B12 deficiency impairs the development of young children and the food aid we provide is insufficient

Summary: Studies show that vitamin B12 deficiency not only leads to anemia in children, but also interferes with brain development and movement.

A source: University of Copenhagen

According to a study conducted by the University of Copenhagen and Médecins Sans Frontières in Burkina Faso, vitamin B12 deficiency in infants leads to poor motor development and anemia. B12 deficiency is a major but neglected problem and the food we currently provide does not help. Researchers say the problem requires new solutions.

In Denmark, poor psychomotor development is common in young children on a vegetarian diet, but such effects can be prevented daily with B12 supplements. In low-income countries, children are less likely to meet vitamin B12 requirements.

According to a joint study by Doctors Without Borders at the University of Copenhagen, this is reflected in the prevalence of B12 deficiency among young children in Burkina Faso.

The results were published in a popular magazine Plos Medicine.

Vitamin B12 deficiency can not only lead to anemia, but also damage the nervous system. And for young children, B12 is very important for brain development.

“Among the many children in our study, we found a strong correlation between vitamin B12 deficiency and poor motor development and anemia,” said Henrik Fries, the study’s first author and professor of nutrition and exercise at the University of Copenhagen. and Sports.

For many years, vitamin A, zinc, and iron deficiencies have been the focus of nutrition around the world, and there are few studies on B12 deficiency.

“B12 deficiency is one of the problems that goes unnoticed during a poor diet. “Unfortunately, the food aid we provide today is inadequate,” said Henrik Fries, who has worked in nutrition and health in low-income countries for many years.

The study involved more than 1,000 malnourished children aged 6-23 months. Children’s B12 levels were measured before and after three months of the daily diet containing the recommended B12 content. At the start of the study, two-thirds of the children had low or limited levels of B12.

Short-term food aid does not replenish B12 stores

“Their B12 levels increased during the period when the children were provided with food, but it dropped significantly after we stopped the program. Despite providing them with food for three months, their stores were not replenished. This regular food aid program only lasts four weeks, ”said Henrik Fries.

Even after three months of feeding, one-third of children had low or limited levels of B12. Unfortunately, there is a limit to which B12 can be digested.

“A baby’s intestines can only absorb 1 microgram of B12 when they eat. So if a child is short of 500 micrograms, it will take more than a few weeks for them to get to the emergency room, ”said Vibeke Brix Christensen, a pediatrician and medical consultant at Médecins Sans Frontières and author of the study.

“Furthermore, long-term care programs are unrealistic, and humanitarian organizations are trying to reduce the duration of treatment to serve more children for the same amount of money,” said Vibeke Brix Christensen.

According to him, dividing the required amount of vitamin B12 into several meals will probably allow children to absorb the same amount of vitamin B12 each time. But the problem is that if B12 deficiency occurs among children in low-income countries, it is difficult to do anything about it.

New solutions needed on the table

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

Because our bodies cannot produce B12 on their own, we need to give it through animal products or synthetic supplements. However, in many low-income countries, access to animal food is incredibly difficult for the general population. Are pills or fortified foods a way to prevent it?

“It may be, but in low-income countries, the problem is poor resources and a poor health care system. It is not economical to give tablets to millions of people. In order to enrich food with B12, it should be added to the food available to the poor. This requires the expansion of the industry, because many people now eat only what they produce. In addition, it requires laws that are not based on voluntary participation, ”said Henrik Fries, who is more confident in other types of decisions.

Vitamin B12 deficiency can not only lead to anemia, but also damage the nervous system. And for young children, B12 is very important for brain development. Image in public domain

“Private households can be encouraged to raise chickens and goats, which can be managed by the mother and provide access to animal feed. Finally, work needs to be done to develop products fermented with B12-producing bacteria – this is not yet the case, but researchers and companies are already working on it, ”concludes Henrik Fries.

Researchers are in a dialogue with UNICEF’s Copenhagen-based Delivery Unit on how to improve products to treat moderate to acute malnutrition.

Notes:

KYRGYZ AIRAM

  • B12 deficiency can be passed from mother to child. If the mother is deficient in B12, her baby will be born deficient in B12, and B12 is very low in breast milk. B12 deficiency in children affects the formation and regeneration of their intestinal cells. Consequently, the child’s ability to absorb B12 and other important nutrients decreases. Thus, B12 deficiency contributes to the development of malnutrition.

ABOUT SPICY FOOD

  • Since 2010, the Department of Nutrition, Exercise and Sport (NEXS) at the University of Copenhagen has been working with WHO and UNICEF to focus on improving emergency food aid used to combat malnutrition in children.
  • According to UNICEF, an estimated 200 million children under the age of five worldwide are malnourished. Malnutrition kills three million children every year.
  • Acute malnutrition in children is characterized by very thin children depending on their height. Globally, an estimated 50 million children are malnourished, two-thirds with moderate malnutrition and one-third with severe malnutrition.
  • Today, only about 20% of malnourished children receive emergency food assistance.

It’s about diet and neuronal development research reports

Author: Maria Hornbeck
A source: University of Copenhagen
The connection: Maria Hornbeck – University of Copenhagen
Photo: Image in public domain

Original study: Open access.
“Cobalamin in serum of moderately malnourished children in Burkina Faso: a secondary analysis of a randomized trial” by Henrik Fries et al. PLOS Medicine


Abstract

See also

It shows the mother and child

Cobalamin yolk in children with moderate acute malnutrition in Burkina Faso: a secondary analysis of a randomized trial

Background

Serum cobalamin (CC) levels and effects of dietary supplements are unknown among children with moderate acute malnutrition (MAM). We aimed to assess the prevalence and correlation of SC in children with MAM, its association with hemoglobin and development, and the effect of dietary supplements on SC.

Methods and findings

A randomized 2 × 2 × 3 factor test was performed in Burkina Faso. Children from 6 months to 23 months with MAM are 500 kcal / day lipid-based nutritional supplement (LNS) or corn-soy mixture (CSB), containing peeled soy (DS) or soy isolate (SI) and 0%, 20%, or It makes up 50 percent of the total protein in milk for 3 months.

Randomization has led to a basic equivalence between intervention groups. Data on hemoglobin and development were initial. SC was initial and available after 3 and 6 months. SC was available for 1,192 (74.1%) of the initial 1,609 children.

The mean (± SD) age was 12.6 (± 5.0) months and 54% were women. Low mid-upper arm circumference (MUAC; <125 mm) was found to have a longitudinal z-score (WLZ; <−2) for low weight in 80.4% (958) and 70.6% (841) of children. Stunting was observed in 38.2% (456). Only 5.9% did not breastfeed.

The median (IQR) SC was 188 (137; 259) pmol / L. Two-thirds had SC ≤222 pmol / L, which was associated with low hemoglobin. After age and sex adjustment, 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-points, fine and coarse motor development, respectively.

SC data were available from 1,330 (85.9%) of 1,548 children observed after 3 months and from 398 (26.5%) of 1,503 children after 6 months. Based on Tobit regression, left censored data accounting, and correlation of missing data, the mean (95% CI) in the SC ranged from baseline to 3 and 6 months of observation at 72 (65; 79, P <0.001) and 26 (16; 37, P <0.001) pmol / L, respectively.

The changes were similar among 310 children who had SC data at all 3 time points. However, growth 39 (20; 57, P <0.001) Smol (interaction, if pmol / L is greater in children given LNS, if P <0.001). No effect of milk was found. Four children died and none had an allergic reaction to the supplements.

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

Conclusions

Low SC is common among children with MAM and can contribute to erythropoiesis disorders and child development. During the addition, the increase in SC was insufficient. The bioavailability and adequacy of cobalamin in food supplements should be reconsidered.

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