What is it
What is vitamin D
Vitamin D is a group of fat-soluble secosteroids necessary for the intestinal absorption of minerals such as calcium, magnesium, phosphate, and many other biological functions.
In humans, the most important compounds of this group are vitamin D3 (also known as cholecalciferol) and vitamin D2 (known as ergocalciferol). Which, however, must be mutated to calcitriol (the active hormonal form).
The primary natural source of vitamin D is the endogenous production of cholecalciferol (Vit D3) at the skin level, starting from cholesterol, by a chemical reaction. Which depends on exposure to sunlight (in particular UVB irradiation). However, cholecalciferol and ergocalciferol can also be taken with diet and supplements. Still, only a few foods can be considered good sources of vitamin D (especially fish, liver, and egg yolk; second, some mushrooms).
The dietary recommendations for vitamin D have a large margin of safety. Generally, they do not consider the extent of sun exposure, totally based on nutritional intake. Due to the variability linked to different latitudes (light and dark hours are seen in the Nordic countries), the uptake of UVB rays in the population is quite variable. Moreover, let us not forget that excessive sun exposure can increase the risk of skin cancer.
Both vitamin D is introduced with food and the vitamin produced in the skin. They are biologically inactive and necessarily require the intervention of a protein enzyme able to hydroxyl them by converting them into the biologically active form. This occurs in the liver and kidneys. Since vitamin D can be synthesized enough in most mammals that are sufficiently exposed to sunlight. It should not be considered an essential dietary factor – it should not even be considered a vitamin. Instead, it has the characteristics of a pro-hormone, activated in the calcitriol hormone, which produces its effects by interacting with a nuclear receptor located in multiple cells of different tissues.
Cholecalciferol (Vit D3) is converted to calcifediol (25-hydroxycholecalciferol), while ergocalciferol (Vit D2) is converted to 25-hydroxyergocalciferol. These two metabolites of vitamin D (called 25-hydroxyvitamin D or “25(OH) D”) can be measured in the blood serum to determine a person’s total vitamin D level. Calcifediol is then further hydroxylated by the kidneys to form calcitriol (also known as 1,25-dihydroxycholecalciferol), the biologically active form of vitamin D.
Calcitriol circulates as a natural hormone in the blood, playing a significant role in homeostasis and calcium and phosphate metabolism. Regulating blood concentrations and promoting the physiological growth of the skeleton, bone remodeling, and preventing degeneration with advanced age. Calcitriol also has other biological effects, including cell growth, various neuromuscular and immune functions, and the reduction of inflammation.
The discovery of vitamin D occurred by searching for the missing dietary substance in children suffering from rickets (the infantile-onset form of osteomalacia). Vitamin D supplements are therefore given to treat or prevent osteomalacia, rickets, and osteoporosis. Still, scientific evidence regarding other health effects in the general population is weak or nil. The effect of vitamin D supplementation on mortality is not yet apparent. However, almost all research groups agree that there is no justification for recommending that vitamin D supplements various diseases as a preventative measure.
Chemical
Vitamin D structure and chemistry
Vitamin D is defined as all secosteroids (steroids where one of the links in the steroids is open) which exhibit the biological activity of calciferol and are characterized by the derivatives of cyclopentanoperhydrophenanthrene. There are several forms of this, with two main forms: vitamin D2 or ergocalciferol and vitamin D3 or cholecalciferol. The structural difference between vitamin D2 and vitamin D3 is that the D2 side chain contains a double link between carbon 22 and 23 and a methyl group on carbon 24.
Calciferol is 50-100 times more active than ergocalciferol (D3 is more active than D2). Both ergocalciferol and calciferol are inactive vitamin D. Therefore, active liver and kidney function is required. Man can synthesize cholecalciferol from a precursor, with a function of provitamin: dehydrocholesterol (derived from cholesterol by reduction). This provitamin is found in the skin to absorb the solar radiant energy that causes the isomerization to cholecalciferol (see the skin synthesis of vitamin D). Proper sun exposure thus reduces the need for vitamin D.
Note: When vitamin D or calciferol is used, without specifying any referenced index, it is either vitamin D2 or vitamin D3 or both. Vitamin D2 was differentiated in 1931 and, after irradiation of 7-dehydrocholesterol, vitamin D3 was discovered in 1935.
Biology
Vitamin D biology
The active metabolite of vitamin D (calcitriol) performs its biological effects by binding to the vitamin D receptor (VDR.), mainly found in the target cell nucleus. The calcitriol binding to VDR. Enables it to act as a transcription factor that modulates the gene expression of transport proteins (e.g., TRPV6 and calbindin), which are involved in the absorption of calcium in the intestine. The vitamin D receptor belongs to the steroid/thyroid hormone superfamily. It is expressed by cells in most organs, including the brain, heart, skin, gonads, prostate, and breasts.
Activation of VDR. in intestinal cells, bones, kidneys, and parathyroids leads to the maintenance of calcium and phosphorus levels in the blood (with the help of the parathyroid hormone and calcitonin) and bone retention.
One of the most important roles of vitamin D is to maintain skeletal calcium balance by promoting the absorption of calcium in the intestine, bone resorption by increasing the number of osteoclasts, maintaining calcium and phosphate levels for bone formation, and allowing the proper functioning of the parathyroid hormone to maintain serum calcium levels. A vitamin D deficiency can lead to a lower bone mineral density and an increased risk of a reduction in bone density (osteoporosis). Or bone fracture because the lack of vitamin D alters the mineral metabolism in the organism. Therefore, vitamin D is also crucial for bone remodeling through its role as a potent stimulator of resorption.
VDR. also regulates cell proliferation and differentiation. Vitamin D interacts with the immune system, and VDR. is expressed in different white blood cells, including activated T and B cells. In vitro, vitamin D increases the expression of the thyroxine hydroxylase gene in adrenal cord cells and affects the synthesis of neurotrophic factors, nitric oxide synthetase, and glutathione.
Functions
What is Vitamin D for?
Calciferol acts by a hormonosile action mechanism, since:
- It is self-synthesized by the human organism
- Acts on a target organ
- It has a structure that resembles steroid hormones.
Vitamin D is essential for the homeostasis of calcium and phosphate and is crucial for the growth and maintenance of the skeleton. The metabolically active form is 1,25-(OH)2-cholecalciferol, which works by:
- Absorption of calcium and phosphate in the intestine
- Bone calcium deposition
- Maintaining cartilaginous trophy
- Renal resorption of calcium and phosphorus in the proximal contorted tubules.
Vitamin D and calcium
1,25-(OH)2-cholecalciferol stimulates the synthesis of CaBP (the protein that carries calcium) in the target organ (enterocytes), acting at the level of the transcription of the intestinal DNA that codes for protein and RNA polymerase plasma. The use of actinomycin D and a-amanitin transcription inhibitors, respectively, and RNA polymerase confirmed this action. This synthesizes new RNA that promotes the synthesis of CaBP necessary to promote the absorption of calcium. In this process, it is now certain that it is involved cyclic AMP, which increases in tissues by the action of active vitamin D.
Food Sources
Where is vitamin D?
Foods rich in vitamin D are liver, fish oil, sea fish (herring, salmon, sardine), and egg yolk; minor quantities are present in mushrooms.
To learn more
9 High Vitamin D Foods
Note: almost all vitamin D is synthesized on the skin. Appropriate sun exposure is therefore recommended, especially for the elderly.
Vitamin D: how to intake
The health benefits of vitamin D supplementation are uncertain. A 2013 review found no effect from the integration on disease rates, apart from a ten-year decrease in mortality in the elderly. Vitamin D supplements do not alter outcomes for myocardial infarction, stroke or cerebrovascular disease, cancer, bone fractures, or knee arthritis. Low levels of vitamin D can result from a condition rather than being the cause of it.
A report by the “United States Institute of Medicine” states: “Results related to cancer, cardiovascular disease and hypertension, diabetes and metabolic syndrome, falls, immune efficiency and autoimmune diseases, infections, neuropsychological functioning, and preeclampsia cannot be reliably linked to the intake of calcium or vitamin D and are often conflicting.”
United States
| Age | RDA (IU / day) | mcg / day |
| Babies 0-6 months | 400 * | 10 |
| Children 6-12 months | 400 * | 10 |
| 1-70 years | 600 | 15 |
| over 70 years | 800 | 20 |
| Pregnant and nursing | 600 | 15 |
| Age | Maximum tolerable dose (IU / day) | mcg / day |
| Babies 0-6 months | 1000 | 25 |
| Children 6-12 months | 1500 | 37.5 |
| Children 1-3 years | 2500 | 62.5 |
| Children 4-8 years old | 3000 | 75 |
| over 9 years | 4000 | 100 |
| Pregnant and nursing | 4000 | 100 |
Canada
| Age | RDA (IU) | Maximum Tolerable Dose (IU) |
| Babies 0-6 months | 400 * | 1000 |
| Children 7-12 months | 400 * | 1500 |
| Children 1-3 years | 600 | 2500 |
| Children 4-8 years old | 600 | 3000 |
| children and adults 9-70 years | 600 | 4000 |
| over 70 years | 800 | 4000 |
| Pregnant and nursing | 600 | 4000 |
Australia and New Zealand
| Age | Adequate intake (mcg) | Maximum tolerable dose (mcg) |
| Babies 0-12 months | 5 * | 25 |
| Children 1-18 years old | 5 * | 80 |
| Adults 19-50 years old | 5 * | 80 |
| Adults 51-70 years | 10 * | 80 |
| Adults over 70 years old | 15 * | 80 |
European Food Safety Authority
| Age | Adequate intake (mcg) | Maximum tolerable dose (mcg) |
| Babies 0-12 months | 10 | 25 |
| Children 1-10 years | 15 | 50 |
| Children 11-17 years old | 15 | 100 |
| Adults | 15 | 100 |
| Pregnant and nursing | 15 | 100 |
To learn more:
Supplements of Vitamin D
Vitamin D3 Supplement by Nature’s Bounty 2000IU
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Absorption
Absorption of vitamin D
Calciferol is absorbed in the intestine in the same way as lipids. It is, therefore, part micelle (formed by a combination of the bile salts with the products resulting from the hydrolysis of the lipids). Absorbed by passive diffusion into the enterocytes and later incorporated in the chylomicrons and transported in circulation through the mesenteric lymphatic vessels. Unlike other fat-soluble vitamins, calciferol is not stored in the liver. However, the amount of calciferol from food is very low. Most vitamin D is synthesized at the skin level by the action of ultraviolet light.
Requirements
Vitamin D requirements
Under normal conditions, exposure to sunlight is sufficient to satisfy the body’s calciferol needs.
The following are the recommended levels tables in the United States, Canada, Australia, New Zealand, and the European Food Safety Authority.
Deficiency
Vitamin D deficiency: when to worry?
An absolute deficiency of this vitamin is assessed by blood tests and confirmed by low concentrations.
A diet lacking vitamin D combined with inadequate sun exposure causes osteomalacia in the adult and rickets in the child, consisting in the rarefaction of bone tissue. In the Western world, these conditions are now infrequent. However, for the elderly, vitamin D deficiency has become a global problem. It remains common in children and adults in less developed countries. The low calcifediol content (25-hydroxy-vitamin D) mainly results from insufficient solar exposure. Deficiency involves reduced bone mineralization and skeletal damage that leads to the above diseases. A vitamin D deficiency can reduce the intestinal absorption of calcium to only 15%. When it is not deficient, an individual usually absorbs between 60-80% of food calcium.
Vitamin D and bone health
Vitamin D and rickets
Rickets, typical of childhood age, is a disease characterized by reduced growth and long, soft, weak, and deformed bones – which bend under the weight when children start to walk. This condition, typically characterized by the inarching of the females outwards, can be caused by a deficiency of calcium and/or phosphorus, as well as a lack of vitamin D.
Today it is widespread in most low-income countries like Africa, Asia, or the Middle East, or in people with genetic disorders like pseudo vitamins D deficiency.
Vitamin D deficiency in the mother can cause a bone disease manifested before birth and impaired skeletal quality after birth. Nutritional rickets is typically found in countries with intense sunlight throughout the year, such as Nigeria. It can occur even without vitamin D deficiency (e.g., calcium and phosphorus deficiency).
Although rickets and osteomalacia are now rare in the UK, there have been outbreaks in some immigrant communities. Where women with supposedly adequate exposure in daylight wore mainly covered clothes. Darker skin and reduced sun exposure will not usually cause rickets. Unless your diet deviates from the Western omnivorous model of high intakes of meat, fish, and eggs. The most significant dietary risk factor for rickets includes elimination from animal foods – as happens in the vegan diet.
Vitamin D deficiency remains the leading cause of rickets among young children in most countries because breast milk is poor in vitamin D.
Social habits and climatic conditions can prevent adequate sun exposure. In sunny countries like Nigeria, South Africa, and Bangladesh, rickets occurs in small and large children. It is more responsible for an inadequate calcium level – typical of cereal-based diets with scarce dairy products.
Rickets has been a major public health problem in the past, in Denver (USA). Where ultraviolet rays are about 20% stronger than sea level at the same latitude, nearly two-thirds of 500 children had a slight form of rickets in the late 1920s. An increase in the proportion of animal and plant in the American diet in the twentieth century, coupled with an increase in the consumption of fortified milk in vitality amine D, coincided with a sharp decrease in the number of cases rickets. Also, in the United States and Canada, vitamin D-fortified milk, childhood vitamin supplements, and vitamin supplements have helped eradicate most rickets for children suffering from specific fat malabsorption.
Vitamin D, osteoporosis and osteomalacia
Osteomalacia is a disease of adults that results from a vitamin D deficiency. The characteristics of this disease are the softening of the bones, which leads to the flexion of the spine, the incursion of the legs, proximal muscle weakness, bone fragility, and an increased risk of fractures. Osteomalacia reduces calcium absorption and increases bone demineralization, increasing the risk of fractures. It usually occurs when levels of 25-hydroxyvitamin D are less than about 10 ng/mL. Although it is hypothesized that the effects of osteomalacia contribute to chronic musculoskeletal pain. There is no persuasive evidence that low vitamin D levels are responsible for chronic pain or that supplementation may alleviate it.
Vitamin D and skin pigmentation
Dark-skinned people living in temperate climates have been shown to have low levels of vitamin D.
Probably due to lower efficiency in its production due to abundant melanin in the skin, which would hinder the synthesis of the skin.
Signs of a vitamin D deficiency
Early signs of calciferol deficiency are:
- serum reduction of calcium and phosphorus
- secondary hyperparathyroidism and increase in alkaline phosphatase in serum.
Later signs include:
- inadequate mineralization of the skeleton (rickets in children, osteomalacia in adults)
- muscle weakness
- abdominal pain.
Rickets occurs in children between 4 and 24 months of age and is essentially in inadequate mineralization of the growing bone, resulting in deformations of the skeleton.
In the first months of life, the symptoms essentially concern the skull with:
- softening in the western, temporal, and parietal regions
- delay in closing the front fontanel (it becomes pathological after the fifteenth month of life)
- cartilage hypertrophy (in older children) with no dosage, especially in wrists and ankles
- long bones of the lower limbs swarf and knee.
Osteomalacia occurs in adults with:
- muscle weakness
- back-lumbar pain of the spine, pelvic belt, and thighs
- insecure gait and bone fragility, especially of the spine, shoulders, ribs, and pelvis
- extremely low bone density and pseudo-fractures, especially the backbone, femur, and humerus (which can be detected by X-ray examination)
- increased risk of fractures, especially to the pelvis and wrists.
Toxicity
Vitamin D toxicity
Cases of vitamin D toxicity are rare and caused by supplementation with high doses of vitamin D – not from food or excessive sun exposure. According to some research, the threshold for the toxicity of vitamin D has not yet been established; according to some research. The tolerable higher intake level (UL) would be 4000 IU / day by age 9-71 years (100 µg / day). However, other studies conclude that prolonged intake of 1250 µg/day (50,000 IU). In healthy adults may produce evident toxicity after several months and increase serum levels of 25-hydroxyvitamin D to 150 ng/mL and beyond. Those with certain medical conditions, such as primary hyperparathyroidism, are much more sensitive to vitamin D and develop hypercalcemia to increase vitamin D.
In contrast, maternal hypercalcemia during pregnancy can increase sensitivity to mental retardation syndromes and facial deformities.
A review published in 2015 found that adverse effects were reported only at serum concentrations of 25(OH)D greater than 200 nmol/L.
Published cases of hypercalcemia toxicity in which the dose of vitamin D and the level of 25-hydroxy-vitamin D are known, all-cause a consumption of ≥4000 IU (1,000 µg) per day.
Pregnant or breastfeeding women should consult their doctor before taking a vitamin D supplement. The Food and Drug Administration (FDA) has recommended that vitamin D fluid supplement manufacturers enter a marked dropper for 400 international units. 1 IU is the biological equivalent of 25 ng cholecalciferol/ergocalciferol. Also, for infant formula, the FDA recommends that the dropper does not contain more than 400 IU. For children (from birth to 12 months), the tolerable upper limit (the maximum amount that can be tolerated without harm) is set at 25 µg/day (1,000 IU). A thousand micrograms per day in children produces toxicity within a month. After being commissioned by the Canadian and American governments, the Institute of Medicine (IOM) increased the tolerable ceiling (UL) to 2,500 IU per day for ages 1-3 years, 3,000 IU per day for ages 4-8 years, and 4,000 IU per day for ages 9-71 years (including pregnant or breastfeeding women) ).
The concentration of calcitriol is self-regulated by a negative feedback loop. It is also influenced by parathyroid hormone, fibroblasts 23 growth factor, cytokines, calcium, and phosphate.
Signs and symptoms of excess vitamin D
Hypervitaminosis (excess vitamin D) leads to increased intestinal absorption and calcium resorption, resulting in hypercalcemia, easily identifiable for increased urination and thirst.
If untreated, hypercalcemia causes excess calcium deposits in soft tissues and organs such as the kidneys, liver, and heart, causing pain and organ damage. This is associated with a decrease in serum PTH (the amount of parathormone in the blood, see: calcium and osteoporosis) and finally loss of calcium homeostasis with consequent:
- anorexia, nausea, vomiting, and diarrhea
- hypercalcaemia and hypercalciuria
- nephrocalcinosis, cardiac calcinosis, and soft tissue calcification.
These can be followed by polyuria, polydipsia, weakness, insomnia, nervousness, itching, and, finally, renal failure. Also, proteinuria, urinary stones, azotemia, and metastatic calcification (especially in the kidneys) may develop. Other symptoms of vitamin D toxicity include mental retardation in young children, abnormal bone growth and formation, diarrhea, irritability, weight loss, and severe depression.
The toxicity of vitamin D is treated by disrupting the integration of vitamin D and limiting the intake of calcium. Kidney damage can be irreversible. Exposure to sunlight for long periods does not usually cause vitamin D toxicity. The concentrations of vitamin D precursors produced in the skin reach a balance, and further production is degraded.
Excessive dietary calciferol intake is extremely unlikely, considering the reduced amount of vitamin D in food. There are no known cases of hypervitaminosis due to excessive sun exposure. In contrast, intoxication following administration of calciferol for therapeutic purposes is possible.
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