Why do we need vitamin D. The noncalcemic effects of vitamin D

Chemical structure and properties . In 1936 A. Windaus from fish oil a drug that cured rickets was isolated. It was named vitamin D 3, since earlier by A. Hess and M. Weinstock ergosterol was isolated from vegetable oils, called vitamin D 1, When exposed to UV rays on vitamin D 1, a compound that cures rickets was formed - vitamin D 2, ergocalciferol ( calciferol means calcium carrier). In plants under UV irradiation, other vitamers of ergosterol are synthesized (D 4 - 7). The most important vitamin D group is vitamin D 3 - cholecalciferol. Cholecalciferol is formed as an intermediate in the biosynthesis of cholesterol (from 7-dehydrocholesterol) in human skin cells under the influence of UV rays.

The daily requirement of vitamin D. Food sources of vitamin D. Vitamin D 3 is found exclusively in animal food. Fish oil is especially rich in it. It is contained in the liver, yolk of eggs. Vitamin D 2 is present in vegetable oils and milk. There is a lot of it in yeast. It is biologically less active. The daily requirement for children ranges from 10 to 25 μg (500-1000 IU), in adults it is less.

Vitamin D metabolism. Group D vitamins are absorbed like vitamin A. In the liver, vitamins are hydroxylated by the microsomal system of oxygenases at C-25 (25 (OH) -D 3 is formed from vitamin D 3, i.e. 25-hydroxycholecalciferol), and then carried by current blood by means of a specific transport protein to the kidneys. In the kidneys, the second reaction of hydroxylation at C-1 is carried out with the help of mitochondrial oxygenases (1.25 (OH) 2-D 3 is formed, i.e., 1.25-dihydroxycholecalciferol, or calcitriol). This reaction is activated by parathyroid hormone secreted by the parathyroid gland when the level of calcium in the blood decreases. If the calcium level is adequate to the physiological needs of the body, secondary hydroxylation occurs at C-24 (instead of C-1), while an inactive metabolite 1,24 (OH) 2-D 3 is formed. Vitamin C takes part in hydroxylation reactions.

Vitamin D 3 is stored in adipose tissue. It is excreted mainly in the feces in unchanged or oxidized form, as well as in the form of conjugates.

Biochemical functions of vitamin D. Vitamin D 3 can be considered as a pro-hormone, since it is converted into 1.25 (OH) 2-D 3, which acts similarly to steroid hormones. So, penetrating into target cells, it binds to protein receptors that migrate into the cell nucleus. In enterocytes, this hormone-receptor complex stimulates the transcription of mRNA, which carries information for the synthesis of a calcium ion carrier protein. Probably, the vitamin is also responsible for the synthesis of Ca2 + -ATPase in different cells. In the intestine, calcium absorption is carried out both by facilitated diffusion (with the participation of calcium-binding protein) and by active transport (with the help of Ca2 + -ATPase). At the same time, the absorption of phosphorus is accelerated.
V bone tissue 1,25 (OH) 2-D 3 stimulates the process of demineralization (synergistically with parathyrin). In the kidneys, activation by vitamin 1.25 (OH) 2-D 3 calcium ATPase of the renal tubular membranes leads to an increase in the reabsorption of calcium ions; phosphate reabsorption also increases. Calcitriol is involved in the regulation of growth and differentiation of bone marrow cells. It has antioxidant and anticarcinogenic properties.

Vitamin D hypovitaminosis. Lack of vitamin D in children leads to rickets. The main manifestations of this disease are reduced to the symptoms of calcium deficiency. First of all, osteogenesis suffers: there is a deformation of the skeleton of the limbs (their curvature as a result of softening - osteomalacia), the skull (late infestation of fontanelles), chest(the appearance of a kind of "rosary" on the bone-cartilaginous border of the ribs), teething is delayed. Muscle hypotension (enlarged abdomen) develops, neuromuscular excitability increases (in the infant, a symptom of baldness of the back of the head is revealed due to frequent rotation of the head), seizures may occur. In an adult, calcium deficiency in the body leads to caries and osteomalacia; in the elderly - to the development of osteoporosis (a decrease in bone density due to impaired osteosynthesis). The destruction of the inorganic matrix is ​​explained by the increased "leaching" of calcium from bone tissue and impaired calcium reabsorption in renal tubules with a deficiency of vitamin D. The diagram below shows inhibition (dashed arrow) of absorption, a decrease in calcium intake into the bone and a decrease in calcium excretion with a lack of vitamin D. At the same time, in response to hypocalcemia, parathyrin is secreted and increases (solid arrow) calcium intake from the bone into the bloodstream (secondary hyperparathyroidism).

Hypervitaminosis D. Excessive intake of vitamin D leads to intoxication and is accompanied by pronounced demineralization of bones - up to their fractures. The calcium content in the blood rises. This leads to calcification of soft tissues, kidneys are especially prone to this process (stones are formed and renal failure develops).

The increase in the level of calcium (and phosphorus) in the blood is explained as follows: 1) bone resorption (solid arrow); 2) an increase in the intensity of absorption of calcium and phosphorus in the intestine and 3) an increase in their absorption in the kidneys (i.e., inhibition of urinary excretion - dotted line).

Under normal conditions, an increase in blood calcium will lead to the formation of inactive 24.25 (OH) 2-D 3, which does not cause bone resorption ("resorption"), but with hypervitaminosis D this mechanism becomes ineffective. Interestingly, skin pigmentation (sunburn) is a protective factor that protects against excessive formation of vitamin D when the skin is exposed to UV radiation. However, in fair-skinned northern countries, lacking solar insolation, vitamin D-deficiency states, as a rule, do not develop, since their diet includes fish oil.

Assessment of the body's supply of vitamin D. The provision of the body with vitamin D is assessed on the basis of determining the active forms of vitamin D in the blood and tissues by the method of radio competitive analysis; the content of calcium, phosphorus and activity of alkaline phosphatase in the blood serum; the level of urinary phosphate excretion. Stress tests are also used with the intake of fixed doses of calcium for parenteral administration, followed by the determination of the calcium content in the blood and its excretion in the urine.

I gave a link to a cool vitamin complex. I chose it on the basis of a combination of many useful factors, which I immediately wrote about. But there is one question that needs to be spent more time, namely: how is skin aging related?

Why such a topic? But because in my spring complex as many as 1000 IU units of vitamin D, and, given the scanty dosages of this wonderful vitamin in our pharmacy options, many will have a question - is such a concentration of vitamin D dangerous?

Let's figure it out together!

What do we know about vitamin D, except that its deficiency causes rickets in children of the "North"? 🙂

Basically, vitamin D is synthesized in the skin under the influence of UV light, unless it is ingested with food or special supplements. Its metabolism begins in the epidermis from 7-dehydrocholesterol (a substance constantly present in the skin). With the help of sunlight, cholecalciferol (vitamin D3) is formed from it in the skin - a hormonally active form of vitamin D, which is transported to various organs.

Vitamin D from food identical to cholecalciferol formed in the skin, with the exception of the replacement of one or two atoms in the molecule, which does not in any way affect its functionality for the body.

It is the general aging process of the skin that leads to a REDUCTION of the ability to synthesize vitamin D with the help of sunlight! Over the years, the synthesis process drops by 75%.

And then, after 37-40 years, it becomes extremely important "Get extra" necessary for younger skin vitamin D from "external sources".

What are the benefits of vitamin D for the skin?

Optimal level of vitamin D in the skin:

Helps improve firmness
stimulates collagen production
enhances the healthy glow of the skin
reduces the depth of wrinkles and fine lines
reduces dark dark spots
has a beneficial effect on improving the situation with skin diseases such as psoriasis, eczema and acne

How does vitamin D affect the beauty of our skin?

Now I will explain more simply this complex sentence))).

It has now been scientifically proven that chronic inflammation is the cause of premature skin aging.

⇒ Chronic inflammation in the body can be a response to environmental and psycho-emotional stress, constant physical and emotional fatigue, smoking, dirty city air, improper skin care regimens, as well as harmful preservatives in cosmetics, various allergens and irritants, plus UV radiation (which, by the way, seems to be necessary for the production of vitamin D, but at the same time has a catastrophic effect on the youth and beauty of the skin ...).

⇒ Chronic inflammation can last from several weeks to several years... Moreover, it is not at all necessary that it will begin with any specific skin infection! And it is also not necessary that you will notice that it goes on and accelerates the aging of the skin.

Chronic inflammation can also be caused by weakening and aging. immune system.

So how does chronic inflammation lead to premature skin aging?

This is largely due to matrix metalloproteinases (MMPs), enzymes associated with inflammatory responses in the body. MMPs are proteolytic endopeptidases that break skin proteins into fragments, accelerating their destruction. Skin proteins are our favorite collagen and elastin.

Why do metalloproteinases break down collagen?

it necessary restorative response of the body for skin damage after injury. As you remember (of course you remember!))))) From my, the process of creating and breaking down collagen is fundamental in the body so that our skin is healthy and elastic for as long as possible. This process must be proportional in time: i.e. the creation of young collagen should not be longer than the process of destruction by metalloproteinases of the old, and vice versa.

Once the skin has been damaged by burns or other trauma, inflammation and immune response begin to stimulate the accelerated decomposition of old, damaged skin and scars, and the formation of a new, young and "pink". * Remembering our burns. *

When chronic inflammatory process in the skin for the reasons indicated here above, metalloproteinases "mechanically", due to the constant "work" of immunity, break down and destroy collagen and elastin proteins... This leads to VISIBLE SKIN AGING, expressed by a network of fine wrinkles and lines on the face, loose skin and general tissue atrophy.

By the way! Prolonged acne is a CAUSE OF PREMATURE SKIN AGING. I often write about this in various posts. There is a chronic constant inflammatory process in the skin, and all immune enzymes are actively working to break down and utilize important proteins of youth. And therefore, I remind you once again: first we cure acne, then we start using "rejuvenating" care products. Girls, our unfortunate acne skin is aging, alas, faster, and the fight against acne should be at the forefront.

An important takeaway: prevention and reversal chronic inflammation should be the main skin care strategy to counteract its accelerated and visible aging.

For this we must obligatory and daily take antioxidant vitamins in human dosages, observe the correct diet, and use competent cosmetics.

And since it is vitamin D that regulates the action of genes and molecules in the immune response to the inflammatory process, increases Negative influence inflammation on the skin, increasing the destructive effect of metalloproteinases on collagen.

Active vitamin D stimulates certain factors that are important for suppressing inflammatory processes in the skin.

In order to understand what the phrase "skin renewal" means, consider the "visual aid" on important processes occurring in our epidermis.

⇒ We see that the epidermis has several layers which are made up of cells "Keratinocytes"... Keratinocytes are constantly moving in the "bottom-up" direction: they originate in the basal layer, and gradually move upward to the uppermost layer of the epidermis - the stratum corneum. As long as the keratinocyte moves from the basal layer to the granular layer, it is alive.

⇒ In grainy keratinocyte "dies", i.e. loses its nucleus and becomes an ordinary "bag" filled with keratin. A "dead" keratinocyte is called a "corneocyte".

Corneocytes, although they are "morally dead", they still continue to move like zombies ...)))

⇒ From the “granular” layer they move to the “stratum corneum”, where they stick together with a special fatty (lipid) composition (we often call it "Skin cement"). This special "sticky" composition consists of ceramides (ceramides) and phospholipids.

If the skin is healthy and the formation of the stratum corneum takes place "according to the regulations", then microbes that damage it do not penetrate through the normal skin cement. That is why we so often remind you how important it is to restore the lipid-skin cement (the lipid barrier of the skin) and use that “replenish” it. But this retreat ...

⇒ But also in stratum corneum the path of our "zombie" corneocyte does not end. It "floats" out of the viscous lipid cement "phospholipids + ceramides", and already completely dry, dead cell appears on the surface of the face, where it gets into the "company" exfoliating cells.

Exfoliating cells- this is permanently dead corneocytes that simply fall off the skin in different ways: by themselves, after washing or after scrubbing.

This is the way the keratinocyte goes. And this process is happening all the time. True, with different durations in time in different years ... And this is called "Skin renewal".

• with dead and exfoliated cells, toxins, salts and bile are released from the skin
• bacteria do not penetrate through healthy skin with a strong lipid barrier (stratum corneum)
• skin looks fresher and lighter

Skin cell renewal up to 25 years old in about 28 days(from the birth of a new keratinocyte cell to the exfoliation of a dead corneocyte).

After 25 years skin renewal slows down and by the age of 40 it reaches 40 days in time about. A after 50 years skin renewal occurs on average in 60 days and more ...

What causes skin renewal to slow down?

• chronological aging
• photoaging (the effect of UV rays on the skin, see)
• lack of certain vitamins, including vitamin D
• lack of estrogen in the body (menopause or other reasons)
• increased oily or dry skin
• chronic inflammatory diseases

A very important point for those "who are over 30")))). The renewal of epidermal cells stretches over time in comparison with the skin up to 25 years.

⇒ Vitamin D regulates the work of epidermal growth factor and other molecules participating in the process of division of skin cells, and is just the same vitamin necessary for the skin, which regulates and normalizes the skin renewal time, keratinocyte formation rate, and their timely "advancement" upward to rejuvenate the skin surface.

This is why vitamin D deficiencies need to be replenished regularly to keep our skin looking healthy and beautiful!

I want to say that vitamin D is no worse (and if you look at a bunch of studies, then even better) vitamin E reduces lipid peroxidation in the skin under the influence of UV rays, and protects skin cell membranes from destruction.

Girls, who, like me, "are inseparable from acne in life." US it is imperative to replenish vitamin D deficiencies daily! Especially if you, again like me, are afraid of the sun (and with acne, the sun is contraindicated!) And do not leave the house without sun protection, or try to stay in open sunlight as little as possible.

Vitamin D helps fight acne along with other vitamins!

It activates specific genes that code for antimicrobial receptors. And also, which is very important to know, activates the production of antimicrobial peptide - cathelicidin, with the help of which the skin with acne overcomes this infection and accelerates its healing, stimulating angiogenesis.

Vitamin D norm

⇒ For an adult who is in the sun every day, the norm of vitamin D from vitamins is 400 IU per day.

But absolutely different picture in a case like mine:

Natural climate with little sunny days
high air pollution
the presence of acne and, accordingly, constant protection from direct sunlight on the skin
not so young to spend enough time in the sun again, because it accelerates the visible aging of the skin (the process of photoaging)

⇒ In this case, daily intake of vitamin D from 2000 to 4000 IU.

Important! Excess vitamin D, especially if the body does not have enough MAGNESIUM, can create conditions for the development of cardiovascular diseases.

That is why, I personally take vitamin D not separately, but in the best vitamin complex, where its balance with magnesium is observed, and therefore taking vitamin D is not dangerous, but on the contrary, it is extremely useful for beautiful, healthy skin!

Vitamin D is one of the most popular and widely discussed vitamins in recent decades. Since vitamin D was first recommended as a key nutrient in 1943, it has a long history of research.

Initially, the daily requirement for vitamin D was approximately 200 IU (5 mcg cholecalciferol). Over the years, this level has gradually increased. First, up to 400 IU (10 μg cholecalciferol), and then up to 400-800 IU (10-20 μg cholecalciferol). However, the latest recommended daily intake remains controversial for three reasons.

First, good known fact that human skin cells can synthesize vitamin D in the sun. Under the influence ultraviolet radiation B (UVB) our skin cells (keratinocytes) convert 7-dehydrocholesterol into a form of provitamin D called cholecalciferol. The amount of pigments in skin cells, the strength of UV radiation, the use of sunscreens, the general health of our skin and other factors affect the production of the vitamin. Therefore, it is difficult to accurately predict the amount of vitamin D produced.

Second, cholecalciferol is not the same as active vitamin D. For its formation, cholecalciferol must be transported to the liver cells, where 25-hydroxycholecalciferol is formed. The 25-hydroxycholecalciferol is then transported to the kidneys, where it is converted to 1,25-dihydroxycholecalciferol. It is this form of vitamin D that is active.

Finally, the recommended dosage remains an issue, as there is still no known protective level of vitamin D for the prevention of disease. Early research on the effects of vitamin D focused on preventing rickets (osteogenesis disorders in children). Recent vitamin D research focuses on the immune and cardiovascular systems as well as blood sugar levels.

The role of vitamin D in health

Bone health. Vitamin D deficiency can lead to softening or malformations of the bones. In children, this condition is called rickets. In adults, this is called osteomalacia. The relationship between vitamin D and bone metabolism is more complex than one might think. Vitamin D increases blood calcium levels, aiding the absorption of calcium from food and decreasing the excretion of calcium in the urine. In addition, vitamin D can extract calcium from bones to maintain proper blood levels, and this affects bone strength.

Obviously, if our goal is to build strong bones, we do not want to allow calcium to be excreted from the bone tissue. For this reason, we need to ensure that vitamin D is adequately supplied from food or produced in skin cells by exposure to sunlight. Any bony fish, including sardines or salmon, is potentially a rich source of both vitamin D and calcium.

Blood sugar control. Researchers have found that the risk of hyperglycemia and diabetes is higher in people with low vitamin D. More recent studies have shown that increasing the concentration of vitamin D in the body can lower sugar levels and the risk of developing diabetes.

Immunity. Vitamin D is one of the many substances involved in the maturation of white blood cells - our first line of defense against most infections. Specifically, researchers found a link between low vitamin D levels and the risk of respiratory infections.

Vitamin D is found in foods

The list of foods containing vitamin D is short. In addition, one of the best food sources of vitamin D, it loses its benefits during processing. However, it will be easier for you if you like fish. Salmon, for example, contains only one serving of vitamin D daily. Sardines contain over 40% of the norm, and tuna contains just under 25%.

Eggs from free-range hens are good source vitamin D (about 10% of the norm per egg). Vitamin D is concentrated in the yolk, so eat a whole egg.

Also keep in mind that vitamin D is a very stable nutrient. It is not destroyed by most cooking methods. Scrambled eggs lose about 20% of their vitamin D. A slight loss of vitamin D can be expected when cooking in oil. Either way, most of the vitamin D will end up on your plate.

One research team found that when foods were baked at 232 ° C for 10 minutes, vitamin D was almost unaffected. Another study reported that eggs baked at 163 ° C for 40 minutes lost more than half of their vitamin D. In other words, prolonged exposure may be the culprit.

Deficiency risk

The risk of vitamin D deficiency is substantial. In every age and gender group surveyed, the reported vitamin D levels did not meet the daily requirement even with the consumption of supplements and fortified foods. Since vitamin D can form in sunlight, it is preferable not to exclude this source.

Worst of all, vitamin D deficiency has tripled since the 1980s. This trend is likely due to reduced sun exposure and increased use of sunscreens.

The geography of your residence also matters. The further north you go, the less likely you are to meet your vitamin D needs. North of the 37th parallel, you get virtually no vitamin D from natural sunlight during the winter months. The darker the skin, the less efficiently you synthesize vitamin D. Therefore, it is better for people with dark skin color to live closer to the equator.

Sunscreen interferes with the production of vitamin D in the skin. One research team found that applying SPF8 sunscreen as recommended completely blocked vitamin D production.

Diseases with deficiencyvitamin D

• Osteoporosis
• Rickets
• Osteomalacia
• Imbalance
• Diabetes
• Rheumatoid arthritis
• Bronchial asthma
• Depression
• Epilepsy
• Weak immunity

Relationship with other nutrients

As stated above, the activity of vitamin D and is very closely related. There is reason to believe that vitamin D in the absence of adequate calcium in the body can lead to bone loss by increasing the rate of calcium resorption.

Vitamin D also appears to slightly increase intestinal absorption of magnesium. Since calcium and magnesium compete with each other for absorption, magnesium deficiency can be considered an aggravating factor. Vitamin D and vitamin K work together in bone metabolism. Low levels of vitamin K pose a risk of bone problems.

Risk of toxicity

The acceptable upper limit for vitamin D is 4000 IU for adults. Considering that it is quite difficult for many people to reach the 400 - 800 IU norm, this is not so scary. As an example, you need to eat a pound of salmon a day in order to reach a normal level.

In 2010, the U.S. National Academy of Sciences updated its vitamin D intake guidelines.

• 0-12 months: 400 IU (10 mcg cholecalciferol)
• 1-70 years: 600 IU (15 mcg cholecalciferol)
• 70+ years: 800 IU (20 mcg cholecalciferol)
• Pregnant women: 600 IU (15 mcg cholecalciferol)
• Breastfeeding women: 600 IU (15 mcg cholecalciferol)

Of course you need to sunbathe: in moderate sun, at the right time and not for long. Unfortunately, whether you tan or not, between the ages of 20 and 70, our skin loses about 75% of its ability to produce vitamin D. In addition, the use of sunscreens reduces the body's ability to synthesize vitamin D. For example, with SPF-8 by 95%, and if you use sanskrin with SPF-15, then this figure increases to 98%.

In addition, the skin is the last organ to receive vitamins and antioxidants from the food and supplements used. Our body has its own priorities, and the received vitamin D is primarily used to maintain the correct level of calcium in the blood, bone formation processes and neuromuscular functions. But when using preparations with vitamin D directly on the skin, its protective capabilities will expand and a rejuvenating effect will be achieved.

Dermal application of vitamin D analogs causes a decrease in anti-inflammatory cytokines and, at the same time, evens out the expression of the antimicrobial peptide cathelicidin LL-37. This major peptide, produced by keratinocytes, has many important functions required to maintain skin function. It controls the microbial flora, attracts cells of the adaptive immune system, promotes epithelial restoration and supports the processes of angiogenesis. All this is necessary for the blood supply and the provision of skin cells with oxygen and nutrients. The importance of this peptide is evidenced by the fact that in diseases such as atopic dermatitis, psoriasis, rosacea, eczema and trophic ulcers of the legs, its correct expression is impaired. For example, it is well known that topical application of vitamin D supplements reduces inflammation and morphological changes in psoriasis spots and plaques.

Creams with vitamin D3

Now a little about what options are there for replenishing vitamin D directly in the skin itself. Probably, many have noticed that while on vacation at the sea, if we sunbathe moderately, without burning, our skin looks healthier and denser, despite the "harmful" sunburn. Moderate daily sun exposure, when the body is saturated with vitamin D and begins to give excess to the skin, has visible positive benefits. We look refreshed, rejuvenated and energetic. Of course, not everyone has the opportunity to tan in moderation every day, and the line between a healthy tan and excessive sun exposure is very easy to cross. Therefore, the use of cosmetics with vitamin D3 becomes a safe necessity. Our keratinocytes activate this precursor into its active form, directly in the skin itself.

So, unfortunately, there are still few options for such cosmetics on the market. The most famous is Life Flo Vit D3 Body Cream, one press of the pump will give us 1000 units of vitamin D3.

Is this a lot? Not at all. For example, when you are in summer time in the sun for 20-30 minutes, our skin is capable of producing 10,000 - 20,000 IU of vitamin D. When replenishing a deficiency, treating osteoprosis and cancer, the doses, standard calcitriol used internally, range from 50,000 and more international units. External use, in comparison with oral administration, is not able to significantly increase the level of vitamin D inside the body, and basically all the benefits go directly to the skin itself.

Another good option is Vitamin D3 Cream 10,000 IU, it often disappears from the market and cannot be bought on the iHerb. Let's hope that someday they will include it in their base.

Variants of vitamin D3 in liquid formulas, you can add a few drops to your favorite face and body creams or increase their concentration in Life Flo Vit D3 Body Cream. For example, Thorne Research D / K2 makes good oil solutions, 2,000 IU - ten drops of such a concentrate contain 5000 IU of vitamin D and 1 mg of vitamin K2.

Or, for example, natural, lichen-synthesized vitamin D3 - Vitamin D3 Vegan. One measured dose contains 1000 IU. This is my favorite formula. Firstly, there is a natural vitamin, and secondly, it is dissolved not in long-chain triglecerides (ordinary oils), but in medium-chain ones.

Medium-chain trigleceride molecules are much shorter than oil ones. Oily oils are not completely absorbed into the skin and remain a shiny film on it. Like any vegetable oil, say, corn oil or sunflower oil.

Medium chain does not leave a greasy feeling when applied to the skin - it feels like silk and is absorbed without a trace. Ideal for under-eye or neck areas. A couple of drops of this vitamin D can also be used as a hand moisturizer.

And inside, such triglecerides are absorbed by a completely different mechanism that does not require energy consumption. Since the molecule is short, it simply diffuses. Anything hidden in medium chain triglycerides will be fed into tissues almost instantly.

In winter, it is advisable to use higher concentrations of vitamin D, especially on those areas of the skin that are always closed from sunlight. Naturally, such liquid formulas can also be taken orally.

Internal intake of vitamin D3

The main function of vitamin D in the body is calcium homeostasis. The importance of its use in the prevention and treatment of osteopenia and osteoprosis is well known. This is one of the main ways to get calcium directly into the bone and not into the blood vessels. For women who have entered menopause, taking similar drugs becomes vital. They will also undoubtedly be pleased that vitamin D is able to change body composition, namely, to minimize the amount of fat that is deposited on organs in the abdominal part of the body and in the upper arms.

The following formula is desirable for women from the period of perimenopause for the prevention of osteopenia and osteoporosis. SEDDS, Vitamin D3 + Ca. Vitamin D with calcium, which is absorbed in the right way due to the special delivery system Self Emulsified Drug Delivery System. SEDDS - pretty new system Many pharmaceutical companies use it to better absorb fat-insoluble ingredients.

And here is the natural form of vitamin D, synthesized by fungi or yeast. Source of Life Garden Vit D3 contains 2500 IU per capsule and is good for internal use during winter. This supplement is also supplemented with organic mixtures of vegetables, mushrooms, plants and enzyme ingredients. All this will have a beneficial effect on the body and will allow you to get as many positive changes as possible. A very good buy, naturally synthesized vitamins are usually very expensive. And an excellent choice for replenishing vitamin D deficiency at any time for both adults and children.

I would also like to note the liposomal forms of vitamin D - Liposomal Vitamin D. Liposomes are special forms of lipids that contain phosphorus and are completely analogous to phospholipids that make up cell membranes. Liposomes are often used to increase bioavailability and improve absorption, delivery into the bloodstream and even into cells of various drugs, peptides, vitamins or nutrients. Phospholipids form a special membrane around the delivered molecules. This protective shell will repel substances that can damage them, as a result of which liposomal absorption can reach 90%.

Liposomal forms of drugs are undoubtedly more effective and can quickly increase the level of vitamin D in the body very quickly. When serious diseases, chemotherapy, problems with assimilation, liposomal form of vitamin D - the best choice compared to normal.

Mostafa WZ, Hegazy RA. Vitamin D and the skin: Focus on a complex relationship: A review.

Vitamin D and Skin: A Complex of Interactions

Mostafa WZ, Hegazy RA - Department of Dermatology, Faculty of Medicine, Cairo University, Cairo, Egypt

Introduction

It looks a bit ironic that vitamin D, through a historical accident, began to be classified as a "vitamin", because vitamin is conventionally defined as "an essential essential element in the diet." The paradox with "vitamin D" is that the diet itself is usually poor in vitamin D, except for cod or other fish, oils, or food fortified with this vitamin.

Vitamin D is actually a fat-soluble prohormonal steroid that is involved in endocrine, paracrine and autocrine regulation. The endocrine effects of vitamin D are mainly associated with serum calcium homeostasis. Vitamin D and calcium are often used in describing the same processes because they are functionally related, the main role of vitamin D is to regulate calcium levels in the bloodstream, constantly supporting the absorption of calcium and phosphate from the intestine or taking calcium from the bones. In addition, vitamin D is beneficial when present at optimal concentrations without significantly affecting calcium absorption; however, it triggers or facilitates a flexible physiological response to changes in calcium levels.

The paracrine and autocrine effects of vitamin D depend on the genetic transcription of a unique cell type expressing nuclear receptors for vitamin D. in many organs and systems,,,,. The potential myriad effects of this vitamin on human health and disease have led to a growing interest in vitamin D deficiencies and ways to normalize low levels of vitamin D.

Sources of Vitamin D

There are only 3 known sources of vitamin D: sunlight, diet, and vitamin D supplements (Fig. 1),,.

sunlight

The most famous source of vitamin D is its synthesis in the skin, under the influence of the sun. The first mention of this physiological action sunlight on the synthesis of vitamin D belongs to the Greek historian Herodotus. He visited the battlefield where Cambyses (525 BC) defeated the Egyptians and examined the skulls of the slain Persians and Egyptians. He noted that the skulls of the Persians were so fragile that they broke even when struck by pebbles, while the skulls of the Egyptians were strong and could hardly be damaged even when struck by a stone. Herodotus's explanation was that the Egyptians walked bareheaded since childhood, exposing their heads to sunlight, while the Persians covered their heads by shading them from the sun, resulting in weaker skull bones. Later, in the mid-17th century, Francis Gleeson, professor of physics at Cambridge University, noted in his treatise on rickets that the disease was common among infants and young children of farmers who ate well and whose diet included eggs and butter but they lived in rainy, foggy parts of the country and were indoors during long, harsh winters.

Synthesis of vitamin D in the skin. According to the International Commission of Illumination (ILC), the effective radiation for the synthesis of vitamin D (i.e. the efficiency of each wavelength for the synthesis of vitamin D in the skin) covers the spectral range (255-330 nm) with a maximum of about 295 nm (UVB). Exposure to UV radiation inducing skin redness at a minimum erythemal dose for 15-20 minutes can induce the production of up to 250 μg of vitamin D (10,000 IU).

Its precursor 7-dehydrocholesterol is converted into provitamin-D 3 in the plasma membrane of basal and suprabasal keratinocytes and dermal fibroblasts. Vitamin D3 synthesized in the skin is released from the membrane and enters the systemic circulation associated with vitamin D-binding protein (DBP). Serum vitamin D3 concentration peaks 24 to 48 hours after exposure to UV radiation. Thereafter, serum vitamin D3 levels decline exponentially with half-lives ranging from 36 to 78 hours. As a fat-soluble molecule, vitamin D3 can be accumulated by adipocytes and contained subcutaneously or in the omentum for later use. The distribution of vitamin D3 in adipose tissue extends its half-life to two months, which was first discovered in experiments with the participation of submarine personnel,,.

Once in the bloodstream, vitamin D is converted in the liver by hydroxylase to 25-hydroxyvitamin D (25 (OH) D; calcidiol). The circulating 25 (OH) D level is a measure of the vitamin D content. This level reflects the UV dose and dietary intake of vitamin D. Serum half-life of 25 (OH) D is approximately 15 days. 25 (OH) D is biologically inactive except at very high, non-physiological levels. As needed, 25 (OH) D is converted in the kidneys to the active hormonal form 1,25-dihydroxyvitamin D (1,25 (OH) 2D; calcitriol), this process is usually tightly controlled by parathyroid hormone, the concentration of which begins to increase when a 25 (OH) D level of 75 nmol / L or less. Despite this, inadequate dietary intake of vitamin D lowers circulating calcitriol levels. Circulating calcitriol levels are also negatively impacted by a decrease in the number of viable nephrons, high serum concentrations of fibroblast growth factor-23, and high levels of pro-inflammatory cytokines such as interleukin (IL) -1, IL-6, and tumor necrosis factor-alpha (TNF-α) ,.

It is important to know that the conversion of provitamin D3 into inactive metabolites lumisterol and tachysterol balances the skin biosynthesis of vitamin D3 by a feedback mechanism. This mechanism prevents an “overdose” of vitamin D 3 by UV exposure. After less than 1 minimum erythemal dose (DER; i.e., the radiation dose required to redden the skin 24 hours after exposure), the concentration of provitamin D 3 reaches its maximum level and further UV radiation only leads to the production of inactive metabolites.

Food Sources and Supplements

Vitamin D is available in 2 different forms, ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Exposure to light provides the need for vitamin D only in the D3 form, while dietary intake is able to provide both forms, which are officially regarded as equivalent and interchangeable,. However, for several reasons, objections to this assumption were expressed, in particular, differences in their effectiveness differ in their effectiveness with an increase in serum 25-hydroxyvitamin D with a decrease in the level of metabolites of vitamin D2 and vitamin D-binding protein in plasma, as well as the detection of non-physiological metabolism and a shorter lifetime of vitamin D2. However, to this day, the main vitamin D supplements are in the form of vitamin D2, not vitamin D3. Multivitamins can contain either vitamin D2 or vitamin D3, but most companies have now reformulated their product names to contain vitamin D in D3.

There are only a few natural sources of vitamin D, including fish oil, cheese, egg yolks, mackerel, salmon, tuna, beef, and liver. Because it is not easy for many people to get enough vitamin D from natural food sources, many countries consume foods such as orange juice, milk, yogurt, and vitamin D cereals. Many inexpensive vitamin D supplements and forms are available over the counter in both forms of vitamin D3 and vitamin D2 and forms with or without calcium,.

Vitamin D levels

Various cut-off values ​​for vitamin D have been used until recently. The 50 nmol / L level is widely used in the determination of the 25 (OH) D content, although in some studies the 37.5 nmol / L level was used as the minimum allowable,,. Further research, however, have shown that a 25- (OH) D level of 75 nmol / L or higher is necessary to cover all physiological functions vitamin D and, therefore, should be considered as optimal,,,,.

Factors affecting vitamin D levels

Nutrient deficiencies are usually the result of nutritional deficiencies, malabsorption and use, increased demand, or increased excretion. Vitamin D deficiency can occur when there is a lack of it in the diet for some time, limited exposure to sunlight, impaired renal function of converting 25 (OH) D into an active form, or insufficient absorption of vitamin D in the gastrointestinal tract. Dietary vitamin deficiencies are associated with milk allergy, lactose intolerance, ovo vegetarianism, and veganism.

As for the amount of vitamin D synthesis in human skin, it depends on several factors, including environmental factors such as geography of residence, season, time of day, weather conditions (cloud cover), amount of air pollution and surface reflections that can interfere with UV radiation. reaching the skin,,,.

Individual characteristics represent another group of factors that influence the synthesis of vitamin D in the skin, including age, for example, older people have thinner skin and, therefore, are less able to synthesize vitamin D, overweight and obesity reduce vitamin levels D. It should also be noted that the type of human skin determines the efficiency of vitamin D synthesis. Light skin (type I) synthesizes six times more vitamin D than dark skin (type VI). Also, clothes, habits, lifestyle, workplace(for example, indoor versus outdoor), and avoiding the sun have a strong effect on vitamin D synthesis,,,.

The effect of certain methods, such as the use of sunblock or tanning beds, on the synthesis of vitamin D contains some interesting characteristics. Sunscreens are known to effectively block UVB radiation. However, it is questionable whether sunscreen actually causes vitamin D deficiency. It is rare to completely cover the body with sunscreen. Some areas of the skin are always free of cream. In regions where the sun is intense and the temperature is high enough for the population to use sunscreen, vitamin D levels are generally satisfactory. On the other hand, the use of tanning beds is controversial, but despite this, subjects who regularly visit tanning beds that are exposed to UVB radiation are likely to have a higher concentration of 25 (OH) D. However, there is a trend towards limiting the use of tanning beds due to fear of melanoma and non-melanoma skin cancer.

Vitamin D and skin: what besides its synthesis and metabolism?

The skin is a unique organ in that it is not only a source of vitamin D for the body, but also is able to respond to the active metabolite of vitamin D, 1,25 (OH) 2D. Both 1,25 (OH) 2D and its receptor (VDR) play an essential role in the skin.

Differentiation and proliferation of skin cells

Both calcium and 1,25 (OH) 2D have important and interacting functions in regulating the process of skin cell differentiation. 1,25 (OH) 2D increases the expression of involucrin, transglutaminase, loricrin and filaggrin, stimulates the formation of the stratum corneum, while suppressing hyperproliferation,. These processes are due to the ability of 1,25 (OH) 2D to increase intracellular calcium levels, which is achieved by induction of the calcium receptor, and phospholipase C, which play an important role in the ability of calcium to stimulate keratinocyte differentiation. VDR-deficient mice show a defect in epidermal differentiation consisting of decreased levels of involucrin and loricrin and loss of keratohyalin granules.

Skin antibacterial effects

1,25 (OH) 2D and its receptor regulate the long chain processing of glycosylceramides, which are essential for skin barrier formation and skin protection. In addition, they induce type 2 toll-like receptors (TLR2) and its coreceptor CD14, which initiates an innate immune response in the skin. Activation of these receptors leads to the induction of CYP27B1, which in turn induces cathelicidin, resulting in the death of foreign microorganisms. Mice lacking VDR or enzyme (CYP27B1) show decreased lipid content, resulting in a defect in the permeability of skin barriers and a defective response of the innate immune system to invading infectious agents.

Vitamin D and cutaneous innate immunity

The historical link between vitamin D and innate immune function originally stemmed from the use of fish oil as a treatment for tuberculosis (TB). More recent studies describe the cellular and molecular mechanisms underlying the action of vitamin D on the causative agent that causes tuberculosis, Mycobacterium tuberculosis (M. TB). In the first of these studies, performed 25 years ago, active 1,25 (OH) 2D appeared to reduce the proliferation of M. TB in macrophages; contributed to this m interferon-γ (IFNγ) - a stimulant of macrophages. However, an important step forward in our understanding of how vitamin D forms an antibacterial response to TB emerged after much more recent research aimed at studying the ways in which monocytes and macrophages, key cells in the formation of an immune response, respond to the introduction of M. TB. These data showed that monocytes promoted localized activation of vitamin D in response to M. TB invasion by binding 1,25 (OH) 2D to endogenous VDR. Thus, vitamin D can modulate gene expression in response to the introduction of M. TB - a classic intracrine mechanism. Functional studies have shown that 25OHD-mediated induction of cathelicidin coincides with increased killing of M. TB in monocytes. Naturally, the occurring changes in serum 25OHD correlated with the induction of monocyte cathelicidin expression. The takeaway from these studies was that individuals with low serum 25OHD levels would be less able to maintain monocyte induction, antibacterial activity, and would be at greater risk of infection. Conversely, in vivo supplementation of vitamin D deficiency in individuals with vitamin D deficiency has been shown to improve TLR-mediated induction of monocytic cathelicidin and, therefore, to protect against infection (Fig. 2).

Research has shown that T-cell cytokines play a key role in enhancing and attenuating vitamin D-mediated cathelicidin production. Indeed, cytokine production by monocytes themselves may be central to intracrine vitamin D metabolism in this cell type. Thus, it seems likely that the ability to provide an appropriate response to an invasion of infection will be highly dependent on the availability of vitamin D in conjunction with other components of the normal human immune response.

Vitamin D can also influence the innate immune response to invading pathogens by affecting antigen presentation on the membrane of macrophages or dendritic cells (DC) (Fig. 2). These cells are known to express VDR and treatment with 1,25 (OH) 2D has been shown to inhibit DC maturation, suppress antigen presentation, and promote a T-cell immune response.

Vitamin D and cutaneous adaptive immunity

Previous studies of vitamin D and the immune system showed VDR expression in both T and B lymphocytes (Fig. 2). In particular, VDR expression was expressed only in immunologically functionally active proliferating cells, which suggests an antiproliferative role for 1,25 (OH) 2D in these cells. Helper T cells (Th) are the main target for 1,25 (OH) 2D, which can suppress Th proliferation as well as the production of modulating cytokines by these cells. Activation of naive Th antigen, in turn, leads to the activation of the Th subgroup with separate cytokine profiles: T h1 (IL-2, IFN-γ, tumor necrosis factor alpha) and T h2-type immune response (IL-3, IL-4 , IL-5, IL-10), which, respectively, are responsible for cellular and humoral immunity,.

In vitro, 1,25 (OH) 2D inhibits Th1 cytokines by stimulating the production of T h2 cytokines. The third Th group, as is known, is under the influence of vitamin D is interleukin-17 (IL-17) -secreting T cells (Th17 cells). Type 1 diabetic mice treated with 1.25D exhibit lower levels of IL-17 and 1.25 (OH) 2D-mediated suppression of autoimmunity manifests itself in inhibition of Th17 activity. In addition, subsequent studies have shown that 1,25 (OH) 2D suppresses the production of IL-17 through direct transcriptional suppression of interleukin-17 gene expression.

Another group of T cells known to be induced by 1,25 (OH) 2D regulatory T cells (Tregs). Part of the Th cell family, Tregs suppress the immune response of other T cells as part of a mechanism to prevent excessive or autoimmune reactions... Recent studies have highlighted the importance of Tregs as a mediator of the immunoregulatory action of vitamin D. Systemic administration of 1,25 (OH) 2D in kidney transplant patients has been shown to increase the circulating Treg population.

Studies of vitamin D and T-cell function to date are focused primarily on the response of these cells to active 1,25 (OH) 2D. Less clear are the mechanisms by which fluctuations in vitamin D levels may also affect T lymphocytes, despite reports of serum 25OHD levels being associated with a specific T lymphocyte population. For example, the level of circulating 25OHD correlated with the activity of Tregs in patients with multiple sclerosis,. There are four potential mechanisms by which serum 25OHD affects T-cell function; I) direct effects on T cells through systemic 1,25 (OH) 2D; (Ii) indirect effects on antigen presentation to T-lymphocytes through localized expression of CYP27B1 DC and intracrine synthesis of 1,25 (OH) 2D; (Iii) direct effects of 1,25 (OH) 2D on T cells after synthesis of the active form of vitamin D by CYP27B1-expressing monocytes or DC - by a paracrine mechanism; (Iv) intracrine conversion of 25OHD to 1.25 (OH) 2D by T cells. It is still unclear whether one or more mechanisms are involved in the regulation of specific types of T cells. For example, the effects of 1,25 (OH) 2D on Tregs may occur indirectly through exposure to DC, but may also include direct effects on Tregs. However, DCs also express CYP27B1 and can therefore act as a vehicle to target 25OHD on Tregs. Interestingly, that the expression of CYP27B1 by T cells is described, it can be assumed that 25OHD may also influence the function of these cells through an intracrine mechanism, although precise data on specific types of T cells are not available.

Although the expression of VDR B cells has been known for many years, the ability of 1,25 (OH) 2D to suppress B cell proliferation and immunoglobulin (Ig) production was initially perceived as an indirect Th-mediated effect. However, more recent studies have confirmed a direct effect of 1,25 (OH) 2D on B-cell homeostasis, with marked effects including inhibition of plasma cells and activation of memory cell differentiation. These effects contribute to the action of vitamin D in B-lymphocyte-associated autoimmune disorders such as systemic lupus erythematosus. Other B cell targets are known to be modulated by 1,25 (OH) 2D and include IL-10 and CCR10, and B cell responses to vitamin D are thought to go beyond its effects on B cell proliferation and Ig synthesis.

Hair follicle cycle

In vitro studies support the concept that VDR may play a vital role in postnatal life support hair follicle... The cells of the mesodermal papilla and the external root sheath (NRV) of epidermal keratinocytes express VDR to varying degrees depending on the stage of the hair cycle. And in the anagen and catagen stages, an increase in VDR is observed, which is associated with a decrease in proliferation and an increase in keratinocyte differentiation. These changes are thought to be conducive to changing hair growth cycles.

Limited studies have been done in humans to investigate the role of vitamin D in the hair growth cycle. Topical calcitriol has been shown to be effective in chemotherapy-induced alopecia induced by paclitaxel and cyclophosphamide. However, topical calcitriol does not provide protection against chemotherapy-induced alopecia caused by the combination of 5-fluorouracil, doxorubicin, cyclophosphamide and the combination of cyclophosphamide, methotrexate, and 5-fluorouracil. The ability of topical calcitriol to prevent chemotherapy-induced alopecia may be dependent on which chemotherapeutic agents are used. It should be noted that studies that did not find any effects used small doses of vitamin D, which are inadequate to protect against chemotherapy-induced alopecia.

Sebaceous glands

Incubation of human sebaceous gland cells with 1.25OH2D has been reported to result in a dose-dependent suppression of cell proliferation. Using real-time PCR, it has been shown that the key components of vitamin D (VDR, 25OHase, 1aOHase, and 24OHase) are strongly expressed in such cells. It was concluded that local synthesis or metabolism of vitamin D may be important for the regulation of growth and various other cellular functions of the sebaceous glands, which are promising targets for vitamin D therapy or analogs for pharmacological modulation of calcitriol synthesis / metabolism.

Photoprotection

Photodamage refers to damage to the skin induced by ultraviolet (UV) light. Depending on the dose of ultraviolet light, there can be DNA damage, an inflammatory response, apoptosis of skin cells (programmed cell death), skin aging and cancer. Several studies, mainly in vitro (cell cultures),, and studies in mice, where 1,25-dihydroxyvitamin D3 was topically applied to the skin before or immediately after irradiation, have shown that vitamin D has a photoprotective effect. Reported effects on skin cells include a decrease in DNA damage, a decrease in apoptosis, an increase in cell survival, and a decrease in erythema. The mechanisms of these effects are not known, but one mouse study showed that 1,25-dihydroxyvitamin D3 caused the expression of metallothionein (a protein that protects against free radicals and oxidative damage) in the basal layer. In addition, the extragenomic mechanism of action of vitamin D has been shown to promote photoprotection; such effects of vitamin D include cellular signaling cascades through which calcium channels open.

Healing wounds

1,25-dihydroxyvitamin D3 regulates the expression of cathelicidin (MP-37 / hCAP18), an antimicrobial protein that appears to activate the innate immunity of the skin to stimulate wound healing and tissue repair. One study showed that human cathelicidin is expressed during the early stages of normal wound healing. Other studies have shown that cathelicidin modulates inflammation in the skin, induces angiogenesis, and improves re-epithelialization (the process of repairing the epidermal barrier that protects underlying cells from environmental influences). Active forms of vitamin D and its analogs have been shown to activate the expression of cathelicidin in keratinocyte culture. However, it is necessary additional research to determine the role of vitamin D in wound healing and epidermal barrier function, and whether oral vitamin D supplementation or topical treatment with vitamin D analogues aids surgical wound healing.

Vitamin D and skin conditions

Based on the aforementioned facts regarding the relationships that exist between vitamin D and skin, it seems that only a “natural” vitamin D deficiency leads to a long list of skin diseases including skin cancer, psoriasis, ichthyosis, autoimmune skin diseases such as vitiligo, cystic dermatoses, scleroderma and systemic lupus erythematosus, as well as atopic dermatitis, acne, hair loss, infections, and photodermatosis. However, it remains controversial whether vitamin D deficiency is primarily at the root of the disease's pathogenesis or is simply an indirect event contributing to the inflammatory process. A recent systematic review of 290 prospective cohort studies and randomized studies of 172 key health indicators and physiological parameters associated with the risk of disease or inflammation highlighted one important fact; Vitamin D deficiency is a marker of poor health despite being an actual cause or association with other factors.

Skin cancer

A number of epidemiological studies have shown that vitamin D may have a protective effect, reducing the risk of cancer and cancer-associated mortality,,,,. Adequate vitamin D levels have been linked to a reduced risk of certain cancers, including cancers of the esophagus, stomach, colon, rectum, gallbladder, pancreas, lungs, breast, uterus, ovary, prostate, bladder, kidney, skin. thyroid and hematopoietic system (eg, Hodgkin's lymphoma, non-Hodgkin's lymphomas, multiple myeloma). For skin cancer, epidemiological and laboratory research gave conflicting results: some reveal a link between high level vitamin D and an increased risk of skin cancer, others show a reduced risk of skin cancer,,,, and still others do not show any association. The main findings pointing to the role of vitamin D in the prevention of initiation and progression of death from skin cancer are the involvement of vitamin D in the regulation of multiple signaling pathways that are important in carcinogenesis, including inhibition of the signaling pathway underlying the development of basal cell carcinoma, and activity of enzymes of excisional repair of nucleotides. In addition, vitamin D induces triggers of apoptotic pathways, inhibits angiogenesis, and alters cell adhesion. Another thing is that skin cancer metastasis depends on the tumor microenvironment, where vitamin D metabolites play a key role in preventing certain molecular interactions involved in tumor progression. A key factor complicating the association between vitamin D and skin cancer is ultraviolet B-radiation... The same UVB spectrum that catalyzes the production of vitamin D in the skin also leads to DNA damage, which can lead to epidermal malignancies. Overall, there is some evidence that vitamin D may play a role in the development of non-melanoma skin cancer (NSC), including basal cell and squamous cell carcinoma, as well as prevention of melanoma, although there is still no direct evidence to speak of a protective effect.

Psoriasis

Psoriasis is chronic inflammatory disease skin, which affects 2-3% of the world's population, there is a tendency for a significant increase in the incidence. Although the pathogenesis of psoriasis is not fully understood, there is sufficient evidence to indicate that impaired immune regulation in the skin, in particular T cells, plays a key role in the development of psoriasis. A number of studies have focused on the possible role of vitamin D deficiency in psoriasis,,.

The exact mechanism by which vitamin D deficiency contributes to pathogenesis is not fully understood. Several pathways have been identified, including the loss of the antiproliferative function of vitamin D, as found in cultured human keratinocytes, when exposed to calcitriol, there was a marked inhibition of growth and accelerated maturation. In addition, since inflammation and angiogenesis are cornerstones in the pathogenesis of psoriasis, the loss of anti-inflammatory and anti-angiogenic activity of vitamin D may represent another explanation for the contribution of vitamin D deficiency in psoriasis. Since 1α, 25-dihydroxyvitamin D3 is known to inhibit the proliferation of Th1 and Th17 cells, as well as induce Tregs, another pathway has been proposed by which vitamin D deficiency may play a role in the pathogenesis of psoriasis in the uncontrolled proliferation of Th1 and Th17 cells on the one hand. and inhibition of Tregs on the other hand. Topical treatment with calcipotriol has shown significant reductions in skin levels of human beta-defensin (HBD) 2 and HBD3, as well as IL-17A, IL-17F, and IL-8, which play an important role in psoriasis, which also links vitamin D deficiency to the pathogenesis of psoriasis.

With these findings on the role of vitamin D in the pathogenesis of psoriasis, it is not surprising that it is one of the most indicated topical agents for the treatment of this disease, either alone or in combination with betamethasone; Numerous studies have documented the efficacy and safety of the use of topical calcipotriol in the treatment of localized plaque psoriasis.

Acne and rosacea

Acne vulgaris is the most common skin condition affecting millions of people around the world. Inflammation resulting from the immune response to Propionibacterium acnes (P. Acnes) plays a significant role in the pathogenesis of acne. In a recent study, it was demonstrated that P. acnes is a potent inducer of Th17, and that 1.25OH2D inhibits P. acnes-induced Th17 differentiation, and thus can be considered as an effective factor in acne correction. In addition, sebocytes have been identified as 1.25OH2D-sensitive target cells, indicating that vitamin D analogs may be effective in treating acne. Another recent study showed that the expression of inflammatory biomarkers was observed under the influence of vitamin D treatment in sebocyte culture, but not through the VDR.

Another study found relatively high serum vitamin D levels in patients with rosacea (a common chronic condition affecting the skin of the face) compared with controls, suggesting that increased vitamin D levels may lead to rosacea.

Hair loss

The role of vitamin D in hair can be explained by the fact that the optimal concentration of vitamin D in the body was calculated on the basis of compensating for the phenomena of aging, including hair loss. Recently, 1.25OH2D / VDR has been shown to increase the ability of β-catenin to stimulate differentiation of hair follicle cells. In addition, extensive data from animal studies clearly show that VDR activation plays an important role in the hair follicle cycle, specifically in the initiation of anagen. Interestingly, in experiments in mice, it was not possible to achieve normalization of mineral homeostasis with a diet high in calcium and phosphorus and prevent baldness, suggesting that the mechanism of alopecia is not correlated with mineral levels, but depends on the level of vitamin D. In addition, recent evidence suggests that VDR directly or indirectly regulates the expression of genes responsible for the hair growth cycle, including the signaling pathway.

A recent study on eighty female patients showed that low vitamin D2 levels are associated with both common types of hair loss in women, namely; telogen and androgenetic hair loss in women. It was assumed that testing for vitamin D levels and prescribing vitamin D supplementation in cases of vitamin D deficiency would be warranted in the treatment of these conditions.

Contrary to the suggestion that vitamin D plays an important role in hair loss, a placebo-controlled study in 26 patients showed that calcipotriol did not affect the anagen / telogen ratio after 6 weeks of treatment in patients with scalp psoriasis. It should be noted that the optimal effect of calcipotriol on psoriasis was not observed until 8 weeks, thus this effect may have been too limited to assess the effect of calcipotriol on hair loss. In addition, a study of 296 healthy men was conducted to assess the possible association between alopecia in men and serum 25-hydroxyvitamin D levels. The severity and severity of hair loss were not associated with serum 25-hydroxyvitamin D levels. In this regard, there is an assumption about the real significance of the level of vitamin D on hair loss, and, perhaps, the mechanisms of interaction with the receptors, rather than the level of vitamin D, are of primary importance.

Vitiligo

Vitiligo is a common pigmentation disorder characterized by well-defined depigmented areas or spots of various shapes and sizes, which are based on the destruction of melanocytes in the epidermis.

Vitamin D protects epidermal melanin and restores melanocyte integrity through several mechanisms, including controlling melanocyte activation, proliferation, migration, and pigmentation by modulating T cell activation, which appears to correlate with melanocyte disappearance in vitiligo. The mechanism by which vitamin D acts on melanocytes is not yet fully understood. Vitamin D is thought to be involved in melanocyte physiology by coordinating the production of melanogenic cytokines [most likely endothelin-3 (ET-3)] and SCF / c activity, which is one of the most important regulators of melanocyte vitality and maturation. In addition, the proposed mechanism involving vitamin D in protecting the skin in vitiligo is based on its antioxidant properties and regulatory function in relation to reactive oxygen species, which are formed in excess in vitiligo in the epidermis. On the other hand, the active form of vitamin D reduces the activity of apoptosis of keratinocytes and melanocytes induced by UVB, which is reported to reduce the melanin content of the skin. In addition, vitamin D can have an immunomodulatory effect by inhibiting the expression of IL-6, IL-8, TNF-α and TNF-γ, modulate the maturation of dendritic cells, their differentiation and activation, and also induce to inhibit antigen presentation, thereby weakening the autoimmune component. in the pathogenesis of vitiligo.

It remains to be seen if vitamin D deficiency plays a role in the onset of vitiligo, as it does in others. autoimmune diseases... In 2010, Silverberg and Silverberg conducted a study of serum 25-hydroxyvitamin D (25 (OH) D) in the blood of 45 patients with vitiligo and found that 55.6% had a deficiency (22.5-75 nmol / L) and 13.3% was very low (<.22.5 нмо/л), что было повторно продемонстрировано другими исследователями . Тем не менее, другое исследование показало отсутствие корреляции между 25(OH)D и витилиго .

Despite controversy, topical vitamin D3 analogs are the recommended therapeutic agents for vitiligo. The use of vitamin D analogues in the form of a combination of PUVA and topical calcipotriol for the treatment of vitiligo has been described by Parsad et al. ... Subsequently, a number of studies have reported treatment of vitiligo with vitamin D analogs alone or in combination with ultraviolet light or corticosteroids for repigmentation, with some conflicting results.

Pemphigus vulgaris and bullous pemphigoid

Pemphigus vulgaris and bullous pemphigoid are potentially fatal autoimmune bullous diseases caused by acantholysis of keratinocytes as a result of antibody production by B cells. Vitamin D, due to its participation in the modulation of immune functions, including apoptosis of B cells, cell differentiation of the T h2 immune response, regulation of Tregs function, can take an active part in the immune regulation of such diseases. Several recent studies have demonstrated that patients with pemphigus vulgaris and bullous pemphigoid have significantly lower serum vitamin D levels compared to controls, regardless of age, body mass index, or phototype. In addition, it has been suggested that lower levels of vitamin D may explain the increased incidence of fractures in these patients and should be taken into account in patients who should be taking corticosteroids.

Atopic dermatitis

Atopic dermatitis (AD) is a common chronic inflammatory type of eczematous skin lesions. Several studies have shown an initial dysfunction of the epidermal barrier followed by immune activation as the underlying mechanism. Animal studies, case reports, and randomized clinical trials have suggested that vitamin D, through a variety of mechanisms, including immunomodulation, may relieve symptoms of AD. Most of these studies indicate an inverse relationship between the severity of atopic dermatitis and vitamin D levels. In addition, studies have shown that in people with AD who are deficient in vitamin D, vitamin D saturation leads to improvements and a decrease in the severity of the disease.

Should Vitamin D Be In Every Prescription?

The answer to this question is still far from clear, but at least we can clearly recommend a routine assessment of its level, with particular emphasis on those at risk of deficiency, such as older people who are obese who do not have regular sun exposure. or malabsorption. Vitamin D supplementation can be an important adjunctive treatment if deficiency is present.

conclusions

In conclusion, there is a unique link between vitamin D and dermatology. On the one hand, our skin is a source of this important vitamin, and on the other hand, all available data indicate its important effect on the health of our skin and the involvement of its deficiency in the pathogenesis of many dermatological diseases. Several factors are responsible for maintaining its optimal level, therefore, the sunny climate zone is far from a guarantee of protection against vitamin deficiency. This is described in several epidemiological studies conducted in areas close to the equator,,,. Based on the available evidence, it is clear that vitamin D supplementation should be the preferred recommendation towards achieving normal serum levels, thereby avoiding the problems associated with vitamin D deficiency. More research is still needed to examine its complex links to dermatological conditions and to provide clear guidelines and recommendations for taking it.

Vitamin D and the skin: Focus on a complex relationship: A review Abstract in English: The “sunshine” vitamin is a hot topic that attracted ample attention over the past decades, specially that a considerable proportion of the worldwide population are deficient in this essential nutrient. Vitamin D was primarily acknowledged for its importance in bone formation, however; increasing evidence point to its interference with the proper function of nearly every tissue in our bodies including brain, heart, muscles, immune system and skin. Thereby its deficiency has been incriminated in a long panel of diseases including cancers, autoimmune diseases, cardiovascular and neurological disorders. Its involvement in the pathogenesis of different dermatological diseases is no exception and has been the subject of much research over the recent years. In the current review, we will throw light on this highly disputed vitamin that is creating a significant concern from a dermatological perspective. Furthermore, the consequences of its deficiency on the skin will be in focus.