The following article was selected as the winner for Fitness Savvy’s 2019 Scholarship Award.
This submission was received from Ashwin Venkatakishnan, who is studying Medicine.
Vitamin D Deficiency – Symptoms, Treatment and Causes
Vitamins are organic compounds that are essential for humans. There are 13 types of vitamins in total.1 In this article, we will focus on what constitutes Vitamin D deficiency and examine its symptoms, treatments and causes.
Vitamin D is a hormone, meaning that it binds to specific receptors (Vitamin D Receptors – VDRs) to have an effect on the body. It exists naturally as either Vitamin D2 or Vitamin D3. Vitamin D2 is produced by plants and mushrooms while Vitamin D3 is found in animal-sourced foods such as fatty fish and eggs. Interestingly, our own skin also produces Vitamin D3 when exposed to ultraviolet radiation from sunlight.2
Both forms first undergo hydroxylation in the liver to form 25-hydroxyvitamin D [25(OH)D] before being further hydroxylated in the kidney to form the biologically active 1,25-hydroxyvitamin D [1,25(OH)2D]. 25(OH)D has a half-life of 15 days. This means that the time taken for its concentration to reduce to half its original level is 15 days. In contrast, 1,25(OH)2D has a half-life of just 15 hours. As such, serum concentration of the former serves as the better long-term indicator of the amount of Vitamin D in our bodies. This concentration is measured in ng/ml or nmol/l, with 1 ng/ml roughly equal to 2.5 nmol/l. Take note that this conversion is only for Vitamin D!
Members of the medical community are divided over what is the optimum serum level, ranging from 12 ng/ml to 40 ng/ml.3 However, the consensus is that Vitamin D deficiency occurs when the 25(OH)D level is less than 20ng/ml and one should strive to maintain a level of around 30ng/ml.4 Vitamin D deficiency has many side effects as listed and explained below.
- Impaired Immune System – Our body has 2 main types of immune responses, namely innate (nonspecific) and adaptive (antigen-specific). Vitamin D is helpful in both. It increases production of many antimicrobials and enhances the function of our existing macrophages and neutrophils. These are large white blood cells which ‘eat’ foreign matter indiscriminately. In addition, Vitamin D activates specialised immune defence cells like T-cells and is thought to help prevent tissue damage by limiting the inflammatory response of our immune system. Lack of Vitamin D can compromise our immune system, making us more susceptible to pathogens.5
- Bone Weaknesses and Disorders – Vitamin D promotes the absorption of calcium and phosphorous in our intestines which keeps our bones strong and healthy. When there is too little Vitamin D, there is less calcium uptake and this can result in osteoporosis, where the patient is afflicted with thin, brittle bones.6
In addition, Vitamin D helps correct hypocalcaemia (low blood calcium level) and hypophosphatemia (low blood phosphorous level) by stimulating bone resorption (breaking down of bone) to release calcium and phosphorous into the blood. When Vitamin D is deficient, an alternate homeostatic pathway occurs. More parathyroid hormone (PTH) is synthesised which helps correct hypocalcaemia but worsens hypophosphatemia by enhancing urinary phosphate excretion. This leads to even greater bone resorption7 and can cause osteomalacia, a condition, where the bones become soft and more prone to fracture, increasing both the initiation and propagation of cracks in bones by up to 31%.8
Osteomalacia in adults has less obvious symptoms which disappear once treated. When it occurs in children, it is called rickets and has more severe symptoms. In addition to obvious skeletal deformities such as an oddly shaped skull and a curved spine, stunted growth and muscle cramps have been observed in rickets-afflicted children.9
- Hair Loss – Vitamin D plays an important role in creating new hair follicles. New follicles not only help maintain hair thickness, but also prevent the premature fall of existing hair.10 Vitamin D deficiency can cause hair loss and has been linked with alopecia areata.11 This is an autoimmune disease in which the immune system mistakenly attacks the body’s own hair follicles, causing hair on the scalp to fall out in patches. Hair on other parts of the body is also susceptible.12
- Muscle Pain – Pain-sensing nerve cells called nociceptors contain these specific Vitamin D receptors (VDRs). Vitamin D binds to these VDRs and inhibits the growing of these nerves into muscle fibres (innervation). Vitamin D deficiency leads to hyperinnervation by nociceptors, inducing musculoskeletal pain. 13
- Blood Sugar Issues – Beta cells in the pancreas produce the hormone insulin that allows our body to make use of the sugars in the food we eat. It directs the absorption of sugars from our blood into our cells where the sugars are either broken down to produce energy or stored in the form of glucose for future use. Vitamin D deficiency can lead to decreased sensitivity to insulin. Insulin is now less effective in regulating blood sugar levels and this can lead to Type II Diabetes. 14
- Depression – Vitamin D is thought to also affect our emotional well-being. VDRs exist in several regions in our brain and are particularly abundant in the hypothalamus, which is in charge of regulating emotional responses.15 Vitamin D deficiency has been linked to depression, though whether it causes depression remains to be rigorously proven.16Vitamin D deficiency is not to be taken lightly. One requires approximately 2200-3000 IU (International Units) of vitamin D per day, obtained from all sources including sunlight, to maintain a 25(OH)D level of 30-32 ng/ml.17In 1972, 1 IU of Vitamin D was formally defined as having the same amount of biological activity as 65 pmol of Vitamin D2 or D3 which translates to approximately 25.78 ng of the former or 25 ng of the latter.18 However, recent studies have shown Vitamin D3 to have much higher potency than Vitamin D219,20. 50,000 IU of Vitamin D2 is equivalent to 5,000-15,000 IU of Vitamin D3 and not 50,000 IU of Vitamin D3 as previously thought.19
The recommended dietary allowance (RDA) of Vitamin D from foods alone is 600 IU/day for youths and adults and 800 IU/day for those aged above 70 years.4 Vitamin D deficient people need to consume way more in order to raise their 25(OH)D level to at least 30ng/ml in the short term. One can increase his Vitamin D intake through the following ways.
- Eat Vitamin D-rich foods – Vitamin D is fat-soluble, meaning it is absorbed best when taken with higher-fat foods. Fatty fish like salmon and herrings provide up to 1600 IU of Vitamin D per serving.21
Cod liver oil can also be taken. One teaspoon alone provides 450 IU of vitamin D. Besides, it is rich in multiple essential nutrients, making it an excellent choice all round. The only problem (other than its taste!) is a problem of plenty. Just one teaspoon contains 90% of the RDA for vitamin A. When too much vitamin A is taken in, one can suffer symptoms ranging from drowsiness to nausea and respiratory infection.22
People who don’t eat seafood can consider egg yolks and mushrooms. Egg yolks from chickens raised indoors contain less than 40 IU, while those from chickens free to roam outdoors have up to 160 IU of vitamin D. However, they pale in comparison to egg yolks from chickens given Vitamin D enriched food, which have up to 6000 IU! Mushrooms grown in the wild or under UV light have up to 2300 IU per serving and 130-450 IU per serving respectively.21
Since natural sources of food are hard to come by, several common food items have been fortified with Vitamin D. Examples include cow’s milk (130 IU per cup), soy milk (99-119 IU per cup), orange juice (142 IU per cup) and some cereal and oatmeal (55-154 IU per ½ cup serving).21
To increase the 25(OH)D level by a large amount quickly, one would be better served by the following method.
- Take Vitamin D supplements – Capsules come in various dosages, ranging from 400 IU all the way to a maximum of 50,000 IU (prescription only). The patient’s 25(OH)D level is first checked before deciding the dosage. The prescribed capsules usually have to be taken either daily or weekly.
There are two important things to take note. Firstly, supplements do not straightaway raise the 25(OH)D level. Secondly different patients respond in different ways to the same dosage. One factor affecting the patient’s response is his BMI. Since Vitamin D is fat-soluble, it tends to get absorbed by fatty tissue. A rule of thumb is that every 1000 IU of vitamin D3 taken daily will raise a 25(OH)D level of a healthy person by 10 ng/ml in a few weeks’ time. Obese people have to take in more Vitamin D to raise their serum level by the same amount and are thus prescribed higher doses.23
The patient has to recheck his vitamin D level around 3 months after starting treatment to ensure he is on the right track. Even if the patient’s 25(OH)D level has become optimal, he will need to continue taking supplements, albeit of a lower dose, to maintain his 25(OH)D level.
Certainly, taking Vitamin D supplements to raise the 25(OH)D level seems more appealing than eating the same few foods over and over again. Supplements are also cheap, with an entire bottle of capsules priced in the vicinity of $20.
The only real disadvantage that supplements have is that there is a risk of vitamin D toxicity (25(OH)D level above 150 ng/ml).17 Such high levels can only be achieved if patients take their high dose capsules daily when they were supposed to take them weekly instead. This is either the patient’s fault (misreading the prescription) or the medical practitioner’s fault (mislabelling the prescription). Possible vitamin D toxicity is one reason for patients needing to recheck their 25(OH)D level after 3 months of taking supplements.
Symptoms of vitamin D toxicity include hypercalcemia (elevated blood calcium levels), nausea, kidney failure and surprisingly, bone loss.24 Although Vitamin D is crucial for maintaining strong bones, excessive amounts are thought to drastically lower the level of Vitamin K2, another vitamin instrumental to bone health, leading to bone resorption.24 Fortunately, these problems are reversible if proper medical care is sought upon the appearance of symptoms.25
If you are put off by the risk of Vitamin D toxicity, you can consider the following method.
- Get more sunlight – There are three types of ultraviolet radiation in sunlight, namely UVA, UVB and UVC. As UVB rays hit cholesterol in our skin cells, Vitamin D3 is synthesized. Not only is this method completely free, but there is also absolutely no risk of Vitamin D toxicity, no matter how long one stays under the sun. UVB-induced Vitamin D production in skin is a self-limiting process, with sunlight degrading any excess Vitamin D produced.26
UVB rays have low penetrating power. They cannot pass through glass windows, so merely sitting in an office building next to a closed window will have no effect on Vitamin D production in the skin. They are also blocked by sunscreen so one has to go unprotected under the sun to maximise the speed of Vitamin D production.27 In addition, thick clothing hinders UVB rays, so wearing a thin t-shirt and shorts allows one to absorb more Vitamin D.28
This method is also quick-acting. A mere thirteen minutes of sunlight exposure in midday, three times a week during summer, is sufficient to maintain healthy levels among Caucasian adults in the UK!29 However, the recommended duration under the sun is much longer for people with dark skin as they have more melanin that reduces the amount of UVB rays absorbed. People living further from the equator also have to be outdoors longer as they get exposure to fewer UVB rays per unit time.30,31
Receiving just one mineral erythemal dose (lowest dose of UV light that causes slight reddening of the skin) was found to have the same effect on the 25(OH)D level as ingesting approximately 15,000 – 20,000 IU of Vitamin D in a single dose. The 25(OH)D level also remained elevated for a longer time.32 It is not recommended to stay unprotected under the sun longer than necessary as there is a possible risk of skin cancer. It is thus good to start seeking shelter once your skin starts to redden.
If being exposed to the sun is not possible (during winter months for instance), one can get a light box, preferably one that can supply 10,000 lux of full spectrum light. Sitting in front of a box 30 minutes a day is sufficient. If symptoms such as eyestrain or headaches due to bright light occur, one can consider shifting further away from the light box or using it in shorter intervals instead.33 A light box is not cheap, with prices being as high as $1000, but note that this is a one-time investment that can be used for life.
It can now be understood how some cannot meet their minimum daily Vitamin D requirement without supplements. Vegans have limited Vitamin D-rich food choices. Obese people have to consume way more Vitamin D due to its tendency to get stored in fatty tissues instead of remaining in the blood. People having a 9-5 desk job or living far away from the equator are less likely to spend enough time under the sun. This also applies for those who regularly wear sunscreen or cover most of their skin outdoors. We will now examine 3 new causes of Vitamin D deficiency.
- Impaired Digestive System – Fat-digesting juices are needed to break down Vitamin D. Hence, disorders such as obstructive jaundice and cystic fibrosis,34 where there is low release of fat-digesting bile juices, are risk factors of Vitamin D deficiency. In addition, conditions like Coeliac Disease, Crohn’s Disease35 and gastric bypass drastically reduce absorption of nutrients like Vitamin D into the bloodstream. Therefore, even if sufficient Vitamin D is ingested into the body, the amount that actually makes it into the blood is ultimately insufficient.
- . Impaired Kidney and Liver – The liver and kidney are needed to metabolise the ingested Vitamin D into its biologically active form of 1,25(OH)2D. Any problem with these 2 organs will affect the synthesis of 1,25(OH)2D. Furthermore, kidney disorders involving proteinuria (excessive protein in urine) such as Nephrotic Syndrome and renal Fanconi Syndrome also play a role in Vitamin D deficiency. This is because one of the many proteins being wrongly excreted in the urine is Vitamin D-Binding Protein (VDBP). As VDBP is usually bound to Vitamin D, excretion of VDBP also means excretion of Vitamin D.36 Renal disorders involving tubules can be inherited, and some can result in major organs becoming resistant to 1,25(OH)2D.37
- Usage of certain catabolism-promoting drugs – Drugs like glucocorticoids and anti-epileptic agents enhance the synthesis of hydroxylases that degrade 25(OH)D and 1,25(OH)2D, resulting in possible Vitamin D deficiency.38
- Old Age – As people age, their skin produces less Vitamin D when under the sun. Elderly people are also more likely to be homebound and get below-average exposure to sunlight. Since they get less Vitamin D through sunlight, they have to get more through food, which is why their RDA of Vitamin D is significantly higher than for other age groups. However, even if the elderly manage to consume enough Vitamin D, the combination of factors 1 and 2 naturally make them more vulnerable to Vitamin D deficiency due to their organs being more susceptible to failure.39
In conclusion, Vitamin D is crucial to humans as the multitude of symptoms arising from its deficiency would attest. There are numerous reasons for it to be lacking in humans but there are also numerous ways to correct the problem.
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2 Bordelon, Paula, et al. “Recognition and Management of Vitamin D Deficiency” American Family Physician. 80.8 (2009): 841. American Academy of Family Physicians. Web. 01 Mar. 2019.
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21 Jones, Taylor. “9 Healthy Foods That Are High in Vitamin D.” Healthline, Healthline Media, 12 Sept. 2018, www.healthline.com/nutrition/9-foods-high-in-vitamin-d.
22 Pietrangelo, Ann. “Hypervitaminosis A: Causes, Symptoms, and Diagnosis.” Healthline, Healthline Media, 2017, www.healthline.com/health/hypervitaminosis-a.
23 Lee, Paul, et al. “Adequacy of Vitamin D Replacement in Severe Deficiency Is Dependent on Body Mass Index.” The American Journal of Medicine, vol. 122, no. 11, 2009, pp. 1056–1060., doi:10.1016/j.amjmed.2009.06.008.
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References for images
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