The influence of group B vitamins on the nervous system

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The influence of group B vitamins on the nervous system

B1 (thiamine): the key to the energy support of nerve cells

Tiamin, or vitamin B1, plays a fundamental role in maintaining the health of the nervous system, primarily due to its participation in carbohydrate metabolism. Carbohydrates are the main source of energy for the brain and nerve cells, and thiamine is a cofactor for several key enzymes involved in this process. In particular, it is necessary for the work of the enzymes of pyruvate dehydrogenase (PDH), alpha-metoglutaratratdehydrogenase (α-kgdh) and transcetolase.

• The role in glucose metabolism: PDH catalyzes the transformation of the pyruvate into acetyl-koa, which then enters the Crebs cycle (citric acid cycle) for energy production in the form of ATP. Tiamine deficiency leads to a decrease in PDH activity, which limits the flow of energy into the brain.
• Alpha-kooglutardroadsta α-kgdH is also a key enzyme in the Crebs cycle, and its activity also depends on thiamine. A decrease in α-kgdh activity further violates the production of energy in nerve cells.
• Transcetolasa and pentosophosphate paths: Transcophosphate pathos plays a role in the pentosophosphate path, which is important for the synthesis of nucleotides (necessary for DNA and RNA) and NADPH (NADPH), an important reducing agent that protects the cell from oxidative stress. Tiamin deficiency reduces transcetolase activity, violating these processes.
• Myelination: Tiamin can also play a role in myelinization of nerve fibers, although accurate mechanisms are still studied. Myelin is a fat shell surrounding the nerve fibers, which provides fast and effective transmission of nerve impulses.

Clinical manifestations of thiamine deficiency:

Tiamine deficiency can lead to serious neurological disorders, the most famous of which are:

• Vernika-Korsakov’s disease: This is a severe neurological disorder, which is often observed in people who abuse alcohol. Alcohol prevents the absorption of thiamine and increases its excretion from the body. Vernik’s disease is characterized by a triad of symptoms: encephalopathy (confusion), ataxia (impaired coordination of movements) and ophthalmoplegia (paralysis of the eye muscles). Korsakova syndrome, which often follows the disease of Wernick, is characterized by memory disorders, especially anterograd amnesia (inability to form new memories) and retrograde amnesia (loss of past memories), as well as confabulations (false memories). The pathophysiology of Vernika-Korsakov’s disease includes damage to the mamillalar bodies, thalamus and cerebellum.
• Since Beri-Bury is a disease caused by a deficiency of thiamine, which can manifest itself in various forms. There is dry Beri Berie, which is characterized by peripheral neuropathy (damage to the peripheral nerves), manifested by weakness, numbness and tingling in the limbs. There is also a moist Beri-Bury, which is characterized by heart failure, edema and shortness of breath. Cerebral Beri-Bury also exists and includes neurological manifestations similar to Wernik’s disease.
• Optical neuropathy: Tiamine deficiency can also lead to optical neuropathy, causing vision of vision.

Diagnosis and Treatment Deficit Thiamine:

Diagnosis of thiamine deficiency may include measuring the level of thiamine in the blood or transcetic activity in red blood cells. Treatment includes the introduction of thiamine, usually intravenously or intramuscularly, in high doses. It is important to start treatment as early as possible to prevent irreversible damage to the nervous system.

B2 (riboflavin): role in redox reactions

Riboflavin, or vitamin B2, is the predecessor of two important coofers: Flavmononucleotide (FMN) and Flavideninindinucleotide (FAD). These coenzymes are involved in a wide range of redox reactions that are necessary for the production of energy and the functioning of the nervous system.

• Participation in the electron-transport circuit: FAD is a component of the II complex in the electron-transport circuit, which is located in mitochondria. The electron-transport chain plays a key role in the production of ATP, the main source of energy for cells.
• Metabolism of fatty acids: FAD is necessary for the enzyme Acil-Coa dehydrogenase, which is involved in the beta-oxidation of fatty acids. Beta-oxidation of fatty acids is an important source of energy, especially for the brain during starvation.
• Metabolism of other vitamins: Riboflavin is involved in the metabolism of other B vitamins, such as folic acid and vitamin B6. It is necessary to turn folic acid into its active form and for the formation of the pyridoxal-5-phosphate coofficient (PLP) from vitamin B6.
• Antioxidant Protection: FAD is also involved in the functioning of glutathioneductase, an enzyme that plays an important role in antioxidant cell protection.

Clinical manifestations of riboflavin deficiency:

Riboflavin deficiency is rarely found in isolation, often accompanied by a deficiency of other vitamins of group B. Symptoms of deficiency may include:

• Heyrozy: Cracks and ulcers in the corners of the mouth.
• Glossit: Inflammation of the tongue.
• Seborrheic dermatitis: Inflammation of the skin with peeling, especially on the face and folds of the skin.
• Anemia: Reducing the level of red blood cells.
• Neurological symptoms: Include peripheral neuropathy, weakness and depression. Rarely, can lead to ataxia.

Diagnosis and Treatment Fisheries Deficit:

Diagnosis of riboflavin deficiency may include measuring the level of riboflavin in the blood or the activity of glutathioneductase in red blood cells. Treatment includes riboflavin oral intake.

B3 (niacin): role in energy metabolism and DNA of reparation

Niacin, or vitamin B3, is the predecessor of two important coofers: nicotinydenindininicleotide (above) and nicotinindinindinoucleotidfosphate (NADF). These coofers participate in hundreds of enzymatic reactions, including energy metabolism, DNA and RNA synthesis, and cell alarm.

• Energy metabolism: Above and NADF are involved in glycolis, the Crebs cycle and the electron-transport chain, playing a key role in the production of ATP.
• DNA Reparation: Above is a substrate for PARP enzymes (polymerase), which are involved in DNA reparations. DNA damage is one of the factors that contribute to aging and the development of neurodegenerative diseases.
• Cell alarm: Participates in cell alarm, affecting the expression of genes and protein activity.
• Antioxidant Protection: NADF is involved in the functioning of glutathioneductase, which plays an important role in the antioxidant protection of cells.

Clinical manifestations of niacin deficiency:

The severe shortage of niacin leads to Pellagra, the disease characterized by the “triad d”: dermatitis, diarrhea and dementia.

• Dermatitis: Symmetric dermatitis, especially in areas of skin, exposed to sunlight.
• Diarrhea: Inflammation of the mucous membrane of the gastrointestinal tract, leading to diarrhea.
• Dementia: Neurological symptoms, including depression, anxiety, confusion and dementia.

A less pronounced Niacin deficiency can manifest with fatigue, weakness, headaches and irritability.

Diagnosis and Treatment Niacina Deficit:

Diagnosis of Pellagra is based on clinical manifestations. The level of niacin in the blood is not always a reliable indicator of deficiency. Treatment includes niacin oral intake.

Niacin and cholesterol:

Niacin (in the form of nicotinic acid) in high doses (1-3 grams per day) was used to reduce the level of LDL cholesterol (poor cholesterol) and increase the level of HDL cholesterol (good cholesterol). However, due to side effects, such as tides, itching and hepatotoxicity, its use is limited.

B5 (pantothenic acid): key to Coenzym A

Pantotenic acid, or vitamin B5, is the predecessor of cooferment A (COA), which plays a central role in the metabolism of carbohydrates, fats and proteins.

• Metabolism of carbohydrates, fats and proteins: KOA is involved in the cycle of Krebs, beta-oxidation of fatty acids and synthesis of fatty acids. It is also necessary for the synthesis of acetylcholine, a neurotransmitter, playing an important role in teaching and memory.
• Cholesterol synthesis: KOA is also involved in cholesterol synthesis.
• Detoxification: COA is necessary for detoxification of some drugs and toxins.

Clinical manifestations of pantothenic acid deficiency:

The deficiency of pantothenic acid is extremely rare, since it is widespread in food. Symptoms of deficiency may include:

• Fatigue:
• Headaches:
• Insomnia:
• Numbness and tingling in the arms and legs (paresthesia):
• Irritability:
• Abdominal pain:

Diagnosis and treatment of pantothenic acid deficiency:

Diagnosis of pantothenic acid deficiency is complex, since there are no reliable laboratory tests. Treatment includes oral intake of pantothenic acid.

B6 (pyridoxin): neurotransmitter synthesis and nerves protection

Pyridoxine, or vitamin B6, is a group of compounds, including pyridoxine, pyridoxal and pyridoxamine. All these compounds can be converted into pyridoxal-5-phosphate (PLP), a coherent that is involved in more than 100 enzymatic reactions, many of which are important for the functioning of the nervous system.

• Synthesis of neurotransmitters: PLP is necessary for the synthesis of many neurotransmitters, including serotonin, dopamine, norepinephrine and GABA (gamma-aminobatic acid). These neurotransmitters play an important role in the regulation of mood, sleep, appetite and cognitive functions.
• Amino acid metabolism: PLP is involved in amino acid metabolism, including transamination, decarboxylation and desulfhydrination.
• GEMA synthesis: PLP is necessary for the synthesis of hem, a hemoglobin component that transfers oxygen in the blood.
• Myelination: PLP can play a role in myelinization of nerve fibers.
• Gluconeogenesis: PLP is involved in gluconeogenesis, the process of glucose synthesis from non-carb sources.

Clinical manifestations of pyridoxine deficiency:

Pyridoxine deficiency can lead to various neurological symptoms, including:

• Depression:
• Irritability:
• Anxiety:
• Confusion:
• Peripheralic neuropathy: Numbness, tingling and pain in the arms and legs.
• Convulsions: Especially among infants.
• Seborrheic dermatitis:
• Glossit:
• Stomatitis: Inflammation of the mucous membrane of the mouth.
• Anemia:

Medicinal interactions:

Some drugs may disrupt vitamin B6 metabolism, increasing the risk of deficiency. These include:

• Isaonazid: Used to treat tuberculosis.
• Penicillamin: Used to treat the disease of Wilson and rheumatoid arthritis.
• Oral contraceptives:

Diagnosis and Treatment Pyridoxine Deficiency:

Diagnosis of pyridoxine deficiency may include measuring the level of pyridoxal-5-phosphate (PLP) in the blood. Treatment includes the oral intake of pyridoxine.

Overdose by vitamin B6:

High doses of vitamin B6 (more than 100 mg per day) for a long time can lead to sensory neuropathy, characterized by numbness and tingling in the arms and legs. Symptoms usually disappear after the cease of taking vitamin B6.

B7 (BIOTIN): Support for metabolic pathways and cell growth

Biotin, or vitamin B7, is a cooferment for several carboxylase, enzymes that participate in important metabolic tracks, including:

• Gluconeogenesis: Synthesis of glucose from non -nuclear sources. Biotin is a cofactor for pyruvatkarboxylase, which catalyzes the first stage of gluconeogenesis.
• Synthesis of fatty acids: Biotin is a cofactor for acetyl-coal carboxylase, which catalyzes the first stage of synthesis of fatty acids.
• Amino acid metabolism: Biotin is involved in the metabolism of some amino acids such as leucin.

Biotin also plays a role in the regulation of genes expression and cellular growth.

Clinical manifestations of biotin deficiency:

Biotin’s deficiency is rare, but can occur in people who consume raw eggs in large quantities for a long time. Raw eggs contain avidine, protein, which is associated with biotin and prevents its absorption. Other causes of biotin deficiency include:

• Genetic defects: Some genetic defects may disrupt biotin metabolism.
• Long -term parenteral nutrition:
• Reception of some drugs: For example, anticonvulsants.

Symptoms of biotin deficiency may include:

• Dermatitis: Especially around the mouth, nose and eyes.
• Hair loss (alopecia):
• Fitty nails:
• Neurological symptoms: Depression, fatigue, numbness and tingling in the arms and legs.

Diagnosis and Treatment Biotin Deficit:

Diagnosis of a biotin deficiency may include measuring the level of biotin in the blood or urine. Treatment includes oral intake of biotin.

Biotin and hair loss:

Biotin is often advertised as a means of treating hair loss. However, studies show that biotin is effective only for the treatment of hair loss caused by biotin deficiency. If hair loss is not associated with a deficiency of biotin, the intake of biotin is likely not to bring any benefit.

B9 (folic acid): development of the nervous tube and neurotransmissance

Folic acid, or vitamin B9, is the predecessor of tetrahydrofolat (TGF), a coherent that is involved in single -iron metabolism. A single -iron metabolism is necessary for the synthesis of DNA and RNA, amino acids and neurotransmitters.

• Synthesis DNA and RNA: TGF is necessary for the synthesis of purines and pyrimidins, construction blocks of DNA and RNA.
• Amino acid metabolism: TGF is involved in the metabolism of some amino acids such as homocysteine.
• Synthesis of neurotransmitters: TGF is necessary for the synthesis of serotonin, dopamine and norepinephrine.

Clinical manifestations of folic acid deficiency:

Folic acid deficiency can lead to serious health problems, especially during pregnancy.

• Nervous tube defects: The deficiency of folic acid during pregnancy increases the risk of defects in the nervous tube in the fetus, such as spinal splitting (spina bifida) and anencephaly. The nervous tube is formed in the early stages of pregnancy and is the predecessor of the brain and spinal cord.
• Megaloblastic anemia: Folic acid deficiency leads to a violation of DNA synthesis in blood cells, which leads to the formation of large and immature red blood cells (megaloblasts).
• Neurological symptoms: Folic acid deficiency can cause neurological symptoms such as depression, fatigue, irritability, peripheral neuropathy and cognitive disorders.

Folic acid and homocysteine:

Folic acid is involved in the metabolism of homocysteine, amino acids, which in high concentrations is associated with an increased risk of cardiovascular diseases, dementia and osteoporosis. Folic acid deficiency can lead to an increase in the level of homocysteine ​​in the blood.

Recommended dose of folic acid:

The recommended daily dose of folic acid for adults is 400 mcg. Women planning pregnancy or pregnant women are recommended to take 600-800 μg of folic acid per day to prevent defects of the nervous tube in the fetus.

Diagnosis and treatment of folic acid deficiency:

Diagnosis of folic acid deficiency may include measuring the level of folic acid in the blood or red blood cells. Treatment includes oral intake of folic acid.

B12 (cobalamin): myelination, DNA synthesis and neurological function

Cobalamin, or vitamin B12, plays a critical role in the functioning of the nervous system and bloodiness. He is a cofactor for two important enzymes: methylmalonil-cooa mutazy and methioninsyntase.

• Methylmalonil-Coa mutase: This enzyme catalyzes the transformation of methylmalonil-cooa into succinyl-Coa, which is involved in the Crebs cycle. Vitamin B12 deficiency leads to the accumulation of methylmalonic acid (MMA), which can be toxic for the nervous system.
• Methioninsintase: This enzyme catalyzes the transformation of homocysteine ​​into methionine. Metionine is necessary for the synthesis of S-adenosylmetionine (SAME), which is an important donor of methyl groups in various biochemical reactions, including DNA methylation and neurotransmitters. Vitamin B12 deficiency leads to the accumulation of homocysteine ​​and a decrease in the level of SAME, which can negatively affect the function of the nervous system.
• Myelination: Vitamin B12 is necessary to maintain the integrity of the myelin shell that surrounds and protects the nerve fibers. Vitamin B12 deficiency can lead to demyelinization, the process of destruction of the myelin shell, which violates the transmission of nerve impulses.
• DNA synthesis: Vitamin B12 is necessary for the synthesis of DNA, especially in rapidly dividing cells, such as blood cells.

Clinical manifestations of vitamin B12 deficiency:

Vitamin B12 deficiency can lead to various neurological and hematological symptoms.

• Megaloblastic anemia: Like a deficiency of folic acid, vitamin B12 deficiency leads to a violation of DNA synthesis in blood cells, which leads to the formation of large and immature red blood cells (megaloblasts).
• Neurological symptoms: Neurological symptoms of vitamin B12 deficiency can be varied and include:
  • Peripheralic neuropathy: Numbness, tingling and pain in the arms and legs.
  • Subanarious combined degeneration of the spinal cord: Damage to the spinal cord, which leads to a violation of coordination of movements (ataxia), weakness and spasticity.
  • Cognitive disorders: Reduced memory, confusion of consciousness and dementia.
  • Depression:
  • Psychosis:
  • Optical neuropathy:

Causes of vitamin B12 deficiency:

Vitamin B12 deficiency can be caused by various factors, including:

• Insufficient consumption: Vitamin B12 is mainly contained in animal products, so vegans and vegetarians are at risk of deficiency.
• Distribution of absorption:
  • Personic anemia: Autoimmune disease in which the body produces antibodies to the inner factor of Cabas, the protein that is necessary for the absorption of vitamin B12 in the intestine.
  • Gastroctomy: Removing part or the entire stomach.
  • Atrophic gastritis: Inflammation of the mucous membrane of the stomach, which leads to a decrease in the production of the internal factor of calamas.
  • Malbsorbs syndrome: Diseases that disrupt the absorption of nutrients in the intestines, such as the disease of the crown and celiac disease.
  • Reception of some drugs: Metformin (used to treat diabetes) and proton pump inhibitors (used to reduce the acidity of the stomach) can disrupt the absorption of vitamin B12.
• Increased need: Pregnancy and lactation increase the need for vitamin B12.

Diagnosis and treatment of vitamin B12 deficiency:

Diagnosis of vitamin B12 deficiency may include:

• Measurement of vitamin B12 in the blood:
• Measurement of the level of methylmalonic acid (MMA) in the blood or urine: An increased MMA level indicates a deficiency of vitamin B12.
• Measurement of the level of homocysteine ​​in the blood: An increased level of homocysteine ​​may indicate a deficiency of vitamin B12 or folic acid.
• Blood test for the presence of antibodies to the internal factor of Kla: For diagnosis of pernicious anemia.

Treatment of vitamin B12 deficiency includes:

• Vitamin B12 injections: Injections are usually used to treat vitamin B12 deficiency caused by a violation of absorption.
• Vitamin B12 oral reception: High doses of vitamin B12, taken orally, can be effective for the treatment of deficiency, especially if it is caused by insufficient consumption.
• Dietary changes: An increase in the consumption of products rich in vitamin B12, such as meat, fish, eggs and dairy products. For vegans and vegetarians, enriched products and additives of vitamin B12 are available.

The interaction of B vitamins B:

It is important to note that B vitamins work synergically. The deficiency of one vitamin group B can affect the metabolism of other B vitamins, which can aggravate the symptoms. Therefore, in some cases, it can be useful to take a complex of B vitamins, and not individual vitamins.

Conclusion (not included, according to the assignment)

Attention: This article is intended only for information purposes and should not be considered as a medical consultation. Before taking any additives, especially in high doses, consult your doctor. Self -medication can be dangerous for your health.