Lipoic acid: analogues, sources and beneficial properties of the substance. Alpha lipoic acid and DMAE What determines the cost

In order to always be healthy, feel less tired and enjoy your life to the fullest, a person must not only eat right regularly and spend time outdoors every day. To keep our body in proper shape, we need vitamins and healthy supplements.

The role of superfoods in human life

There are also so-called superfoods that have a fantastic effect on the human body. They got their name due to the fact that they contain a huge amount of vitamins and minerals. Superfoods are extremely beneficial for health. These include, for example, barley, spirulina (a type of blue-green algae), root vegetable), coenzyme Q10, lipoic acid, ginseng.

Significance for the body

Alpha-lipoic acid (analogues in tablets will be presented below) is found in every cell of the human body. After all, we get it from food, and our body, in turn, synthesizes it. Thanks to her, a person leads a full, energetic life. Its advantage is the ability to function in both water and fat.

For the first time, alpha-lipoic acid was obtained from beef liver cells in the fifties of the last century. Nowadays, scientists have learned how to get this product within the walls of the laboratory.

Foods that contain lipoic acid:

  • offal (liver, heart, kidneys);
  • broccoli, spinach, Brussels sprouts, peas, tomatoes;
  • unpolished rice.

But still, the lipoic acid contained in food will not be enough for the body. Therefore, it is recommended, after consulting a doctor, to take it additionally, as an additive to the main food. The specialist will select the dosage that is right for you.

Thanks to lipoic acid, the human body increases the production of the beneficial substance glutathione, which is an antioxidant that neutralizes human exposure to potentially harmful chemicals. Regular consumption of lipoic acid increases the body's ability to fight toxins. The unique advantage of alpha lipoic acid is its ability to enhance the properties of its "allies" - vitamins C and E - in the fight against toxins.

Lipoic acid also improves digestion (metabolism), which promotes weight loss. By acting on areas of the brain that cause appetite, lipoic acid, analogues block the feeling of hunger. Also, this substance reduces the accumulation of fat by the liver. Of course, the best results can be achieved by combining the intake of alpha lipoic acid with physical activity and an appropriate, well-chosen diet.

Some scientists also call lipoic acid the secret of eternal youth, because it prevents the destruction of DNA molecules, that is, it prevents the aging of the body to some extent. Moreover, lipoic acid analogues prevent the process of brain degradation.

Lipoic acid: analogues

In its effect, lipoic acid is similar to B vitamins. It improves liver function and, as already indicated above, promotes detoxification of the body.

Lipoic acid analogues will be useful in the following cases:

  • Chronic pancreatitis caused by alcohol.
  • chronic hepatitis.
  • Active cirrhosis of the liver caused by alcohol abuse.
  • Chronic heart failure.
  • Chronic cholecystopancreatitis.
  • Viral hepatitis of moderate severity (in the absence of jaundice).
  • Various poisonings (sleeping pills, mushrooms, carbon) that caused acute liver failure.
  • Diabetic polyneuritis.

by application

Children over 6 years of age are prescribed a dose of lipoic acid 12-24 mg 2-3 times a day, orally after meals. Adults - 50 mg 3 times a day. Usually the drug is taken for 20-30 days. If necessary, the course of admission can be extended by a doctor.

Lipoic acid is produced (its analogues too) in tablets and can be hidden under different names.

The healing effect of lipoic acid appears only after eight weeks of regular use.

"Octolipen"

Now you know how useful lipoic acid analogues are for the human body. "Octolipen" is one of the analogues of lipoic acid and is used for medicinal purposes, as well as for weight loss. Helps reduce the amount of glucose in human blood, as well as increase the level of production of glycogen in the human liver, which forms an energy reserve in the body that can make up for a sharp drop in blood sugar levels.

"Octolipen" contains thiocotic (alpha-lipoic) acid and excipients. It is sold in 300 mg capsules and 600 mg film-coated tablets, as well as in injection ampoules.

The use of the drug is contraindicated during pregnancy and lactation. In the case of the use of the drug by people suffering from diabetes, on initial stage reception it is recommended to constantly monitor the level of sugar in the blood. Also, during treatment, the use of alcohol, which reduces the therapeutic effect of lipoic acid, is prohibited.

R-alpha lipoic acid

Under laboratory conditions, scientists have learned how to obtain the r-isomer of lipoic acid, which contains the highest concentration of this substance. This variety is less common, but it is better absorbed by the body and, accordingly, it costs more. Sold, for example, as food additive for athletes.

R-alpha lipoic acid (R-ALA/R-isomer) is the biologically active form of alpha-lipoic acid (ALA/RS-isomer) that acts as a natural substrate in damaged cell metabolism and glucose excretion while optimizing action insulin.

Alpha lipoic acid (ALA) participates in many chemical reactions, but speaking plain language, it helps to store energy and nutrients from the food we eat. The human body needs ALA for energy production. ALA starts acting like antioxidant only when present in excess in the body; then it is in the cells in the so-called "free" state.

However, if you do not take ALA as a supplement, you will never get the antioxidant effect of ALA. As antioxidant ALA deactivates free radicals, known for their damaging effects. ALA protects mitochondria and DNA, thus delaying the aging process. Also, ALA interacts with vitamins C and E and some other antioxidants, making them more effective.

Application ALA in the form of an additive leads to a noticeable increase in mass and strength. Taking ALA before and during your workout increases your performance in the gym, and it also helps nutrients get into your muscles faster. Alpha lipoic acid is one of the best antioxidants today.

The amount of nutrients in one serving (1 capsule) of the product:

  • R-Alpha Lipoic Acid - 150 mg

Other Ingredients: gelatin, cellulose, silicon dioxide.

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R-lipoic acid is the biologically active form of alpha-lipoic acid. The supplement normalizes the balance of oxidative and reduction processes and is the official cure for diabetes, diseases of the liver, heart and blood vessels, as well as a means for weight loss.

Lipoic acid (alpha-lipoic acid, r-lipoic acid, thioctic acid, ALA) is a fatty acid found in mitochondria and is involved in energy metabolism.

The difference between thioctic acid and other fatty acids is that its antioxidant properties are preserved in both aqueous and fatty media; both in oxidized and reduced forms. This distinguishes it from water-soluble vitamin C and fat-soluble antioxidant - vitamin E. The supplement increases the level of glutathione and coenzyme Q10 in the intercellular space and enhances the process of protein glycosylation.

Scope of alpha lipoic acid:
- insulin resistance
- type 2 diabetes
- dyslipidemia and atherosclerosis (prevention and treatment)
- liver disease of any etiology
- elderly age
- chronic stress
- excess background radiation
- severe infections, heavy metal poisoning
- polyneuropathy of any etiology

R-lipoic acid is the active isomer of alpha lipoic acid and is best absorbed by the body. Thorne uses sodium bound R-lipoic acid to further enhance its stability and absorption.

1 capsule contains 100 mg of r-lipoic acid, it has more activity than alpha-lipoic acid and does not irritate the stomach, unlike the latter. For me it matters.
I took 1 capsule 2 times a day. One jar lasted me for a month.

When taking ALA, it should be borne in mind that, while freeing the body from harmful substances, it can also take useful ones with it - therefore, it is necessary to dilute r- or alpha-lipoic acid with magnesium, iron, calcium, potassium, etc., at least in time for 2 hours.

R-lipoic acid is one of the healthiest supplements out there, but the price isn't exactly humane. Therefore, I limit myself to a course of 1 month twice a year. I didn’t observe weight loss for a month of taking it, but somehow I didn’t feel like sweets. Perhaps, with prolonged use, the weight will decrease. But for weight loss, along with alpha-lipoic acid, it is desirable to take L-carnitine, it contributes to a greater effectiveness of ALA.

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Catad_tema Complications of diabetes - articles

Alpha lipoic acid - spectrum of clinical applications

O. V. Vorobieva
Professor of the Department of Nervous Diseases of the Faculty of Postgraduate Professional Education of the State Educational Institution of Higher Professional Education "Moscow Medical Academy. I. M. Sechenov" Roszdrav RF

Summary
Alpha Lipoic Acid (ALA), a natural antioxidant, is a fatty acid found in every cell of the human body. For medicinal purposes, ALA has been used since the mid-twentieth century. The paper provides an overview of clinical studies on the effectiveness of ALA in various clinical conditions associated with oxidative stress.
Keywords: alpha lipoic acid, oxidative stress, diabetic neuropathy.

Summary
Alpha lipoic acid (ALA) is a natural antioxidant, a fatty acid that is found in every cell of human body. ALA is used for treatment since the mid-twentieth century. The article provides an overview of the clinical studies of ALA effectiveness in different clinical conditions associated with oxidative stress.
key words: alpha-lipoic acid, oxidative stress, diabetic neuropathy.

The history of the discovery of ALC
Alpha lipoic acid (ALA) was discovered by Snell et al. in 1937 when he discovered that certain bacteria needed potato extract to grow. In 1951, Reed et al. isolated the so-called potato growth factor (ALA), and soon the participation of ALA as a coenzyme in the Krebs cycle and in the elimination of free radicals was shown. ALA was originally known as an essential biochemical cofactor for mitochondrial enzymes. However, in the last decade, ALA and its metabolic intermediate, dihydrolipoic acid, have been found to be powerful antioxidants. Since about the 1980s, ALA has been recognized by most researchers as one of the most powerful antioxidants.

Hyperglycemia-induced oxidative stress and ALA
The role of oxidative stress has been studied in depth in experimental diabetes models and in diabetic patients. An increase in glucose levels in people with diabetes leads to an increase in advanced glycation end products (AGEs). This process, defined as auto-oxidative glycolysis, is considered to be the main cause of increased free radical production in diabetic patients. In addition, auto-oxidative glycolysis may be responsible for the reduced availability and activity of antioxidant enzymes. In addition, fructose, which is elevated due to the activation of the polylogo metabolic pathway, serves as a source of AGE precursors. The damaging effect of accumulated glycation end products (AGEs) is mediated by their binding to specific nerve fiber sheath receptors and activation of nuclear factor kB (NF-kB). One of the effects of NF-kB is to stimulate the release of substances that impair blood flow, such as endothelin-1. In contrast, antioxidants inhibit NF-kB. Oxidative stress induced by hyperglycemia contributes to the programmed death of Schwann cells, which is an additional pathogenetic factor in the development of diabetic neuropathy. For example, when glucose is added to a dorsal root ganglion cell culture, the frequency of programmed Schwan cell death increases. Free radicals disrupt the activity of cellular structures, including the endothelium, causing endoneural hypoxia and accelerating the development of neuropathy.

ALA, a natural antioxidant, is a fatty acid found in every cell of the human body. ALA is produced in the body naturally and is defined chemically as 1,2-dithiolan-3-pentanoic acid (C8 H14 02S2). In humans, ALA is synthesized in the liver and other tissues. Food is an additional source of ALA. It is found in the following foods: red meat, liver, green vegetables, potatoes, yeast. The endogenous level of ALA in healthy individuals is 1-25 ng/ml. But its synthesis decreases with age, as well as in persons with chronic diseases including diabetes mellitus and its complications such as diabetic neuropathy.

This acid plays a critical role in the process of converting glucose into energy. At the same time, ALA is a powerful lipophilic antioxidant, the effectiveness of which has been proven both in laboratory conditions and in the body. The main effect of acid is the absorption of various reactive oxidized substances. ALA is a versatile antioxidant because it is both water and fat soluble. This property provides the advantage of ALA in the protection of various forms of oxidative stress, in particular, intracellular protection. An additional benefit of ALA is its synergistic interaction with other antioxidants, including vitamins C and E. In addition, ALA is involved in the recycling of other antioxidants such as vitamin C, E and glutathione. For example, ALA may be involved in the regeneration of vitamin C and glutathione. Glutathione is one of the main non-enzymatic defense mechanisms, which can both directly react with free radicals, destroying them, and is part of the glutathione peroxidase enzyme system. Together with ALA, glutathione plays an important role in various cellular redox reactions. An additional effect of ALA is the stimulation of nerve growth factor and, accordingly, fiber regeneration. The natural form of ALA consists of the R isomer, but the synthetic form is a racemic mixture of two isomers of the R form and the S form. Both isomers have different potential. The R-form has great potential for glucose utilization. On the other hand, the S-form shows the best affinity for glutathione reductase.

An analysis of the above facts demonstrates that oxidative stress is the final pathway in nerve fiber damage. Therefore, antioxidants may protect against glycemia-induced nerve fiber dysfunction or improve diabetic neuropathy. The uniqueness of ALA as an antioxidant lies in the following properties:

1) the ability to directly eliminate free radicals;
2) the ability to regenerate endogenous antioxidants such as glutathione, vitamins E and C;
3) the ability to reduce the production of free radicals due to metal chelate activity.

ALC in clinical practice
With therapeutic purposes, ALA was first used in 1966 by German clinicians for the treatment of diabetic polyneuropathy and cirrhosis of the liver, because there were observations of low levels of ALA in this category of patients. In animal models of experimental diabetes, ALA has been shown to improve neural circulation and nerve signal conduction. These positive results prompted the immediate conduct of clinical studies on the efficacy of ALA in the treatment of diabetes-induced polyneuropathy. Decades of ALA use have accumulated a wealth of evidence for its effectiveness in treating symptoms of diabetic polyneuropathy. The drug is well tolerated by patients, their therapy is safe.

ALA is the drug of choice for the treatment of diabetic neuropathy.
In the 1990s, seminal studies were conducted on the efficacy and safety of ALA for the treatment of diabetic neuropathy in an evidence-based manner. The first major ALADIN study evaluated three doses of ALA. The study included 328 patients with type 2 diabetes. Patients received 1,200 mg, 600 mg, 100 mg, or placebo intravenously for three weeks. Improvement in symptoms by 30% or more was observed in 71% of the patient who received 1200 mg of ALA per day; in 82% of patients who received 600 mg of ALA per day; in 65% of patients who received 100 mg of ALA per day; in 58% of patients receiving placebo. The second study, called ALADIN II, looked at the outcomes of 65 patients who received two doses of ALA tablets (600 mg/day or 1,200 mg/day) or placebo for over two years. The study provided strong evidence for clinical improvement in neuropathic symptoms. The main indicator of the severity of DPN was the Total Symptom Score (TSS) score, which assessed the intensity and frequency during the last 24 hours of the main positive neuropathic symptoms, such as shooting pain, burning, numbness, and paresthesia. Based on these positive results, the ALADIN III study was designed to test the hypothesis of the effectiveness of a short course of intervenous ALA followed by a long course of oral ALA for the treatment of diabetic neuropathy. In this study, patients received 600 or 1,200 mg of ALA per day for three weeks, followed by a tablet form of 1,800 mg/day for six months. The results showed a steady trend in pain improvement but did not reach statistical significance. But the ORPIL trial, in which patients with type 2 diabetes received 1,800 mg/day, showed a significant improvement in endoneural function after three weeks of treatment. In addition, the SYDNEY study demonstrated the effect of ALA on the sensory symptoms of diabetic polyneuropathy. The SYDNEY study included patients with stable diabetes complicated by sensorimotor neuropathy who received intravenous ALA 600 mg or placebo five days a week for a total of 14 infusions. After treatment, there was a significant improvement in the Total Symptom Score (TSS, assesses the main positive neuropathic symptoms) by 5.7 points in the active treatment group compared with the placebo group by 1.8 points (P< 0,001). Помимо быстрого улучшения сенсорных симптомов наблюдалась редукция процессов дегенерации нервных волокон. Авторы заключили, что АЛК может успешно использоваться для лечения сенсорных симптомов диабетической полиневропатии.

Another complication of diabetes is cardiovascular autonomic neuropathy, which is found in at least 25% of diabetic patients. Cardiovascular autonomic neuropathy is characterized by a reduction in heart rate variability and is associated with an increased risk of mortality in diabetic patients. Of interest in this regard is the DEKAN study, which evaluated the efficacy of a four-month course of 800 mg/day ALA on cardiovascular autonomic neuropathy. At the end of the study, an improvement in heart rate variability was shown in the active drug group compared to placebo. Thus, there is evidence of the benefit of a long-term course of oral forms of ALA for the treatment of diabetic sensorimotor neuropathy (600-1800 mg/day) and cardiac autonomic neuropathy (800 mg/day). The effectiveness of a combined course (600 mg/day IV for 10 days followed by a tablet form of 600 mg/day for 50 days) was also evaluated in patients with various forms of autonomic neuropathy. The authors noted a regression of symptoms of diabetic enteropathy, a decrease in complaints of dizziness/unstability while standing, and an improvement in sexual function. In the control group, there were no changes in the intensity of symptoms of autonomic (autonomous) insufficiency. The data allowed the authors to conclude that ALA is effective in the treatment of various forms of diabetic autonomic neuropathy.

In 2004, data from a meta-analysis based on four randomized placebo-controlled trials (ALADIN I, ALADIN III, SYDNEY, NATHAN II) with a total of over 1,000 patients were published. A meta-analysis convincingly showed that after three weeks of intravenous administration of ALA at a dose of 600 mg positive effect observed in more than 50% of patients. Moreover, improvement was observed both in relation to positive neuropathic symptoms and in relation to neurological deficit. These are very encouraging findings, as neurological deficits are a major risk factor for foot ulceration.

A daily tablet dose of 600 mg showed optimal ratio safety/efficacy (clinical study SYDNEY 2) . At a daily dose of 1,200 mg, 21% of patients experienced mild nausea, which is higher than in the ALADIN I (15%) and ALADIN II (7%) clinical trials at the same dose. Post-marketing observations have confirmed the highly safe profile of ALA. The results of the conducted clinical trials made it possible to formulate an algorithm for the treatment of diabetic patients with diabetic polyneuropathy with intravenous administration of alpha-lipoic acid. Treatment begins with intravenous administration of ALA in a single dose of 600 mg for 14-15 days. In the future, tablet forms are used.

Four of the RCTs cited above (ORPIL, SYDNEY, SYDNEY 2, ALADIN) are rated as high-quality evidence (level 1b). A meta-analysis based on these studies has shown that ALA leads to a significant and clinically significant reduction in the severity of neuropathic pain, when used for three weeks at a dose of 600 mg / day. (Level A recommendation) .

Russian neurologists and endocrinologists have also accumulated extensive clinical experience in the use of ALA in diabetic neuropathy. It should be noted that domestic and foreign injectable and tablet preparations of ALA are currently available in Russia. Among domestic drugs, the drug "Thiolepta" stands out, which has shown effectiveness against diabetic and alcoholic neuropathy, as well as a significant economic advantage. A comparative study showed that the additional use of "Thiolepty" at a dose of 600 mg / day. (two 300 mg tablets once) for two months in patients treated with euglycemic supportive baseline therapy provides a greater trend towards regression of diabetic polyneuropathy symptoms compared with patients receiving baseline therapy alone. By the end of treatment, the severity of DPN was less in the main group of patients who received Thiolept: normalization of the index on the NDS scale in 50% of patients (in the control group only in 30%); disappearance of neurological symptoms according to the TSS scale in 30% of patients (neurological symptoms persisted in the control group). An electroneuromyographic study showed a statistically insignificant (p > 0.05) trend towards a more pronounced increase in the speed of impulse conduction along the sensory and motor nerves, as well as the amplitudes of motor and sensory responses in the main group.

Additional clinical options for using ALA
Of course, the main indication for the use of ALC is diabetes mellitus and complications associated with impaired glucose metabolism, including primarily neuropathy and cataracts. Additionally, ALA improves the body's ability to utilize glucose, which helps reduce insulin dependence. But due to its properties, ALA provides high protection against oxidative processes, which makes it possible to use ALA for medicinal purposes in a wide range of diseases.

ALC and compression-ischemic radiculopathy
In animal models (compression of the sciatic nerve of the rat), the protective effect of ALA on the reduction of oxidative stress in traumatic nerve fiber injury has been proven. These findings allow discussion of the use of ALA for the treatment of back pain associated with radiculopathy. The most common cause of radiculopathy and radicular pain is lumbar hernia. intervertebral disc. Damage to the nerve fiber depends on the duration of compression. A consistent pattern of axonal degeneration and myelin degradation and subsequent rapid regeneration is characteristic of peripheral nerve injury. An indisputable fact is the increase in free radicals after tissue damage. Increased production of free radicals under conditions of inefficient balance of cellular antioxidant systems leads to additional direct damage to cell membrane phospholipids, mitochondria, and cellular proteins. Peroxide dismutase is one of the protective systems that protects cells from damage associated with free radicals. Peroxide dismutase belongs to the family of metatalloproteinases. It catalyzes the dismutation of free radicals, the end products of which are water and hydrogen peroxide, the latter being neutralized by the activity of catalase. An experimental model of a damaged nerve fiber showed an increase in the activity of peroxide dismutase and catalase, which may be a response that levels oxidative stress. Despite the lack of a complete understanding of the subtle mechanisms of nerve fiber damage, the evidence available to date is sufficient to suggest that ALA may increase the antioxidant defense of the damaged fiber. Indeed, recent studies have shown the effectiveness of ALA in relation to clinical symptoms such as pain, paresthesia, hypoesthesia in patients with compression radiculopathy due to disco-radicular conflict. These data from Senoglu et al. (2009) correlates with another study that evaluated the efficacy of additional use of a combination of ALA and gamma-linolenic acid in a six-week rehabilitation program in patients with discogenic radiculopathy compared with a similar group of patients who received only a rehabilitation program. Additional benefits of antioxidant therapy have been demonstrated in terms of pain reduction and associated functional impairment (Visual Analogue Scale, Oswestry Low Back Pain Disability Questionnaire, Aberdeen Back Pain Scale, Revised Leeds Disability Questionnaire, Roland and Morris Disability Questionnaire), as well as improved quality of life (Short Form Health Survey .

ALC and alcoholic neuropathy
Antioxidant therapy is considered as one possible way to treat the toxic effects of alcohol on the nervous system. However, although there are many publications on the proven therapeutic effect of ALC in diabetic polyneuropathy, studies on the effectiveness of ALC in AP are still rare. It has been shown that ALC is effective in 70% of patients with AP, influencing sensory and motor symptoms and also having a positive effect on painful and paresthetic manifestations of AP, which are painful for patients. When analyzing the efficacy and tolerability of ALC in comparison with thiamine, it was found that ALC is significantly more effective than vitamin B1 in terms of clinical and electrophysiological parameters and is recommended for widespread use in the treatment of AP. Treatment of ALC can be considered etiotropic, since the drug affects one of the main etiological factors in the formation of polyneuropathy in chronic alcoholism - oxidative stress. In addition, there is evidence of a direct effect of ALA on ethanol-mediated neurotoxicity in vivo.

ALC and vibration sickness
The main symptoms of vibration disease include vascular disorders, manifested by violations of the peripheral circulation, changes in capillary tone, impaired general hemodynamics, as well as the development of vegetative-sensory polyneuropathy of the extremities. Endoneurial ischemia triggers oxidative stress processes that play an important role in nerve fiber damage. This fact opens up new possibilities for the use of antioxidant therapy for the treatment of vibrational disease. At the Department of Occupational Diseases of the St. Petersburg State Medical Academy. II Mechnikov conducted a comparative, open randomized study of the effectiveness of "Thiolepty" at a dose of 600 mg / day. (course duration 21 days) for the treatment of vibration disease with vegetative-sensory polyneuropathy. Additional introduction of Thiolepty into therapy led to a decrease in the frequency of subjective complaints of patients, to a steady decrease in the recurrence of pain in the extremities, and to a decrease in the frequency of angiospasm attacks. In the group of patients treated with Thiolepta, there was a significant positive trend (p< 0,05) электрофизиологических показателей, тестирующих состояние нервного волокна. После лечения наблюдалось возрастание скорости распространения возбуждения по моторным и сенсорным волокнам.

ALC and the immunodeficiency virus
Some experimental data suggest that ALA may have a positive effect in people infected with HIV. For example, ALA has been shown to significantly (30-70%) increase glutathione in individuals infected with HIV. This may be important for hepatocyte recovery since the immunodeficiency virus induces glutathione deficiency. Moreover, ALA inhibits viral replication during the acute and chronic periods of cell infection. In vitro, ALA shows a synergistic antiviral effect when combined with azathiaprine. This combination results in a stronger inhibition of viral replication than either drug alone. Separate studies have shown that ALA reduces the activity and invasiveness of the HIV gene.

ALA and skin aging
Some experts are considering the possibilities of ALA in relation to the inhibition of skin aging processes. It is assumed that ALA can promote the elimination of damaged collagen, have a preventive effect on the processes of protein glycosylation, which prevent premature aging and skin damage. Clinically, ALA appears to be superior to vitamins C and E for symptoms such as improved skin color, tone, and texture. ALA has traditionally been used in creams to improve skin texture and reduce pores and wrinkles.

ALC and the cardiovascular system
Oxidation of low-density lipoproteins (LDL) with the formation of free radicals contributes to the deposition of cholesterol in the arterial wall, which is associated with atherosclerosis. Since 1992, studies have been published demonstrating the synergistic effect of ALA with vitamins C and E against free radical oxidation of LDL. Clinical work confirms the ability of ALA to reduce ischemia and reperfusion injury of the heart muscle and brain.

ALA as a possible substance for the treatment of multiple sclerosis
Many researchers believe that oxidative damage may be associated with multiple sclerosis. In a model of experimental autoimmune encephalomyelitis in mice, ALA has been shown to be effective in reducing the clinical symptoms of encephalomyelitis (effectiveness between 23-100%), reducing inflammation, demyelination, and loss of axons in the spinal cord. It is hypothesized that the effectiveness of ALA is related to the inhibition of lymphocyte transport across the blood-brain barrier and possibly due to the inhibition of metalloproteinases. However, consideration of ALA as a potential drug for the treatment of multiple sclerosis needs further research.

Possibilities of ALA for the treatment of olfactory disorders
Usually, a violation of the sense of smell is associated with an infectious lesion of the upper respiratory tract. Separate studies show an improvement in post-viral olfactory dysfunction under the influence of a course (4.5 months) of ALA at a dose of 600 mg / day in approximately 60% of patients.

Chronic Fatigue Syndrome and ALC
Chronic fatigue syndrome (CFS) is characterized by a persistent or fluctuating feeling of fatigue, often associated with a variety of multisystem symptoms. The exact causes of the disease are not known, but several studies show clinical findings that suggest a possible relationship between CFS and free radical levels. This suggests the possibility of using antioxidant therapy in individuals suffering from CFS. Research by Canadian clinicians has shown the success of ALA and other antioxidants in the treatment of CFS.

Possibilities of ALC in the prevention of symptoms of drug toxicity
Neuropathy can be a dose-limited side effect of most drugs used in the treatment of life-threatening conditions such as cancer, HIV infection. Epidemiological studies support earlier reports that cytotoxic agents cause axonal sensorimotor neuropathy or, less commonly, fine fiber involvement in some patients. Cytostatic-induced neuropathy can be acute or chronic. Symptoms of acute neuropathy appear during or shortly after a course of therapy with drugs containing platinum. Chronic neuropathy may occur weeks or months after chemotherapy. The prognosis of drug-induced neuropathies is unfavorable, in some patients the symptoms remain irreversible. Some antiviral drugs can also cause sensory neuropathy.

Recently there have been observations of a beneficial effect of ALA on neuropathies induced by cytostatics. Patients with cytostatic-induced neuropathy were administered during the next course of ALA at a dose of 600 mg IV for 3-5 weeks, and then 1,800 mg in tablet form until resolution of neuropathic symptoms, up to a maximum of six months. The average duration of treatment was two months. Improvement in neuropathic symptoms was observed on average after four weeks of treatment. The authors conclude that the preventive use of ALA in combination with cytostatics is useful for the treatment and prevention of damage to the peripheral nervous system. Randomized trials also support the benefits of prophylactic use of ALA tablets (1,800 mg/day, three doses) for at least 24 weeks.

Separate studies demonstrate the positive effect of ALA in reducing the risk of cytotoxic cardiotoxicity. For example, administration of ALA five days before and two days after Doxrubicin injection resulted in a clinically significant reduction in plasma creatine phosphokinase and plasma lactate dehydrogenase.

Side effects of ALA
ALA is characterized by excellent tolerance. However, high doses of ALA can cause nausea, indigestion, and reduce mineral levels. Among side effects ALA has described headache, skin rash, muscle cramps, and low blood glucose levels. Therefore, diabetic patients are advised to regularly monitor their sugar levels while taking ALA.

Conclusion
Thus, a review of foreign and Russian studies (RCTs), both past years and modern ones, showed the effectiveness and high safety of using ALC in diabetic neuropathy. The drug Thiolept (thioctic acid), being a powerful antioxidant, has been proven to reduce the symptoms of DPN (pain, numbness, paresthesia), improving the quality of life of patients and has a pathogenetic effect, demonstrating a high profile of efficacy and safety.

LITERATURE

1. Snell EE, Strong FM, Peterson WH. Growth factors for bacteria. VI: Fractionation and properties of an accessory factor for lactic acid bacteria. Biochem J 1937. 31(10):1789-1799.
2. Reed LJ, DeBusk BG, Gunsalus IC, Hornberger CSJr. Cristalline alpha-lipoic acid: a catalytic agent associated with pyruvate dehydrogenase. Science 1951. 114(2952):93-94.
3. Reed L.J. The chemistry and function of lipoic acid. Adv Enzymol 1957. 18:319-347.
4 Sen.CK. Redox signaling and the emerging therapeutic potential of thiol antioxidants. Biochem Pharmacol 1998.55 (11): 1747-1758.
5. Kihara M, Low P A Impaired vasoreactivity to nitric oxide in experimental diabetic neuropathy Experimental Neurology, 1995, v 132, 180-185.
6. Kowluru RA. Effect of advanced glycation end products on accelerated apoptosis of retinal capillary cells under in vitro conditions. life sci. 2005 Jan 14;76(9):1051-60.
7. Miinea C, Eichberg J. Antioxidant protection mechanisms and arachidonic acid synthesis are altered in Schwann cells grown in elevated glucose. Fifth Diabetic Neuropathy Satellite Symposium 2000. 32.
8. Teichert J, Preiss R. HPLC-methods for determination of lipoic acid and its reduced form in human plasma. Int J Clin Pharmacol Ther Toxicol. 1992;30:511-512.
9. Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med. 1997;22:359-378.
10. Packer L, Witt EH, Tritschler HJ. „ Alpha-Lipoic acid as a biological antioxidant. Free Radic Biol Med 1995 Aug;19(2):227-50.
11. Murase K, Hattori A, Kohno M, Hayashi K. Stimulation of nerve growth factor synthesis/secretion in mouse astroglial cells by coenzymes. Biochem Mol Biol Int 1993.30:615-621.
12. Biewenga GP, Haenen GR, Bast A. The pharmacology of the antioxidant lipoic acid.//Gen Pharmacol 1997;29:315-331.
13. Coppey LJ, Gellett JS, Davidson EP, et al. Effect of antioxidant treatment of streptozotocin-induced diabetic rats on endoneurial blood flow, motor nerve conduction velocity, and vascular reactivity of epineurial arterioles of the sciatic nerve. diabetes. 2001;50:1927-1937.
14. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a 7-month multicenter randomized controlled trial (ALADIN III Study). ALADIN III Study Group. Alpha Lipoic Acid in Diabetic Neuropathy. Diabetes Care. 1999;22:1296-1301.
15. Ruhnau KJ, Meissner HP, Finn JR, et al. Effects of 3-week oral treatment with the antioxidant thioctic acid (alpha-lipoic acid) in symptomatic diabetic polyneuropathy. Diabetes Med. 1999;16:1040-1043.
16. Ametov AS, Barinov A, Dyck PJ, et al. SYDNEY Trial Study Group. The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid: the SYDNEY trial. Diabetes Care. 2003;26:770-776.
17. Yadav V, Marracci G, Lovera J, et al. Lipoic acid in multiple sclerosis: a pilot study. Multi Scler. 2005;11:159-165.
18. Ziegler D, Nowak H, Kempler P, Vargha P, Low PA. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis.//Diabet Med 2004;21(2):114-121.
19. Ziegler D, Ametov A, Barinov A, Dyck PJ, GurievaI, Low PA, Munzel U, Yakhno N, Raz I, Novosadova M, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy. The SYDNEY 2 trial. Diabetes Care 2006. 29:2365-2370.
20. Ziegler D. Thioctic acid for patients with symptomatic diabetic neuropathy: a critical review. Treat Endocrinol 2004.3(3):173-189.
21. Strokov I. A., Akhmetzhanova L. T., Solokha O. A. The effectiveness of the treatment of diabetic polyneuropathy with alpha-lipoic acid tablets. Difficult patient 2010; 8#3:17-21.
22. Barantsevich E. R., Posokhina O. V. Approaches to the treatment of neurological manifestations of diabetes mellitus. Journal neurol. and psychiatrist. S. S. Korsakova 2010;110 No. 4:63-66.
23. Senoglu M, Nacitarhan V, Kurutas EB, Senoglu N, Altun I, Atli Y, Ozbag D. Intraperitoneal Alpha-Lipoic Acid to prevent neural damage after crush injury to the rat sciatic nerve. J Brachial Plex Peripher Nerve Inj. 2009;4:22.
24. Ranieri M, Sciuscio M, Cortese AM, Santamato A, Di Teo L, Ianieri G, Bellomo RG, Stasi M, Megna M. The use of alpha-lipoic acid (ALA), gamma linolenic acid (GLA) and rehabilitation in the treatment of back pain: effect on health-related quality of life. Int J Immunopathol Pharmacol. 2009;22(3 Suppl):45-50.
25. Ranieri M, Sciuscio M, Cortese AM, Santamato A, Di Teo L, Ianieri G, Bellomo RG, Stasi M, Megna M. The use of alpha-lipoic acid (ALA), gamma linolenic acid (GLA) and rehabilitation in the treatment of back pain: effect on health-related quality of life. Int J Immunopathol Pharmacol. 2009;22(3 Suppl):45-50.
26. Sklyar I. A., Vorobieva O. V., Sharyapova R. B., Sadekov R. K. Thioctacid in the treatment of alcoholic polyneuropathy. Treatment of nervous diseases 2001; 2:39-41.
27. Kovrazhkina E. A., Airiyan N. Yu., Serkin G. V., Glushkov K. S., Pavlov N. A., Gekht A. B., Stakhovskaya L. V., Skvortsova V. I. Opportunities and prospects for the use of Berlition for the treatment of alcoholic polyneuropathy. Zhurn Nevrol and psychiatrist. S. S. Korsakova 2004; 104:2:33-37.
28. Pirlich M, Kiok K, Sandig G, Lochs H, Grune T. Alpha-lipoic acid prevents ethanol-induced protein oxidation in mouse hippocampal HT22 cells. Neurosci Lett. 2002 Aug 9;328(2):93-6.
29. Artamonova V. G. Lashina E. L. The use of the drug thiolept (thioctic acid) in combination therapy of vibration disease. Zhurn Nevrol and psychiatrist. S. S. Korsakova 2011; 111:1:82-85.
30. Han D, Tritschler HJ, Packer L. Alpha-lipoic acid increases intracellular glutathione in a human T-lymphocyte Jurkat cell line. Biochem Biophys Res Commun 1995 Feb 6;207(1):258-64.
31. Baur A et al., Alpha lipoic acid is an effective inhibitor of human immuno-deficiency virus (HIV-1) replication, Klin Wochenschr 69 (1991): 722-4.
32. Perricione N. The Wrinkle Cure, Chapter 6 "Alpha Lipoic Acid" pp.71-72. Warner Books., 2000.
33. Cao X and Phillis JW. Free Radical Research 1995; 23:365.
34. Marracci GH, Jones RE, McKeon GP, ​​Bourdette DN. "Alpha Lipoic Acid inhibits T cell migration into the spinal cord experimental and suppresses and treats autoimmune encephalomyelitis." Journal of Neuroimmunology, October2002;131(1-2):104-14.
35. Hummel T, Heilmann S, Huttenbriuk KB., "Lipoic acid in the treatment of smell dysfunction following viral infection of the upper respiratory tract." Laryngoscope 2002 Nov;112(11):2076-80.
36. Logan AC, Wong C. "Chronic fatigue syndrome: oxidative stress and dietary modifications." Alternative Medicine Review Oct 2001;6(5):450-9.
37. Peltier AC, Russell JW. Advances in understanding drug-induced neuropathies. Drug Saf 2006;29(1):23-30.
38. Gedlicka C, Kornek GV, Schmid K, Scheithauer W. Amelioration of docetaxel/cisplatin induced polyneuropathy by alpha-lipoic acid. Annals of Oncology 2003;14:339-340.
39. Phase III Randomized Study of Alpha-Lipoic Acid in Preventing Platinum-Induced Peripheral Neuropathy in Cancer Patients Receiving a Cisplatin- or Oxaliplatin-Containing Chemotherapy Regimen (MDA-CCC-0327).
40. Al-Majed, AA. Gado, AM, Al-Shabanah, OA, and Mansour, AM. "Alpha-lipoic Acid Ameliorates Myocardial Toxicity Induced by Doxorubicin." Pharmacol Res December 2002;46(6):499-503.
41. Mijnhout G. S., Alkhalaf A., Kleefstra N., Bilo H. J. G. The Netherlands Journal of Medicine 2010; 68(4): 158-162.