B12 deficiency harms the development of young children and the food aid we provide is not enough

Summary: A study reveals that vitamin B12 deficiency not only leads to anemia in children, it also impairs brain development and motor function.

Source: University of Copenhagen

Vitamin B12 deficiency in infants leads to poor motor development and anemia, according to a Burkinabé study conducted by the University of Copenhagen and Médecins Sans Frontières. B12 deficiency is a huge but neglected problem, and the food aid we are currently providing is not helping. According to the researchers, the problem calls for new solutions.

In Denmark, cases of poor psychomotor development are regularly seen in young children brought up on vegan diets, although such outcomes can be prevented with daily vitamin B12 supplements. But for children in low-income countries, the odds of meeting their vitamin B12 needs are much worse.

This is reflected in widespread B12 deficiency among young children in Burkina Faso, according to a study by the University of Copenhagen conducted in collaboration with Médecins Sans Frontières.

The results were published in the renowned journal Medicine from Plos.

A lack of vitamin B12 not only leads to anemia, it can also damage the nervous system. And for young children, B12 is crucial for brain development.

“Among the many children who participated in our study, we found a strong correlation between vitamin B12 deficiency and poor motor development and anemia,” says Henrik Friis, first author of the study and professor in the Department of nutrition, exercise from the University of Copenhagen. and Sports.

For many years, the focus has been on vitamin A, zinc and iron deficiencies as they relate to malnutrition across the world, while research on vitamin B12 deficiency is sparse.

“Vitamin B12 deficiency is one of the most overlooked issues when it comes to malnutrition. And sadly, we can see that the food aid we provide today is not up to the task,” says Henrik Friis, who has worked for many years in the field of nutrition and health in low-income countries.

More than 1,000 acutely malnourished children aged 6 to 23 months participated in the study. Children’s vitamin B12 levels were measured before and after three months of daily food rations containing the recommended vitamin B12 content. At the start of the study, two-thirds of the children had low or marginal levels of vitamin B12.

Short-term food aid does not replenish B12 reserves

“During the time the children were receiving food relief, their B12 levels increased, before dropping dramatically once we stopped the program. Although they were supplied with food for three months, their reserves remained far from being filled. This, while a typical food relief program only lasts four weeks,” explains Henrik Friis.

Even after three months of relief food, a third of the children continued to have low or marginal vitamin B12 stores. The unfortunate explanation is that there is a cap on how much B12 can be absorbed.

“A child’s gut can only absorb 1 microgram of vitamin B12 per meal. So if a child is 500 micrograms short, it will take much longer than the few weeks they will have access to emergency food aid,” says Vibeke Brix Christensen, pediatrician and medical advisor at Médecins Sans Frontières. and co-author of the study. .

“Furthermore, longer-term relief programs are unrealistic as aid organizations try to reduce the length of treatment regimens in an effort to be able to serve more children for the same amount of money. “, continues Vibeke Brix Christensen. .

She points out that it might make a difference to spread the needed amount of vitamin B12 over multiple meals, which would likely allow children to get the same amount of vitamin B12 each time. But the problem is that if a widespread B12 deficiency appears in children in low-income countries, it is difficult to remedy.

New solutions needed on the table

Preventing vitamin B12 deficiency would be the best course of action. Unfortunately, sustainable solutions are not yet readily available according to Professor Friis.

Because our bodies cannot produce B12 on their own, we must obtain it through animal products or synthetic supplements. However, in many low-income countries, access to animal source foods is incredibly difficult for the general population. One wonders if pills or fortified foods are the way to prevention?

“It is possible, but the problem in low-income countries is the lack of resources and weak health care systems. Distributing tablets to millions and millions of people is not profitable. And to fortify foods with B12, it must be added to foods accessible to the poor. This requires industrial expansion, as many people currently only eat what they can produce themselves. In addition, this requires legislation that is not based on voluntary action,” explains Henrik Friis, who trusts other types of solutions more:

It shows a sad child
A lack of vitamin B12 not only leads to anemia, it can also damage the nervous system. And for young children, B12 is crucial for brain development. Image is in public domain

“Individual households could be encouraged to raise chickens and perhaps goats, which a mother could manage and use to provide access to animal-source foods. Finally, work needs to be done to develop fermented products with bacteria that produce B12, which does not yet exist, but towards which researchers and companies are already working,” concludes Henrik Friis.

Researchers are in dialogue with UNICEF’s Supply Division, based in Copenhagen, on how to improve products to treat moderate to acute malnutrition.



  • Vitamin B12 deficiency can be passed from mother to child. If a mother is deficient in B12, her child will also be born deficient in B12, before receiving breast milk containing too little B12. A child’s B12 deficiency can affect the formation and regeneration of their intestinal cells. Consequently, the child’s ability to absorb vitamin B12 and other vital nutrients will be reduced. Thus, a vitamin B12 deficiency contributes to the development of malnutrition.


  • Since 2010, the Department of Nutrition, Exercise and Sports (NEXS) at the University of Copenhagen has been working with WHO and UNICEF, among others, with a focus on improving the emergency food aid used to combat child malnutrition.
  • According to UNICEF, approximately 200 million children under the age of five suffer from malnutrition worldwide. Malnutrition contributes to the death of three million children each year.
  • Acute malnutrition in children is characterized by children who are too thin for their height. Globally, approximately 50 million children are estimated to suffer from acute malnutrition, with two-thirds suffering from moderate malnutrition and the remaining third from severe acute malnutrition.
  • Today, only around 20% of severely malnourished children receive emergency food aid.

About this diet and neurodevelopment research news

Author: Maria Hornbek
Source: University of Copenhagen
Contact: Maria Hornbek – University of Copenhagen
Picture: Image is in public domain

Original research: Free access.
Serum cobalamin in children with moderate acute malnutrition in Burkina Faso: secondary analysis of a randomized trial” by Henrik Friis et al. OLP Medicine


See also

This shows a mother and her baby

Serum cobalamin in children with moderate acute malnutrition in Burkina Faso: secondary analysis of a randomized trial


In children with moderate acute malnutrition (MAM), the level of serum cobalamin (SC) and the effect of dietary supplements are unknown. Our aim was to assess the prevalence and correlates of low CS in children with MAM, associations with hemoglobin and development, and the effects of dietary supplements on CS.

Methods and results

A 2 × 2 × 3 randomized factorial trial was conducted in Burkina Faso. Children aged 6 to 23 months with MAM received 500 kcal/d as a lipid-based nutritional supplement (LNS) or corn-soya blend (CSB), containing dehulled soy (DS) or soy isolate (SI) and 0%, 20%, or 50% total milk protein for 3 months.

Randomization resulted in baseline equivalence between intervention groups. Data on hemoglobin and development were available at baseline. SC was available at baseline and after 3 and 6 months. SC was available to 1192 (74.1%) of the 1609 children at baseline.

The mean (± SD) age was 12.6 (± 5.0) months and 54% were female. Low arm circumference (MUAC; < 125 mm) was observed in 80.4% (958) of the children and a low weight-for-height z-score (WLZ; <-2) in 70.6% (841). Growth retardation was observed in 38.2% (456). Only 5.9% were not breastfed.

The median CS (IQR) was 188 (137; 259) pmol/L. Two-thirds had an SC ≤ 222 pmol/L, which was associated with lower hemoglobin. After adjustments for age and sex, a very low CS (<112 pmol/L) was associated with 0.21 (95% CI: 0.01; 0.41, p = 0.04) and 0.24 (95% CI: 0.06, 0.42, p = 0.01) z-score of lower fine and gross motor development, respectively.

SC data were available for 1330 (85.9%) of 1548 children followed after 3 months and 398 (26.5%) of 1503 children after 6 months. Based on tobit regression, accounting for left-censored data and adjustments for correlates of missing data, the mean (95% CI) increases in SC from baseline to 3- and 6-month follow-up were 72 (65; 79, p < 0.001) and 26 (16; 37, p < 0.001) pmol/L, respectively.

Changes were similar among the 310 children with SC data at all 3 time points. Yet the increase was 39 (20; 57, p < 0.001) pmol/L greater in children who received LNS compared to CSB if based on SI (interaction, p < 0.001). No effect of milk was found. Four children died and no children developed an allergic reaction to the supplements.

The main limitation of this study was that only CS was available as a status marker and was missing in a quarter of the children.


Weak CS is common in children with MAM and may contribute to impaired erythropoiesis and child development. The increase in SC during supplementation was inadequate. The bioavailability and suitability of cobalamin in dietary supplements should be reconsidered.

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