B vitamins: role in the nervous system

B vitamins: role in the nervous system

B vitamins are a complex of eight water -soluble vitamins, each of which plays a unique and vital role in maintaining the health of the nervous system. They interact closely with each other, forming the synergistic effect necessary for the optimal functioning of the brain, nerves and mental well -being. The deficiency of any of these vitamins can lead to a variety of neurological and psychiatric disorders, emphasizing their irreplaceability.

This detailed exploration delves into the individual roles of each B vitamin, their mechanisms of action within the nervous system, the consequences of deficiencies, methods for assessment and supplementation, and the latest research in this critical area.

1. Tiamin (vitamin B1): the key to energy metabolism of the nervous system

Tiamin, also known as vitamin B1, plays a central role in carbohydrate metabolism, a key source of energy for the nervous system. Nerve cells, having high metabolic activity, are extremely dependent on the constant influx of glucose and its effective transformation into energy. Tiamine acts as a coofer for several key enzymes involved in this process.

• The mechanism of action: Tiamin in the form of thiamindifosphate (TDP) participates in:

  • Decarboxylation of alpha coat acids: TDP is necessary for the operation of the pyruvate-heated complex (PDH), a key enzyme in glycolysis, which ensures the transformation of the pyruvate into acetyl-koa, which then enters the Krebs cycle. The deficiency of thiamine leads to the accumulation of pyruvat and lactate, violating the energy balance in the nerve cells.
  • Pentosophosphate path: TDP is involved in transcetolas, the enzyme necessary for the pentosophosphate path, which provides the formation of riboso-phosphate, an important component of nucleotides (DNA and RNA), and nicotinindinindinucleotidfosphate (NADPH), a key restorer that protects the nerve cells from oxidizing stress.
  • Metabolism of branched amino acids: TDP is also important for the metabolism of leucine, isolacin and valine, which play a role in neurotransmission.

• The consequences of the deficit: Tiamine deficiency can lead to serious neurological disorders, such as:

  • Vernika-Korsakov’s disease: This is a severe neurological disorder characterized by encephalopathy of Wernik (acute phase) and the psychosis of Korsakov (chronic phase). Vernika encephalopathy is manifested by confusion, ataxia (impaired coordination) and ophthalmoplegia (paralysis of the eye muscles). The psychosis of Korsakov is characterized by anterograd and retrograde amnesia, confabulations (false memories) and apathy. Alcoholism is the main cause of thiamine deficiency, since alcohol prevents the absorption and absorption of vitamin B1.
  • Since This is a condition characterized by peripheral neuropathy (damage to the peripheral nerves), heart failure and edema. There are several types of Beri Berie: dry Beri Beri (damage to the nervous system), wet Beri-Beri (defeat of the cardiovascular system) and acute Bari Beri (acute heart failure).
  • Optical neuropathy: Tiamine deficiency can contribute to the development of optical neuropathy, leading to visual impairment.

• Diagnostics and treatment: Diagnosis of thiamine deficiency is based on clinical symptoms, anamnesis (especially in people who abuse alcohol) and laboratory studies, such as determining the level of thiamine in the blood and transcetolasis activity in red blood cells. Treatment includes intravenous or intramuscular administration of thiamine, especially in cases of Vernika-Korsakov’s disease. It is important to note that before the introduction of glucose to patients with suspected deficiency of thiamine, they must first introduce thiamine in order to avoid aggravation of neurological symptoms.

2. Riboflavin (vitamin B2): Support for redox reactions in the nervous system

Riboflavin, or vitamin B2, is a flavinmononucleotide cofactor (FMN) and flavideninindininucleotide (FAD), which are involved in many redox reactions that are critical for energy metabolism and protecting nerve cells from oxidative stress.

• The mechanism of action: FMN and FAD participate in:

  • Electronic transport: FAD is a component of the II complex in the electron transfer circuit in mitochondria, playing the role in the development of ATP (adenosinerifospeta), the main energy currency of the cell.
  • Metabolism of fatty acids: FAD is necessary for beta-oxidation of fatty acids, a process that provides energy for nerve cells, especially in conditions of glucose deficiency.
  • Glutation’s restoration: FAD is a cofacor of glutathioneuctase, an enzyme that restores glutathione, a powerful antioxidant that protects the nerve cells from damage to free radicals.
  • Transformations of other vitamins of group B: Riboflavin is necessary for converting vitamin B6 (pyridoxine) into its active form, as well as for folic acid metabolism.

• The consequences of the deficit: Riboflavin deficiency is rarely found in isolation and is often accompanied by a deficiency of other vitamins of group B. The symptoms of riboflavin deficiency include:

  • Heit: Inflammation and cracks in the corners of the mouth.
  • Glossit: Inflammation of the tongue.
  • Seborrheic dermatitis: Inflammatory skin disease, manifested by redness, peeling and itching, especially in the face and scalp.
  • Photophobia: Sensitivity to light.
  • Neurological symptoms: Although less specific, riboflavin deficiency can aggravate neurological problems, especially in combination with a shortage of other vitamins of group B.

• Diagnostics and treatment: Diagnosis of riboflavin deficiency is based on clinical symptoms and laboratory studies, such as determining the level of riboflavin in the blood and the activity of glutathioneuctase in red blood cells. Treatment includes riboflavin oral intake.

3. Niacin (vitamin B3): The importance for energy and neurotransmitters

Niacin, represented by nicotinic acid and nicotinamide, is the predecessor of nicotinindinindininindinulesotide (NAD+) and nicotinindinindinindininicoleotidfosphate (NADP+), key coofers involved in hundreds of metabolic reactions, including energy metabolism, synthesis of fatty acids and cholesterol, and cell protection from cell protection from oxidative stress. NAD+ and NADP+ are especially important for the functioning of the nervous system.

• The mechanism of action: NAD+ and NADP+ participate in:

  • Glycolize and Crebs cycle: NAD+ is an electrons acceptor in glycolis and a Crebs cycle, ensuring the production of ATP.
  • Respiratory chain: NAD+ is involved in the transfer of electrons in the respiratory chain, ensuring the effective production of energy in mitochondria.
  • Synteze neurotransmitted: NAD+ is necessary for the synthesis of serotonin, dopamine and norepinephrine, key neurotransmitters that regulate mood, sleep, appetite and cognitive functions.
  • DNA refraps: NAD+ is a substrate for enzymes involved in DNA reparations, protecting the nerve cells from genetic damage.
  • Signal transduction: NAD+ is involved in a signal transduction through the activation of sirtuins, proteins that regulate aging, stress resistance and metabolism.

• The consequences of the deficit: A severe shortage of niacin leads to Pellagra, characterized by “three D”: dermatitis, diarrhea and dementia. Neurological symptoms of pellagra include:

  • Depression: The deficiency of serotonin, dopamine and norepinephrine caused by niacin deficiency can lead to depression.
  • Apathy: Reducing motivation and interest in the world around us.
  • Irritability: Increased sensitivity to irritants and a tendency to outbreaks of anger.
  • Anxiety: Feeling anxiety and tension.
  • Confusion: Violation of orientation in time and space.
  • Dementia: Progressive deterioration in cognitive functions.

• Diagnostics and treatment: Diagnosis of Pellagra is based on clinical symptoms and anamnesis (for example, insufficient nutrition). Laboratory studies may include determining the level of niacin in the blood and excretion of Niacin metabolites in urine. Treatment includes niacin oral intake.

4. Pantotenic acid (vitamin B5): the indispensable component of Coenzyme A

Pantotenic acid, or vitamin B5, is the predecessor of Coenzyme A (COA), a key cofactor involved in the metabolism of carbohydrates, fats and proteins, as well as in the synthesis of acetylcholine, neurotransmitter, which plays an important role in memory, training and muscle control.

• The mechanism of action: COA participates in:

  • Crebs cycle: COA is necessary for the receipt of acetyl-koa into the Crebs cycle, ensuring energy production in mitochondria.
  • Synthesis of fatty acids: COA is involved in the synthesis of fatty acids, important components of cell membranes and myelin, an isolation layer surrounding the nerve fibers.
  • Cholesterol synthesis: COA is involved in the synthesis of cholesterol necessary for the structure of cell membranes and the synthesis of steroid hormones.
  • Acetylcholine synthesis: COA is necessary for the synthesis of acetylcholine, neurotransmitter, which plays an important role in transmitting nerve impulses in the brain and muscles.

• The consequences of the deficit: Pantothenic acid deficiency is extremely rare, since this vitamin is widespread in food products. Symptoms of deficiency may include:

  • Fatigue: Reducing energy and increased fatigue.
  • Headache:
  • Irritability:
  • Sleep violation:
  • Numbness and tingling in the arms and legs: Peripheral neuropathy.

• Diagnostics and treatment: Diagnosis of pantothenic acid deficiency is difficult due to the nonspicuousness of symptoms and the absence of reliable laboratory methods. Treatment includes oral intake of pantothenic acid.

5. Pyridoxine (vitamin B6): Central vitamin for the synthesis of neurotransmitters and Milin

Pyridoxine, pyridoxal and pyridoxamine are forms of vitamin B6, which acts as a coherent for more than 100 enzymes involved in amino acid metabolism, neurotransmitter synthesis (serotonin, dopamine, norepinephrine and range), hem synthesis (hemoglobin component) and the formation of myelin. Vitamin B6 plays a key role in maintaining the health of the nervous system.

• The mechanism of action: Pyridoxal-5-phosphate (PLP), the active form of vitamin B6, participates in:

  • Transamination: PLP is involved in the transamination of amino acids, the process necessary for the synthesis of essential amino acids and the removal of an excess of amino acids.
  • Decarboxylation: PLP is involved in the decarboxylation of amino acids necessary for the synthesis of neurotransmitters: triptophanes in serotonin, histidine in histamine, glutamate in GABA.
  • GEMA synthesis: PLP is involved in the synthesis of hem, a hemoglobin component necessary for the transfer of oxygen in the blood.
  • Mielin synthesis: PLP is involved in the synthesis of sphingolipids, important components of myelin, an isolation layer surrounding the nerve fibers.
  • Glycogenolise: PLP is involved in glycogenolysis, the process of splitting glycogen into glucose, providing energy for nerve cells.

• The consequences of the deficit: Vitamin B6 deficiency can lead to:

  • Peripheral neuropathy: Numbness, tingling and pain in the arms and legs.
  • Convulsions: Especially in children.
  • Depression: Deficiency of serotonin, dopamine and norepinephrine.
  • Anemia: Disruption Synthesis Gem.
  • Seborrheic dermatitis:
  • Glossitu:

  High doses of vitamin B6 (more than 200 mg per day) can also cause peripheral neuropathy.

• Diagnostics and treatment: Diagnosis of vitamin B6 deficiency is based on clinical symptoms and laboratory studies, such as determining the level of pyridoxal-5-phosphate (PLP) in the blood. Treatment includes oral intake of vitamin B6. It is important to observe the recommended doses to avoid neurotoxicity caused by an excess of vitamin B6.

6. BIOTIN (vitamin B7): An important cofactor for the metabolism of fatty acids and glucose

Biotin, or vitamin B7, is a cofactor of carboxylase, enzymes involved in the metabolism of fatty acids, glucose and amino acids. Although the Biotin deficiency is rare, it can affect the nervous system.

• The mechanism of action: Biotin participates in:

  • Gloundogenesis: Biotin is necessary for pyruvatkarboxylase, an enzyme involved in gluconeogenesis, the process of glucose synthesis from non-carb sources.
  • Synthesis of fatty acids: Biotin is necessary for acetyl-coal carboxylase, an enzyme involved in the synthesis of fatty acids.
  • Leucine catabolism: Biotin is necessary for beta-methylcronel-coal of carboxylase, an enzyme participating in the catabolism of leucine, amino acids, which plays a role in neurotransmissions.

• The consequences of the deficit: Biotin deficiency can lead to:

  • Dermatitis: Especially in the face.
  • Hair loss:
  • Neurological symptoms: Depression, fatigue, convulsions.
  • Parestesis: Numbness and tingling in the limbs.

  Biotin’s deficiency can occur with excessive use of raw eggs, since avidine contained in raw eggs binds biotin and prevents its absorption.

• Diagnostics and treatment: Diagnosis of biotin deficiency is based on clinical symptoms and laboratory studies, such as determining the level of biotin in the blood and excretion of biotin metabolites in urine. Treatment includes oral intake of biotin.

7. Folic acid (vitamin B9): necessary for the synthesis of DNA and neurotransmitters

Folic acid, or vitamin B9, plays a key role in the synthesis of DNA, RNA and amino acids, as well as in the metabolism of homocysteine. It is absolutely necessary for the normal development of the nervous system, especially during pregnancy.

• The mechanism of action: Folic acid in the form of tetrahydrofolat (ThF) is involved in:

  • Nucleotides synthesis: ThF is necessary for the synthesis of purines and pyrimidins, construction blocks of DNA and RNA.
  • Amino acid metabolism: ThF is involved in the metabolism of homocysteine, turning it into methionine. A high level of homocysteine ​​is associated with an increased risk of cardiovascular diseases and neurological disorders.
  • Synteze neurotransmitted: WF is involved in the synthesis of serotonin, dopamine and norepinephrine.

• The consequences of the deficit: Folic acid deficiency can lead to:

  • Megaloblastic anemia: Violation of the formation of red blood cells.
  • Fruit nervous tube to defects: The back of the bifid (cleft spine) and anencephalus (lack of brain).
  • Depression: Deficiency of serotonin, dopamine and norepinephrine.
  • Cognitive disorders: Deterioration of memory and attention.
  • Increased level of homocysteine: Increasing the risk of cardiovascular diseases and dementia.

• Diagnostics and treatment: Diagnosis of folic acid deficiency is based on clinical symptoms and laboratory studies, such as determining the level of folic acid in the blood and homocysteine ​​level. Treatment includes oral intake of folic acid. Pregnant women are recommended to take folic acid to prevent defects in the nervous tube in the fetus.

8. Kobalamin (vitamin B12): Critically important for myelinization and functioning of nerve cells

Cobalamine, or vitamin B12, plays a key role in the formation of myelin, isolation layer surrounding the nerve fibers, as well as in the synthesis of DNA and RNA, and in the metabolism of homocysteine. Vitamin B12 deficiency can lead to serious and irreversible neurological disorders.

• The mechanism of action: Cobalamin participates in:

  • Mielin synthesis: Cobalamin is necessary for the synthesis of sphingolipids, important components of myelin. Demielinization (destruction of myelin) leads to a violation of the transmission of nerve impulses and the development of neurological symptoms.
  • Homocysteine ​​metabolism: Cobalamin is involved in the transformation of homocysteine ​​into methionine. Vitamin B12 deficiency leads to an increase in homocysteine ​​levels, which increases the risk of cardiovascular diseases and neurological disorders.
  • Synthesis of succinyl-KOA: Cobalamin is necessary for the transformation of methylmalonyl-koa into a succinyl-cooa, which enters the Krebs cycle for energy production.

• The consequences of the deficit: Vitamin B12 deficiency can lead to:

  • Megaloblastic anemia: Violation of the formation of red blood cells.
  • Peripheral neuropathy: Numbness, tingling and pain in the arms and legs.
  • Myelopathies: The damage to the spinal cord, leading to weakness, impaired coordination and incontinence of urine and feces.
  • Dementia: Cognitive disorders, worsening memory and attention.
  • Mental disorders: Depression, psychosis.
  • Optical neuropathy: Vision of vision.

  Vitamin B12 deficiency is more common in elderly people, vegetarians and vegans, as well as in people with diseases of the gastrointestinal tract, violating the absorption of vitamin B12 (for example, atrophic gastritis, Crohn’s disease). Pernicious anemia is an autoimmune disease in which the body produces antibodies to the inner factor of casla, the protein necessary for the absorption of vitamin B12 in the intestine.

• Diagnostics and treatment: Diagnosis of vitamin B12 deficiency is based on clinical symptoms and laboratory studies, such as determining the level of vitamin B12 in the blood, homocysteine ​​and methylmalonic acid level (MMA). Treatment includes intramuscular or subcutaneous administration of vitamin B12, especially in cases of severe deficiency or impaired absorption. The oral intake of vitamin B12 can be sufficient for the treatment of mild deficiency.

Assessment and additional sources of group B vitamins

An adequate assessment of the status of B vitamins B is crucial for the early detection of deficiency and prevent the development of serious complications. A comprehensive assessment usually includes a history of anamnesis, a physical examination and laboratory research.

• A history of history: A detailed history should include information about the diet, taking drugs, the presence of diseases of the gastrointestinal tract and other risk factors for the deficiency of vitamins of group B.
• Physical examination: Physical examination can reveal signs of deficiency of B vitamins, such as glossitis, heit, dermatitis, neurological disorders and mental disorders.
• Laboratory research: Laboratory studies may include determining the level of group B vitamins in the blood, homocysteine ​​levels, methylmalonic acid (MMA) and the activity of enzymes dependent on vitamins of group B.

After confirming the deficiency of B vitamins, it is necessary to start the appropriate treatment. Treatment usually includes oral intake of group B vitamins, but in some cases intramuscular or subcutaneous administration of vitamins may be required. It is important to consider the possible interactions of group B vitamins with other drugs.

Providing sufficient consumption of group B vitamins through food or additives is important for maintaining the optimal functioning of the nervous system. Good dietary sources include:

• TIAMIN (B1): Pork, whole grain products, legumes.
• Riboflavin (b2): Dairy products, eggs, meat, green vegetables.
• Niacin (B3): Meat, fish, poultry, peanuts, mushrooms.
• Pantotenic acid (B5): Widely distributed in food products, especially in meat, eggs, milk and vegetables.
• Pyridoxin (B6): Meat, fish, poultry, bananas, potatoes.
• Biotin (B7): Eggs, liver, nuts, seeds.
• Folic acid (B9): Green leafy vegetables, legumes, citrus fruits.
• Kobalamin (B12): Meat, fish, poultry, dairy products.

Recent studies

Active studies continue to study the role of group B vitamins in the nervous system, especially in the context of aging, neurodegenerative diseases and mental disorders. Results show the potential role of group B B Vitamins:

• Slow down cognitive decline: Some studies show that taking B vitamins can slow down a cognitive decline in older people, especially in those who have increased homocysteine ​​levels.
• Improving mood and reducing depression symptoms: B vitamins can play a role in regulating mood and reduce symptoms of depression, especially in combination with other treatment methods.
• Reducing the risk of defects in the nervous tube: Taking folic acid during pregnancy reduces the risk of defects in the nerve tube in the fetus.
• Protection from neurodegenerative diseases: Studies show that group B vitamins can have a protective effect against neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, but further studies are needed to confirm these results.

Conclusion

B vitamins are absolutely necessary to maintain the health of the nervous system. The deficiency of any of these vitamins can lead to a variety of neurological and mental disorders. An adequate assessment of the status of B vitamins and timely treatment of deficiency are crucial to prevent the development of serious complications. Maintaining a balanced diet rich in group B vitamins, or taking appropriate additives can help ensure the optimal functioning of the nervous system and the general state of health. Recent studies continue to expand our understanding of the role of group B vitamins in the nervous system and open up new opportunities for the prevention and treatment of neurological disorders.