Vitamin D is a group of fat-soluble vitamin which can be obtained from a few foods, sunlight and supplements (Office of Dietary Supplements, 2009). The main role of Vitamin D is to assist the metabolism of Calcium and Phosphorus and also involve in mineralization of bone. Till now, different forms of Vitamin D have been discovered, they are named Vitamin D1, D2 , D3, D4 and D5 respectively.
They are prohormones. It means they are originally inactive, they have to undergo certain modifications to convert into active form. The figure below shows the two steps activation of Vitamin D prohormones (Figure 1). Two hydroxylation reactions for the Vitamin D prohormones for activation, the first hydroxylation takes place in the liver and intermediate called 25-hydroxyvitamin D (also called Calcidiol) are formed. The second hydroxylation takes place in the kidney and the intermediate 25-hydroxyvitamin D are then converted to active form known as 1,25-dihyroxyvitamin D (also called Calcitriol).
Figure 1: Pathway for the activation of Vitamin D
Source: Mana, B., 2008
They are secosteroids. It means they are steroids with one of the bonds in the rings broken. Steroid is a group of substances with a sterane core which consists of four rings (Figure 2). Vitamin D has the similar structure as steroid. However, some of the bonds in the rings of Vitamin D are broken (Figure 3).
Figure 2: Structure of Sterane
Source: Wikipedia, Steroid
Figure 3: Structure of Vitamin D2, D3, D4, D5
Source: Wikipedia, Vitamin D
There are two major forms of Vitamin D. They are Vitamin D2 and D3. The structure of Vitamin D2 and D3 are very similar, except the presence of a double bond between c22 and c23 and a methyl group in the C24 in the side chain of Vitamin D2 (Wikipedia Vitamin D).
Both Vitamin D2 and D3 are essential to Human. However, Vitamin D2 (also called ergocalciferol) cannot be produced by vertebrates included Human and should be obtained from external environment. They are believed to have a high efficiency to absorb UV radiation and protect the organisms (Holick, 2009)
Different from Vitamin D2, Vitamin D3 (also called cholecalciferol) can be made by UVB at wavelengths 270 – 300 nm (Wikipedia, Vitamin D). Furthermore, Vitamin D3 is more effective than Vitamin D2 in human since both duration and potency of Vitamin D3 are higher than that of Vitamin D2 (Laura et al.,2004).
Source of Vitamin D
There are three ways to get Vitamin D such as sunlight, food and supplements and medications. Sunlight can help our skin to make Vitamin D from ultra-violet light (UVB rays). We can also through food to absorb Vitamin D like fatty fish, egg yolks and liver.
Source of Vitamin D – Sunlight
Sunlight is the best and only natural source of Vitamin D. When you get Vitamin D from sunshine, your body takes what it needs atomically and de-metabolizes any extra. Furthermore, 90 percent of our Vitamin D can naturally absorb from sunlight especially ultraviolet B exposure to our skin. It initiates the conversion of cholesterol in the skin to Vitamin D3. Sun exposure to the arms and legs for 10-15 minutes can produce thousands of units of Vitamin D which is 90% of our needed amount of Vitamin D. In addition, Full body exposure to sunlight is fortified with 3,000-20,000 IU (International Units) of Vitamin D (unshineVitamin.org, n.d). However, the sun is not a reliable source for everyone as the season, time of day, geography, latitude, level of air pollution, skin color, and age all affect our skin’s ability to produce Vitamin D.
Limitation of Sunlight
UV-B can be called the “burning ray”. It is the primary cause of sunburn and is caused by overexposure to sunlight. But UV-B sunlight can produce Vitamin D on the skin. The amount of UV-B is not a constant. It is a variable and can be affected by a number of factors:
* Latitude – The further north you are, the less there is
* Altitude of location – The higher up you are, the more UV-B reaches you
* Amount of skin surface exposed – The actual dosing of your sun expose is quite complex, since it involves knowing the amount of UV-B and one’s skin color
* Skin pigmentation – The darker the pigmentation or more tanned your skin, the less UV-B penetrates. Window glass allows only 5 percent of the UV-B light range that produces Vitamin D to get into your home or auto
* Season – Virtually less UV-B radiation in winter
* Clouds – Can block UV-B
* Pollution – Smog and ozone can block UV-B (Lee, 2008)
Alternative to UV exposure
Humans make and store abundant amounts of Vitamin D when skin is exposed to UVB from most indoor tanning equipment. E.g. tanning bed / sun bed. A single indoor tanning session (Maximum 20 mins) makes as much Vitamin D as 100 8-ounce glasses of whole milk (Uvsun, 2000). What’s more, UV exposure to tanning bed irradiation can increase pre-Vitamin D at a linear rate of 1 percent per minute. One week of exposure can lead to an increase in 25(OH) D by 50 percent, and five weeks of exposure can increase the level by 150 percent (Liu, 2008).
Source of Vitamin D – Food
Based on World’s healthiest Foods ranked as quality sources of Vitamin D, it indicated that salmon is excellent and also contains the highest nutrient density. Shrimp and milk are very good. Cod and egg are good too. Besides, some fortified and non-fortified food sources also contain Vitamin D such as cereal, orange juice, mackerel, sardines and tuna. Take orange juice and tuna as examples. If humans drink 8 oz of it, they can absorb 100 IU of Vitamin D. If humans eat 3.6 oz of canned tuna, they can absorb 300 IU of Vitamin D.
World’s Healthiest Foods ranked as quality sources of Vitamin D
World’s Healthiest Foods Rating
Salmon, chinook, baked/broiled
Cow’s milk, 2%
Egg, whole, boiled
Source: Whfood.com. (2010) from http://www.whfoods.com/genpage.php?tname=nutrient&dbid=110
Vitamin D content
100 IU per serving
100 IU per 8 oz
100 IU per 8 oz
Non-fortified food sources
20 IU per L
Cod liver oil
400 IU per teaspoon
250 IU per 3.5 oz
300 to 600 IU per 3.5 oz
Salmon (fresh, farmed)
100 to 250 IU per 3.5 oz
Salmon (fresh, wild)
600 to 1,000 IU per 3.5 oz
300 IU per 3.5 oz
230 IU per 3.6 oz
Source: Bordelon, P., Ghetu, M.V. & Langan, R. (2009).from http://www.aafp.org/afp/2009/1015/p841.html
Importance of Vitamin D
Vitamin D plays an important role in maintaining our bone for lifelong health. Also, it helps to maintain the level of calcium and phosphorus in human bodies. Vitamin D works with estrogen in the kidney regulating renal tubular from reabsorption of calcium and phosphorus. At the same time, Vitamin D works with PTH (parathyroid hormone) as to regulate the release of calcium and phosphorus from the bones into the bloodstream. Figure 4 shows how Vitamin D is processed within the human body to help the absorption of calcium.
Figure 4: the Vitamin D endocrine system
Source: Higdon, 1994 http://lpi.oregonstate.edu/infocenter/vitamins/vitaminD/dendocrine.html
Adequate storage levels of Vitamin D can maintain the strength of bone and help to prevent osteoporosis from elderly. Moreover, sufficient intake of Vitamin D can help to prevent risk of fall. Study showed that nursing home patients intake 800IU of Vitamin D daily would experience less falls when compared with the placebo group (Broe et al, 2007).
Vitamin D has a multitude of other biologic functions in the human body. Laboratory, animal evidence and epidemiologic data showed that Vitamin D plays a role in the prevention of colon, prostate, and breast cancers. Not only it helps to balance the mineral metabolism, it has direct effects on various nuclear receptors of different cells like prostate, liver, thyroid and brain (Vitamin & Herb University, Holick, 2003).
In vitro the studies of animal and epidemiological, Vitamin D might exhibit in the prevention and treatment of type 1 diabete and type 2 diabete, hypertension, glucose intolerance, multiple sclerosis, and other medical conditions (Office of Dietary Supplements).
How much is needed
Some researchers in the Vitamin D suggested that approximately 5-30 minutes of sunlight exposure between 10am and 3pm at least twice a week to the face, arms, legs, or back without sunscreen usually lead to sufficient Vitamin D in human body (Office of Dietary Supplements). However, since there are many factors reducing the ability of the skin to provide the total needs of Vitamin D, it is impossible to estimate the total intake of Vitamin D at the basis of skin exposure to sunlight.
There are very few foods in nature contain Vitamin D. The fatty fish and fish liver oils are the best sources. Moreover, there is no accurate data of food composition for estimation of Vitamin D in the dietary intakes. Therefore the WHO and Food and Agriculture Organization have established recommended nutrient intakes (RNIs) for Vitamin D (Table 1) , assuming no Vitamin D is being synthesized in the skin through exposure to sunlight. Recently, many experts and professional associations have recommended an increase in the Vitamin D intake from 200IU (5ïg) to 1000IU (25ïg) for an adult. Institute of Medicine is currently reviewing this newly recommendation (Vitamin & Herb University).
Table 1: Recommended nutrient intakes (RNIs) for vitamin D, by group
Source: WHO, 2004
What happens if we take excessive Vitamin D? If we intake too much Vitamin D, the following nonspecific symptoms may occur: nausea, vomiting, poor appetite, constipation, weakness, and weight loss.
Vitamin D toxicity is more likely to occur from high intakes of supplements. It is unlikely to result in Vitamin D toxicity from excessive sun exposure and high intakes of dietary Vitamin D.
Vitamin D Deficiency
Because of reduced dietary intake or inadequate exposure to sunlight, there will be deficient of Vitamin D in human body. Some studies reported “deficiency is defined as a serum 25-hydroxyVitamin D level of less than 20 ng per mL (50 nmol per L), and insufficiency is defined as a serum 25-hydroxyVitamin D level of 20 to 30 ng per mL (50 to 75 nmol per L)” (Bordelon et al, 2009). If insufficient 25 hydroxy-
cholecalciferol was brought to the kidney or the kidneys themselves being diseased, human can be repeatedly hidden more “parathyroid hormone” (Barasi, 1997, p.153-154).
Thus kidney cannot respond naturally and it fails to connect with blood calcium. The levels of calcium phosphate crystals begin getting low and forming soft tissue in the body (Richardson J.P., 2005). Such removal of calcium from the circulation also creates the bone releasing all available calcium for its normality of blood calcium level. The bones as a result turn into soft and bendable (Richardson J.P., 2005). Calcium in the bone activates the action of the osteoclasts and works as synthesizer to the bone as well. But Vitamin D deficiency can cause dematerialize the bone. Some significant symptoms are bone pain & soft bones, frequent bone fractures, bone deformities or growth retardation in children (A.D.A.M., Inc. (2003).
The deficiency in Vitamin D may have chronic pain and lower extremity weakness to people. It can negatively affect bone development and human health. In figure 5, the diagrams showed various bone fractures for patients who suffered from insufficiency or lack of Vitamin D at different degrees.
Figure 5: various bone fractures
Source: A.D.A.M., Inc. (2003)
The prevalence of Vitamin D deficiency has been reported to be 21 % in adolescents and 58 % in adults, 54 % in homebound older adults, and 84 % in elderly black women (Richardson J.P., 2005). However, the signs and symptoms of Vitamin D deficiency are insidious or nonspecific sometimes. Having been carried the studies of symptomatic patients, some are commented more susceptible to their characteristics. See table 2.
Table 2. Risk Factors for Vitamin D Deficiency
*Age older than 65 years
*Breastfed exclusively without Vitamin D supplementation
* Dark skin
* Insufficient sunlight exposure
* Medication use that alters Vitamin D metabolism
(e.g., anticonvulsants, glucocorticoids)
* Obesity (body mass index greater than 30 kg per m2)
* Sedentary lifestyle
(Source: Bordelon et al, 2009)
In addition, people at low Vitamin status can also be associated with other diseases (Bordelon et al, 2009). They are common manifestations of Vitamin D deficiency relating to other pathologic conditions in all ages.
* Reduced lower extremity neuromuscular function
* Increased risk of type 1 diabetes
* Impaired insulin sensitivity
* Increased risk of multiple sclerosis
* Impaired immune response
* Increased risk of various cancers
* Rickets (children)
* Osteomalacia (adults)
* Elevated serum PTH
* Decreased serum phosphorus
* Dlevated serum alkaline phosphatase
* Epidemiological evidence of increased risk of colon, breast, and prostate cancer
Case Study: Rickets and Osteomalacia
Classically, rickets and osteomalacia are metabolic bone diseases attributed primarily to Vitamin D deficiency, resulting in impaired calcium absorption and secondary phosphorus depletion. Both diseases cause softening and weakening of bones because of defective or inadequate bone mineralization. Rickets and osteomalacia are actually the same condition; rickets is the name used when it occurs in children with premature bones whereas osteomalacia is the term used for adults with mature bones.
Causes of Rickets and Osteomalacia
Rickets is among the most frequent childhood diseases in many developing countries. It mostly stems from nutritional insufficiency of Vitamin D, Calcium and Phosphates. A deficiency of Vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones. Lifestyles or cultural practices that decrease time spent outdoors or increase the amount of body surface area covered by clothing when outdoors further limit sunlight exposure. Rickets and osteomalacia can develop in people who spend little time in the sunlight, wear very strong sunscreen, live in areas where sunlight hours are short, or where the air is smoggy.
It was recognized that Vitamin D must be metabolized in the liver and kidneys before it can carry out its biologic effects on calcium, phosphorus, and bone metabolism. Therefore, a defect in the kidneys and liver would lead to problems with the break down of Vitamin D, thus causing rickets in patients with liver and kidneys defects (Thacher, 2006). Some rickets and osteomalacia cases are related to hereditary syndromes, cancer, or use of medication. Drugs, for examples Cadmium, Fluoride and Aluminum are expected to reduce the human’s abilities for Vitamin D absorption.
Clinical features and symptoms of Rickets and Osteomalacia
The clinical features for rickets and osteomalacia are usually associated with bone deformity (Annex 1). In serious cases, rib bending, wrist enlargement, knock knees, bog legs could be noticed from the patients’ appearance.
Rickets can cause significant morbidity including delays in growth and motor development, failure to thrive, short stature, skeletal deformities such as tibial bowing gibbus and pigeon chest. Patient with rickets may feel difficulty in breathing due to the deformity of ribs.
Symptoms of osteomalacia include bowing of the legs, a decrease in height, bone pain and muscle weakness (Spence, 2004).Osteomalacia may cause weakness and stiffness in the arms and legs, decreased muscle tone and discomfort during movement. Some people also walk with a waddling motion. Bone fractures may also occur in patients.
World’s prevalence of Nutritional rickets
Nutritional rickets has been described from at least 59 countries in the last 20 years. Its spectrum of causes differs in different regions of the world (Annex 2). Recently attention has been focused on the apparently high prevalence of rickets in Asia and Africa (Annex 3). In Mongolia and Tibet, rickets appears to be mainly due to Vitamin D deficiency associated with the high latitude, cold winters and limited skin exposure of sunlight (Annex 4).
Treatment of Rickets and Osteomalacia
To treat rickets or osteomalacia, Stoss Therapy can be used. This therapy will apply a single dose of vitamin D ranged from 300,000 IU to 500,000 IU (7,500?g to 12,500?g) to the patient for boosting the vitamin D level. The effects of the large dose of vitamin D should usually respond within 5 to 7 days. However, if the patient use it as the only treatment method the symptoms of bones bowing, knock knees, pathological fractures, or saber skin may still persist (Reinhold Vieth,1999).
Besides Stoss Therapy, there are many treatment methods available to heal rickets and osteomalacia but the idea behind them is to increase the Bone Mineral Density (BMD) by fullilling the ability of mineral absorption (Kwok, 2008).
First of all, drugs can be used for the rickets and osteomalacia patients. There are many different medicines for choices. A very well known example of medicine for this is the Biphosphonate. The advantage for taking medicines for the treatment is that they are not very expensive. However, the limitation of this is due to the drug from non-compliance of the patients.
Another treatment method developed for longer time is hormonal replacement. However, it is not recommended for menopausal women since it has risks from causing breast cancer. For middle-aged women, selective oestrogen receptor modulators (SERM) can be very efficient. Normally, the BMD in the patient will increase considerably and can prevent vertebral fractures. It also can protect the patient from getting breast cancer. However, the downside is that there are chances to stimulate venous thrombosis and fatal stroke to the patients.
Parathyroid hormone (PTH) therapy is another treatment option. The advantage of it is the high efficiency for increasing BMD in the patients. On the other hand, these therapies of this method are quite expensive and unlikely to everyone can afford it. Also, long term use of PTH may also lead to bone cancer.
As there are many different choices from rickets treatments, the doctor will choose a suitable one based on the age, gender and different body condition of the patient.
Prevention of Rickets and Osteomalacia
To reduce the risk of Rickets and Osteomalacia, and obtain adequate amount of to maintain good health, people are advised to be exposed to sunlight for at least 15 minutes each day. Foods like oily fish, eggs, fortified cereals and breads are all sources of vitamin D, but these may still be inadequate when sunshine hours are limited. Women, who are pregnant or breastfeeding, are encouraged to take vitamin supplements, to minimize the risk of developing vitamin D deficiency and other conditions and to prevent their child suffering rickets (Carvel,2007).
Recommendations for adequate Vitamin D intake
There is good evidence to support dietary supplementation of around 20 µg/day of vitamin D to people over 65 years of age appears to reduce problems related to vitamin D deficiency (Mosekilde,2008). Several countries have published recommendations for the dietary intake of vitamin D (Annex 5). The dietary recommendations are typically defined in terms of target intakes. Most of these studies recommend each person should consume 5-15µg Vitamin D from food per day. If these target intakes are applied at an individual level, they are supposed to meet the needs of the majority, especially for the high-risk groups. Nevertheless, these recommendations differ depending on the source, reflecting variations in the approach to providing general dietary guidelines. Moreover, these recommendations focus mainly on Caucasian whites, there is no specific recommendation for different ethnicity. It is also largely unknown whether vitamin D insufficiency in these populations leads to the same clinical consequences as in Caucasians (Mosekilde,2008). These findings underline the need to adjust recommendations to meet the estimated needs and to improve vitamin D status in the populations.
According to the Vitamin D, there have no regulations to make it clear that how much Vitamin D should be obtained between Hong Kong and China. However, World Health Organization (WHO) has recommended nutrients intakes (RNIs) for vitamin D in 2004. What’s more, the National Academy of Sciences established the Adequate Intake (AI) levels for Vitamin D in 1997. All of the guidelines mentioned above are constructive and useful for people to follow suitably in their daily life.
Vitamin D deficiency is common in all age groups. Even young children and young and middle-aged adults are at significantly increased risk of vitamin D deficiency. It is believed that there is very little vitamin D in the diet, and increased use of sunscreens and diminished outdoor activity also contribute to this problem. For prevention the problem of vitamin D deficiency in some geographical regions, e.g., countries in Southern European and the Middle East, public measures should be increasing the use of fortification of foods such as Milk with vitamin D, supplementation to high-risk groups.
As we know that Vitamin D deficiency will constitute adverse effect to our health. Consequently, we should pay much attention to avoid having skin cancer by over exposure under the sunlight. Besides, if we take vitamin D, do not take fish oil and fish oil capsules. These can be very allergenic and contained high levels of unneeded vitamin A. It is highly recommended to seek advice from some experts in connection with the vitamin D intake and it will do well to the health.
From Craviari T, Pettifor JM, Thacher TD, Meisner C, Arnaud J, Fischer PR, Rickets Convergence Group, “Rickets: an overview and future directions, with special reference to Bangladesh. A summary of the Rickets Convergence Group meeting, Dhaka, 26-27 January 2006” Journal Of Health, Population, And Nutrition [J Health Popul Nutr], ISSN: 1606-0997, 2008 Mar; Vol. 26 (1), pp. 112-21
Source : Thacher, Tom D; Fischer, Philip R, Strand, Mark A; Pettifor, John M. Nutritional rickets around the world: causes and future directions. Annals of Tropical Paediatrics: International Child Health, Volume 26, Number 1, March 2006, pp. 1-16(16).
Source: Thacher, Tom D; Fischer, Philip R, Strand, Mark A; Pettifor, John M. Nutritional rickets around the world: causes and future directions. Annals of Tropical Paediatrics: International Child Health, Volume 26, Number 1, March 2006, pp. 1-16(16).
Source: Thacher, Tom D; Fischer, Philip R, Strand, Mark A; Pettifor, John M. Nutritional rickets around the world: causes and future directions. Annals of Tropical Paediatrics: International Child Health, Volume 26, Number 1, March 2006, pp. 1-16(16).
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