Vitamins and minerals. Seizures: A Nutraceutical Approach

Vitamins for epilepsy are simply necessary for the body, strengthening and maintaining the immune system, but you need to know which of them should be consumed.

Vitamins are substances necessary for the normal functioning of patients with epilepsy. However, epilepsy requires controlled intake of vitamins.

Why you need to take vitamins

Firstly, some hereditary metabolic diseases can provoke the development epileptic seizures. For example, a disorder of vitamin B6 (pyridoxine) metabolism, which was diagnosed at the birth of a child using a biotic blood test, may be the cause of convulsive attacks in children. early age(calls them pyridoxine).

Secondly, a variety of antiepileptic drugs with prolonged use can affect the level of vitamins such as E, D, C, B22, B6, B2, biotin, beta-carotene, folic acid in the body.

In addition, research recent years suggests that a deficiency of these vitamins in the body of patients who suffer from epilepsy may affect the development of certain behavioral disorders.

How to take vitamins correctly

But in case of epilepsy, constant replacement vitamin intake is also controversial, and uncontrolled use of vitamins as self-medication and according to an inconsistent treatment regimen (combined vitamin therapy or monotherapy, duration of vitamin therapy, daily dose of vitamin preparations, etc.) with a doctor is simply unacceptable.

Vitamins for epilepsy should be taken under close supervision. This should be remembered, because unbalanced or prolonged use of certain vitamins may reduce the effectiveness of antiepileptic drugs, and it is also possible to provoke epileptic seizures (for example, uncontrolled and long-term use of drugs folic acid).

Vitamins for pregnant women suffering from epilepsy However, at the same time, prescribing folic acid to women childbearing age who suffer from epilepsy and who are taking carbamazepine or valproic acid, is indicated to prevent the teratogenic effects of antiepileptic drugs on the fetus and to reduce the risks of miscarriage or the birth of a baby with a congenital malformation.

What vitamins are used in the treatment of epilepsy?

Vitamin B2 (riboflavin, lactoflavin)

One of the most important water-soluble vitamins, a coenzyme of many biochemical processes. Vitamin B2 is necessary for the formation of red blood cells, antibodies, and for regulating growth and reproductive functions in the body. It is also essential for healthy skin, nails, hair growth, and overall health of the entire body, including thyroid function. Vitamin B2 also promotes the absorption of pyridoxine (vitamin B6).

Riboflavin deficiency primarily affects tissues rich in capillaries and small vessels (for example, brain tissue). With vitamin B2 deficiency, a frequent manifestation may be cerebral insufficiency of varying severity, manifested by a feeling of general weakness, dizziness, decreased tactile and pain sensitivity, increased tendon reflexes, etc. The need for riboflavin increases with increased physical activity, as well as when taking riboflavin antagonists - oral contraceptives and some antiepileptic drugs. Therefore, a diet rich in riboflavin or vitamin therapy may be prescribed to patients with epilepsy.

Foods high in riboflavin include liver, kidney, yeast, egg white, cheese, fish, almonds, champignons, porcini mushrooms, chanterelles, cottage cheese, broccoli, buckwheat, meat, milk, germ of cereals, peas, leafy green vegetables. Riboflavin is found in small amounts in refined rice. pasta, white bread, fruits and vegetables.

The human body does not store riboflavin “in reserve”, and any excess is excreted in the urine (with an overdose of riboflavin, the urine turns bright yellow).

Vitamin B5 (pantothenic acid)

Necessary for the metabolism of fats, carbohydrates, amino acids, the synthesis of vital fatty acids, cholesterol, histamine, acetylcholine, hemoglobin. Pantothenic acid gets its name from the Greek "pantothene", meaning "everywhere", due to its extremely wide distribution. Pantothenic acid, entering the body, is converted into pantethine, which is part of coenzyme A, which plays an important role in the processes of oxidation and acetylation. Vitamin B5 is necessary for the normal absorption and metabolism of folic acid (vitamin B9).

Vitamin B1 (thiamine) increases the effectiveness of vitamin B5.

Homopantothenic acid is a natural homologue of pantothenic acid (vitamin B5) and is a compound in which β-alanine is replaced by γ-aminobutyric acid (GABA). It is quite widespread in the plant and animal world and is found in the brain in an amount of 0.5-1% of the total content of GABA in tissues. The cause of vitamin B5 deficiency can be a low content of proteins, fats, vitamin C, B vitamins in food, diseases small intestine with malabsorption syndrome, as well as long-term use of certain antiepileptic drugs (for example, barbiturates), many antibiotics and sulfonamides. The concentration of the vitamin decreases from exposure to caffeine and alcohol. For alcohol poisoning and sunburn There may be a condition close to vitamin B5 deficiency.

Symptoms of vitamin B5 deficiency: fatigue, depression, sleep disturbance, increased fatigue, headaches, nausea, muscle pain, burning, tingling, numbness of the toes, burning, excruciating pain in the lower extremities, mainly at night, redness of the skin of the feet, dyspepsia, decreased body resistance to infections (frequent occurrence of acute respiratory diseases).

A person’s daily need for vitamin B5 is satisfied with a normal mixed diet, since pantothenic acid is found in many animal products and plant origin(buckwheat and oatmeal, peas, garlic, fish roe, egg yolk, green parts of plants, milk, carrots, cauliflower, bran bread, etc.). In its most concentrated form, it is found in brewer's yeast and royal jelly. In addition, vitamin B5 is synthesized by intestinal flora.

Side effects when taking pantothenic acid are very rare, and occasionally dyspepsia may occur. An overdose of vitamin B5 is possible with long-term use not only of single drugs, but also with uncontrolled use multivitamin complexes with high doses of vitamin.

Vitamin B6

Vitamin B6 is common name three substances: pyridoxine, pyridoxal, pyridoxamine, as well as their phosphates, among which the most important is pyridoxal phosphate. In the human body, any of these substances is converted into the phosphorylated form of pyridoxine - pyridoxal phosphate, which takes part in the formation of red blood cells, participates in the processes of glucose uptake by nerve cells, and is necessary for protein metabolism and transamination of amino acids. Pyridoxal phosphate ensures the processes of decarboxylation, transamination, deamination of amino acids, participates in the synthesis of protein, enzymes, hemoglobin, prostaglandins, the metabolism of serotonin, catecholamines, glutamic acid, gamma-aminobutyric acid (GABA), histamine, improves the use of unsaturated fatty acids, reduces cholesterol and lipids in the blood, improves myocardial contractility, promotes the conversion of folic acid into its active form, and stimulates hematopoiesis. A sufficient amount of vitamin B6 is necessary for normal functioning liver.

Possible consequences of vitamin B6 deficiency: seizures, depression, irritability, increased anxiety; dermatitis on the face, above the eyebrows, near the eyes, sometimes on the neck and in the scalp, dry dermatitis in the nasolabial fold, seborrhea, glossitis, cheilitis with vertical cracks in the lips, stomatitis; decreased appetite, nausea and vomiting (especially in pregnant women), conjunctiva, polyneuritis, decreased T-lymphocyte population.

Diet therapy with a high content of pyridoxine or courses of vitamin therapy can be prescribed by an epileptologist for secondary pyridoxine deficiency and drug-induced hepatopathy caused by long-term use of various antiepileptic drugs (for example, valproic acid drugs). Therefore, pyridoxine can be included in combination potentiated therapy with antiepileptic drugs. However, uncontrolled high doses of pyridoxine or prolonged use may reduce the effectiveness of antiepileptic therapy. The need for pyridoxine increases when taking antidepressants and oral contraceptives, during stress and increased exercise, as well as in people who drink alcohol and smoke. Corticosteroid hormones (hydrocortisone, etc.) can also lead to the leaching of vitamin B6, and when taking estrogen-containing drugs, a pronounced deficiency of vitamin B6 occurs.

In addition, vitamin B6 is prescribed in high doses conditions for hereditary disorders of pyridoxine metabolism with the development of pyridoxine-dependent seizures, which debut in young children.

Foods high in pyridoxine include unrefined cereal grains, leafy greens, yeast, buckwheat and wheat cereals, rice, legumes, carrots, avocados, bananas, walnuts, molasses, cabbage, corn, potatoes, soybeans, meat, fish, oysters, cod and cattle liver, kidneys, heart, egg yolk.

Self-medication and unreasonable prescription of vitamin B6 are unacceptable; with an overdose of pyridoxine, allergic reactions may develop in the form of urticaria, increased acidity of gastric juice, numbness and tingling in the arms and legs, up to loss of sensitivity (exogenotoxic polyneuropathic syndrome). Excessive (high) doses of vitamin B6 can lead to severe toxic effects.

Vitamin B7 (biotin, vitamin H, coenzyme R)

A water-soluble vitamin that is a cofactor in the metabolism of fatty acids, leucine and in the process of gluconeogenesis. Biotin improves the functional state of the nervous system. It also helps in the absorption of protein and is an important ally of other B vitamins in metabolism, such as folate and pantothenic acid and vitamin B12. In addition, it is involved in the breakdown of fatty acids and fat burning. Biotin is also produced by beneficial intestinal microflora, but the question of the amount of vitamin we get from this source remains debatable.

A small risk of biotin deficiency may exist in people who for a long time live on intravenous nutrition. If a person receives long-term treatment antiepileptic drugs, antibiotics or drinking alcohol, biotin synthesis can be sharply reduced due to the death of beneficial intestinal bacteria, which makes additional intake necessary.

With a lack of biotin, the following are observed: nervousness, irritability, skin lesions, pale smooth tongue, drowsiness, lethargy, depression, muscle soreness and weakness, arterial hypotension, high cholesterol and blood sugar, anemia, loss of appetite and nausea, deterioration of hair condition, growth slows down. The richest foods in biotin are yeast, tomatoes, spinach, soybeans, egg yolk, mushrooms, liver, milk, and cauliflower.

Vitamin B9 (folic acid)

A water-soluble vitamin necessary for the growth and development of the circulatory and immune systems. Humans do not synthesize folic acid, receiving it through food or through synthesis by intestinal microflora. Folic acid is found in green leafy vegetables, legumes, wholemeal bread, yeast, liver, and is part of honey. Folic acid is necessary for the creation and maintenance of new cells in a healthy state, so its presence is especially important during periods of rapid development of the body - at the stage of early intrauterine development and in early childhood.

The administration of folic acid is indicated for women of childbearing age suffering from epilepsy and taking valproic acid and carbamazepine in order to prevent the teratogenic effect of antiepileptic drugs on the fetus and reduce the risk of miscarriage (spontaneous miscarriage) or the birth of a child with congenital malformations of the neural tube, heart and urogenital tract , as well as chromosomal abnormalities.

In this case, the prescription of folic acid, the selection of the dose and treatment regimen are carried out by neurologists-epileptologists, neurogeneticists or medical geneticists under the control of the level of folic acid in the blood and the presence/absence of gene mutations that further disrupt the metabolism of folates in the woman’s body (for example, mutations of the methylenetetrahydrofolate reductase gene) .

The decision on the choice of vitamin therapy for women planning a pregnancy or pregnant women should be individualized and must be discussed with the attending physician, a neurologist-epileptologist, since prolonged and uncontrolled use of folic acid preparations leads to hypervitaminosis and provocation of epileptic seizures.

Vitamin B23 (carnitine)

It is an amino acid found in all tissues of the body. L-carnitite is one of the main essential substances, since it plays a major role in the transport of fatty acids to mitochondria (the “energy” station of cells), where fatty acid are broken down to produce the energy necessary for the functioning of the entire organism. Fatty acids on their own are not able to penetrate into mitochondria, therefore the efficiency of energy metabolism depends on the content of L-carnitine in cells. Only L-carnitine has biological activity. D-carnitine has no effect positive influence on the body and interferes with the absorption of L-carnitine, increasing carnitine deficiency.

A quarter of the daily requirement of carnitine is produced in our body from lysine and methionine, vitamins (C, B3 and B6) and iron. A deficiency of any of these substances leads to carnitine deficiency. The remaining 75% of the daily carnitine requirement should be obtained from food. The name "carnitine" (from the Latin word "caro" - meat) indicates the main source of this amino acid. Most carnitine is found in meat, poultry, and seafood. Grains, fruits and vegetables contain carnitine in small quantities.

The level of vitamin carnitine in the blood plasma may decrease in patients with epilepsy taking valproic acid drugs (Depakine, Convulex, Convulsofin, etc.) both in monotherapy and in combination with other antiepileptic drugs (phenobarbital, phenytoin or carbamazepine), as well as in ketogenic diet. Therefore, the administration of vitamin B23 is sometimes used in combination with taking antiepileptic drugs or against the background of a ketogenic diet.

One of the indications for the use of L-carnitine is hereditary mitochondrial diseases, including clinical picture which include epileptic seizures. Mitochondrial diseases are accompanied by profound disturbances in energy metabolism, which leads to the development of lactic acidosis and the accumulation of toxic metabolic products. L-carnitine affects the processes of cell bioenergetics through the correction of key links in energy metabolism. A feature of therapy is the need for long-term (in in some cases lifelong) use of carnitine and prescription of doses exceeding physiological ones. Generalized experience of clinical observation of patients with mitochondrial diseases (carnitine deficiency, diseases associated with defects of the respiratory chain) shows that carnitine-based drugs are very effective and contribute to either regression of clinical manifestations of the disease or a decrease in their intensity

The main signs of L-carnitine deficiency are: fast fatiguability, drowsiness and muscle weakness; hypotension; depression; in children - a lag in physical and psychomotor development; among schoolchildren – a decrease in academic performance; dysfunction of the heart and liver.

With low effectiveness of diet therapy, vitamin B23 is prescribed in the form of biological active additives to food or medicines. Dosages of carnitine should be selected by the attending physician, a neurologist-epileptologist, for each specific case, depending on the individual characteristics of the patient, health status, nutrition and level of physical activity.

With uncontrolled or long-term use of vitamin B23, undesirable drug reactions may develop: increased activity, problems falling asleep, nausea, vomiting, abdominal cramps and diarrhea (diarrhea); less often - bad smell body and other gastrointestinal symptoms.

Vitamin C (ascorbic acid)

Necessary for the normal functioning of connective and bone tissue, performs biological functions a reducing agent and coenzyme of certain metabolic processes, considered as an antioxidant. Ascorbic acid is involved in the formation of collagen, serotonin from tryptophan, the formation of catecholamines, the synthesis of corticosteroids, and is involved in the conversion of cholesterol into bile acids.

Vitamin C is necessary for detoxification in hepatocytes with the participation of cytochrome P450, therefore it can be prescribed against the background of long-term use of antiepileptic drugs metabolized in the liver in order to prevent or reduce the severity of drug-induced hepatopathy (for example, with long-term use of drugs valproic acid, phenytoin, carbamazepine, oxcarbazepine, etc.). Vitamin C itself neutralizes the superoxide anion radical to hydrogen peroxide, restores ubiquinone and vitamin E, stimulates the synthesis of interferon, thereby participating in immunomodulation. In nature, significant amounts of ascorbic acid are found in citrus fruits, as well as many vegetables. The richest ascorbic acid kiwi fruits, rose hips, red peppers, citrus fruits, black currants, onions, tomatoes, leafy vegetables (for example, lettuce and cabbage).

Vitamin therapy should be carried out under the supervision of the attending physician (neurologist-epileptologist), since an overdose of vitamin C can cause irritation of the urinary tract, itchy skin, diarrhea

Vitamin D (ergocalciferol – vitamin D2, cholecalciferol – vitamin D3)

Regulates the exchange of calcium and phosphorus in the body. If a person has hypovitaminosis D, then it is excreted from the body a large number of salts of calcium and phosphorus, while bone, which is almost the only place where they accumulate, begins to quickly lose these elements. Osteoporosis and osteopenia develop, bones become soft, curved and break easily. A person receives vitamin D in two ways: from food and from one’s own skin, where it is formed under the influence of ultraviolet rays.

Vitamin D deficiency with the development of osteoporosis, osteopenia and osteomalacia has been shown as a result of numerous studies in patients with epilepsy who have been taking drugs of the carbamazepine group for a long time (finlepsin, tegretol, carbaleptin, etc.), oxcarbazepine (Trileptal), phenytoin, and also (less often) with long-term use high doses of valproic acid drugs. Therefore, vitamin D can be prescribed by an epileptologist in conjunction with antiepileptic drugs in the form of short and repeated courses in individually selected dosages.

However, self-medication with vitamin D is dangerous. Ergocalferol (vitamin D2) is very toxic and is poorly excreted from the body, which leads to a cumulative effect. The main symptoms of overdose: nausea, dehydration, malnutrition, lethargy, increased body temperature, muscle hypotension, drowsiness, followed by severe anxiety, convulsions. Cholecalciferol (vitamin D3) is less toxic, but even with its prophylactic use it is necessary to keep in mind the possibility of overdose (accumulation in the body - cumulation), especially in children (this vitamin should not be prescribed more than 10-15 mg per year).

During treatment with vitamin D (especially when taking combination drugs vitamin D with calcium, for example Calcium D3, etc.), biochemical control of the calcium content, as well as active metabolites of vitamin D in the blood and urine, is required. Biochemical control is also required when simultaneously prescribing vitamin D with antiepileptic drugs with a predominantly renal elimination route, for example: topiramate drugs (Topamax, Topsaver, Torial, etc.), since the risk of nephrolithiasis—the formation of urinary tract stones—increases. In adult patients suffering from epilepsy and related arterial hypertension, you should remember the risk of overdose (cumulation) of vitamin D when combined with the use of antihypertensive drugs - thiazide diuretics. Diphenine and barbiturates reduce the effectiveness of vitamin D.

With hypersensitivity and an overdose of vitamin D, hypercalcemia, hypercalciuria and symptoms caused by them may be observed - heart rhythm disturbances, nausea, vomiting, headache, weakness, irritability, weight loss, extreme thirst, frequent urination, kidney stone formation, nephrocalcinosis, soft tissue calcification, anorexia (lack of appetite), arterial hypertension, constipation, kidney failure.

At chronic poisoning vitamin D - demineralization of bones, calcium deposition in the kidneys, blood vessels, heart, lungs, intestines, dysfunction of organs, which can lead to death.

Vitamin E (tocopherol)

Vitamin E (tocopherol) combines a number of unsaturated tocopherol alcohols, of which alpha-tocopherol is the most active. Vitamin E is involved in ensuring adequate reproductive function, improves blood microcirculation, is necessary for tissue regeneration, and is useful for premenstrual tension syndrome and the treatment of fibrotic breast diseases. It ensures normal blood clotting and healing, reduces the risk of keloid scar formation after injury, lowers blood pressure, helps prevent the development of cataracts (clouding of the lens of the eye), relieves leg muscle cramps (cramps), supports healthy nerves and skeletal muscles, prevents anemia. As an antioxidant, vitamin E protects cells from damage by slowing down the oxidation of lipids (fats) and the formation of free radicals, slows down the aging process, and reduces the risk of developing Alzheimer's disease.

Food sources of vitamin E are vegetable oils (sunflower, cottonseed, corn), apple seeds, nuts (almonds, peanuts), turnips, green leafy vegetables, cereals, legumes, egg yolk, liver, milk, oatmeal, soybeans, wheat and its sprouts . Herbs rich in vitamin E: dandelion, alfalfa, flaxseed, nettle, oats, raspberry leaf, rose hips.

The first and earliest sign, which appears quite quickly with insufficient intake of vitamin E from food and excess intake of unsaturated fatty acids, is muscular dystrophy. Necrosis has been described in the liver with vitamin E deficiency, fatty degeneration, expansion of sinusoids, decrease in glycogen content. May suffer reproductive system and myocardium.

Vitamin E can be included in combination potentiated therapy with antiepileptic drugs, since it enhances their anticonvulsant effect, reduces the risk and degree of menstrual irregularities during long-term use of valproic acid drugs, reduces the threat of miscarriage, and reduces the severity of menopausal vegetative syndrome. The role of vitamin E in reducing the risk of catamenial attacks associated with premenstrual tension syndrome in women of childbearing age has not been sufficiently studied.

Self-medication with vitamin E is unacceptable, since it requires individual and slow titration of the dose, starting with minimal dosages, under the supervision of the attending neurologist-epileptologist. Supplemental tocopherol may cause an increase in blood pressure and serum triglycerides, and may reduce the need for insulin in concomitant insulin-dependent patients. diabetes mellitus. With long-term intake of vitamin E, additional biochemical screening of the level of tocopherol in the blood serum is advisable to exclude its accumulation and reduce the risk of developing intoxication.

Folic acid is a water-soluble substance belonging to the B vitamins, it is also known as folacin or vitamin B9. It is not synthesized in the human or animal body; the source is food and normal intestinal flora. Derivatives of folic acid - folates - are the results of its metabolism in the body, they participate in many metabolic processes and are cofactors in many enzymatic reactions for the synthesis of amino acids. Folic acid is important for normal processes of tissue growth, development and proliferation, including erythropoiesis and embryogenesis. In addition, folic acid has an estrogen-like effect and therefore makes it possible to reduce the amount of hormones taken during hormone replacement therapy.

Taking folic acid is thought to reduce the risk of cervical cancer in women taking oral contraceptives. Until recently, folate deficiency was associated to a greater extent with pathology of the development of the central nervous system and folate deficiency anemia. Today it is also correlated with the risk of developing acute coronary syndrome and strokes. It is believed that folic acid provides prevention of deep venous thrombosis and embolism.

The fact that folic acid deficiency in pregnant women leads to the development congenital pathology central nervous system in children has been known for 50 years. Neural tube defects are one of the most serious birth defects, with spina bifida and anencephaly being the most common among them. According to statistics, every year 500,000 children are born in the world with such anomalies. Already in 1964, the Lancet published the results of a Liverpool study, in which out of 98 women who gave birth to children with defects of the central nervous system, 54 were found to have a disorder of folic acid metabolism. Normally, within 28 days after fertilization, the development of the fetal neural tube is completed, and it is very important that pregnant women take folic acid during this period. Often, however, at this time women do not yet know about their pregnancy.

Neural tube defects develop as a result of problems with its closure or, in some cases, as a result of reopening. Anencephaly results in either stillbirth or early death after birth, while newborns with spina bifida today survive, especially with intensive treatment and surgery. These children most often become severely disabled with paralysis and pelvic dysfunction. In the mild version, these are kyphosis and scoliosis. Such children are lagging behind in mental development, psychologically they are less adaptive to environment. Folic acid occupies a special place in epilepsy. Firstly, because antiepileptic drugs reduce the level of folic acid in the blood plasma. And secondly, because after the epileptic attack itself, the content of folic acid in the brain drops. Both of these factors contribute to an increase in the duration of attacks.

According to WHO recommendations, daily requirement in folic acid for adults and children over 12 years of age is 400 mcg (0.4 mg), the same dose is recommended for pregnant women and women wishing to become pregnant. Some WHO experts recommend increasing the dose to 5 mg during pregnancy and lactation.

In recent years, data have emerged on the important role of hyperhomocysteinemia (HHC) in the pathogenesis of microcirculatory and thrombotic complications in various diseases, including obstetric practice, and its connection with folic acid deficiency. K. McCully proved the connection between increased level homocysteine ​​in the blood, metabolic disorders or lack of folic acid and early development atherosclerosis. Subsequently, many studies have proven the role of HHC in the pathogenesis of early myocardial infarction and thrombovascular disease, the development of deep and superficial vein thrombosis, carotid artery thrombosis, Crohn's disease, and some mental illness(epilepsy), etc. There is evidence of a connection between HHC and the development of Down syndrome. In recent years, HHC has been associated with obstetric pathology, including recurrent miscarriages, gestosis, premature detachment normally located placenta (PONRP), placental insufficiency, intrauterine growth retardation (IUGR).

Homocysteine ​​is an amino acid containing a sulfhydryl group, which is a product of the metabolism (demethylation) of dietary methionine, which is abundant in animal protein. In plasma it is found in 4 forms, and the term “total plasma (serum) homocysteine” refers to the pool of all forms of homocysteine ​​(HC). Homocysteine ​​is metabolized by remethylation or transsulfuration. The metabolic process occurs with the participation of vitamins - folic acid and its derivatives, folates, as cofactors, as well as B2, B6, B12, etc. Normal content homocysteine ​​in the blood of non-pregnant women is 5-15 µmol/l. If the level is higher, then they speak of mild (16-30 µmol/l), moderate (31-100 µmol/l) and severe (more than 100 µmol/l) HHC. However, in pregnant women, the concentration of GC in the blood is significantly lower than in non-pregnant women, and is 3-4 µmol/l (up to 5 µmol/l). HHC can be caused by many factors. These include various diseases and medications leading to a decrease in plasma folate, genetic abnormalities (mutations in the genes of such important enzymes as cystathione B synthetase (CBS), methylenetetrahydrofolate reductase (MTHFR)), dietary deficiency of folate and B vitamins.

Special attention deserve genetic defects. The most common genetic cause of severe HHC and classic homocystinuria (congenital) is a homozygous CBS mutation. The incidence of this pathology in the general population is 1 in 300 thousand, and the result is an increase in the fasting HC level up to 40 times the norm. This defect is inherited in an autosomal recessive manner. Clinical manifestations include lens dislocation and others eye complications, mental retardation (in approximately 50% of cases), skeletal deformities, early atherosclerosis and atherothrombotic (vascular) complications. Approximately half of untreated homozygous patients experience vascular complications before the age of 30 years. The heterozygous form manifests itself as moderate HHC, is more common and accounts for 0.3-1% in the general population.

The most common enzyme defect associated with mildly elevated GC levels is a mutation in the gene encoding MTHFR. MTHFR catalyzes the conversion of folic acid to its active form. To date, 9 mutations of the MTHFR gene located in the 1p36.3 locus have been described. The most common of them is the C677T substitution (in the MTHFR protein - substitution of alanine for valine), which is manifested by thermolability and a decrease in the activity of the MTHFR enzyme. It has been noted that increasing the folate content in food can prevent an increase in the concentration of GC in plasma.

An increase in the level of homocysteine ​​in the blood plasma directly correlates with the inhibition of thrombomodulin synthesis, a decrease in the activity of AT III and endogenous heparin, as well as with the activation of the production of thromboxane A2. In the future, such changes cause microthrombosis and microcirculation disorders, which, in turn, plays a significant role in the pathology of the spiral arteries and the development of obstetric complications associated with changes in the uteroplacental circulation.

In the early stages of pregnancy, HHC may be associated with impaired placentation, fetoplacental blood flow and, consequently, with miscarriage. At later stages (II, III trimesters) - with the development of chronic placental insufficiency, PONRP, chronic intrauterine fetal hypoxia, fetal malnutrition and a number of complications of the newborn period. According to A.D. Makatsaria (2001), the MTHFR mutation and the accompanying HHC were found in 45% of the examined women with recurrent pregnancy loss. In patients with pregnancy complicated by placental insufficiency, IUGR, antenatal fetal death, HHC is detected in 22% of cases. HHC is also associated with the development of generalized microangiopathy in the second half of pregnancy, manifested as late gestosis. With gestosis, there is a significant increase in the content of GC in the blood compared to uncomplicated pregnancy and there is a direct correlation with the severity of gestosis. All these statements in equally also refer to the MTHFR mutation, which is the most common cause GGC. Thus, according to the literature, in pregnant women with preeclampsia, the frequency of detection of the MTHFR C677T mutation is significantly increased. It occurs most often when severe forms gestosis (77.8%) and repeated gestosis (86.7%). Also, women with the mutation have a significantly increased risk of developing severe gestosis in subsequent pregnancies (53.8%).

With all the variety of manifestations and causes pathogenetic prevention and treatment of HHC of various origins imply the administration of folic acid both before conception and throughout pregnancy and lactation at a dose of at least 4-5 mg/day, and with severe folate deficiency, homozygous MTHFR mutation and moderate and severe HHC, the dose of folic acid is increased to 6-8 mg per day. If necessary, conventional anticoagulant and antiplatelet therapy is added. In addition, it is necessary to prescribe B vitamins: B1, B6, B12 (1 mg/day). Therapy is so simple and safe drugs allows you to significantly reduce or even normalize the level of GC.

MTHFR mutation and HHC certainly play an important role in the structure of reproductive losses and obstetric complications. Therefore, screening in risk groups is necessary, which will allow us to establish the cause and pathogenetically correctly carry out the prevention of complications to reduce maternal and perinatal morbidity and mortality.

In the clinic of obstetrics and gynecology of City Clinical Hospital No. 1 named after. N.I. Pirogov examined 55 pregnant women with varicose veins veins lower limbs and 63 pregnant women with varicose veins of the lower extremities with thrombotic complications during this pregnancy or in history. The percentage of MTHFR mutations was 12% in group 1, 38% in group 2, and HHC mutations were 15.7 and 48.9%, respectively. The data obtained indicate sufficient big role HHC in the development of thrombotic complications in pregnant women.

Together with the laboratory of clinical immunology (headed by corresponding member of the Russian Academy of Medical Sciences, MD G.T. Sukhikh), 120 women aged 18 to 38 years were examined. Group I consisted of 40 patients with undeveloped pregnancy; Group II - 40 patients with progressive pregnancy and symptoms of incipient miscarriage, of which 77.5% suffered from recurrent miscarriage, and Group III - 40 healthy pregnant women. All pregnant women underwent a comprehensive examination, including examination for infections, hormonal, immunological examinations, etc. The hemostasis system was also examined: thromboelastogram with the determination of r + k, ma, ITP; aggregation activity of platelets with ADP, indicators of fibrinogen concentration, APTT, AVR, PTI, RKMF were determined. An examination was carried out for genetic factors of thrombophilia (mutations C677T in the MTHFR gene, G1691A (Leiden) in the factor V gene, G20210A in the prothrombin gene) using allele-specific PCR. As a molecular factor of thrombophilia, the level of homocysteine ​​in venous blood plasma was determined by ELISA. All pregnant women received complex therapy taking into account the examination results. If hyperhomocysteinemia was detected, folic acid (Folacin) at a dose of 5 mg per day and B vitamins were prescribed; HHC was monitored after 2 weeks. Thrombophilia correction was carried out according to well-known schemes depending on the hemostasiogram parameters. The hemostasiogram was monitored every 10-14 days throughout pregnancy.

The following results were obtained: a mutation in the MTHFR gene was detected in 60 and 50% of patients in groups I and II, respectively, in the control group - in 10% of pregnant women. The average level of GC in groups I and II was 8.92 ± 1.21 and 8.72 ± 1.5 μmol/l, respectively, which is almost 2 times higher than the norm for pregnant women; in the control group it was 5.15 ± 0. 05 µmol/l. Already 2 weeks after the start of therapy with folic acid and B vitamins, there was a decrease in the level of GC to standard values ​​- 2.32 ± 0.5 and 2.1 ± 0.3 μmol/l in groups II and III, respectively. When studying hemostasiograms of patients with HHC and genetic forms Thrombophilia most often (in 86% of cases) revealed an increase in the activity of prothrombin complex factors and hypercoagulation along the internal pathway. The average level of ITP in this group of pregnant women was 17.4 ± 2.6 conventional units, PTI - 111.4 ± 0.6. At the same time, the average concentrations of fibrinogen, APTT and AVR were within normal limits. Hyperaggregation and activation of intravascular coagulation were detected in 26 and 42% of cases, respectively, and directly correlated with the presence of other factors of thrombophilia and miscarriage in patients (APS, anti-CG sensitization, hyperandrogenism, etc.). Platelet aggregation activity averaged 38.2 ± 2.8%. Correction of thrombophilic conditions was carried out taking into account the severity of changes in hemostasiograms according to generally accepted schemes.

The data obtained indicate the important role of HHC in the genesis of miscarriage and the development of thrombotic complications, and therefore the need for their diagnosis. The HC level in risk groups is significantly higher than in healthy pregnant women. The administration of folic acid and B vitamins allows normalizing homocysteine ​​levels within 2 weeks after the start of therapy. It is important to add adequate doses of folic acid to the complex of medications when treating epilepsy in pregnant patients.

In general important role folic acid in normal course pregnancy in various groups of pregnant women is beyond doubt, as a result of which it is recommended to prescribe folic acid (Folacin) at a dose of 5 mg per day.

The capabilities of our brain are such that its potential remains to be understood and understood. Today, many publications compare the speed of information processing by the brain with the work of a high-speed computer. This is not entirely true - rather, the capabilities of a computer are approaching the capabilities of our brain.
From school curriculum We know that the work of the brain is carried out by transmitting low-precision electrical signals, which contain information in encrypted form about what needs to be done at a given moment in time. Moreover, the speed of information transfer is such that we perform these actions as if “automatically”. In fact, all our actions are conscious, but we don’t even have time to realize them when we perform them. This is especially true for situations where you need to act “without thinking.” This does not mean that we are all stupid and do not understand what we are doing. We are talking about the mechanism of brain activity. And we have the same one not only for the functioning of the brain: everything metabolic processes at the ionic level they follow the laws of interaction of weak electric fields and, accordingly, weak currents. In order for the electrical signal to be transmitted correctly, the “wire” system must be debugged. Although our body also has “wireless” communication. But the “wires” system is the main one. The role of signal conductors is the nervous system, all of whose endings are covered with myelin “insulation”. Myelin is produced from lecithin, which is discussed in some detail in the book. Each nerve ending (I ask medical readers to forgive the primitiveness of the presentation, since the book is intended mainly for the average person) is washed with at least three blood vessels. This is necessary because metabolic processes in the nervous system occur at speeds that are beyond ordinary understanding. All brain activity of the nervous system is subject to strict laws of coordination. Therefore, when electrical processes in the brain are disrupted for some reason, a “short circuit” occurs - a burst of discharge in individual nerve cells. These bursts of activity cause conditions called epileptic seizures. Epilepsies are characterized by various external manifestations:

1. objective loss of consciousness followed by prolonged convulsions;
2. temporary loss of consciousness without convulsions;
3. partial loss of consciousness with preservation motor activity and speech; in this case, speech is controlled, although with great difficulty;
4. lack of perception of reality, hallucinations and lack of control over one’s own actions, which is characteristic of impaired activity temporal lobe brain;
5. partial non-perception of something (temporary “switching off” of the senses).

Epilepsy can be caused either by a genetic predisposition (Morphan's syndrome - “disease of geniuses”) or acquired. The acquired disease manifests itself mainly after a head injury or after severe viral infection brain (encephalitis, meningitis, stroke, tumor).
Among the non-drug drugs for epilepsy, we recommend special diet, based on the body’s production of excess ketone bodies - a product of the breakdown of fats. At the same time, the consumption of sugar and starch-containing carbohydrates is practically eliminated. A person gets energy almost exclusively from consumed fats. There is even a technique described in medical literature, which prescribes a diet: for 1 g of proteins and carbohydrates - 4 g of fat. Ketone bodies, by reducing appetite, cause chemical changes in the saturation center of the brain. In some way that is not fully understood, they reduce electrical activity in the brain as a whole, which partially improves the condition. Although those suffering from epilepsy should not experience emotional swings and outbursts, “quenching” with ketone bodies is not best way out, because an excess of fats is also harmful. It’s more logical to build yourself balanced diet according to the principle of the maximum permissible and minimum necessary energy costs according to the regime of their life activity. This diet allows for quite a few adjustments. wide range, because it is tied to energy costs, and not just to therapeutic measures.
Folic acid, about the importance of which for the body a lot is said in the text, is lost by the body in epilepsy: according to at least, after each attack its content in the brain drops. But, on the other hand, its use can reduce the level of anticonvulsants taken in the blood. Therefore, your doctor should monitor your folic acid levels from time to time and adjust the appropriate dose of your anticonvulsant drug. For example, if you take phenobarbital, then folic acid will neutralize it and, on the contrary, will provoke a seizure. Nicotinic acid increases the effectiveness of medications, but your doctor should prescribe the dosage, because you are unique. What suits you may not suit anyone else in the world. You may know about many drugs, but yours is the one that helps you. In general, deficiency of B vitamins (thiamin, pyridoxine) stimulates seizures. Anticonvulsants, in turn, remove them from the body. Replenishing the norm of this particular vitamin group weakens the occurrence of seizures and reduces their frequency. Independence in taking vitamin complexes is useless, since overdoses can lead to nervous disorders. (Symptoms of over- and under-dosing, see “Desperation Therapy”). Typically, B vitamins are prescribed in combination with fin-lepsin and phenobarbital. To reduce the convulsive readiness of the brain, Depaten is prescribed. Finlepsin itself begins to have a therapeutic effect only against the background of a targeted increase in immunity, restoration of the salt composition of the blood and the absence of problems with the intestines. This is due to the fact that the body functions as if “on its own,” and the electrical activity of the brain is restrained “on its own,” which does not interfere with the normal functioning of the body (together with the brain, of course) generally. Preventive administration of the drug has a proactive effect. As you remember, the speed of signal transmission in the brain is such that a short delay is not perceived in any way. Magnesium, whose role in brain function is also well documented, also affects the frequency of attacks: the less magnesium, the more frequent they are. There is a lot of magnesium in fresh greens. In some cases, medications (magnesium aspartate) are taken. Greens and bile acids, as you remember, stimulate the formation of antihemorrhagic vitamin K, which reduces the danger internal bleeding(bleeding). At the same time, it is advisable to take tocopherol (vitamin E). The amino acid taurine, which objectively suppresses the electrical activity of the brain, can only be recommended by your attending physician. It reduces the frequency of attacks and allows you to reduce the dosage of anticonvulsants, but overdoses can worsen the encephalogram. The provocation of attacks can be influenced by some nonspecific allergens, including those necessary for cerebral circulation, such as Omega-6 fatty acids. This applies to attacks of the temporal lobe. The phenomenon is rare, but it must be kept in mind when choosing a treatment method. Some proteins are also provocateurs, but which ones will be determined by the results of analyzes and studies.
Epilepsy attacks in children were relieved after several courses of treatment with complexes of Tibetan herbal formulas, including those intended only for adults, but according to the dosage of “Desperation Therapy”. For example, in Krivoy Rog, neurologist I. A. Vinnichek has a case where a seven-year-old child with epilepsy did not get results with the help of finlepsin, and herbal formulas made it possible to completely abolish anti-convulsant therapy ( brochure “Doctors - about NEWAYS products.” Based on materials from the Second All-Russian Conference of Doctors, Moscow, 1998). The most studied new drug from the “Tibetan series” is today “Engineer” (the old name is “Einstein”). Its composition:
ginkgo biloba extract - 3.80%;
lecithin - 3.50%;
bacopa manniera extract - 2.55%;
phosphotidylserine - 2.50%;
centella asiatica - 1.90%;
ginseng extract - 0.90%.
This drug, used sublingually (injected under the tongue), is an improved modification of herbal formulas that have been used since ancient times in Tibetan and Ayurvedic medicine for disorders cerebral circulation. It improves inter-synaptic transmission of nerve impulses and neuron trophism. Bacopenes and ginkgo-sides improve memory, especially operational memory, when you need to quickly navigate a large volume of changing information. It is used as an auxiliary drug for long-term intense workloads by accountants, tax officers, customs officers, businessmen, and people simply tired of brain overload. As a parapharmaceutical drug, it is used for cerebral palsy, hydrocephalus and other diseases of the nervous system in children. For adults it is used mainly for acute and chronic cerebrovascular accidents. For ischemic strokes, it is taken together with drugs that relieve inflammatory processes in the nervous system. It is clear that these drugs must be compatible. Due to its powerful cleansing and restorative effect on the vascular system of the brain, the drug naturally causes a sharp improvement in brain activity. The results are noticeable literally in the first tens of hours. Therefore, with increased convulsive readiness it is advisable to take it under the supervision of a specialist in brain pathologies. This is a necessary precaution: it is unknown how this particular brain will behave with a sharp improvement in its blood. Undoubtedly, activity will increase, but is it necessary in this particular situation? Changes in the tissues of the brain matter that provoke the appearance of epilepsy can be eliminated provided that the usual rehabilitation scheme is followed, which is the opposite of the appearance of the diagnosed disease: disorder - infection - chronic inflammatory course - disorder at the cellular level (genocode). That is, in order to eliminate the cause of the disease, it is necessary to go through its development, “restoring bridges” along the way.

Related Terms
Generalized Seizures; Partial Complex Seizures; Epileptic Seizures; Temporal lobe epilepsy
Basic Suggested Natural Methods Treatments
Ketogenic Diet; Nutritional Support
Other Suggested Natural Treatments
Acupuncture; electromagnetic therapy (transcranial magnetic stimulation); fish fat; Food Allergens Identification and Avoidance; ; Melatonin; Kalinji; taurine; traditional chinese vegetable medicines(Saiko-Keishi-i sho-Saiko-k); Yoga
Herbs and Supplements to Avoid
; 2-Dimethylaminoethanol (DMAE); ; glutamine; Hyssop; Ipriflavone; Japanese star anise; Nicotinamide; Willow White

Epilepsy is a brain disorder that causes repeated episodes of seizures called. A seizure is sometimes referred to as an electrical storm in the brain, leading to abnormal movements, sensations and states of consciousness. In reality, however, it is more orderly than the storm. During a seizure, the nerves function in an abnormally synchronized manner, a sort of parallel, that can last for seconds or minutes. Results range from mild changes in awareness to severe convulsions.

Isolated seizures can occur for many reasons. Term epilepsy used when a person has recurrent seizures without known treatable causes. If the capture occurs in a localized part of the brain, it is called partial capture. If it affects a large part of the brain, it is called epileptic seizures.

The most common forms of generalized seizures are non-convulsive (Petit mal) and tonic-clonic seizures (Grand mal). Petit mal seizures involve a brief period of consciousness that occurs suddenly and lasts for a short time before disappearing; There are usually no symptoms afterwards. A severe attack includes: loss of consciousness, body spasms, tongue biting, and frequent urination. A state of confusion follows capture.

Partial seizures come in three main types. They can be simple (involving only the arm, for example) or complex (involving more complex movements and loss of consciousness). Finally, some may develop into a generalized attack. There are several medications used to treat epilepsy, usually with significant success. Most of these drugs can cause serious side effects, Although. Fortunately, some of these side effects can be partially corrected with nutritional supplements (see nutritional support section).

Key Suggested Natural Treatments

There is no established herb or supplement for the treatment of epilepsy. However, a number of supplements may be useful in treating nutritional deficiencies caused by anticonvulsants. In addition to the herb and supplement, the ketogenic diet may be helpful for controlling seizures in children.

Note: Epilepsy is too serious a condition to self-medicate. For this reason, none of the procedures listed below should be used without the advice and supervision of a physician.

Ketogenic Diet

Before drugs to treat epilepsy were invented, scientists noticed that fasting led to a reduction in the frequency of seizures. Subsequent investigation suppressed a metabolic state called ketosis as causative factor. Ketosis occurs during fasting and also when consuming a diet high in fat and very low content carbohydrates (ketogenic diet).

Once effective anticonvulsant drugs were developed, the ketogenic diet fell out of favor, but in recent years medical interest has returned. Today, the diet is seeing increased use in treating people who do not respond completely to standard medications. Most studies have involved children because they tend to have a more enjoyable diet than adults.

Evidence suggests that a ketogenic diet can almost completely stop seizures in about half of all children with epilepsy and reduce seizure frequency less dramatically in another third. Unfortunately, the ketogenic diet can cause side effects such as nausea, decreased immunity, confusion, dehydration, constipation, and an increased tendency to bruise. Serious side effects seen occasionally with certain forms of the ketogenic diet include kidney stones, gallstones, impaired liver function, severe hypoproteinemia (dangerously low levels of protein in the blood), and kidney damage. Vitamin and mineral deficiencies can occur with some ketogenic diets, but using a multivitamin/multimineral supplement can easily prevent this.

Nutritional Support

Numerous anticonvulsant medications can reduce fat levels of the essential vitamin biotin, perhaps by interfering with its absorption. Valproic acid may affect biotin less than other anticonvulsants.

It is not clear whether it was actually the biotin deficiency that caused any problems. However, it is not good to be short on any of the important nutrients, and for this reason biotin supplementation is recommended during long-term anticonvulsant therapy. Keep in mind, however, that the effects of anticonvulsants may be, at least in part, related to their effects on biotin levels. For this reason, medical supervision is strongly recommended before adding biotin to an anticonvulsant regimen.

Many anticonvulsants increase the risk of osteoporosis and other bone diseases. This is thought to be partly because they impair calcium metabolism (see also sections on vitamin D and vitamin K below). Effects on calcium may also increase tendency to seizures due to a decrease in calcium levels in the blood.

Calcium supplements may thus be beneficial for people taking anticonvulsants. However, some studies indicate that antacids containing calcium carbonate may interfere with the absorption of phenytoin and other anticonvulsants. For this reason, calcium supplements and anticonvulsants should be taken over several hours.

Vitamin D

Anticonvulsants may interfere with vitamin D activity; this may be another contributing factor to anticonvulsant-induced bone problems.

Supplementing with vitamin D may help prevent bone loss. Adequate exposure to sunlight may also help because sunlight causes the body to produce vitamin D.

Vitamin K

Phenytoin, carbamazepine, phenobarbital and primidone accelerate the normal breakdown of vitamin K into inactive byproducts, thereby depriving the body active form Vitamin K. Use of these anticonvulsants by a pregnant mother may result in vitamin K deficiencies in their unborn children, resulting in bleeding disorders or facial bone abnormalities in newborns. For this reason, mothers who take these anticonvulsants may need to supplement with vitamin K during pregnancy.

In other circumstances, anticonvulsants rarely destroy vitamin K enough to cause bleeding problems. However, vitamin K deficiency may contribute to anticonvulsant-induced osteoporosis.

Carnitine

Valproic acid (Depakene) and possibly other anticonvulsants can reduce carnitine levels in the body. For this reason, it has been suggested that people using these drugs should take supplemental carnitine. However, there is no evidence that taking will carnitine provide any noticeable benefits; One study that attempted to evaluate this possibility failed to find any significant effect.

Other proposed treatments for epilepsy

Herbs and Supplements

In traditional Chinese herbal medicines known, the Japanese surnames Saiko-keishi-to and Sho-saiko-to have also been proposed for epilepsy, but the evidence for their use remains very preliminary. Both of these treatments consist of a combination of vodka, peony root, pinellia root, cassia bark, ginger root, unabi fruit, Asian ginseng root, Asian skullcap root, and licorice root, but the proportions are different.

A double-blind study conducted in Iran reportedly found that use of the seed extract Kalinji The plant helped control seizures in children.

Weak evidence suggests that the amino acid taurine may offer modest, short-term benefits in epilepsy.

There are conflicting results that fish oil supplementation may reduce the frequency of seizures in people with epilepsy.

Several studies from one research group hint that melatonin supplements may improve the quality of life of children with epilepsy.

People with epilepsy have lower than normal levels of the mineral manganese in their blood. This suggests (but does not prove) that manganese supplements may be beneficial for epilepsy

Other supplements sometimes suggested for epilepsy (but without significant supporting documentation) include vitamin B 1 , vitamin B 6 , beta-carotene glycine. Herbs that are traditionally regarded as “nervines” or nerve relaxants are also sometimes suggested, for example the following:

• Skullcap
• Lobelia
• Lady's slipper
• Valerian
• Passionflower
• Melissa

However, there is no convincing evidence that they can help, and some of these herbs pose significant safety concerns.

Note A: Most herbs used for epilepsy are sedatives, as are many anticonvulsants. Combination treatments may result in dangerous oversedation. People suffering from epilepsy should therefore seek medical supervision before using any herbs or supplements.

Alternative Treatments

A special form of electromagnetic therapy called transcranial magnetic stimulation has shown promise for epilepsy. In a double-blind, placebo-controlled study, 24 participants suffering from epilepsy localized to a specific part of the brain and not fully responding to drug treatment were given twice-daily treatment with transcranial magnetic stimulation or sham transcranial magnetic stimulation for a week. The results showed a moderate reduction in seizures among participants in this MTP. However, the benefits quickly disappeared when treatment was stopped.

Evidence weakly suggests that food allergen identification and avoidance may be beneficial for people with both migraine and epilepsy.

Acupuncture showed promise for reducing the frequency of seizures in some people with epilepsy in a review of 17 randomized trials with 1,538 people. Lawsuits comparing acupuncture (alone or with medication) to placebo or sham acupuncture; either medication or no treatment. Although some had lower seizure incidence rates with acupuncture alone or with medications, the quality of the studies was low, reducing the validity of the results. Current evidence does not support the use of acupuncture to treat epilepsy.

Yoga has also been studied as a potential treatment. An analysis of 2 randomized trials involving 50 people found mixed results, though. One trial comparing real yoga to yoga scam or not treatment found that real yoga did not reduce the frequency or duration of attacks. But, other research does not support the use of yoga. The researchers stressed the need for more research.

Herbs and Supplements to Avoid for Epilepsy

Numerous herbs and supplements have been associated with unexpected or unexpectedly severe cramps. In most cases, however, evidence implicating any specific natural product Increased seizure activity remains random. Some of the more dangerous "pro-capture" agents are discussed here. Additionally, we discuss herbs and supplements that may interact with medications used for seizures. See also the discussion of folate and biotin above.

The seeds contain a seizure-promoting substance called 4-methoxypyridoxine (MPN). Although seeds Rarely used today, cramps have also been reported using a more normal form of the herb: ginkgo leaf extract. One possible explanation is that the ginkgo leaf products may have been contaminated with ginkgo seeds. Another possibility has been suggested as good: ginkgo may have effects on brain function similar to tacrine, a drug also used to improve memory and which has been linked to seizures. Finally, it has been suggested that ginkgo may negatively affect the effectiveness of Dilantin and Depakote. Regardless of the explanation, people with epilepsy should probably avoid ginkgo.

Many anti-epilepsy drugs work by blocking the action of a substance called glutamate; For this reason, high dosages of the closely related amino acid glutamine may presumably inhibit these drugs and pose a danger to people with epilepsy.

Manufacturers of the DMAE supplement warn that it may increase the risk of seizures.

Tea made from the herb hyssop is considered safe, but hyssop essential oil, like most essential oils, is toxic in excessive doses. Some of the constituents in hyssop oil are believed to increase the risk of seizures. For this reason, hyssop essential oil should not be used by people suffering from epilepsy.

Japanese star anise contains substances that may provoke seizure activity.

Some evidence hints that the supplement may potentially initiate or worsen attack-related illnesses called myoclonic seizures.

Grapefruit juice slows the body's normal breakdown of several drugs, including the anticonvulsant carbamazepine, allowing it to build up potential dangerous levels in blood; this effect may last for 3 days or more after the last glass of juice.

In addition, ipriflavone may increase carbamazepine and phenytoin levels, potentially increasing the risk of side effects.

White willow herb, also known as willow bark, is used to treat pain and fever. White willow contains a substance closely related to aspirin known as salicin. Aspirin is known to increase phenytoin levels and toxicity when long-term use both drugs. This raises concern that white willow may have similar effects to phenytoin, although this has not been proven.

Nicotinamide increases blood levels of carbamazepine and primidone, possibly requiring a dose reduction to prevent toxic effects.

Early reports suggest the possibility that gamma-linolenic acid (GLA) supplementation may worsen temporal lobe epilepsy. However, there was no later confirmation of this.

Aug 18, 2015 HerbApteka

Vitamins for epilepsy are simply necessary for the body, strengthening and maintaining the immune system, but you need to know which of them should be consumed. In this article you can find out why vitamins are needed and which ones epilepsy does not “like”.

Vitamins are substances necessary for the normal functioning of patients with epilepsy. However, epilepsy requires controlled intake of vitamins.

Why you need to take vitamins

Firstly, some hereditary metabolic diseases can provoke the development of epileptic seizures. For example, a disturbance in the metabolism of vitamin B6 (pyridoxine), which was diagnosed at the birth of a child using a biotic blood test, can be the cause of convulsive seizures in early childhood (called pyridoxine).

Secondly, a variety of antiepileptic drugs with prolonged use can affect the level of vitamins such as E, D, C, B22, B6, B2, biotin, beta-carotene, folic acid in the body.

In addition, recent research suggests that a deficiency of these vitamins in the body of patients who suffer from epilepsy may affect the development of certain behavioral disorders.

How to take vitamins correctly

But in case of epilepsy, constant replacement vitamin intake is also controversial, and uncontrolled use of vitamins as self-medication and according to an inconsistent treatment regimen (combined vitamin therapy or monotherapy, duration of vitamin therapy, daily dose of vitamin preparations, etc.) with a doctor is simply unacceptable.

Vitamins for epilepsy should be taken under close supervision. This should be remembered, because unbalanced or prolonged use of certain vitamins may reduce the effectiveness of antiepileptic drugs, and it is also possible to provoke epileptic seizures (for example, uncontrolled and long-term use of folic acid drugs).

Vitamins for pregnant women with epilepsy However, at the same time, prescribing folic acid to women of childbearing age who suffer from epilepsy and who are taking drugs carbamazepine or valproic acid is indicated to prevent the teratogenic effects of antiepileptic drugs on the fetus and to reduce the risks of miscarriage or birth of a baby with a congenital malformation.