboratory confirmation, according to the same review, includes measuring zinc in the blood plasma. In the 2009 Italian case, the baby's blood zinc was 0.5 mg/L against a normal range of 0.70 to 1.50 mg/L. The level is not always low, though. In a 2020 Chinese report of 16-month-old twin boys with acrodermatitis enteropathica, plasma zinc and alkaline phosphatase were both normal, and the diagnosis was made by gene testing. The 2010 Tunisian series found no significant link between blood zinc levels and how the disease looked.

Alkaline phosphatase. Alkaline phosphatase is an enzyme that needs zinc to work, and it is part of the standard Comprehensive Metabolic Panel. The 2019 review describes it as a supplementary measure. In a 2025 Canadian case of a 3-month-old breastfed girl, and in the 2026 American case, the diagnosis rested on the combination of low zinc and low alkaline phosphatase in the baby's blood.

The mother's milk. Measuring zinc in the mother's breast milk separates the milk route from the others. In the 2013 Italian case, the mother's milk zinc was lower than that of two other mothers of babies born at the same stage of pregnancy. In the 2026 American case, milk samples from the mother were compared with samples from 7 unrelated mothers; her milk zinc was 265, 144 and 46 micrograms per decilitre below the expected level at 0, 5 and 7 months after birth, against an average of 29 below expected in the comparison mothers.

Gene testing — of the mother. The 2026 American report highlights a trap. Testing usually looks at the baby, but in this condition the baby does not have to carry the mother's gene change. In their case the mother carried an SLC30A2 change of uncertain significance that was absent in the baby, and the diagnosis came from sequencing mother, father and baby together. In the 2025 Canadian case, testing of the mother also found only a variant of unknown significance, so the gene result was inconclusive.

What Case Reports Describe After Zinc Is Given

The evidence on treatment comes from case reports and small series, not from randomized trials. Across these reports, zinc given to the baby by mouth is followed by fast improvement. The 2017 review states that zinc supplementation of these babies effectively and rapidly resolves the signs, and a 2015 review states that in both transient neonatal zinc deficiency and acrodermatitis enteropathica, the signs are improved by daily oral zinc. The 2019 German review reports that oral zinc replacement frequently leads to remission within a few days.

The individual reports give a sense of the time course and of the doses used:

For comparison, the inherited disease. A 2025 review of 231 children with acrodermatitis enteropathica, drawn from 190 published articles, found zinc deficiency in 75.9% of them. Of the 174 who received zinc at various doses, 159 (91.4%) responded, and 1 to 3 mg per kilogram per day was the most commonly used effective dose. The review notes that there is no consensus on the best dose, and that zinc was often ineffective when the rash came from an underlying metabolic disorder.

Giving zinc to the mother. The 2006 Davis paper reports that the genetic form is not corrected by giving the mother zinc, and the 2012 Shanghai paper states that milk zinc is known to be independent of how much zinc the mother eats. The 2020 Indian case is the exception on record here: the mother's blood and milk zinc rose after she took zinc, which the authors took as a sign of a non-genetic form.

The doses above are the ones these case reports describe for individual babies under medical care. Decisions about zinc for an infant belong with the infant's clinician.

Later Brothers and Sisters Can Be Affected

Because the problem in the genetic form lies in the mother's milk, every baby she breastfeeds receives the same low-zinc milk. Case reports show this happening:

The 2026 American authors point out a further reach: a woman carrying a disease-causing SLC30A2 change carries a risk for her future breastfed children and for any other baby who receives her milk. They suggest that carrier screening could identify such women in advance. The 2017 review similarly proposes early genetic diagnosis, so that affected babies can receive zinc without delay.

The pattern in the inherited disease is different. There the faulty genes belong to the baby, and the 2011 German report shows a newborn brother found to carry the same two changes, and treated before signs appeared.

How Common It May Be

Transient neonatal zinc deficiency has long been described as rare. Several research groups now think it is under-recognized. The 2007 Austrian authors called it a rare but probably underrecognized disorder; the 2016 Japanese study concluded that its frequency may be higher than previously thought; and the 2017 review states that it is more frequent than initially thought, noting a growing number of cases reported worldwide.

A 2019 Israeli study tried to put a number on it. The researchers examined 115 changes in the SLC30A2 gene listed in a large public gene database, carried on 668 gene copies among 60,706 healthy people of diverse ethnicity. Using computer prediction and laboratory zinc-transport tests, they found 14 changes that markedly damaged zinc transport. Together with two other clearly damaging changes, 26 gene copies carried harmful changes, which the authors interpreted as suggesting that at least 1 in 2,334 newborn infants is at risk of developing the condition. This figure is a calculated estimate from gene data, not a count of sick babies. The 2026 American authors describe the true frequency of disease-causing SLC30A2 changes as unclear.

What Is Not Known

Key Research Papers

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PubMed Topic Searches

  1. PubMed: Transient neonatal zinc deficiency
  2. PubMed: SLC30A2 (ZnT2) and breast milk zinc
  3. PubMed: Zinc deficiency in breastfed preterm infants
  4. PubMed: Acrodermatitis enteropathica and SLC39A4

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