2023-09-19 10:31:21
The effect of iron on the central nervous system
Iron is an essential microelement, influencing on the functioning of all body systems. Its key functions include transport of electrons, oxygen, DNA synthesis, and tissue respiration. Lack of iron in the body has many negative effects, including decreased immunity, chronic fatigue and deterioration in the functioning of the central nervous system.
Organism does not produce iron independently and receives it through food. Most of this trace element is contained in the hemoglobin of red blood cells. Iron is deposited in the cells of the liver, spleen, bone marrow and other tissues in the form of ferritin, a complex protein complex (iron protein).
Iron penetrates into the brain through the blood-brain barrier using the transport protein transferrin. Its highest concentration is observed in the basal ganglia, a complex of large brain structures surrounding the central limbic system. The basal ganglia, in addition to regulating motor skills, also regulate emotions, behavior and motivation.
Iron is involved in many processes important to the central nervous system, including the generation of nerve impulses, the formation of the myelin sheath of axons, and the production of neurotransmitters. The normal functioning of the hypothalamus, the main regulator of the neuroendocrine system, depends on it.
Iron deficiency in the brain leads to depression and anxiety disorders. Low iron levels in the central nervous system provokes death of brain mitochondria – the main producers of ATP necessary for the functioning of neurons. Mitochondrial dysfunction is a provocateur of decreased mental abilities and intelligence.
Iron deficiency during gestation associated with psychopathologies, neurological diseases and abnormal brain structure in the offspring.
Effects of iron deficiency on the developing brain
Every third child does not reach their development potential by preschool age. The first 1000 days of life, from conception to 2 years of age, are the most important period for the development of the central nervous system.
Iron deficiency occurring during this time impairs brain formation and neurotransmitter production, leading to irreversible neurocognitive and behavioral changes.
In pregnant women at 19–24 weeks of gestation increases the risk of latent iron deficiency, which, if untreated, progresses to IDA in 65% of cases. In Russia, anemia occurs in almost every third pregnant woman. This high prevalence of IDA is largely due to the increased need for iron during gestation.
A pregnant woman’s blood volume increases, which means the production of hemoglobin increases. For every additional gram of hemoglobin, 3.46 milligrams of iron are required. Part of this nutrient is used for the development and metabolism of the fetus. In addition, the fetus stores maternal iron in reserve to use it following birth.
With a slight iron deficiency in the mother’s body, the unborn child is not in danger, since the placenta deposits iron and, if necessary, directs it to the needs of the fetus. When severe iron deficiency occurs in a pregnant woman, it occurs throughout the mother-placenta-fetus system, which leads to serious consequences, including a decrease in mental abilities and the development of mental disorders in the offspring.
With fetal iron deficiency, a number of pathological processes occur in the fetal brain:
The synthesis of serotonin, dopamine, and norepinephrine—neurotransmitters on which the normal functioning of the central nervous system largely depends—is reduced. Serotonin is responsible for emotional stability, memory and learning, and normal sleep quality. The lack of neurotransmitters that arose during fetal development persists into adulthood. The formation of important brain structures, including the hippocampus, which is responsible for recognition memory, is disrupted. Children born with low blood ferritin levels demonstrate poor recognition memory both in infancy and at age 3.5 years. During school age, they have problems with academic performance, planning and attention. Myelination of nerve fibers is impaired. The myelin sheath “insulates” the long processes of neurons—the axons—to conduct signals at high speed. Iron is involved in the synthesis of fatty acids that make up myelin. With its deficiency, demyelination occurs, increasing risk of delayed physical and mental development, a number of mental illnesses. Gene expression changes. Fetal iron deficiency reduces the expression of genes responsible for synaptic plasticity and increases the activity of genes that provoke neurological diseases and psychopathologies. Insufficient maternal iron intake in the first trimester of gestation is associated with an increased likelihood of autism in the offspring, and in the second trimester with a 30% increase in the risk of schizophrenia. Also exists correlation between fatal iron deficiency and the onset of ADHD in childhood.
In 68% of children in the first year of life born to mothers with IDA, may occur anemia. Iron deficiency in young children is a provocateur of delayed mental, physical and speech development, decreased immunity and high morbidity.
IDA and cognitive function in adolescents and adults
Puberty connected with intensive growth and hormonal changes in the body, therefore during this period the need for all nutrients increases. Iron deficiency is a common phenomenon during puberty: it occurs in 26.4% of girls and 16.5% of boys.
Girls often develop both latent iron deficiency and iron deficiency anemia. The first often remains undiagnosed, which creates favorable conditions for its transformation during pregnancy into IDA, which increases the risk of maternal mortality and fetal development abnormalities.
Iron deficiency is negative influences on the somatics, psyche, and mental abilities of adolescents. It reduces memory, concentration, motivation to learn, and provokes emotional lability.
If iron deficiency is not corrected in a timely manner, these disorders tend to progress into adulthood. Examination of adult patients with IDA using special scales and EEG revealedthat iron deficiency also negatively affects the developing brain, leading to a decrease in memory and intelligence. Normalizing blood ferritin levels through iron supplementation correlates with improved cognitive function.
Iron deficiency and depression
According to the classical theory of depression, in the pathogenesis of this disease lies insufficient production of dopamine, norepinephrine and serotonin. Patients with depressive disorder are often prescribed antidepressants that increase the concentration of these neurotransmitters in the brain. The most effective drugs are selective serotonin reuptake inhibitors (SSRIs).
Since iron is involved in the synthesis of dopamine, norepinephrine and serotonin, with its deficiency, little of these neurotransmitters are produced, which leads to the development of depression.
In patients with depressive disorder, iron deficiency occurs almost three times more often than in people without psychopathologies, and its severity correlates with the severity of depressive symptoms.
In addition to depression, iron deficiency is associated with anxiety and psychotic disorders. In people with IDA who take iron supplements, the risk of psychopathology is significantly reduced.
Iron deficiency and insomnia
Insomnia suffers from 10 to 30% of the world population, while in half of the cases it is chronic. Genome-wide association search showed that the MEIS1 gene, associated with restless legs syndrome and IDA, has a pleiotropic effect in insomnia. Pleiotropy is a type of inheritance in which a gene determines the expression of several traits.
The relationship between iron deficiency and sleep disturbances in childhood has been well studied, and several studies have found it in adults as well.
A large-scale study of more than 12,000 adults found that anemia is a risk factor for insomnia.
IDA provokes insomnia through several mechanisms:
Anemia reduces blood flow in the frontotemporal region of the brain, which regulates sleep duration. The quality of sleep largely depends on the synthesis of dopamine. With anemia, little of it is produced, which leads to insomnia. One of the symptoms of IDA is chronic fatigue, which causes sleep problems.
Prevention and treatment of iron deficiency
With proper treatment of IDA is cured in 100% of cases. The goal of treatment is not only to normalize hemoglobin levels, but also to replenish iron stores, which are determined by the level of serum ferritin.
Discontinuation of IDA treatment when only the hemoglobin level is normalized leads to relapses of anemia.
Normalizing the iron content in the body helps alleviate mental problems caused by its deficiency. In particular, treatment with iron-containing drugs improves mental state of patients with depression and iron deficiency.
For the treatment of IDA, preparations of divalent or trivalent iron are prescribed. Both are effective for adult anemia. In the treatment of childhood IDA, ferric iron preparations work better.
Previously, high doses of iron supplements, taken daily or several times a day, were used to treat anemia. Often this dosage regimen led to side effects. Today, safer treatment regimens are recommended: taking low doses in short courses (2 weeks a month) or every other day for a month. Such dosing regimens not only reduce the risk of side effects, but also show higher efficacy compared to high-dose treatment.
The basis for the prevention of iron deficiency is a sufficient intake of iron from food. The daily requirement of an adult for this microelement is 1–2 mg, for a child – 0.5–1.2 mg. Only 10–15% of dietary iron is absorbed in the gastrointestinal tract, so the diet should contain enough foods containing it.
Exists two forms of dietary iron: heme and non-heme. The first is found in meat products, the second in plant products. Heme iron is four times better absorbed by the body than non-heme iron.
The main sources of iron are beef and veal liver, white fish, eggs, and shellfish. Buckwheat, green leafy vegetables, carrots, white and cauliflower, and legumes are also rich in it.
Preventive administration of iron supplements is recommended for all breastfed and mixed-fed children from 4 months of age until the transition to artificial feeding. By the age of 4 months, the child’s iron reserves received from the mother are depleted. Breast milk contains little iron, so infants need supplements containing it. Formula-fed babies get enough iron from formula or complementary foods.
All pregnant women must pass screening to detect iron deficiency in the fifth to sixth week of gestation. The most important hematological indicator is serum ferritin. Multicenter randomized studies have proven that the information value of this indicator for identifying iron deficiency is two times higher than that of serum iron.
Preventive intake of iron supplements is necessary for pregnant women who had heavy menstruation before conception, with a short interval between pregnancies (a year or less), multiple pregnancies and the presence of latent iron deficiency.
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