The Role of Nutrition in Brain Development

The best possible development of a child’s cognitive, social, and emotional/behavioral skills is guaranteed. All throughout life, the brain’s cognitive, social, and emotional regions continue to develop. However, the trajectory of the brain’s growth and development varies over time. Before the age of three, the brain begins to shape most of its final structure and capacity. The identification and clarification of this particularly delicate window of time has helped public initiatives supporting healthy brain development become more focused. The implications are significant since it appears that delaying optimum brain development until later in life may have long-term effects on education, employment prospects, and adult mental health2. The “ultimate cost to society” of childhood is these long-term effects.

Three elements that have a substantial impact on early brain development stand out: the absence of toxic stress and inflammation, the existence of strong social support and a stable bond, and the supply of optimum nutrition3. This article focuses on the latter by first describing the significant aspects of brain development in late fetal and early postnatal life, going over the fundamental ideas by which nutrients control brain development during that time period, and presenting the human and pre-clinical evidence that emphasizes the significance of early life nutrient sufficiency in promoting optimal brain development.

An homogenous organ, the brain is not. Instead, it is made up of many anatomical regions and functions (including myelination), each with distinct developmental trajectories1. The developmental paths of several of these regions start out slowly and then pick up speed during foetal life or soon after birth. For instance, myelination suddenly rises from 32 weeks gestation and is most active in the first two postnatal year 1

Nutrients that Affect Brain Development

Iron

A significant function for iron in brain development has been shown in more than 50 human investigations, including observational studies, supplementation trials, and iron therapy studies 2,15. Overall, there is broad agreement that iron deficiency prevention is preferable to treatment and that the earlier the brain is protected from inadequate iron status, such as during pregnancy and the first few months of life, the better. 8 Children who had their mothers take iron/folic acid supplements while they were pregnant performed better on numerous tests of intellectual, executive, and motor function than placebo-controlled children in a series of trials conducted in Nepal30.

According to a recent 10-year follow-up study of a Chilean baby iron supplementation research, excessive iron may result in inferior neuro developmental results. In that study, children with low hemoglobin who received iron-fortified milk at 6 months of age fared considerably better on a battery of neuro developmental tests at 10 years of age than infants with high hemoglobin33. These findings highlight the fact that a nutrient can be useful at one dose or time but hazardous at another.

Myelination, the growth and operation of the dopamine, serotonin, and norepinephrine systems, as well as iron are all required for the normal morphological development of the embryonic brain 34–36. Additionally, iron alters the brain’s epigenetic structure36.

Iodine

The creation of thyroid hormone is the only function of iodine in the development of the brain. The first trimester, when foetal T3 production is completely dependent on maternal T4 supply, is the time when the developing fetal brain is most susceptible to an iodine deficit.

Cretinism, characterized by hearing, speech, and movement impairments with an IQ of about 3045, can be brought on by iodine deficiency. Children’s cognitive development improves when iodine supplementation is given to pregnant women who are at risk for iodine deficiency 45–47.

Neurogenesis, neuronal migration, glutamatergic transmission, and brain weight are all shown to be negatively impacted by prenatal iodine deficiency in preclinical investigations, while dendritogenesis, synaptogenesis, and myelination are impacted by postnatal models 48,49.

In lesser deficiencies, sensory gating, increased anxiety, and global abnormalities might be seen in addition to worse learning and memory.

Zinc

Zinc is required for healthy neurogenesis, migration, myelination, synaptogenesis, modulation of neurotransmitter release in GABA-ergic neurons, and ERK1/2 signalling, according to preclinical model 41,42, particularly in the fetal cortex, hippocampus, cerebellum, and autonomic nervous system43. Early life zinc insufficiency has behavioural effects on learning, attention, memory, and mood44.

Studies and meta-analyses It is probable because there is a large deal of variety in the effect sizes and research designs that the studies 37,38 of zinc supplementation fail to establish a substantial effect on child cognition or motor development.

The prevention of zinc shortage in early infancy, as well as the good effects of zinc when combined with iron, are revealed in individual research, however 39,40.

Protein

One of the most typical effects of malnutrition is failure to grow. It is known as intrauterine growth restriction (IUGR) in its fetal form when the foetus weighs less than the 10th percentile for gestational age. Numerous macro- and micronutrients are probably deficient in IUGR. Therefore, undernutrition in protein or energy, as well as deficits in important micronutrients, may contribute to poorer developmental outcomes after IUGR.

According to consensus panels, IUGR and postnatal growth failure during the first three years have a significant impact on neurodevelopment. Children with IUGR who were born at 35 weeks of gestation or later had worse neuro developmental scores overall, according to a recent systematic review of 38 studies17.

According to pre-clinical models of early life malnutrition, protein or protein-energy restriction causes smaller brains with lower concentrations of neurotransmitters and growth factors, fewer neurons, simpler dendritic and synaptic head architecture, and less RNA and DNA in the brains’ tissues 20,21. IUGR alters the brain’s epigenetic profile, offering a potential pathway for long-term neuro developmental effects22.

Clinical Implications

Priority should be given to screening for common nutrient deficiencies, dietary advice for women of reproductive age, and maintaining a healthy maternal body weight during the preconception phase. More over 15% of American women of reproductive age are iron-deficient50, making screening for and treating maternal iron deficit particularly high yield. Recent research showing that obesity during pregnancy poses a risk to embryonic brain development (51, 52) has made weight management and obesity reduction a focus.

The nutritional health of the embryonic brain can be impacted by non-nutritional variables such as maternal high blood pressure, diabetes mellitus, and stress during pregnancy. Maternal hypertension is the cause of 75% of IUGR cases in the United States. All newborns with IUGR have protein deficiency, and 50% of them have inadequate iron reserves at birth53. Pre-gestational or gestational diabetes mellitus complicates 10% of pregnancies, and up to 65% of babies delivered to diabetic moms have iron reserves that are below the 5th percentile54. The foetal brain is directly impacted by maternal stress, but it also changes how some nutrients are transported in the maternal-fetal dyad52.