It is quite difficult to briefly outline all the factors that influence a child’s cognitive development—specialists on this topic are given a year-long course of lectures at universities. But we can identify several main ones, which play a decisive role in the development of the child as an individual (and, consequently, his future fate) and at the same time are entirely dependent on the parents.
Personality development factors
All factors that in one way or another influence the emotional and intellectual development of a child can be divided into 2 large groups: organic and sociocultural. Organic factors include genetic inclinations that a child inherits from his parents. Of course, this heredity is not unconditional and largely depends on how the pregnancy proceeded. Continuous stress, bad habits of the mother, lack of oxygen and nutrients and other potentially dangerous circumstances of the child’s intrauterine development can subsequently lead to various pathologies in his mental and personal development.
A good socioeconomic status means that parents have enough time and money at their disposal to provide their child with everything necessary for his successful mental development - first of all, their attention.
But no less important in the formation of a healthy emotional and intellectual constitution of a child is his social environment, which is primarily characterized by such a concept as socioeconomic status. Despite the definition of “economic” in the name of this factor, it has a very indirect relationship to the material well-being of the family, although it is partly determined by it. A good socioeconomic status means that parents have enough time and money at their disposal to provide their child with everything necessary for his successful mental development - first of all, their attention. If parents are constantly busy with their own affairs - regardless of whether they make ends meet, working three jobs, or are focused on their own career in a large and successful company - and pay critically little attention to communication with their child, this will inevitably affect on its development in a negative way. That is, socioeconomic status as a factor of cognitive development means the ability of parents to provide their child with due attention, to be sensitive to not only his material, but also emotional needs.
What plays a decisive role: heredity or social environment?
The role of parents in shaping the child’s personality
The formation of cognitive abilities, although genetically determined, does not occur without the participation of parents. Unfortunately, the modern way of life imposes certain restrictions and requirements on this participation. The rhythm of life and the development of technology today often divide parents and children. Instead of communicating, engaging in their upbringing and development, parents replace their direct participation with technological gadgets or countless sections and groups of the so-called early development, where the child is sent almost from birth. Why are both dangerous for normal cognitive development? Technological gadgets (smartphones, computers and tablets) are designed in such a way that they operate mainly with visual information: icons and virtual objects are interpreted symbols, information that does not require any effort from the brain to recognize and perceive it. Thus, it deprives the child of the function of abstract thinking as unnecessary. The graphic information that a child sees in a book is more abstract - it forces the brain to work: it must interpret the image and its description, connect them together in its imagination, visualize the action or concept that they describe. This process involves certain parts of the cerebral cortex, which are responsible for the formation of abstract thinking, which is the pinnacle of cognitive development at an early age.
Introduction
In recent years, the role of micronutrients in the cognitive development of children has been actively studied.
A significant evidence base has been obtained on the effectiveness of using B vitamins [1], omega-3 polyunsaturated fatty acids (PUFAs), magnesium, etc. to improve cognitive function [2]. Vitamin D is known to play an important role in calcium homeostasis and musculoskeletal health. Research over the past 10 years has indicated the important role of vitamin D in brain development, cognitive function and memory [3, 4]. The results of epidemiological studies that measured 25(OH)D levels in the blood suggest that currently at least 30–50% of the population in various countries and regions of the world is characterized by low vitamin D levels [5–8]. Let us recall that levels of vitamin 25(OH)D in blood plasma less than 10 ng/ml correspond to severe deficiency and vitamin deficiency, levels of 10–20 ng/ml – vitamin D deficiency, levels of 20–30 ng/ml – vitamin D deficiency, and levels more than 30 ng/ml is the normal level of vitamin D. According to large-scale screenings conducted by Russian researchers, normal levels of vitamin D in the blood (more than 30 ng/ml) are observed in less than 10% of Russian children of different age groups [7, 8]. At the same time, optimal development and functioning of neurons in the cerebral cortex occurs when vitamin D levels in the blood are more than 30 ng/ml [4].
Evidence from basic and clinical studies shows that vitamin D plays an important role in the development and functioning of the central nervous system [9, 10]. Vitamin D is actually a neuroactive steroid hormone necessary for fetal brain development and brain function in children and adults. Vitamin deficiency is associated with decreased cognitive abilities, neuropsychiatric disorders (depression, schizophrenia), and an increased risk of Parkinson's disease and Alzheimer's disease [11].
The development of vitamin D deficiency is facilitated by insufficient consumption of foods containing vitamin D, obesity, low levels of vitamin D in breast milk (for newborns), low insolation, decreased synthesis of biologically active forms of vitamin D due to liver and kidney dysfunction, and many other factors [5, 6 ]. In addition, poor dietary habits contribute to the maintenance of long-term vitamin D deficiency. For example, consumption of cola drinks by children aged 5 years predicts nutrient intake in late childhood and adolescence. Children consuming this type of beverage are characterized by a higher intake of simple sugars and a reduced intake of protein, fiber, calcium, vitamin D, magnesium and potassium (n=170) [12].
Next, the role of vitamin D in maintaining the homeostasis of neurotransmitters, the development of the cerebral cortex, maintaining cognitive abilities and memory function, as well as normalizing the state of the psycho-emotional sphere is examined in a consistent manner.
Neurotransmitter role of vitamin D
Vitamin D is a steroid hormone that is fundamentally necessary for the formation and functioning of neuronal systems [13]. From the prenatal period, vitamin D is an important modulator of brain development. Chronic vitamin D deficiency in the mother-fetus system disrupts the development program of the central nervous system in the fetus; increases the risk of developing psychoneurological disorders in both the fetus and the mother. As a neurosteroid, vitamin D is essential for the division, growth and differentiation of neurons and also has neuroprotective effects.
The neurophysiological effects of vitamin D are mediated primarily through genomic mechanisms: interactions of the vitamin D receptor (VDR) with genomic DNA. Our earlier genome-wide bioinformatic analysis showed that the biological roles of vitamin D in all types of cells, incl. in cells of the nervous system, include maintaining genome stability (including the cell division cycle, DNA repair, chromosome restructuring), supporting the processes of protein synthesis and degradation, immunity, regulation of embryogenesis, and energy metabolism [13].
Genome-wide analysis also showed that the genomic functions of vitamin D include neurosteroid roles and mediation of the effects of neurotrophic and growth factors. Vitamin D deficiency will significantly aggravate the course of hereditary idiopathic neuropathy (G60), incl. Charcot-Marie-Tooth disease, hereditary ataxia (G11), spinal muscular atrophy (G12). The importance of vitamin D as a neurosteroid (i.e., a neuroactive steroid hormone) is confirmed by a number of facts [13–21] shown in the table.
One of the most important neurosteroid effects of vitamin D is its effect on the biosynthesis of the neurotransmitter dopamine. Dopamine is produced in the brain and is fundamentally important for cognitive performance. With insufficient dopamine biosynthesis, children experience slowness of cognitive processes (bradyphrenia), increased inertia, the process of switching attention from one stage of cognitive activity to another is disrupted, and fine motor skills are impaired (in particular, writing skills) [14]. As a result, the child's ability to learn is reduced. In adolescence, normal metabolism of dopamine significantly increases resistance to the formation of addictions (alcohol, drugs, nicotine, etc.).
The effect of vitamin D on dopamine biosynthesis is associated with activation of gene expression of the main enzyme of dopamine biosynthesis, tyrosine hydroxylase (TH gene). The maximum increase in TH gene expression (2–3 times) was observed at a concentration of 1,25(OH)2D of about 10-8 M. The combined effect of 1,25(OH)2D3 and 20 μM nicotine had no additive effect on TH gene expression, which indicates the relationship between the mechanism of activation of the expression of this gene and nicotinic acetylcholine receptors [21]. 1,25(OH)2D3 dose-dependently protects dopaminergic neurons from the neurotoxic effects of glutamate [22].
The active form of vitamin D protects the brain from neurotoxic doses of methamphetamine, which is known to reduce dopamine and serotonin levels. Animals treated with methamphetamine and placebo showed significant decreases in dopamine and serotonin levels in the striatum and nucleus accumbens. In animals treated with methamphetamine and calcitriol, this decrease was significantly reduced [23, 24]. Thus, vitamin D deficiency creates conditions for the rapid formation of dependence and the development of neurotoxic effects of methamphetamine.
In addition to influencing dopamine and serotonin levels, vitamin D plays a role in regulating levels of other monoamine neurotransmitters. For example, experimental vitamin D deficiency has been associated with a significant reduction in endogenous norepinephrine levels, with impaired norepinephrine synthesis/secretion associated with dysregulation of neuronal calcium levels [25]. Reduced levels of endogenous norepinephrine are associated with a decrease in cognitive potential, alexithemia, and a depleted emotional background.
Vitamin D counteracts motor and neuropsychological disorders that occur when dopaminergic neurons in the substantia nigra of the brain are damaged. In an experiment, vitamin D attenuates movement disorders in a rotenone model of dopaminergic neurotoxicity by increasing autophagy of damaged neurons via the LC3 and Beclin-1 signaling pathways [26].
Vitamin D and cortical development
The activated VDR receptor affects the signaling pathways of neurotrophic and growth factor receptors (nerve growth factor, fibroblast growth factor, insulin, transforming growth factor β, vascular endothelial growth factor), which are fundamentally important for the formation of complex cytoarchitecture of the cortex.
The prenatal period of brain development and the period of early childhood are characterized by a huge potential for neuroplasticity, which requires a sufficient synthesis of neurotrophic factors. The effect of vitamin D on dopamine metabolism is inextricably linked with an increase in the expression of glial cell derived neurotrophic factor (GDnF) and brain derived neurotrophic factor (BDnF). GDnF, in particular, has a significant effect on dopamine synthesis in the striatum [26, 27].
The neuroprotective effect of vitamin D includes not only a neurotrophic effect (stimulation of the synthesis/secretion of neurotrophins), but also regulation of the levels of Ca2+ ions (known to be involved in the processes of apoptosis), antioxidant and neuroimmunomodulatory effects [28–30]. This complex neuroprotective effect of vitamin D is especially important for children suffering from cerebral palsy, attention deficit hyperactivity disorder, and for compensating for the effects of traumatic brain injury. In these diseases, children experience chronically increased oxidative stress in the neurons of the central nervous system, impaired immunomodulation, and insufficient regenerative capacity of the brain.
Basic research on the effects of vitamin D on brain development is supported by clinical research. For example, a longitudinal study of mother-child pairs (n = 1020) showed that low 25(OH)D levels during pregnancy increased the risk of disorders in the child's language development. The mean 25(OH)D level in the second trimester was 22.3 ng/ml (95% confidence interval [CI] - 5.9-68.4), 42% of values were less than 20 ng/dl.
Cognitive and language development scores increased stepwise with increasing 25(OH)D levels, which increased from <20 to >30 ng/dL in the second trimester, even after adjusting for socioeconomic status, race, tobacco product use, and gestational age at birth. and the age of the child at the time of examination [31].
In another study, measurements of serum 25(OH)D levels at 18 weeks' gestation (n=743) identified significant linear correlations between quartiles of maternal vitamin D levels and language impairment at 5 and 10 years. Thus, women with insufficient vitamin D levels during pregnancy (<19 ng/ml) were twice as likely to have a child who developed clinically significant language difficulties compared with women with 25(OH)D levels greater than 28 ng /ml (p<0.05) [32] (Fig. 1).
In another study, maternal blood 25(OH)D concentrations were measured at 32 weeks of gestation and infants were followed up at 6 months of age (n=960). Cognitive, motor, social-emotional functioning and language development were assessed using the Bayley Scales (3rd edition). 60% of women have 25(OH)D levels <30 ng/ml at 32 weeks of pregnancy. Infants born to women with 25(OH)D deficiency (<15 ng/mL) had a decreased language score of -3.48 points (95% CI -5.67 to -1.28) compared with infants born to women with 25(OH)D deficiency (<15 ng/ml). born to women with normal vitamin levels during pregnancy (>30 ng/ml) [33].
Vitamin D levels in umbilical cord blood are associated with neurocognitive development in crawling infants (crawling to walking, n=363, 16–18 months). The Cognitive Development Index (CDI) and Psychomotor Development Index (PDI) in young children were assessed using the Bayley Scales of Infant Development. Children with the lowest vitamin D levels (lowest quintile of cord blood 25(OH)D levels) had a lower IPR of -7.6 points (95% CI -12.4 to -2.82; p=0.002; Fig. 2) and IQR are lower by -8.04 points (95% CI - -12.9– -3.11; p=0.001) compared to the 3rd quintile. Unexpectedly, infants in the highest quintile of cord blood 25(OH)D concentrations also had a significant reduction in IFR of -12.3 points (95% CI -17.9 to -6.67; p < 0.001) [34].
Vitamin D and cognitive performance
Vitamin D deficiency is associated with a decrease in the rate of neuropsychic development in children [35] and a wide range of neurological and neurodegenerative diseases [36]. Neurological disorders associated with vitamin D deficiency include cerebral blood flow disorders [37], memory loss and cognitive impairment [38], and a tendency to seizures [39]. A low supply of vitamin D aggravates the course of neurodegenerative pathologies (multiple sclerosis, Parkinson's and Alzheimer's diseases, idiopathic neuropathy, hereditary ataxia, spinal muscular atrophy) [40]. Vitamin D deficiency is an independent risk factor for overall cognitive decline in clinically stable peritoneal dialysis patients [41].
Diabetes mellitus (DM) is associated with memory loss and complicates learning. In an experiment, vitamin D supplementation improved learning and memory in a streptozotocin model of diabetes in mice. The positive effect of vitamin D on cognitive status in diabetes is associated, in particular, with its neuroprotective roles [42] (Fig. 3).
Experimental proteomic studies have shown that vitamin D deficiency in the mother during embryonic growth leads to complex disturbances in the expression of numerous proteins in brain neurons. In offspring born to females exposed to vitamin D deficiency during pregnancy, at 10 weeks, significant impairments were found in the levels of 36 neuronal proteins involved in neuronal energy metabolism, maintenance of redox balance, cytoskeleton, calcium homeostasis, synaptic plasticity and neurotransmission. Systems biology analysis of the results of this proteomic study showed that established expression abnormalities are also characteristic of models of schizophrenia, multiple sclerosis and mitochondrial neuronal dysfunction [43].
In an experiment, vitamin D reduced age-related hyperphosphorylation of tau protein and improved performance on cognitive tests. Rats at 20 months of age (aged) and 6 months of age (young) were randomized to receive vitamin D or subcutaneous injections of 1,25-dihydroxyvitamin D3 for 21 days. Vitamin D reduced age-related tau hyperphosphorylation while improving brain energy metabolism and cognitive testing results [44].
The results of experimental studies were confirmed by clinical and epidemiological data. Serum 25(OH)D levels are significantly lower in children with mental retardation, with correlations between 25(OH)D levels and Wechsler Learning Scale for Children Intelligence score [45].
Vitamin D deficiency [25(OH)D<20 ng/mL] was associated with neuromotor and neuropsychological impairment in older men and women (n=463, 70–90 years). Vitamin deficiency has been associated with decreased upper and lower limb strength, slower reaction times, poor balance, slower gait speed, and impairments in executive function and visuospatial orientation [46]. Low vitamin D levels have been associated with cognitive impairment in hemodialysis patients [47], impair long-term visual memory (Rey test) in multiple sclerosis [48], and have been associated with alexithymia (as assessed by the Toronto Alexithymia Scale) [49].
Vitamin D deficiency is associated with thinning of the cerebral cortex with age. A longitudinal study of changes in cortical thickness based on magnetic resonance imaging in a group of 203 healthy people aged 23–87 years (mean follow-up interval 4 years) found that higher levels of vitamin D, docosahexaenoic acid and physical activity inhibited cortical thinning brain, and higher cholesterol levels and increased body mass index exacerbated cortical thinning [50]. A study of 75 patients found that a 4-fold increase in the risk of cognitive impairment associated with vitamin D deficiency (less than 20 ng/mL) was also associated with decreased volume of various brain regions (eg, white matter and temporal lobes) [51]. ].
The effects of vitamin D deficiency on cognitive performance have been observed across different age groups. Children with poor school performance have lower serum 25(OH)D levels. Low 25(OH)D levels were significantly associated with decreased Benton visual retention test (BVRT) performance [45]. In a cohort of patients born in 1958 (n=6496), children with low vitamin D concentrations (<10 ng/ml) showed a significant deterioration in short-term memory for words [52].
Vitamin D deficiency (25(OH)D<20 ng/ml) corresponds to a more rapid decline in cognitive function with age (n=2777, 70–79 years, 4 year follow-up). When assessing cognitive abilities using the modified Mini-Mental State Examination (3MS), vitamin D deficiency was associated with both a lower 3MS score (-0.9 points; p=0.02) and a faster decline in score for 4 years (by -1.0 point, 95% CI –-1.5–-0.6; p=0.05) [53, 54].
In the Nurses' Health Study (n=1185, 60–70 years), low plasma vitamin D levels were associated with decreased cognitive function. At a 9-year follow-up, low vitamin D levels (lowest quintile, mean levels 14 ng/mL) were associated with a mean 20% reduction in composite scores on all cognitive tests (95% CI 8–33%; p=0.009 ) compared with women in the highest quintile of concentrations (mean - 38.4 ng/ml) [55].
A systematic review of the association between vitamin D and cognitive performance included 25 cross-sectional and 6 prospective studies. Against the background of vitamin deficiency, a significant decrease in the performance of cognitive and functional tests and a higher incidence of dementia were established. Prospective studies with a mean follow-up of 4–7 years have shown a higher risk of cognitive impairment in participants with lower baseline vitamin D levels [56]. Thus, the results of these clinical and epidemiological studies indicate the promise of using vitamin D for the prevention of cognitive decline.
Vitamin D and memory function
The hippocampus and its dentate gyrus are important in supporting memory function. Vitamin D deficiency has been experimentally associated with decreased hippocampal long-term potentiation [57], impairs spatial learning in adult rats (finding a hidden platform in a water maze) [58], and impairs other neurological testing results.
For example, a vitamin D-deficient diet (<10 ng/ml, 6 weeks) in 10-week-old rats resulted in decreased scores on reaction tests (5C-SRT scale) and performance tests (5C-CPT scale). Vitamin D deficiency has been associated with an increase in basal levels of GABA (γ-aminobutyric acid) in the striatum, indicating changes in the systems that regulate compulsive behavior and reward seeking [59]. Vitamin D3 mediates age-related inflammatory changes in the hippocampus by acting as an anti-inflammatory agent and inhibiting the age-related increase in microglial activation and parallel increase in interleukin-1β levels [60].
Prenatal vitamin D deficiency is associated with impairments in synaptic plasticity in the dentate gyrus in adult rats. In particular, prenatal vitamin deficiency led to significant impairment of latent inhibition and impairment of long-term potentiation. These impairments, associated with prenatal vitamin D deficiency, were partly compensated by the use of the antipsychotic haloperidol, which indicates impairments in synaptic plasticity of the hippocampus due to vitamin D deficiency [61].
Vitamin D improves memory and mood in patients with Parkinson's disease (n=286). Correlations were established between vitamin D deficiency, decreased fluency of speech (p <0.001) and verbal memory (p = 0.0083) on the Hopkins Verbal Learning Test, and increased scores on the Geriatric Depression Scale (p = 0.0083). [62].
All neurodegenerative diseases are, to one degree or another, characterized by a decrease in the mnestic function of the brain. Vitamin D receptors have neuroprotective and neurotrophic effects, incl. decreased amyloid plaque deposition is a hallmark of Alzheimer's disease (AD) [63]. The biological effects of vitamin D counteract the pathophysiology of AD, including β-amyloid deposition, inflammation, disturbances of calcium homeostasis and corticosteroid balance in cortical areas and the hippocampus [64], and age-related decline in memory and cognitive abilities by reducing excess inflammation and amyloid deposition [65]. Experimental studies have shown that vitamin D3 (calcitriol) reduces amyloid accumulation in the brain and improves cognitive parameters in experimental models of AD (Tg2576 and TgCRND8 lines with overexpression of amyloid protein). Treatment with 1,25-dihydroxyvitamin increased p-glycoprotein levels and decreased amyloid levels in brain tissue, especially in the hippocampus [66].
Vitamin D and the psycho-emotional sphere
Vitamin D deficiency aggravates neurological diseases and impairs brain recovery after stress, so vitamin D deficiency is associated with a wide range of neuropsychiatric disorders [67]. Conversely, chronic unpredictable stress affects vitamin D metabolism in the hippocampus and myocardium [68].
Vitamin D deficiency has been noted in psychiatric patients. In a screening of patients admitted to a hospital psychiatric unit (n=544), the mean vitamin D level on admission was only 22 ng/mL (4–79 ng/mL), and vitamin D deficiency (<30 ng/mL) was found in 75% of patients [69].
Children with attention deficit hyperactivity disorder (n=37, 6–12 years) had significantly lower serum vitamin D levels (19.1±10.10 ng/ml) than controls (28.67±13. 76 ng/ml; p<0.001) [70]. Taking vitamin D improves the psycho-emotional state of adolescent girls with premenstrual syndrome against the background of severe vitamin D deficiency [71].
In an experiment, vitamin D deficiency during pregnancy leads to an increase in impulsive behavior in the offspring in the absence of inhibitory control [72]. This combination of symptoms is typical of cognitive deficits in schizophrenia. Patients with schizophrenia had significantly lower serum vitamin D concentrations (15.0±7.3 ng/ml; n=50) compared to patients with depression (19.6±8.3 ng/ml; n= 30) and with the control group (20.2±7.8 ng/ml; p<0.05; n=50) [73].
A high incidence of vitamin D deficiency has been noted in individuals with established psychotic disorders. A case-control study of patients with a first episode of acute psychosis (n=69) and a control group (n=69) showed that vitamin D deficiency was 3 times more common among patients (p<0.001) [74].
Low 25(OH)D levels are associated with greater susceptibility to schizophrenia. In particular, vitamin D is a potent transcriptional activator of the proline dehydrogenase (PRODH) gene, which is located at the 22q11 locus of chromosome 22-o1 and is associated with the highest known genetic risk for schizophrenia. Proline dehydrogenase catalyzes the catabolism of proline, which is a neuromodulator of glutamateergic synapses. Hyperprolinemia is associated with decreased IQ, cognitive impairment, and schizophrenia.
Associations between 25(OH)D levels and schizophrenia were examined in 64 patients and 90 controls. In patients, 25(OH)D levels were significantly lower and 25(OH)D deficiency was associated with schizophrenia (RR=2.1, 95% CI 1.0–4.5; p=0.044). Additionally, participants with low 25(OH)D levels had a 3-fold (95% CI 1.08–8.91) higher risk of hyperprolinemia (p=0.035; Figure 4), which is a common symptom in schizophrenia [75].
Vitamin D deficiency is a likely risk factor for autism spectrum disorder [76]. Children with autism spectrum disorders are characterized by learning difficulties and a higher incidence of vitamin D deficiency [77].
Providing vitamin D helps normalize mood swings in the autumn-winter period. An extreme form of seasonal mood dependence manifests as the clinical syndrome of seasonal affective disorder with carbohydrate cravings, hypersomnia, lethargy, and circadian rhythm disturbances. In a small randomized trial, healthy volunteers (n=44) received 400 or 800 IU/day for 5 days in late winter, which was associated with significant improvements in mood compared with controls [78]. Vitamin D can be used to treat seasonal affective disorder (patients' condition was assessed using the SPAQ-SAD - Seasonal Pattern Assessment Questionnaire-Seasonal Affective Disorder) [79].
Low 25(OH)D3 levels in adolescents correlate with suicide rates and depression. It is noteworthy that when examining 59 adolescents who survived a suicide attempt, none of them had normal levels of vitamin D in their blood! 7% of adolescents who survived a suicide attempt had a vitamin D level of less than 10 ng/ml (corresponding to vitamin deficiency), and 58% had a vitamin D level of less than 20 ng/ml (Fig. 5) [80].
Vitamin D reduces perseverative behavior (persistent repetition of erroneous actions) associated with fetal alcohol syndrome. In the experiment, cholecalciferol was given before, during, and after the fetus was exposed to alcohol in the third trimester. Testing of newborn rat pups for spatial learning showed that exposure to ethanol leads to a significant increase in the number of errors compared to the control group. Treatment with cholecalciferol dose-dependently reduced perseverative behavior associated with the development of alcohol exposure [81].
In stroke patients, an association has been established between serum 25-hydroxyvitamin D levels and depression (DSM-IV criteria - Diagnostic and Statistical Manual of mental disorders). At 6 months post-stroke, 91 (37%) patients were diagnosed with depression, and 25(OH)D levels were significantly lower in this group of patients (8.3 ng/ml, 95% CI 6.8–9.5) than in patients without depression (16 ng/ml, 95% CI –13–20; p<0.001). 25(OH)D levels less than 11.2 ng/mL were associated with a 10-fold increased risk of depression (RR = 10.32, 95% CI 4.97–28.63; p < 0.001) [82].
On the correction of vitamin D deficiency in children
In pediatrics and therapy, vitamin D3 preparations are much more in demand, in particular cholecalciferol, which, being a provitamin (prodrug), is converted into the active form of the hormone (calcitriol) in the quantities required by the body. Preparations based on cholecalciferol are divided into two groups: vitamin D3 in an oil solution and an aqueous solution of micellized vitamin D3.
The micellized form of vitamin D3 [83] is important because the physiological absorption of vitamin D3 in the intestine occurs only with the participation of bile acids (which implies the formation of micelles). Reduced secretion of bile acids sharply reduces the absorption of vitamin D (including from oil solutions) and other fat-soluble vitamins. Micellated (“water-soluble”) solutions of vitamin D (cholecalciferol) provide a good degree of absorption in almost all age groups of patients (children, adults, elderly) with minimal dependence on the composition of the diet, medications, liver condition and bile acid biosynthesis.
Neurological applications of vitamin D involve long-term use of drugs (at least 6-12 months). A previous analysis of data from effective clinical studies made it possible to formulate the following stepwise scheme for prescribing vitamin D: children under 4 months of age need a daily intake of 500 IU/day of vitamin D (for premature infants - 800–1000 IU/day); children from 4 months to 4 years – 1000 IU/day; from 4 to 10 years – 1500 IU/day, and over 10 years – 2000 IU/day throughout the year without a break during the summer months (Fig. 6). When using this type of drug regimen (course duration, daily dose), no side effects are observed [4].
Conclusion
The multifaceted effect of vitamin D on the development and functioning of the central nervous system is reflected in cognitive, mnestic abilities and the emotional sphere. The neurosteroid vitamin D promotes the survival of neuronal networks under stress. Developed neural networks are a necessary condition for the formation of associative thinking, speech fluency, and successful learning. Therefore, a sufficient supply of vitamin D is not only necessary in the prenatal period and early childhood, but is also fundamentally important for the development of learning ability, associative thinking, and the formation of fine motor skills at school age. On the contrary, a low supply of vitamin D aggravates seasonal mood swings, depressive states, increases the risk of suicide, contributes to the formation of perseverative erroneous behavior, contributes to the formation of diseases, addiction and unstable psycho-emotional behavior.
The influence of modern technologies on a child’s cognitive development
It cannot be said that if “virtual” information is abused, abstract thinking completely atrophies. But it becomes more difficult for the child to use it, build his own or understand other people’s logical relationships. But real life, where he will need these qualities, takes place outside the screen of a smartphone and computer.
High-quality communication, among other things, implies, for example, answers to endless children's questions that a child asks as he develops.
With the development of Internet technologies, children have gained wide access to all the information that humanity has accumulated over tens of thousands of years of its existence. But will they become smarter from this? The individual level of knowledge, according to the observations of experts, is decreasing, largely due to the fact that the new generation does not need to accumulate and interpret information on their own, when Internet technologies are available for this. But let’s not forget that technology is only a means, a useful tool for those who know how to use it, that is, perceive, compare and process the information received for the purposes they need. It turns out that children are receiving technology that allows them to do without abstract thinking and analytical abilities, but at the same time deprives them of the opportunity to reap its benefits. It is difficult for such children to create associative connections, their horizons are narrowed, so a general developmental delay soon begins. It is difficult to say what reasons it is primarily due to, organic (certain areas of the brain have not developed) or cultural, but based on the obvious, we can make an assumption in favor of the latter. Therefore, parents should pay attention to quality communication with their child, and not replace it with technical surrogates. High-quality communication, among other things, implies, for example, answers to endless children's questions that a child asks as he develops. In this case, it is not the reliable answers that are important, but the very fact of feedback from your child.
Pre-operational stage (from 2 to 6 years)
The second stage generally corresponds to preschool age (it must be taken into account that the age indicated in this theory is approximate). It was called pre-operative, because. At this stage, children do not understand operations - logical manipulations, and do not know how to think logically. Operations refer to procedures such as division, union and other transformations that require logical thinking. In other words, a child at this stage, especially at its beginning, is not able to use logical categories and operations: classify, compare, evaluate, measure, etc.
However, at this stage, a very important feature is observed - children master speech and begin to actively use symbolic thinking. Those. they use words and symbols to represent objects, groups of objects, images and ideas, and actively use imagination and symbolic play. Thus, cubes can become kingdom subjects or buildings, and a child’s hands can become airplane wings. Such play and the ability to “pretend” is actually an important cognitive achievement—a degree of abstraction not available to great apes and other animals.
Jean Piaget believed that children at this stage are unable to maintain attention on more than one aspect of a situation or characteristic, and in addition, children's logic is based on personal experience rather than generally accepted rules and laws. Thus, at the age of 3-4 years, children are not able to understand the concept of conservation of matter. The principle of conservation is the understanding that the amount of a substance will remain the same even if its shape changes. For example, if you pour water from a short and wide glass into a tall and narrow one, there will be the same amount of water in it. And if you roll out a ball of plasticine into an oblong sausage, the amount of plasticine will not change. Such operations become available to children only at the next stage of cognitive development.
To see what the logic of children at an early stage of the pre-operational stage of development (who have not yet mastered the principle of conservation of mass and quantity) looks like in life, watch this video. (https://www.youtube.com/watch?v=ZDNi4z5tdqU)
Another distinctive feature of this stage is children's egocentrism. In this context, this means that a child up to the age of approximately 3 years perceives the world as an extension of himself, exactly as he sees it, without realizing and often with difficulty accepting points of view that differ from his own. At this stage, it is natural for children to believe that everyone sees and perceives the world exactly the same as they do, and has the same feelings, thoughts, preferences and desires.
Between about 3 and 5 years of age, children begin to realize that other people have their own points of view, feelings and thoughts, and they perceive the world differently, in their own way. This phenomenon is called the model of the human psyche (or theory of mind, in English).
The pre-operational stage is replaced by the stage of concrete operations, at which children demonstrate a greater ability for logical thinking. We will consider this, as well as the fourth stage - formal operations, in detail next time, as well as valuable practical considerations and recommendations for parents.
In the meantime, we invite you to our program “Cognitive Science. Development of thinking." This online training will be useful to all those who want to learn to reason logically and consistently, quickly make effective decisions and find innovative approaches to difficult problems.
Good luck!
We also recommend reading:
- Storytelling
- Cognitive sphere of personality
- Genetic psychology
- Cognitive development. Part 2
- Factors in a child’s intellectual development
- Speech thinking in children and adults: what is it and why is it needed?
- Conceptual thinking: by stages of cognition
- A selection of courses for children and parents
- How to teach a child to read: rules, tips and tricks
- Piaget's theory of cognitive development
- Theories of thinking
Key words:1Cognitive science
