Vitamin D Deficiency - Do You Have These Symptoms?
This article educates us what is Vitamin D deficiency, symptoms, importance of Vitamin D, causes, treatment and suggested best helpful supplements.
- What is Vitamin D?
- Importance of Vitamin D
- Symptoms of Vitamin D Deficiency
- Causes of Vitamin D Deficiency
- Treatment for Vitamin D Deficiency
- D Power - Oral Vitamin Spray
- Mechanism of Action
What is Vitamin D?
It is often called as the "Sunshine Vitamin", Vitamin D3 is actually not a vitamin at all. Rather, it is a hormone produced by the body when stimulated by sunlight. It is also occurs naturally in a few foods -- including some fish, fish liver oils, and egg yolks -- and in fortified dairy and grain products.
For various reasons, most people are no longer able to produce the necessary amount of this "vitamin." These reasons include: living in a geographical area in which there is often little sunlight available, using SPF products to protect against the negative effects of too much sunlight, the current state of production, shipping and storage of the few fresh foods that would naturally provide Vitamin D3, certain medical conditions that preclude the synthesis of the vitamin, among many other factors. Although some foods are now being artificially enhanced with Vitamin D, there are not enough of them to provide all we need.
Importance of Vitamin D
A few years ago, Vitamin D was thought to do nothing more than allow calcium to be absorbed for good bone health. New research suggests that vitamin D may be one of the best vitamins of all for your body as scientists have uncovered up to 2,000 different genes-roughly one-sixth of the human genome-that are regulated by the nutrient. That means almost everything in your body relies on it. The problem is that most of us are not spending enough time in the sun for our bodies to produce Vitamin D, nor do our foods any longer provide what we need.
Vitamin D is essential for strong bones, because it helps the body use calcium from the diet. Traditionally, vitamin D deficiency has been associated with rickets, a disease in which the bone tissue doesn't properly mineralize, leading to soft bones and skeletal deformities. But increasingly, research is revealing the importance of vitamin D in protecting against a host of health problems.
Symptoms of Vitamin D Deficiency
Symptoms of bone pain and muscle weakness can mean you have a Vitamin D deficiency. However, for many people, the symptoms are subtle. Yet even without symptoms, too little Vitamin D can pose health risks.
Low blood levels of the Vitamin have been associated with the following:
– Increased risk of death from cardiovascular disease
– Cognitive impairment in older adults
– Severe asthma in children
Research suggests that Vitamin D could play a role in the prevention and treatment of a number of different conditions, including type1 and type 2 diabetes, hypertension, glucose intolerance, and multiple sclerosis.
Causes of Vitamin D Deficiency
Vitamin D deficiency can occur for a number of reasons:
You don't consume the recommended levels of the vitamin over time. This is likely if you follow a strict vegan diet, because most of the natural sources are animal-based, including fish and fish oils, egg yolks, fortified milk, and beef liver.
Your exposure to sunlight is limited. Because the body makes vitamin D when your skin is exposed to sunlight, you may be at risk of deficiency if you are homebound, live in northern latitudes, wear long robes or head coverings for religious reasons, or have an occupation that prevents sun exposure.
You have dark skin. The pigment melanin reduces the skin's ability to make vitamin D in response to sunlight exposure. Some studies show that older adults with darker skin are at high risk of vitamin D deficiency.
Your kidneys cannot convert vitamin D to its active form. As people age, their kidneys are less able to convert vitamin D to its active form, thus increasing their risk of vitamin D deficiency.
Your digestive tract cannot adequately absorb vitamin D. Certain medical problems, including Crohn's disease, cystic fibrosis, and celiac disease, can affect your intestine's ability to absorb vitamin D from the food you eat.
You are obese. Vitamin D is extracted from the blood by fat cells, altering its release into the circulation. People with a body mass index of 30 or greater often have low blood levels of vitamin D.
Treatment for Vitamin D Deficiency
Treatment for vitamin D deficiency involves getting more vitamin D -- through diet and supplements. Although there is no consensus on vitamin D levels required for optimal health -- and it likely differs depending on age and health conditions -- a concentration of less than 20 nanograms per milliliter is generally considered inadequate, requiring treatment.
Guidelines from the Institute of Medicine increased the recommended dietary allowance (RDA) of vitamin D to 600 international units (IU) for everyone ages 1-70, and raised it to 800 IU for adults older than age 70 to optimize bone health. The safe upper limit was also raised to 4,000 IU. Doctors may prescribe more than 4,000 IU to correct a vitamin D deficiency.
If you don't spend much time in the sun or always are careful to cover your skin (sunscreen inhibits vitamin D production), you should speak to your doctor about taking a vitamin D supplement, particularly if you have risk factors for vitamin D deficiency.
D Power - Oral Vitamin Spray
While you’re catching some rays this summer, think about vitamin D. The sunshine vitamin produced in your skin in response to sunlight. Vitamin D is a fat-soluble vitamin in a family of compounds that includes vitamins D1, D2, and D3. It can affect as many as 2,000 genes in the body.Vitamin D has several important functions. Perhaps the most vital are regulating the absorption of calcium and phosphorous, and facilitating normal immune system function. Getting a sufficient amount of the vitamin is important for normal growth and development of bones and teeth, as well as improved resistance against certain diseases.If your body doesn't get enough vitamin D, you’re at risk of developing bone abnormalities such as osteomalacia (soft bones) or osteoporosis (fragile bones).
Up to 78% UAE populations are vitamin D deficient, 77% of Americans are vitamin D deficient and in India the rate is 75%
Low Vitamin D levels will result in your body working far below its potential. Vitamin D has been shown in recent studies to help promote immune health, help support healthy heart function, help muscle function, bone health and skin health.
Mechanism of Action
Vitamin D3 (cholecalciferol) is produced through the action of ultraviolet irradiation (UV) on its precursor 7-dehydrocholesterol. This molecule occurs naturally in the skin of animals and in milk. Vitamin D3 can be made by exposure of the skin to UVB, or by exposing milk directly to UV (one commercial method). Human skin makes vitamin D3 and supplies about 90% of vitamin D. D3 is also found in oily fish and cod liver oil.
Vitamin D2 is a derivative of ergosterol, a membrane sterol named for the ergot fungus, which is produced by some kinds of phytoplankton, invertebrates, yeasts, and higher fungi such as mushrooms. The vitamin ergocalciferol (D2) is produced in all of these organisms from ergosterol, in response to UV irradiation. Like all forms of vitamin D, it cannot be produced without UV irradiation. D2 is not produced by green land plants or vertebrates, because they lack the precursor ergosterol. The biological fate for producing 25(OH)D from vitamin D2 is expected to be the same as for 25(OH)D3, although some controversy exists over whether or not D2 can fully substitute for vitamin D3 in the human diet.
The photochemistry of vitamin D biosynthesis in animal and fungi
Thermal isomerization of previtamin D3 to vitamin D3
The transformation that converts 7-dehydrocholesterol to vitamin D3 occurs in two steps. First, 7-dehydrocholesterol is photolyzed by ultraviolet light in a 6-electron conrotatory ring-opening electrocyclic reaction; the product is previtamin D3. Second, previtamin D3 spontaneously isomerizes to vitamin D3 (cholecalciferol) in an antarafacial sigmatropic hydride shift. At room temperature, the transformation of previtamin D3 to vitamin D3in an organic solvent takes about 12 days to complete. The conversion of previtamin D3 to vitamin D3 in the skin is about 10 times faster than in an organic solvent
Photosynthesis of vitamin D in the ocean by phytoplankton (such as coccolithophore and Emiliania huxleyi) has existed for more than 500 million years and continues to the present. Although primitive vertebrates in the ocean could absorb calcium from the ocean into their skeletons and eat plankton rich in vitamin D, land animals required another way to satisfy their vitamin D requirement for a calcified skeleton without relying on plants. Land vertebrates have been making their own vitamin D for more than 350 million years.
Vitamin D can be synthesized only by a photochemical process, so land vertebrates had to ingest foods that contained vitamin D or had to be exposed to sunlight to photosynthesize vitamin D in their skin to satisfy their vitamin D requirements.
A diet deficient in vitamin D in conjunction with inadequate sun exposure causes osteomalacia (or rickets when it occurs in children), which is a softening of the bones. In the developed world, this is a rare disease. However, vitamin D deficiency has become a worldwide issue in the elderly and remains common in children and adults. Low blood calcidiol (25-hydroxy-vitamin D) can result from avoiding the sun. Deficiency results in impaired bone mineralization and bone damage which leads to bone-softening diseases, including:
Rickets, a childhood disease, is characterized by impeded growth and soft, weak, deformed long bones that bend and bow under their weight as children start to walk. This condition is characterized by bow legs, which can be caused by calcium or phosphorus deficiency, as well as a lack of vitamin D; today, it is largely found in low-income countries in Africa, Asia, or the Middle East and in those with genetic disorders such as pseudovitamin D deficiency rickets. Rickets was first described in 1650 by Francis Glisson, who said it had first appeared about 30 years previously in the counties of Dorset and Somerset. In 1857, John Snow suggested rickets, then widespread in Britain, was being caused by the adulteration of bakers' bread with alum. The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920. Nutritional rickets exists in countries with intense year-round sunlight such as Nigeria and can occur without vitamin D deficiency. Although rickets and osteomalacia are now rare in Britain, outbreaks have happened in some immigrant communities in which osteomalacia sufferers included women with seemingly adequate daylight outdoor exposure wearing Western clothing. Having darker skin and reduced exposure to sunshine did not produce rickets unless the diet deviated from a Western omnivore pattern characterized by high intakes of meat, fish, and eggs, and low intakes of high-extraction cereals. The dietary risk factors for rickets include abstaining from animal foods. Vitamin D deficiency remains the main cause of rickets among young infants in most countries, because breast milk is low in vitamin D and social customs and climatic conditions can prevent adequate sun exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh, where the disease occurs among older toddlers and children, it has been attributed to low dietary calcium intakes, which are characteristic of cereal-based diets with limited access to dairy products. Rickets was formerly a major public health problem among the US population; in Denver, where ultraviolet rays are about 20% stronger than at sea level on the same latitude, almost two-thirds of 500 children had mild rickets in the late 1920s. An increase in the proportion of animal protein in the 20th century American diet coupled with increased consumption of milk fortified with relatively small quantities of vitamin D coincided with a dramatic decline in the number of rickets cases. Also, in the United States and Canada, vitamin D-fortified milk, infant vitamin supplements, and vitamin supplements have helped to eradicate the majority of cases of rickets for children with fat malabsorption conditions.
Osteomalacia is a disease in adults that results from vitamin D deficiency. Characteristics of this disease are softening of the bones, leading to bending of the spine, bowing of the legs, proximal muscle weakness, bone fragility, and increased risk for fractures. Osteomalacia reduces calcium absorption and increases calcium loss from bone, which increases the risk for bone fractures. Osteomalacia is usually present when 25-hydroxyvitamin D levels are less than about 10 ng/mL. The effects of osteomalacia are thought to contribute to chronic musculoskeletal pain, There is no persuasive evidence of lower vitamin D levels in chronic pain sufferers.
Influence of skin pigmentation
Some research shows dark-skinned people living in temperate climates have lower vitamin D levels. Dark-skinned people may be less efficient at making vitamin D because melanin in the skin hinders vitamin D synthesis; however, a recent study has found novel evidence that low vitamin D levels among Africans may be due to other reasons. Recent evidence implicates parathyroid hormone in adverse cardiovascular outcomes. Black women have an increase in serum parathyroid hormone at a lower 25(OH)D level than white women. A large-scale association study of the genetic determinants of vitamin D insufficiency in Caucasians found no links to pigmentation.
However, the uniform occurrence of low serum 25(OH)D in Indians living in India and Chinese in China, does not support the hypothesis that the low levels seen in the more pigmented are due to lack of synthesis from the sun at higher latitudes. The leader of the study has urged dark-skinned immigrants to take vitamin D supplements nonetheless, saying, "I see no risk, no downside, there's only a potential benefit."
Vitamin D toxicity is rare. The threshold for vitamin D toxicity has not been established; however, the tolerable upper intake level (UL) is 4,000 IU/day for ages 9–71. Vitamin D toxicity is not caused by sunlight exposure, but can be caused by supplementing with high doses of vitamin D. In healthy adults, sustained intake of more than 1250 μg/day (50,000 IU) can produce overt toxicity after several months and can increase serum 25-hydroxyvitamin D levels to 150 ng/ml and greater; those with certain medical conditions, such as primary hyperparathyroidism, are far more sensitive to vitamin D and develop hypercalcemia in response to any increase in vitamin D nutrition, while maternal hypercalcemia during pregnancy may increase fetal sensitivity to effects of vitamin D and lead to a syndrome of mental retardation and facial deformities.
Hypercalcemia is a strong indication of vitamin D toxicity, noted with an increase in urination and thirst. If hypercalcemia is not treated, it results in excess deposits of calcium in soft tissues and organs such as the kidneys, liver, and heart, resulting in pain and organ damage. Pregnant or breastfeeding women should consult a doctor before taking a vitamin D supplement. The FDA advised manufacturers of liquid vitamin D supplements that droppers accompanying these products should be clearly and accurately marked for 400 international units (IU). In addition, for products intended for infants, the FDA recommends the dropper hold no more than 400 IU. For infants (birth to 12 months), the tolerable upper limit (maximum amount that can be tolerated without harm) is set at 25 μg/day (1,000 IU). One thousand micrograms per day in infants has produced toxicity within one month. After being commissioned by the Canadian and American governments, the Institute of Medicine (IOM) as of 30 November 2010, has increased the tolerable upper limit (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 lactating women).
Vitamin D overdose causes hypercalcemia, and the main symptoms of vitamin D overdose are those of hypercalcemia: anorexia, nausea, and vomiting can occur, frequently followed by polyuria, polydipsia, weakness, insomnia, nervousness, pruritus, and, ultimately,renal failure. Proteinuria, urinary casts, 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. Vitamin D toxicity is treated by discontinuing vitamin D supplementation and restricting calcium intake. Kidney damage may be irreversible. Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity. Within about 20 minutes of ultraviolet exposure in light-skinned individuals (three to six times longer for pigmented skin), the concentrations of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D produced is degraded.
Published cases of toxicity involving hypercalcemia in which the vitamin D dose and the 25-hydroxy-vitamin D levels are known all involve an intake of ≥40,000 IU (1,000 μg) per day. Recommending supplementation, when those supposedly in need of it are labeled healthy, has proved contentious, and doubt exists concerning long term effects of attaining and maintaining high serum 25(OH)D by supplementation.