B12 deficiency affects the development of young children and the food relief we offer is not good enough

Summary: The study reveals that vitamin B12 deficiency not only causes anemia in children, but also hinders brain development and motor function.

Source: University of Copenhagen

Vitamin B12 deficiency in infants causes poor motor development and anemia, according to a study by Burkina Faso conducted by the University of Copenhagen and Doctors Without Borders. B12 deficiency is a huge but overlooked problem, and the food relief we currently offer does not help. According to researchers, the problem requires new solutions.

In Denmark, cases of poor psychomotor development are observed in young children raised on vegan diets, although these results can be prevented with daily B12 supplements. But for children in low-income countries, the chances of meeting their vitamin B12 requirements are much worse.

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

The results have been published in the well-known journal Plos Medicine.

Vitamin B12 deficiency can not only cause anemia, but can also damage the nervous system. And for young children, vitamin 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, lead author of the study and professor in the Department of Nutrition, Exercise at the University of Copenhagen. and Sports.

For many years, it has focused on vitamin A, zinc, and iron deficiencies when it comes to malnutrition worldwide, while there is little research on B12 deficiency.

“B12 deficiency is one of the most overlooked problems when it comes to malnutrition. And unfortunately we can see that the food relief we offer today is not up to par,” says Henrik Friis, who has worked for many years with nutrition and health in low-income countries.

More than 1,000 children with acute malnutrition between the ages of 6 and 23 months participated in the study. Children’s B12 levels were measured before and after three months of daily food relief rations containing the recommended B12 content. When the study began, two-thirds of the children had low or marginal B12 levels.

Short-term food relief does not fill B12 stores

“During the period when the children received food aid, their B12 levels increased, before decreasing considerably once we stopped the program. Despite having provided them with food for three months, their stores went down. “When a typical food relief program lasts only four weeks,” says Henrik Friis.

Even after three months of food relief, one-third of children still had low or marginal levels of B12 stored. The unfortunate explanation is that there is a limit to the amount of B12 that can be absorbed.

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

“In addition, long-term relief programs are unrealistic, as humanitarian organizations are trying to reduce the length of treatment regimes with the goal of being able to care for more children for the same amount of money.” continues Vibeke Brix Christensen. .

He points out that it could make a difference to divide the required amount of vitamin B12 into several meals, which would probably allow children to absorb the same amount of B12 each time. But the problem is that if there is a widespread B12 deficiency among children in low-income countries, it is difficult to do anything about it.

New solutions are needed on the table

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

Because our body cannot produce B12 on its own, we need to supply it with animal products or synthetic supplements. However, in many low-income countries, access to food of animal origin is incredibly difficult for the general population. One might ask, are pills or fortified foods the way to prevention?

“Possibly, but the problem in low-income countries is weak and under-resourced health systems. Distributing tablets to millions and millions of people is not profitable. And to enrich food with B12, it must be added to food accessible to the poor. “This requires industrial expansion, as many people now eat only what they can produce themselves. It also requires legislation that is not based on voluntary participation,” said Henrik Friis, who has more confidence in other types. of solutions:

Vitamin B12 deficiency can not only cause anemia, but can also damage the nervous system. And for young children, vitamin B12 is crucial for brain development. The image is in the public domain

“Individual households could be encouraged to have chickens and perhaps goats, which a mother could manage and use to provide access to food of animal origin. Finally, work needs to be done to develop products fermented with B12-producing bacteria, something that has not yet been done. it exists, but towards which researchers and companies are already working ”, concludes Henrik Friis.

Researchers are in talks with UNICEF’s Copenhagen-based Supply Division on how products can be improved to treat moderate to acute malnutrition.



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


  • Since 2010, the Department of Nutrition, Exercise and Sports (NEXS) at the University of Copenhagen has worked with WHO and UNICEF, among others, focusing 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 deaths of three million children each year.
  • Acute malnutrition in children is characterized by children who are too thin in proportion to their height. Worldwide, it is estimated that approximately 50 million children suffer from acute malnutrition, with two-thirds of them suffering from moderate malnutrition and the remaining third suffering from severe acute malnutrition.
  • Today, only about 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
Image: The image is in the public domain

Original research: Open Access.
“Serum cobalamin in children with moderate acute malnutrition in Burkina Faso: secondary analysis of a randomized trial” by Henrik Friis et al. PLOS Medicine


See also

This shows a mother and a baby

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


The level of serum cobalamin (SC) and the effect of dietary supplements are unknown among children with moderate acute malnutrition (MAM). Our aim is to evaluate the prevalence and correlations of low SC in children with MAM, the associations with hemoglobin and the development and effects of dietary supplements on SC.

Methods and findings

A 2 × 2 × 3 randomized factorial test was performed in Burkina Faso. Children aged 6 to 23 months with MAM received 500 kcal / day as a lipid-based nutritional supplement (LNS) or a mixture of corn and soybeans (CSB), which contained shelled soybeans (DS) or soy isolate. (SI) and 0%, 20%, or 50% of the total milk protein for 3 months.

Randomization resulted in an initial 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 from 1,192 (74.1%) of 1,609 children at baseline.

The mean age (± SD) was 12.6 (± 5.0) months and 54% were female. The lower middle arm circumference (MUAC; <125 mm) was found in 80.4% (958) of children and the z-weight score for low length (WLZ; <-2) in 70.6 % (841). Growth lag was observed at 38.2% (456). Only 5.9% were not breastfed. The median (IQR) SC was 188 (137; 259) pmol / L. Two-thirds had SC ≤222 pmol / L, which was associated with lower hemoglobin. After age and sex adjustments, very low SC (<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 lower fine and thick motor development, respectively.

SC data were available from 1,330 (85.9%) of 1,548 children followed after 3 months and 398 (26.5%) of 1,503 children after 6 months. From the tobit regression, taking into account the censored data on the left and the adjustments for the correlates of the missing data, the mean increases (95% CI) in SC from baseline to follow-up 3 and 6 months were 72 (65; 79, p <0.001) and 26 (16; 37, p <0.001) pmol / L, respectively. The changes were similar among the 310 children with SC data at 3 times. However, the increase was 39 (20; 57, p <0.001) pmol / L higher in children receiving LNS compared to CSB if based on SI (interaction, p <0.001). No milk effect was found. Four children died and no children developed an allergic reaction to the supplements.

The main limitation of this study was that only SC was available as a status marker and a quarter of children were missing.


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

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