Semax, 1 piece, 3 ml, 0.1%, nasal drops

What causes vitamin D deficiency?

Vitamin D deficiency in many Russian residents is due to:

• location in the northern temperate zone (above 42 degrees north latitude)
• limited exposure to the sun (office work, driving cars)
• eating meat from animals that have not been exposed to the sun (farm)
• use of sunscreens
• chronic diseases (obesity, intestinal pathology, taking a large number of medications)

You can determine the level of vitamin D in your body by taking the following test:

25-OH vitamin D (25-hydroxycalciferol) (amount)

For the curious

Vitamin D

combines a group of vitamins (D1, D2, D3, D4, D5), of which only two forms (D2 and D3) have important biological significance.

The main biological role of calcitriol

(1,25-OH-vitamin D) is to maintain a constant level of calcium in the blood (vitamin D enhances the absorption of calcium in the intestines and, if there is not enough calcium in the blood, ensures the flow of calcium from the bones into the blood).

Over time, receptors for calcitriol, in addition to the intestines and bones, were found in the kidneys, genitals, pancreas, muscles, cells of the immune and nervous systems. Thus, it became clear that vitamin D performs a large number of different functions in the human body:

• regulates the expression of 3% of the human genome (several thousand genes)
• increases the sensitivity of the insulin receptor (prevention of insulin resistance, obesity, diabetes)
• strengthens the skeletal system
• reduces the level of parathyroid hormone in the blood
• promotes the synthesis of sex hormones (testosterone, estrogens, progesterone)
• improves reproductive function
• affects innate and acquired immunity
• prevents the development of tumors, depression, Parkinson's disease

Complivit Aqua D3

Pharmacological properties

Pharmacodynamics
Vitamin D3 is a natural form of vitamin D, which is formed in humans in the skin under the influence of sunlight. Compared to vitamin D2, it is characterized by 25% higher activity.

Vitamin D binds to the specific vitamin D receptor (VDR), which regulates the expression of many genes, including the ion channel genes TRPV6 (ensures the absorption of calcium in the intestine), CALB1 (calbindin; ensures the transport of calcium into the bloodstream), BGLAP (osteo-calcine) ; ensures bone tissue mineralization and calcium homeostasis), SPP1 (osteopontin; regulates osteoclast migration), REN (renin; ensures regulation of blood pressure, being a key element of the renin-angiotensin-aldosterone regulatory system), IGFBP (insulin-like growth factor binding protein; enhances the effect insulin-like growth factor), FGF23 (fibroblast growth factor 23; regulates the levels of calcium, phosphate anion, processes of cell division of fibroblasts), TGFB1 (transforming growth factor beta-1; regulates the processes of cell division and differentiation of osteocytes, chondrocytes, fibroblasts and keratinocytes), LRP2 (LDL receptor-related protein 2; mediates the endocytosis of low-density lipoproteins), INSR (insulin receptor; ensures the effects of insulin on any cell type).

Vitamin D3 is an active antirachitic factor. The most important function of vitamin D3 is to regulate calcium and phosphate metabolism, which promotes proper mineralization and skeletal growth.

Colecalciferol plays a significant role in the absorption of calcium and phosphates from the intestine, in the transport of mineral salts and in the process of bone calcification, and also regulates the excretion of calcium and phosphates by the kidneys. The concentration of calcium ions in the blood determines the maintenance of muscle tone of skeletal muscles, myocardial function, promotes nervous stimulation, and regulates the process of blood clotting.

Lack of vitamin D in food, impaired absorption, calcium deficiency, as well as insufficient exposure to the sun leads to: in children during periods of intensive growth - to rickets, in adults - to osteomalacia, in pregnant women, symptoms of tetany may occur - disruption of the processes calcification of newborn bones.

An increased need for vitamin D occurs in women during menopause, as they often develop osteoporosis due to hormonal imbalances.

Vitamin D has a number of so-called. extraskeletal effects.

Vitamin D is involved in the functioning of the immune system by modulating cytokine levels and regulating the division of T-helper lymphocytes and the differentiation of B-lymphocytes. A number of studies have noted a decrease in the incidence of respiratory tract infections with vitamin D supplementation.

It has been shown that vitamin D is an important part of the homeostasis of the immune system: it prevents autoimmune diseases (type 1 diabetes, multiple sclerosis, rheumatoid arthritis, inflammatory bowel diseases, etc.).

Vitamin D has antiproliferative and prodifferentiating effects, which determine the oncoprotective effect of vitamin D. It has been noted that the incidence of certain tumors (breast cancer, colon cancer) increases against the background of low levels of vitamin D in the blood.

Vitamin D is involved in the regulation of carbohydrate and fat metabolism by influencing the synthesis of IRS1 (insulin receptor substrate 1; participates in the intracellular pathways of the insulin receptor signal), IGF (insulin-like growth factor; regulates the balance of adipose and muscle tissue), PPAR-δ (activated receptor peroxisome proliferators, type δ; helps process excess cholesterol).

According to epidemiological studies, vitamin D deficiency is associated with the risk of metabolic disorders (metabolic syndrome and type 2 diabetes mellitus).

Vitamin D receptors and metabolizing enzymes are expressed in arterial vessels, the heart, and virtually all cells and tissues relevant to the pathogenesis of cardiovascular disease. Animal models show anti-atherosclerotic effects, renin suppression and prevention of myocardial damage, etc. Low levels of vitamin D in humans are associated with unfavorable risk factors for cardiovascular pathology, such as diabetes mellitus, dyslipidemia, arterial hypertension, and are associated with the risk of cardiovascular accidents , incl. strokes.

Studies in experimental models of Alzheimer's disease showed that vitamin D3 reduced amyloid accumulation in the brain and improved cognitive function. Non-interventional human studies have shown that the incidence of dementia and Alzheimer's disease increases with low vitamin D levels and low dietary intake of vitamin D. Cognitive function and the incidence of Alzheimer's disease have been impaired with low vitamin D levels.

Pharmacokinetics.

An aqueous solution of vitamin D3 is absorbed better than an oil solution. In premature babies, there is insufficient formation and flow of bile into the intestines, which interferes with the absorption of vitamins in the form of oil solutions. After oral administration, colecalciferol is absorbed in the small intestine. Metabolized in the liver and kidneys. The half-life of colecalciferol from the blood is several days and may be prolonged in cases of renal failure. The drug penetrates the placental barrier and into mother's milk. Vitamin D3 has the property of cumulation. It is excreted from the body by the kidneys in small quantities, most of it is excreted in bile.

Vitamin D deficiency

A lack of vitamin D in the body can lead to the development of:

• diseases of the cardiovascular system
• immunodeficiency, allergies, psoriasis, bronchial asthma, rheumatoid arthritis
• periodontal disease
• tumors of the large intestine, mammary glands, ovaries, prostate
• chronic fatigue, depression, insomnia
• decreased muscle strength leading to a risk of falls
• decreased motility and number of morphologically normal sperm (male factor infertility)
• risk factor for premature birth, fetopathies (less than 20 ng/ml)

Achieving a vitamin D level of 50 ng/ml (125 nmol/l) reduces the risk of developing:

Vitamin D is important during pregnancy.

Its deficiency is associated with the risk of developing gestational diabetes mellitus, premature birth, preeclampsia, and various intrauterine developmental defects.

There is not a single case of teratogenic (leading to the development of tumors) effect of vitamin D in the world.

Semax, 1 piece, 3 ml, 0.1%, nasal drops

Semax® has an original mechanism of neurospecific action on the central nervous system.

Semax® has a pronounced neurometabolic effect, which manifests itself even when prescribed in very small doses. Higher doses of Semax®, while maintaining the neurometabolic properties of small doses, have a pronounced antioxidant, antihypoxic, angioprotective and neurotrophic effect. When administered intranasally, Semax® penetrates the BBB within 4 minutes, and the therapeutic effect with a single administration lasts 20–24 hours, which is associated with its sequential degradation, in which most of the effects of the neuropeptide are retained in its fragments.

Neurometabolic

The drug affects processes associated with memory formation and learning. Semax® enhances attention when learning and analyzing information, improves the consolidation of the memory trace; improves the body's adaptation to hypoxia, cerebral ischemia, anesthesia and other damaging influences.

Semax® has a stimulating effect on the population of cholinergic neurons of the basal forebrain ganglia.

The targeted effect of Semax® on cholinergic neurons is accompanied by a significant increase in the activity of the acetylcholinesterase enzyme in specific brain structures, which correlates with an improvement in learning processes and memory formation.

Neuroprotective

Semax® affects the processes of delayed neuronal death, including local inflammation, nitric oxide formation, oxidative stress and dysfunction of trophic factors. Powerful, comparable to the effect of NGF, trophotropic effect of Semax® on neurons of the cholinergic group both in a complete environment and in unfavorable conditions caused by deprivation of glucose and oxygen. Semax® at the gene level includes the synthesis of neurotrophins - regulators of growth and differentiation of nervous tissue (BDNF factor).

Semax® has a direct effect on molecular trigger mechanisms, normalizing the balance of cytokines and increasing the level of anti-inflammatory factors, reducing the formation of nitric oxide, causing inhibition of lipid peroxidation (LPO), activation of the synthesis of superoxide dismutase (SOD) and a decrease in the level of cyclic guasine monophosphate (cGMP) ).

Antioxidant, antihypoxic

Semax® has a positive effect on the body's adaptation to hypoxia. The ability of the drug to stop post-hyperventilation EEG effects caused by a compensatory decrease in cerebral blood flow was discovered.

The drug is practically non-toxic with single and long-term administration. Does not exhibit allergic, embryotoxic, teratogenic and mutagenic properties. Does not have a local irritant effect.

Vitamin D standards

Considering the different units of measurement, the recommended level is:

60 - 100 ng/ml

150 – 250 nmol/l

To convert from ng/ml to nmol/l you need ng/ml * 2.5 = nmol/l

Example: 30 ng/ml * 2.5 = 75 nmol/l

Russian Association of Endocrinologists

considers
the optimal concentration
of vitamin D in the blood of an adult to be 30-100 ng/ml,
deficiency
20-30 ng/ml,
deficiency
- less than 20 ng/ml.

According to data presented at the 10th European Congress on Menopause and Andropause (Madrid, 2015), vitamin D levels in obese patients in Russia:

less than 20 ng/ml - 35%

20-30 ng/ml - 30%

more than 30 ng/ml - 35%

Daily Values ​​for Vitamin D

according to the recommendation of the American Society of Endocrinology (2011).

Prophylactic dose

vitamin D (when you can not detect it in the blood and take it calmly) is considered to be 4,000 IU per day.

Without medical supervision, it is not recommended to take vitamin D at a dose of 10,000 IU for more than 6 months. (Russian Association of Endocrinologists)

It is almost impossible to overdose on vitamin D. For example, in Holland, an elderly couple (90 and 95 years old) accidentally took a single dose of cholecalciferol 2,000,000 IU each.

Doctors monitored them for 2 months and did not identify any symptoms of overdose or toxicity. The maximum blood concentration of its form of 25-OH-vitamin D on day 8 was 210 and 170 ng/ml, respectively, which is slightly higher than its target values.