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Effects of vitamin B 6 deficiency on morphological changes in dendritic trees in Purkinje cells in developing cerebellum in rats. High protein and energy drink with increased amounts of micronutrients versus moderate protein and energy drink with standard amounts of micronutrients. However, among three randomized trials of maternal iron supplementation during pregnancy that measured subsequent cognitive development of the children, only one showed positive results. Seven weeks after conception, cell division begins within the neural tube, creating nerve cells neurons and glial cells cells that support neurons. Fatty acids are structural components of myelin.
Nutrition Reviews, vol 72 4 , pp The following provides a short summary of each of these important research studies. A fuller summary of each can be found online at www. What are the current issues regarding nutrition and cognitive abilities of children in especially in Africa, as it seems this continent has not seen much of Global What we know already: Early child development ECD is a key predictor of future social capital and national productivity. Below are short summaries of the recently launched Lancet series of papers on Maternal and Child Undernutrition1.
This high profile series focuses on the disease burden A life cycle approach would be preferable that can break the inter-generation of malnutrition. Summary of research1 Location: Colombia What we know: Poverty and the associated poor nutrition and lack of psychosocial stimulation are associated with poor child This is a little off topic but I am hoping that someone here might know the answer I've read in various places that stunting as a result of nutritional deprivation is Has anyone done any work on adolescent nutrition?
What areas where considered and what indicators were used. I would appreciate reference materials too sorry, the correct Summary of report1 The Saharawi refugee population approximately , living in south Algeria have been in crisis since when conflict over the status of Western Tanya Khara worked as an ENN consultant on the project.
Micronutrients are essential for life and are distinct from macronutrients Summary of published research1 A malnourished child in a therapeutic feeding centre in Kenema Sierra Leone suffers from endemic and pervasive poverty due to long periods of Global What we know: Poor nutrition carries a significant economic burden at individual, national and global levels and prevents poverty Also, undernourished children may be frequently ill and therefore fussy, irritable, and withdrawn, leading caregivers to treat them more negatively than they would treat a happy, healthy child.
Reduced activity due to undernutrition may limit the child's exploration of the environment and initiation of caregiver interactions, which could also lead to poor brain development.
Hypothetical scenario in which the child's experience acts as a mediator between nutritional status and motor, cognitive, and socioemotional development. Adapted from Levitsky and Barnes 58 and Pollitt. Few studies have examined the potential additive, interacting, and mediating effects of nutrition and experiential input from the environment on child motor, cognitive, and socioemotional development.
Studies that have tested all of these in a systematic way could not be located in the existing literature. In future research, datasets that allow the testing of each of these hypotheses are needed. Nutrient deficiency is more likely to impair brain development if the deficiency occurs during a time period when the need for that nutrient for neurodevelopment is high. Various nutrients are necessary for specific neurodevelopmental processes. Each process occurs in different, overlapping time periods in different brain areas.
The timing of five key neurodevelopmental processes is presented in the first row of Table 1. Drawing links between specific nutrients, specific neurodevelopmental processes, and the time period of deprivation or supplementation allows specific hypotheses to be made concerning the effect of nutrient deprivation or supplementation on brain development. For example, myelination of the brainstem auditory pathway occurs from week 26 of gestation until at least 1 year after birth.
This leads to the hypothesis that supplementation with DHA in the third trimester and the first year after birth may improve myelination of this auditory pathway. The latency of auditory-evoked potentials, which measure electrical activity in response to an auditory stimulus through electrodes placed on the scalp, is thought to reflect myelination, among other physiological aspects of brain function.
Much evidence shows that brain development may be compromised when nutrient deficiency is severe to moderate but spared when deficiency is mild to moderate. A number of homeostatic mechanisms protect the developing fetus and the developing brain from nutrient deficiency to a certain degree. For example, in the case of placental insufficiency, when insufficient nutrients and oxygen are available, fetal cardiac output is redistributed such that blood flow to the peripheral tissues decreases and blood flow to the brain, adrenal glands, and heart increases.
This leads to brain sparing, or the sparing of brain growth even when overall fetal growth is reduced. Exactly where this line is drawn is an important question which must be answered for each nutrient individually. Several studies have shown that the effect of nutritional supplementation on brain development depends on initial nutritional status.
For example, in Bangladesh and Indonesia, a positive effect of maternal multiple micronutrient supplementation during pregnancy and postpartum on child motor and cognitive development was found only in children of undernourished mothers.
Even if the timing and the degree of nutrient deficiency are sufficient to alter brain development, one important question is whether these changes can be subsequently corrected. If not, children undernourished in early life would show permanent developmental deficits.
On the other hand, if some or all of these structural alterations can be corrected, children could partly or fully recover cognitive ability. The brain's potential for recovery from early damage has been widely studied in the context of neurological injury during development. When a certain part of the brain is damaged during early life, recovery happens in three ways, depending on the timing of the injury and subsequent experience.
First, there are changes in the organization of the remaining intact circuits in the brain that were left uninjured, involving the generation of new synapses in existing pathways. Second, new circuitry that did not exist before the injury develops.
Third, neurons and glia are generated to replace the injured neurons and glia. In addition to nutrient repletion, enhanced sensory, linguistic, and social interactions may also facilitate recovery.
Data from a group of Korean orphans adopted by middle-class American families provided an opportunity to investigate the possibility of recovery. Children who were undernourished at the time of adoption before age 2 years did not score below the normal range on IQ tests at school age, but their scores were lower than those of Korean adoptees who had not been undernourished in infancy.
Other investigators have studied adults who were born during a period of famine in Holland during World War II when strict food rations were imposed on the entire Dutch population, including pregnant women.
Children born during this period experienced nutrient deprivation in utero but adequate nutrition and health care thereafter. At age 19 years, their average IQ did not differ from that of a group whose mothers did not experience famine during pregnancy.
In these studies, the role of improved nutrition and the role of stimulation from the environment in recovery cannot be distinguished. Other evidence suggests that both of these can contribute to cognitive recovery after early undernutrition. The selection of assessment tools and the age of assessment can also influence whether effects are found in nutrition studies. Global measures, such as the Bayley Scales of Infant Development BSID or IQ tests, are widely used but may be less sensitive to nutritional deficiency than tests of specific cognitive abilities.
Detecting the effects of early nutrient deficiency can also depend on the age of cognitive assessment. For example, a group of children who experienced thiamine deficiency in infancy did not show neurological symptoms at the time of deficiency, but showed language impairment at age 5—7 years. In summary, the long-term effect of nutritional deficiency on brain development depends on the timing and degree of deficiency, as well as the quality of the child's environment.
Recovery is possible with nutrient repletion during a time period when the affected neurodevelopmental process is ongoing and with enhanced interaction with caregivers and other aspects of the environment.
As shown in Table 1 , research in animals has demonstrated the effects of many specific nutrient deficiencies on the development of brain structure and function. However, studies examining the effect of mild to moderate undernutrition on brain development in free-living mothers and children have largely shown mixed or inconclusive results. The factors discussed such as the timing and degree of deficiency and interactions with the amount of stimulation children receive may account for some of these mixed results.
In addition, in many studies, undernutrition is confounded by other factors such as poverty, unstimulating environments, little maternal education, poor healthcare, and preterm birth, which make it difficult to isolate the effects of nutrition. To do this, randomized controlled trials are needed, but few of these specifically examining neurobehavioral outcomes have been conducted.
Many studies have compared school-age children who had suffered from an episode of severe acute malnutrition in the first few years of life to matched controls or siblings who had not. These studies generally showed that those who had suffered from early malnutrition had poorer IQ levels, cognitive function, and school achievement, as well as greater behavioral problems. Chronic malnutrition, as measured by physical growth that is far below average for a child's age, is also associated with reduced cognitive and motor development.
From the first year of life through school age, children who are short for their age stunted or underweight for their age score lower than their normal-sized peers on average in cognitive and motor tasks and in school achievement.
Growth faltering can begin before birth, and the evidence indicates that being born small for gestational age is associated with mild to moderately low performance in school during childhood and adolescence, and with lower psychological and intellectual performance in young adulthood. As discussed earlier, certain protective factors after birth may reduce the risk of long-term effects of low birth weight, such as high socioeconomic status, 52 cognitive stimulation in early life, 81 catch-up growth in height, and increased duration of breastfeeding.
One well-controlled study showed cognitive deficits at 7 years of age in children who had been low-birth-weight infants compared to their normal-birth-weight siblings only if head growth was also compromised. This evidence shows that severe acute malnutrition and chronic malnutrition are clearly associated with impaired cognitive development, while the effects of growth faltering before birth are less clear and may be amenable to cognitive recovery.
Children who experience severe acute malnutrition, chronic malnutrition, and low birth weight tend to face other disadvantages that also affect brain development, such as poverty, poor housing and sanitation, poor healthcare, and less stimulating home environments, making it difficult to draw a causal link from observational studies.
The results of randomized trials of maternal and child food supplementation, which provide stronger evidence of causation, are mixed Table 2. Such trials that provided supplements to both mothers during pregnancy and children throughout the first 2 years of life showed the strongest evidence for long-term positive effects regarding cognition. In a large trial in Guatemala, pregnant women and their children up to the age of 7 years were provided with a milk-based high protein and energy drink with micronutrients or a low protein and energy drink with micronutrients.
In contrast, few long-term effects have been reported when supplementation was provided only to mothers or only to children, though some such trials have demonstrated short-term cognitive and motor effects Table 2. Apart from the trial in Guatemala, only a trial in Jamaica conducted longitudinal assessment at multiple time points throughout childhood and adolescence Table 2. Although this trial did not show long-term effects of the nutrition component of the intervention, the psychosocial stimulation component resulted in sustained effects on IQ, language, and reading ability up to 18 years of age.
They indicated that beginning supplementation at an earlier age or achieving higher compliance with supplement consumption may have resulted in more lasting effects. Together, this evidence suggests that adequate nutrition during pregnancy and throughout infancy is necessary for optimal cognitive development.
However, the most effective timing for nutritional supplementation is not yet clear, since few randomized trials have been conducted and even fewer have evaluated cognition and other outcomes in adolescence and adulthood. Breastfeeding may improve cognitive development through several potential mechanisms, related both to the composition of breast milk and to the experience of breastfeeding.
A suite of nutrients, growth factors, and hormones that are important for brain development are abundant in breastmilk, including critical building blocks such as DHA and choline. Breastfeeding also elicits a hormonal response in mothers during each feeding session, which may reduce stress and depression and thus improve infant caregiving and mother-infant interaction.
In high-income countries, children who are breastfed as infants tend to have higher IQs at school-age than children fed with formula. This problem of confounding is less likely in low- and middle-income countries. For example, among a group of mothers in the Philippines, those from the poorest environments breastfed the longest and in two separate cohorts in Brazil, socioeconomic status was unrelated to breastfeeding practices. Together, these positive associations between longer duration of breastfeeding and higher IQ and school achievement, after controlling for potential confounders, support the idea that a causal relationship exists.
The strongest evidence supporting the conclusion that breastfeeding is beneficial for brain development is from a large cluster-randomized trial in Belarus. Mothers in the breastfeeding promotion group had higher rates of any breastfeeding from birth to 12 months of age and higher rates of exclusive breastfeeding when the infants were 3 months of age.
At a subsequent follow-up mean age, 6. This evidence indicates that promotion of breastfeeding can be an effective strategy to improve children's cognitive development. As shown in Table 1 , essential fatty acids EFA and their derivatives are important for membrane function, synapse function, and myelination.
Researchers have examined whether feeding infants formula containing these fatty acids positively affects cognitive development compared to standard formula that does not contain them. The authors of two recent papers, the first reporting a review and the second a meta-analysis of randomized controlled trials, concluded that EFA-containing formula does not affect general neurobehavioral development in full-term infants. Note that most of the studies included in these two papers examined the effects on BSID scores.
As discussed above, a recently published study showed a positive effect of EFA-containing formula on vocabulary and IQ at the age of 5—6 years even when no effect on month BSID scores was found: However, very little research has been conducted in these countries. Studies in Turkey, Ghana, and China suggest that supplementation with EFA may affect infant neurodevelopment 65 and motor development.
Similarly, the latter trial was conducted in an area near Lake Malawi, where maternal fish consumption may result in relatively high levels of key fatty acids in breast milk, possibly masking any effects of supplementary EFA. The effect of EFA on brain development during pregnancy is also not yet clear. While fatty acids are important for fetal neurodevelopment, randomized trials of maternal EFA supplementation have yielded mixed results.
The meta-analysis on cognitive, language, and motor scores revealed no differences between supplemented and control children from birth to age 12 years, except for cognitive scores in children between the ages of 2 and 5 years. The authors concluded that methodological limitations in the 11 trials reviewed precluded confidence in the results; therefore, additional methodologically sound studies are needed, especially in children from disadvantaged or low-income backgrounds.
Micronutrient deficiency is a critical concern for mothers and children throughout the world. Iron is an essential structural component of the hemoglobin molecule, which transports oxygen to all the organs of the body, including the brain.
IDA, that is, underproduction of hemoglobin due to iron deficiency, is a risk factor for both short-term and long-term cognitive impairment. IDA during infancy is associated with poor mental and motor development and during later childhood, with poor cognition and school achievement.
Longitudinal studies have also consistently demonstrated that children who had been anemic before 2 years of age continued to show deficits in cognition and school achievement from 4 to 19 years of age. These long-term effects of infant IDA may persist even if iron treatment is provided during infancy. In longitudinal studies, adolescents who had been iron-deficient anemic in infancy continued to score lower than their non-anemic peers in IQ, social problems, and inattention, even though they were given iron treatment as infants.
Prenatal iron supplementation may prevent some of these deficits. However, among three randomized trials of maternal iron supplementation during pregnancy that measured subsequent cognitive development of the children, only one showed positive results. Provision of iron to infants in low- and middle-income countries, where rates of iron deficiency are usually high, has consistently led to improved outcomes at the end of the intervention period.
These trials are different from treatment trials in that all children are included, even if they have not been diagnosed with IDA, and the dose of iron is lower. However, two recent follow-up studies reported no effect of iron supplementation in infancy on motor and cognitive ability at age 3.
Further long-term follow-up studies that examine cognitive, motor, and socioemotional skills are needed. Importantly, the provision of iron in malaria-endemic regions should be accompanied by adequate malaria surveillance and treatment. Taken as a whole, the evidence indicates that IDA during infancy is a strong risk factor for cognitive, motor, and socioemotional impairment in both the short and long term.
Avoiding such consequences may require control of iron deficiency before it becomes severe or chronic, starting with adequate maternal iron intake before and during pregnancy and delayed cord clamping at birth.
Iodine is necessary for the synthesis of thyroid hormones, which are essential for central nervous system development, including neurogenesis, neuronal migration, axon and dendrite growth, synaptogenesis, and myelination Table 1.
Pregnant women with severe iodine deficiency may underproduce thyroid hormones, leading to cretinism in the child. Cretinism is a disorder characterized by mental retardation, facial deformities, deaf-mutism, and severely stunted growth. Cretinism cannot be reversed after birth but can be prevented by the correction of iodine deficiency before conception.
Even in the absence of overt cretinism, the evidence suggests that chronic iodine deficiency negatively affects intelligence. A meta-analysis showed a Although striking, these correlational studies may be confounded by uncontrolled factors, and randomized controlled trials of iodine supplementation in school-age children have yielded inconsistent results.
Pregnancy seems to be a sensitive period with regard to the effects of iodine deficiency on neurodevelopment, since cretinism develops during this period. In an iodine-deficient region in China, 4—7-year-old children whose mothers were given iodine during pregnancy performed better on a psychomotor test than those who were supplemented beginning at 2 years of age. Among over 1, 8-year-old children in the UK, those whose mothers had been iodine deficient in the first trimester of pregnancy were more likely to have scores in the lowest quartile for verbal IQ and reading comprehension.
The authors concluded that additional well-designed randomized controlled trials are needed to quantify more precisely the contribution of iodine deficiency to brain development in young children, including trials examining iodized salt.
Though few well-designed controlled studies have been reported, adequate iodine intake is clearly necessary for normal brain development. Prevention of iodine deficiency, especially for pregnant mothers, is an important way to promote healthy brain development in children worldwide.
Zinc is the fourth most abundant ion in the brain, where it contributes to brain structure and function through its role in DNA and RNA synthesis and the metabolism of protein, carbohydrates, and fat. Randomized trials of zinc supplementation during pregnancy in the United States, Peru, Nepal, and Bangladesh have shown no effects , , or negative effects of zinc compared to placebo or other micronutrients on the motor and cognitive abilities of children between the ages of 13 months and 9 years.
Similarly, infant zinc supplementation has not been demonstrated to improve cognitive development. Four of these provided zinc with or without iron or other micronutrients , , — and one provided zinc with or without psychosocial stimulation. In these nine trials, positive effects on motor development were more commonly found. Four of the trials showed that zinc supplementation improved motor development, 56 , , , though one of these found an effect on the motor quality rating of the Bayley Behavior Rating Scale rather than on the Bayley Motor score, and another showed an impact of zinc only when given in combination with iron.
Two other trials in India and Guatemala indicated that zinc supplementation in children under 2 years of age increased activity levels. The available evidence suggests that zinc supplementation during pregnancy does not seem to improve childhood cognitive or motor development.
Zinc supplementation during infancy may positively affect motor development and activity levels, but it does not seem to affect early cognitive ability. A meta-analysis of randomized controlled trials of zinc supplementation in infants did not find any evidence of impact on BSID mental or motor scores; however, the authors concluded that the number of available studies is still relatively small, and the duration of supplementation in these studies may be too short to permit detection of such effects.
Like zinc, B-vitamins, including thiamine, are important for brain development and function through many mechanisms. They play a role in carbohydrate metabolism which helps to provide the brain's energy supply , membrane structure and function, and synapse formation and function. In high-income countries, thiamine deficiency in infants has become a rare condition since food has been enriched with thiamine.
However, recent evidence suggests that the prevalence of thiamine deficiency may be relatively high in some low-income countries. Of infants who were admitted to a hospital in Laos without clinical signs of thiamine deficiency, These children showed impaired language ability compared to control children at 5 years of age, even though they had not displayed any neurological symptoms during infancy.
Other observational studies have demonstrated associations between infant development and maternal niacin and vitamin B 6 intake during pregnancy, maternal riboflavin, niacin, and vitamin B 6 intake during lactation, and infant cobalamin and folate status. Individuals who are deficient in one micronutrient are commonly at risk for deficiencies in others as well. Supplementation with any single micronutrient may not affect cognitive and motor development in individuals who are also deficient in other micronutrients.
In these groups, supplementation with multiple micronutrients may be more beneficial than supplementation with a single micronutrient. The conversion of EFAs to DHA also depends on certain micronutrients and, thus, micronutrient deficiency may influence development through fatty acid status.
Three randomized trials have reported positive effects of multiple micronutrient supplementation during pregnancy on child development between the ages of 6 and 18 months, including motor development in Bangladesh and Tanzania 70 , and cognitive development in China.
As described above, children of mothers in this same study in Nepal who received iron, folic acid, and vitamin A scored higher than those whose mothers received vitamin A alone on five of six cognitive and motor tests. Studies of multiple micronutrient supplementation during infancy have shown some benefits immediately after the supplementation period.
Three randomized trials in Ghana, China, and South Africa demonstrated positive effects on motor development in children between the ages of 12 and 18 months , , and one trial also showed an effect on the overall developmental quotient. When a child is adequately nourished from conception through infancy, the essential energy, protein, fatty acids, and micronutrients necessary for brain development are available during this foundational period, establishing the basis for lifetime brain function.
The well-nourished child is also better able to interact with his or her caregivers and environment in a way that provides the experiences necessary for optimal brain development. Children who are not adequately nourished are at risk for failing to reach their developmental potential in cognitive, motor, and socioemotional abilities. These abilities are strongly linked to academic achievement and economic productivity. Therefore, preventing or reversing developmental losses in early childhood is crucial for fostering economic development in low- and middle-income countries as well as reducing economic disparities in high-income countries.
The evidence is clear that the following conditions are key risk factors for poor motor, cognitive, and socioemotional development: Preventing these conditions should be a global health priority. The following interventions are examples of strategies that have been found to be effective in preventing or improving these conditions: Strategies to promote exclusive breastfeeding during the first 6 months of life and continued breastfeeding thereafter, along with adequate complementary feeding, are also likely to improve cognitive development, though additional evidence for the effectiveness of these strategies is also needed.
Children in food-insecure homes are actually more likely than other children to be overweight. This is often called the hunger-obesity paradox. This pattern appears early in life. Parents facing a shortage of food may encourage their children to eat cheaper, more energy-dense foods. Families may develop a tendency to overeat during periods when food is plentiful. Nutritional shortages during pregnancy and in the early years of life may promote obesity by causing metabolic changes in how energy is used and stored.
Irregular eating patterns can disrupt brain networks involved in energy regulation and hunger signals. Food insecurity is not restricted to families in poverty. Nationally, about 40 percent of poor families are food-insecure, but many poor families avoid food insecurity through the assistance of safety net programs, charitable organizations, and other resources not included in the federal poverty measure.
At the same time, many food-insecure families have incomes well above the poverty line. Low-income families—families with incomes above poverty but below percent of the poverty line—face many of the same difficulties that poor families face, including food insecurity. Moreover, their higher incomes may make them ineligible for many forms of assistance that are available to families in poverty.
Children in food-insecure families are likely to have unhealthy diets and inconsistent eating habits, placing them at risk for cognitive impairment, obesity, and other long-term problems. Effects of prenatal protein malnutrition on the hippocampal formation. Neuroscience and Biobehavioral Reviews. Household food insecurity is a risk factor for iron-deficiency anaemia in a multi-ethnic, low-income sample of infants and toddlers.
Understanding the role of nutrition in the brain and behavioral development of toddlers and preschool children: