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Vitamin B12 in the treatment of diseases of the nervous system.

Vitamin B12 in the treatment of diseases of the nervous system.

Since the second half of the twentieth century. and to the present time, clinical studies are continuing, studying the effectiveness of the use of B vitamins in various neurological diseases. B vitamins (primarily B1 (thiamine), B6 ​​(pyridoxine), B12 (cyanocobalamin)) have been widely used in clinical practice for many years. One of the goals of prescribing vitamins is to replenish their deficiency that develops in various conditions: malnutrition or dietary restrictions in vegetarians, chronic alcoholism, the use of certain medications (for example, isoniazid), after surgical interventions on the gastrointestinal tract, malabsorption syndrome. Studies have shown that a lack of B vitamins, even in developed countries, is not uncommon. Thus, in the USA and Great Britain, vitamin B12 deficiency is observed in 6% of the population, mainly in older age groups [1].

Some genetic diseases, for example, pyridoxine-associated epilepsy, are accompanied by impaired metabolism of vitamins of group B. Lack of essential vitamins of this group leads to a variety of pathologies, including mono- and polyneuropathies, encephalo- and myelopathy of deficient genesis [2]. However, the use of B vitamins is pathogenetically justified even in the absence of their deficiency, due to the fact that, in the form of their coenzymes, they take an active part in biochemical processes that ensure the normal functional activity of various structures of the nervous system. In this regard, B vitamins are often referred to as neurotrophic or neurotropic vitamins. Vitamin B12 (cyanocobalamin) is one of the most important for the normal development and functioning of the nervous system. The history of the discovery of vitamin B12 began in the middle of the 19th century. with a description of the disease, the main manifestation of which was a special form of fatal anemia.

After 20 years, this disease was called “pernicious anemia”. In 1934, doctors D. Maykot and W.P. Murphy received the Nobel Prize for the discovery of the medicinal properties of vitamin B12, and only 12 years later the production of the drug began [3]. Vitamin B12 is the general name for 2 chemical variants of the cobalamin molecule – cyanocobalamin and hydroxycobalamin.

It is the only vitamin that contains essential minerals (mainly cobalt), as well as the only water-soluble vitamin that can accumulate in the body – it accumulates mainly in the liver, but also in the kidneys, lungs and spleen. The human body is not capable of its synthesis. At the same time, vitamin B12 is produced by microorganisms in the digestive tract of any animal, including humans, as a waste product of microflora, but it cannot be absorbed, since it is formed in the large intestine and does not enter the small intestine for absorption [4, 5].

Vitamin B12 in the human body The main sources of vitamin B12 for humans are meat, beef liver, kidneys, fish, milk, eggs. The daily requirement for vitamin B12 for adults is from 2 to 3 μg / day, for children – from 0.3 to 1 μg / day, for pregnant and lactating women – from 2.6 to 4 μg / day [4]. Cyanocobalamin (vitamin B12), being converted in the body with the help of enzyme systems into active coenzymes (methylcobalamin and deoxyadenosylcobalamin), participates in the process of hematopoiesis and maturation of erythrocytes, in the synthesis of creatinine, methionine, nucleic acids, is necessary for the growth and replication of cells.

Vitamin B12 plays an important role in amino acid and carbohydrate metabolism, the biosynthesis of acetylcholine, the formation and functioning of the protein and fat structures of the myelin sheath of the nerve fiber, regulates the work of the blood coagulation system, and reduces the release of excitatory neurotransmitters (glutamate). Vitamin B12 and methionine, as well as vitamin C, play a significant role in the functioning of the central and peripheral nervous system, participating in the metabolism during the production of monoamines [6–8]. The reason for vitamin B12 deficiency in 50–70% of patients (more often in young and middle-aged people, somewhat more often in women) is insufficient secretion of the gastric mucosa of the internal Castle factor (HFK), caused by the formation of antibodies to the parietal cells of the stomach that produce HFK, or to the site of VFK binding with vitamin B12. In about 20% of cases, there is a hereditary complication in relation to HFK deficiency [9].

In these cases, a consequence of vitamin B12 deficiency is the development of the so-called pernicious anemia. In addition, vitamin B12 deficiency can be caused by a stomach tumor, gastrectomy, malabsorption syndrome, helminthiases and dysbiosis, and an unbalanced diet. Other reasons include hereditary diseases characterized by impaired production of proteins that bind to vitamin B12, or a defect in the formation of active forms of the vitamin; metabolic disorders and / or increased need for vitamin



(thyrotoxicosis, pregnancy, malignant neoplasms), as well as long-term use of H2-receptor blockers and proton pump inhibitors.

It should be noted that the reserve of vitamin B12 in the body, even with a limited intake of it, is sufficient for 3-4 years [7-9].

Neurological disorders in vitamin B12 deficiency Cyanocobalamin deficiency, in addition to pernicious anemia, in about a third of patients leads to damage to the nervous system. The main neurological manifestations of vitamin B12 deficiency are: damage to the spinal cord (subacute combined degeneration of the lateral and posterior columns, or funicular myelosis), brain damage (dementia), optic nerves and peripheral nerves of the extremities with the development of distal sensory polyneuropathy [8]. A combined lesion of the central and peripheral nervous system is also possible. Immediate causes of neurological disorders are a violation of methionine synthesis, a slowdown in the oxidation of fatty acids with an odd number of carbon atoms, and the accumulation of methylmalonate, toxic to the nervous system, which causes fatty degeneration of neurons and demyelination of nerve fibers [10]. In addition, the accumulation of neurotoxic substances in the cerebrospinal fluid (CSF) and a decrease in the content of neurotrophic factors were noted.

In experimental studies on laboratory rats, it was found that the lack of vitamin B12 is accompanied by an increase in the content of tumor necrosis factor in the CSF, a decrease in the concentration of epidermal nerve growth factor and interleukin-6. Correction of vitamin B12 intake eliminates these disorders [11]. A number of studies have found that a deficiency of vitamin B12 and vitamin B9 (folic acid) in the mother can lead to defects in the development of the neural tube and the formation of pathology of the nervous system in the fetus. Violation of the formation of the neural tube during pregnancy is manifested by the pathology of the skeletal structures (underdevelopment of the limbs, cleavage of the hard palate, spina bifida), spinal cord (myelomeningocele) and brain (underdevelopment, cysts, malformations, hydrocephalus) of newborns.

Several studies have shown that dietary intake of folate-rich foods during pregnancy and adequate doses of folate and vitamin B12 significantly reduce the risk of fetal neural tube defects [12–14]. It has now been proven that a deficiency of vitamins B6, B12 and B9, resulting from dietary characteristics and / or impaired absorption, is one of the main risk factors for the development of hyperhomocysteinemia, which is an independent risk factor for the development of atherosclerosis, thrombosis, vascular diseases of the brain and dementia. [fifteen].

Pharmacological effects of B vitamins It has been shown that the use of preparations of B vitamins, including B12, can reduce the content of homocysteine ​​in the blood. It was found that the appointment of high doses of B vitamins significantly reduces the progression of atherosclerosis in the early stages of the process. A survey of 779 healthy people and 188 patients with ischemic strokes and transient ischemic attacks showed that a low level of vitamins B9 and B12 in the blood, especially in cases of their combined deficiency, increases the risk of cerebral ischemia [16, 17].

Thus, further prospects for the use of vitamins of group B (B9, B1, B6, B12) in vascular and neurodegenerative diseases of the brain are undeniable, however, it is necessary to conduct controlled clinical studies to assess the effectiveness and safety of drugs. At present, the participation of B vitamins and, in particular, vitamin B12 in the realization of human cognitive abilities has been proven. Thus, at the University of Oxford (Great Britain), the cognitive functions of 1648 subjects in different age groups were assessed for 10 years.

It was found that low levels of vitamin B12 in the blood serum were combined with an increase in the concentration of methylmalonic acid and correlated with a faster rate of decline in cognitive abilities in the examined individuals [17, 18]. J. Kalita and U.K. Misra (India) assessed cognitive functions using the method of cognitive evoked potentials of the brain in 36 patients with megaloblastic anemia aged 16 to 80 years [19].

It was found that clinical and neurophysiological indicators of the state of cognitive functions in the examined subjects were reduced and corresponded to those at the age of 14. An MRI of the head showed changes in white matter and signs of cortical atrophy. Similar changes in the substance of the brain, according to MRI data, have been identified by other researchers [20, 21]. The presence of a correlation between the content of vitamin B12 and methylmalonic acid in blood plasma, the rate of atrophy of the brain substance and a decrease in human cognitive abilities was established. In a prospective study involving 107 subjects aged 61 to 87 years, the above parameters were assessed for 5 years.

Scientists have concluded that low levels of vitamin B12 in blood plasma are the cause of progressive atrophy of the brain substance and subsequent impairment of cognitive functions [22].

Analgesic effect Since 1950s B vitamins are actively used to treat pain syndromes of various etiologies. It should be noted that, until recently, the analgesic effect of vitamins B1, B6 and B12 has been repeatedly questioned. Since the analgesic mechanism of action of these substances for a long time remained unclear, many scientists believed that the analgesic effect of B vitamins was just a placebo effect. However, recent studies have made it possible to create a serious theoretical base confirming the analgesic effect of B vitamins in nociceptive and neuropathic pain. To date, more than 100 studies have been published showing clinical improvement with the use of B vitamins in patients with pain syndromes.

It is assumed that vitamin B12 has the most pronounced analgesic effect [23, 24]. In 2000, the first randomized controlled study of the efficacy of intramuscular vitamin B12 injections for chronic back pain was conducted. The results of a clinical neurological examination of 60 patients aged 18 to 65 years showed a significant decrease in the severity of pain syndrome and an improvement in motor functions. Another controlled study compared the efficacy of vitamin B12 and the antidepressant nortriptyline in treating neuropathic pain in 100 patients with diabetic polyneuropathy (DPN). There was a significant reduction in the intensity of pain on the visual analogue scale (VAS) in the group receiving vitamin B12 injections compared with the group receiving nortriptyline.

In addition, against the background of vitamin B12 therapy in patients with DPN, there was a significant decrease in the severity of paresthesias, burning and chilliness of the legs [23, 25, 26]. A number of experimental studies have shown the presence of an analgesic effect of certain B vitamins and their complexes in neuropathic pain [27, 28]. When the dorsal ganglion was squeezed or the sciatic nerve was ligated, vitamins B1, B6, and B12 administered intraperitoneally reduced thermal hyperalgesia. Repeated administrations of B vitamins produced a persistent decrease in temperature hyperalgesia, with the combination of B vitamins having a synergistic effect in both models of neuropathic pain. The effect of B vitamins on the activity of nociceptive neurons in the central nervous system was studied.

It was found that the activity of nociceptive neurons upon stimulation of sciatic nerve C-fibers decreases dose-dependently against the background of injections of vitamin B6 and a complex of vitamins B1, B6 and B12. In an experiment on laboratory rats, suppression of nociceptive responses was found not only in the posterior horn of the spinal cord, but also in the optic tubercle. Injections of vitamins B6 and B12 reduced nociceptive activity to a greater extent than vitamin B1.

An experimental study of the formaldehyde model of nociceptive pain also revealed the antinociceptive effect of the combination of B1, B6 and B12, which suggests the effect of a complex of B vitamins on the synthesis and functional activity of inflammatory mediators [29]. It was also found that the complex of B vitamins enhances the effect of the main antinociceptive neurotransmitters – norepinephrine and serotonin. Vitamin B12 is able to reduce the release of the excitatory neurotransmitter glutamate in the terminals of the central nervous system [30, 31]. A study by M. Eckert, P. Schejbal (Germany) noted a significant decrease in the intensity of pain and paresthesias during treatment with a complex of B vitamins (pyridoxine, thiamine, cyanocobalamin) in patients with pain syndromes and paresthesias caused by polyneuropathies, neuralgias, radiculopathies and mononeuropathies [32 , 33]. In clinical studies and experimental animal models, it has been shown that in neuropathies, B vitamins enhance the analgesic effect of non-steroidal anti-inflammatory drugs (NSAIDs), as well as the anti-allodynic effect of gabapentin, dexamethasone and valproate [34].

As a result of complex therapy, the duration of treatment and the risk of side effects of the drugs used are reduced. The effectiveness of the combined use of B vitamins and NSAIDs for back pain was especially noted. It was found that the addition of a combination of B vitamins to diclofenac leads to a more rapid achievement of the analgesic effect and allows you to reduce the dose of NSAIDs [35].

In 2009, Brazil conducted a randomized, double-blind study of the efficacy of adding a complex of B vitamins to diclofenac in patients with lumbago. After 3 days of treatment, 46.5% of patients who received diclofenac in combination with a complex of B vitamins showed the disappearance of pain, while with diclofenac monotherapy pain regressed only in 29% of patients [36].

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