Daily vitamins are necessary for toddlers

Vitamin D deficiency / rickets prophylaxis

80 to 90% of vitamin D is formed on the skin by the influence of UV-B light (UV-B with 290 to 315 nm wavelength) and is only slightly absorbed through food.

Cholesterol (dehydroxycholesterol, 7-DHC) stored in the skin is converted into vitamin D3 via intermediate stages under the action of UV-B radiation. The vitamin D3 that gets from the skin into the blood is still inactive and only becomes active vitamin D hormone in the liver and kidneys ((1,25-dihydroxy vitamin D3, 1,25 [OH] 2D3, clacitriol ) transformed.

However, precursors to the biologically active form of vitamin D, calcitriol (1,25- (OH) 2 D3), can also be metabolized in almost all cells. It is then mostly consumed by the cells themselves. Only the kidneys make calcitriol available for bone metabolism via the bloodstream and thus enable the formation and maturation of bone stem cells. In addition, the calcitriol controls the calcium balance by regulating the absorption of calcium from the intestine, and it also influences the phosphate metabolism. As a result, calcium and phosphate are stored in the bones, the actually soft basic bone substance becomes hard (calcification), and the entire skeleton becomes stable.

Vitamin D is stored in muscle and fat tissue. Calcitriol that is not required is converted again and excreted.

Ergocalciferol (vitamin D2), on the other hand, is the plant-based metabolism-relevant substance.

Why is vitamin D so important to the body?

While vitamin D was previously thought to be only important for bone growth, today we know its diverse effects on the body:

  • Strengthening the bones, strengthening the muscles
  • Tooth formation
  • Strengthening of the immune system both in the defense against pathogens and in inhibiting excessive immune reactions and thereby moderating autoimmune diseases such as type 1 diabetes, multiple sclerosis, etc.
  • Protective function for the nerve cells of the brain
  • Positive effect on the cardiovascular system, lowering blood pressure
  • Reduction of vascular disease
  • Protective effect against cancer

Who are the natural vitamin D suppliers?

In the summer months, 15 to 30 minutes or better 10 to 15 minutes of sunlight on the face, arms and hands three to four times a week is enough to produce the necessary amount of vitamin D - when the sun is shining and the skin is not covered with sunscreen is.

In winter, however, people live from the vitamin D depot in their adipose tissue. It is therefore important, especially between November and March, to pay attention to a diet containing vitamin D and possibly also to take a vitamin D supplement.

With the exception of cod liver oil and high-fat sea fish such as herring, eel, mackerel or tuna, there are few foods that contain significant amounts of vitamin D. These include milk, butter, egg yolks, yeast, avocados or beef liver. For example, 100g of hen's eggs contain 2.4 µg of vitamin D. Milk is up to ten times richer in vitamin D in summer than in winter - if the animals are outside in a pasture.

Because vitamin D is resistant to heat and storage, it is artificially added to some foods, especially margarine and baby food. In the USA and Canada, milk is generally fortified with vitamin D.

Causes and Risk Factors for Vitamin D Deficiency

The main reason for a vitamin D deficiency is seldom exposure to the open air and thus little sun radiation on the skin. This is especially true for the winter months, since then in our latitudes the UV radiation is insufficient for vitamin D formation. The discussion about rising skin cancer rates in connection with increasingly aggressive UV radiation means that people are increasingly hiding their skin under clothing and sunscreen. However, preparations with a sun protection factor of 15 already block the production of vitamin D by 99%

It can even be said that the current recommendations of medical professionals regarding sun exposure and adequate supply of vitamin D are contradicting one another. In some cultures, the formation of vitamin D is also difficult, since it is mandatory for women in particular to completely cover their bodies. Basically, however, it can be said that vitamin D deficiency is now a problem for society as a whole.

The further a country is from the equator, the more difficult the body's synthesis of vitamin D becomes due to the decreasing solar radiation. It begins roughly north or south of the 45th parallel, which runs roughly north of the Alps. The smog in industrial areas also reduces the amount of UV radiation that reaches the skin.

Since dark skin pigmentation reduces the formation of the body's own vitamin D, dark-skinned children living in Germany have an increased risk of rickets. Your skin needs 10 to 50 times the amount of UV-B radiation to be able to produce the same amount of calcitriol compared to its fair-skinned peers. A study conducted in 2008 on over 1,000 children between the ages of 0 and 17 living in Germany showed that 29% of boys and 31% of girls with a migration background suffered from vitamin D deficiency, while 18% of boys of German origin and 17% of girls did so German family were affected.

Sufficient intake of calcium through food (e.g. in milk, eggs, sardines, broccoli, spring onions, parsley, watercress) is a prerequisite for the storage of calcium in the bones with the help of vitamin D.

Secondary vitamin D deficiency occurs when disorders in the metabolic process prevent the production or conversion of vitamin D:

  • Inadequate bone formation and disrupted skeletal growth as a result of chronic kidney failure (renal osteodystrophy)
  • Diseases of the digestive tract, such as disorders in bile acid production, liver dysfunction or chronic intestinal inflammation (celiac disease, etc.)
  • Taking medication for epilepsy

How Much Vitamin D Does My Child Need?

If the vitamin D requirement can largely be met by the main supplier, the sun, a daily intake of 5 µg (5 micrograms, 0.005 mg, 200 IU - [1 µg = 40 IU]) for children after the first is sufficient Years of age and adults up to 65 years of age.

In contrast, children in the first twelve months of life have an increased need for healthy bone formation. The German Society for Pediatric and Adolescent Medicine (DGKJ) recommends the daily administration of breast-fed and non-breast-fed infants to prevent rickets, irrespective of the vitamin D produnction through UV light in the skin and the vitamin D supply through breast milk or baby food for rickets prophylaxis a vitamin D tablet of 10-12.5 µg (400-500 IU [international units]; 1µg = 40 IU, 1 IU = 0.025 µg) from the end of the first week of life to the end of the first year of life. The prophylaxis can be continued in the winter months in the second year of life.

After the age of two, an additional dose for primary prevention is no longer necessary. Some preparations of vitamin D can contain a minimal amount of peanut oil, but according to the latest findings this is harmless for allergy sufferers.

The recommendations, from the age of two, presumably have to be reconsidered and modified in view of the general deficiency in all children who were not supplemented, as demonstrated in the measurements by the Robert Koch Institute. The pediatrician can determine whether there is a vitamin D deficiency by examining the blood. To do this, the proportion of 25-hydroxyvitamin D in the blood is measured. The guideline values ​​for assessing the 25-hydroxyvitamin D concentration (in nanomoles per liter, abbreviated nmol / L) apply:

  • below 12.5 nmol / L: severe vitamin D deficiency (usually associated with rickets)
  • 12.5 to below 25 nmol / L: moderate vitamin D deficiency (with a likely effect on bone metabolism)
  • 25 to below 50 nmol / L (depending on age also 25 to below 75 nmol / L): suboptimal vitamin D supply with possible effects on bone metabolism.

While short-term, intense sun exposure (especially sunburns in childhood or extreme exposure to the sun during vacation periods, compared to staying outside the rest of the time) is harmful to health and promotes skin cancer, long-term, less intense sun exposure is apparently more beneficial to health.

Is it possible to overdose on vitamin D?

The organism adjusts its vitamin D production for longer stays in the sun, so that an overdose is actually impossible in a natural way. The same applies to food intake.

Only taking high-dose vitamin D preparations of more than 500 µg over a long period of time would lead to an increased calcium concentration (hypercalcemia) in the blood. The upper safe limit of vitamin D intake was set at 25 µg per day for children (1,000 IU) and 50 µg per day for adults (2,000 IU).

With an even higher, short-term overdose, signs of intoxication such as nausea, vomiting, severe thirst, headache and tiredness occur. Long-term overdose leads to the build-up of calcium in the blood vessels and kidneys, which can lead to kidney stones and kidney failure.

Rickets due to vitamin D deficiency

Sufficient vitamin D production (calcitriol (1,25- (OH) 2 D3) enables calcium phosphate to be incorporated into the bones. This mineralization ensures the stability of the bones. The deficient calcification of the bone tissue due to a vitamin D deficit can lead to rickets (from the Greek “rachis” = back) in children - especially in the very first years of life. The disease, which was described in England in the 17th century, is characterized, among other things, by softening of the bones, curvature of the spine, bending of the leg bones (“X- or Bow legs "), muscle weakness, spasmodic spasms of the muscles (tetany) as well as an upturned chest. The skull flattens out at the back of the head, where there is also softening in some areas, and bulges in the forehead area.

Further symptoms are delayed tooth eruption, tooth decay, tooth enamel defects, flabby abdominal muscles ("frog belly"), swollen joints, general motor development delay, increased susceptibility to infection and constipation. If the chest is severely deformed, lung function and bronchial diseases can be restricted. If the rickets results from a poor diet, iron deficiency and anemia (anemia) occur at the same time.

The symptoms often begin in the third month of life with restlessness, nervousness, bad mood, restricted movements, muscle laxity and sweating at the back of the head.

The diagnosis is made via an X-ray of the wrist and laboratory analysis of vitamin D, calcium and phosphate levels as well as alkaline phosphatase. Among other things, a differential diagnosis must be made for the extremely rare vitamin D-dependent rickets type 1 and type 2, which are based on genetic defects and in which either no calcitriol is formed (type 1) or the intestines and skeleton do not absorb calcitriol (type 2) .

Rickets can also be due to a phosphate deficiency, either due to kidney disease or the congenital so-called phosphate diabetes.

Rickets is treated as follows:

  • First year of life:
    If it occurs in the first four weeks of life: 1,000 IU of vitamin D3 and an additional calcium supplement of 40-80 mg per kilo of weight per day for 12 weeks.
    From the 4th week of life until the end of the 12th month of life: 3,000 IU of vitamin D3 and an additional calcium supplement of 40-80 mg per kilo of weight per day for 12 weeks
    Then the prophylaxis with 500 IU vitamin D3 should be continued until the end of the first year of life
  • Small child:
    After the first year of life: 5,000 IU of vitamin D3 and an additional calcium supplement of 40-80 mg per kilo of weight per day for 12 weeks
    Subsequently adequate sun exposure and calcium intake (e.g. milk)
    If adequate sun exposure cannot be ensured, preventive vitamin D administration should be maintained.

Then the symptoms and laboratory values ​​normalize in the first 6 to 12 weeks. With early detection and treatment, any malalignment of the extremities and axial shifts in the skeleton will heal within a year and surgical corrections are not necessary.

Even if rickets has become rare in Germany, an estimated 400 cases occur annually, more and more among immigrant children with dark skin who did not receive vitamin D prophylaxis in the first year of life.