The Vitamin D Deception

By Daniel Roytas MHSc (Nut), BHSc (Nat), Dip. RM, MANTA

Despite living on the sunniest continent on Earth¹, 25% of all Australians are thought to be vitamin D deficient². Rather than acquiring vitamin D from sensible amounts of sun exposure to maintain optimal levels of vitamin D, it seems the Australian public have turned towards supplementation instead. As of 2010, there were 89 vitamin D manufacturers selling 195 different vitamin D products in Australia. Almost 60 million vitamin D products were sold that year, totalling an eye watering $89.3 million³. Why is all of this money being spent on something that we can literally get for free, right outside our front door?

Could it be that the public health initiatives around sun safety have worked too well? A 2011 paper published in the Medical Journal of Australia found that it is relatively difficult to obtain the equivalent of just 1000 IU (1 capsule worth) of vitamin D from sun exposure when adhering to sun smart recommendations⁴. Whilst these recommendations have been developed with the best intentions, they have driven unnecessary fear in to the hearts and minds of the Australian people, so much so, that many young people are afraid of going out in to the sun⁵. It is important to mention that whilst sensible amounts of sun exposure are beneficial, prolonged periods or excessive exposure are damaging to human health.  

Dr. Robyn Lucas, an epidemiologist at the National Centre for Epidemiology and Population Health in Canberra stated in a 2008 article published in the Journal of Environmental Health Perspective that diseases arising from excessive sun exposure are usually benign and typically occur in older people⁶. She went on to say that despite their high prevalence, skin cancers are associated with a relatively low burden of disease⁶. In that same paper, Dr. Alberto Ascherio an epidemiologist from the Harvard School of Public Health stated that moderate sun exposure (believe it or not) is more beneficial for human health than trying to avoid it⁶. In fact, sun exposure is associated with protective effects against cardiovascular disease, type 2 diabetes, Alzheimer’s disease, multiple sclerosis⁷, prostate, breast, colorectal⁸ and other gastrointestinal cancers⁹. These beneficial effects are due to mechanisms beyond the stimulation of vitamin D synthesis⁸, which supports research suggesting UV exposure is superior to vitamin D supplementation at reducing the risk of disease¹⁰.

Ultraviolet-B radiation exposure (UV-B) from sunshine is the principle source of vitamin D in humans¹¹. One whole body minimum erythema dose (faint skin redness) can generate the equivalent dose of 10 000 – 25 000 IU¹². Just 7 minutes of sun exposure outside of the hours of 10 am – 3 pm in Summer and between 7 – 40 minutes at midday during Winter, is sufficient to maintain adequate vitamin D levels when at least 15% of the skin (arms and hands) is exposed¹³. Therefore, a low vitamin D level might be a good indicator of an individual’s lifestyle habits. That is, that they are spending too much time in doors and not enough time outdoors in the fresh air, enjoying the sun. It is worthwhile to note that UV-B radiation does not penetrate glass, so exposure to sunshine indoors through an office window does not increase vitamin D levels¹⁴.  

This is probably a good time to mention that vitamin D, isn’t actually a vitamin, it is a pleiotropic steroid hormone¹⁵. We shouldn’t let the word “vitamin” fool us. Ask yourself, what other hormone do you take religiously every single day, without a second thought about the potential effects it’s having on your health? It is responsible for the regulation and function of more than 1000 different genes and governs basically every single tissue in the body⁶. It is not known precisely how many genes vitamin d actually regulates and what the true effect of the supplemental vitamin D on our genes is. Our body and the sun have worked this complex inter-relationship out over millennia, however the reality of the matter is that we have no idea what’s really occurring at a genetic level with supplementation. It defies belief that we could be so naïve to think that a synthetic vitamin manufactured in a laboratory (or other exogenous forms) and crammed in to a soft-gel capsule with various other excipients, could take the place of an endogenously produced substance that is formed by a reaction catalysed by the sun. The human body shares an innate relationship with the sun, something not even the wonders of modern medicine may ever come to fully comprehend.

Many readers may not be aware of this, but before vitamin D was popularised as a supplement for humans, it was (and still is) used as the main active ingredient in many commercially available rat poisons and possum baits, albeit at very high doses¹⁶. In high doses, vitamin D has also been shown to be lethal to dogs, cats and birds¹⁶. How can we be absolutely sure, that even at the ‘recommended dose’, vitamin D supplements are not having potentially long term, deleterious effects on our health? The mechanism by which vitamin D toxicity causes death, is by inducing hypercalcemia via increasing  calcium absorption from the small intestine, increasing calcium mobilisation from bones and by inhibiting renal calcium excretion¹⁶. In humans, vitamin D toxicity induced hypercalcemia results in systemic calcification of soft tissue, leading to renal failure, cardiac abnormalities, hypertension, central nervous system depression, and gastro-intestinal dysfunction¹⁷. It should be noted that the reports in the literature of vitamin D toxicity are not common. 

Serum levels of vitamin D (specifically 25(OH)D) plateau at around 150 nmol/L in response to sun light (UV-B) exposure. This is an in-built self-defense mechanism that prevents sun induced vitamin D toxicity as UV-B prevents excessive cutaneous pre-vitamin and vitamin D production¹⁸. Therefore vitamin D toxicity can only be caused by the prolonged ingestion of fortified food and supplementation at high doses over prolonged periods of time¹⁹. There are numerous reports of errors in food fortification of vitamin D, where individuals were exposed to excessive levels of vitamin D leading to toxicity²⁰. For example, a New Zealand study found that only 8 out of 14 products had vitamin D levels within 10% of the listed label dose²¹. A US study found that only a third of all capsules analysed in the study contained vitamin D levels within 10% of the listed dose²². Discrepancies between the listed dose and the actual dose of a range of supplements are responsible for many cases of toxicity reported in the literature. Furthermore, as vitamin D supplements are readily available over the counter, there is a risk for consumers to inappropriately self-medicate which could lead to toxicity, particularly when there is already adequate sun exposure and consumption of fortified foods²³.

Vitamin D is commonly prescribed to patients with vitamin D deficiency, however vitamin D supplementation in such individuals may not necessarily address the underlying cause, and could be equated to putting a band-aid on a gaping wound. In fact, despite vitamin D deficiency being implicated as the cause of disease, there is scant evidence elucidating the pathogenesis^24,25. It has been proposed that vitamin D deficiency is a direct consequence of disease and not a cause of illness²⁶. In fact, vitamin D deficiency may be a marker of deteriorating health, ageing and inflammation, which explains why deficiency could be observed in a wide range of disorders^24,27,28.

Some evidence actually suggests that a chronic inflammatory process caused by persistent bacterial infections^24,29 and chronic disease²⁸ may be the cause of low vitamin D. Paradoxically, whilst inflammation reduces vitamin D levels, supplementation seems to have a negligible effect on ameliorating inflammation^24,27. There is also some evidence indicating that vitamin D could actually up-regulate inflammation^24,29. This is analogous to throwing timber on a raging fire. We know that the body has a self-defence mechanism, where during states of inflammation and infection, it sequesters iron inside the tissue to prevent excessive levels of oxidative stress³⁰. Could it be, that a similar mechanism exists with vitamin D and we have been adding fuel to the fire this whole time through supplementation without realising it? The other train of thought, is that a low vitamin D might actually be an indicator of absence of disease, however further research is required²⁴.  

Furthermore, it has been postulated that adiposity accounts for the lower vitamin D levels seen in overweight & obese individuals due to its sequestration within excess adipose tissue³¹. With 30% of the Australian population now obese and 67% overweight³², could this be one reason why there is high prevalence of vitamin D deficiency in Australia?².

Medicare funded Vitamin D testing is an interesting topic. In 2010, it was reported vitamin D testing cost Medicare $96.7 million, a 95-fold increase compared to the amount spent a decade earlier³³. Incredibly the cost peaked at $151 million in 2012³⁴, which dwarfs the $12.7 million worth of funding by the Australian Government to Cancer Australia that same year³⁵. Consequently, vitamin D testing was restricted to specific, at risk population groups the following year to reduce the expenditure as the cost-benefit analysis did not support widespread use of this test as it is of low clinical value³⁴. Where has the need for such testing come from? 

Understanding the true nature of deficiency is complicated by the fact that vitamin D tests may not be as accurate as we think. Despite the dramatic increase in vitamin D testing, there is considerable uncertainty about the accuracy of these tests³⁶. A report presented at a conference of the Endocrine Society in 2012 stated that at least 40% of all vitamin D tests are inaccurate³⁷. Furthermore, there is no agreement amongst peak regulatory bodies around what actually constitutes vitamin D deficiency²⁴, nor what the optimal serum concentrations should be³⁸. How then, as practitioners, do we interpret the results of a test in a clinically meaningful way?

Surely, despite all of the aforementioned data presented here, there is still a place for vitamin D to be prescribed for patients with a frank deficiency? One of the most common reasons vitamin D is prescribed is in order to reduce the risk of osteoporosis and associated fractures by improving bone mineral density³⁹. Despite commonly held perceptions by clinicians, there is in fact, little evidence to support the use of vitamin D in such cases. A considerable number of systematic reviews and meta-analyses investigating the musculoskeletal effects of vitamin D supplementation have found that it provides very little or no clinically significant benefit (with or without calcium supplementation) in improving bone mineral density or reducing fracture risk^40–46. A 2020 paper published in the Journal of Bone and Mineral Research found that long term, high dose vitamin D supplementation actually reduces bone mineral density and muscle strength in postmenopausal females⁴⁷, the very population group that vitamin D is promoted to protect.

It’s time to get people back out in to the sun and to throw those vitamin D pills in the bin on their way out of the house. 

Note: This article is for general information purposes only. It does not constitute as health advice and does not take the place of consulting with your primary health care practitioner. 

References

1. Fact check: Is Australia the sunniest continent on Earth? Australian Broadcasting Corporation. https://www.abc.net.au/news/2015-08-10/solar-coverage-fact-check-is-australia-sunniest-continent/6659316. Published 2015. Accessed September 17, 2020.
2. Vitamin D. Australian Bureau of Statistics. https://www.abs.gov.au/ausstats/[email protected]/lookup/4364.0.55.006chapter2002011-12#:~:text=The majority of Australian adults,1%25 with a severe deficiency. Published 2014. Accessed September 16, 2020.
3. Bilinski K, Talbot P. Vitamin D Supplementation in Australia: Implications for the Development of Supplementation Guidelines. J Nutr Metab. 2014;2014:1-4. doi:10.1155/2014/374208
4. Stalgis‐Bilinski KL, Boyages J, Salisbury EL, Dunstan CR, Henderson SI, Talbot PL. Burning daylight: balancing vitamin D requirements with sensible sun exposure. Med J Aust. 2011;194(7):345-348. doi:10.5694/j.1326-5377.2011.tb03003.x
5. Lo Presti L, Chang P, Taylor M. Young Australian adults’ reactions to viewing personalised UV photoaged photographs. Australas Med J. 2014;7(11):454-461. doi:10.4066/AMJ.2014.2253
6. Mead MN. Benefits of Sunlight: A Bright Spot for Human Health. Environ Health Perspect. 2008;116(4). doi:10.1289/ehp.116-a160
7. Queirós CS, Freitas JP. Sun Exposure: Beyond the Risks. Dermatol Pract Concept. 2019;9(4):249-252. doi:10.5826/dpc.0904a01
8. van der Rhee H, Coebergh JW, de Vries E. Is prevention of cancer by sun exposure more than just the effect of vitamin D? A systematic review of epidemiological studies. Eur J Cancer. 2013;49(6):1422-1436. doi:10.1016/j.ejca.2012.11.001
9. Garland C, Garland F. Do Sunlight and Vitamin D Reduce the Likelihood of Colon Cancer? Int J Epidemiol. 1980;9(3):227-231. doi:10.1093/ije/9.3.227
10. Mizoue T. Ecological study of solar radiation and cancer mortality in Japan. Health Phys. 2004;87(5):532-538. doi:10.1097/01.HP.0000137179.03423.0b
11. McKinlay A. A reference action spectrum for ultraviolet erythema in human skin. CIE J. 1987;61(1):17-22.
12. Heaney RP, Armas LAG. Quantifying the vitamin D economy. Nutr Rev. 2015;73(1):51-67. doi:10.1093/nutrit/nuu004
13. Nowson CA, McGrath JJ, Ebeling PR, et al. Vitamin D and health in adults in Australia and New Zealand: a position statement. Med J Aust. 2012;196(11):686-687. doi:10.5694/mja11.10301
14. Aydin FN, Aydin I, Agilli M. Factors Affecting the Accuracy of Vitamin D Measurements. Clin Med Res. 2014;12(1-2):4-4. doi:10.3121/cmr.2014.1231
15. Martens P-J, Gysemans C, Verstuyf A, Mathieu C. Vitamin D’s Effect on Immune Function. Nutrients. 2020;12(5):1248. doi:10.3390/nu12051248
16. Eason CT, Wickstrom M, Henderson R, Milne L, Arthur D. Nontarget and secondary poisoning risks associated with cholecalciferol. New Zeal Plant Prot. 2000;53:299-304. doi:10.30843/nzpp.2000.53.3699
17. Tebben PJ, Singh RJ, Kumar R. Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment. Endocr Rev. 2016;37(5):521-547. doi:10.1210/er.2016-1070
18. Binkley N, Novotny R, Krueger D, et al. Low Vitamin D Status despite Abundant Sun Exposure. J Clin Endocrinol Metab. 2007;92(6):2130-2135. doi:10.1210/jc.2006-2250
19. Marcinowska-Suchowierska E, Kupisz-Urbańska M, Łukaszkiewicz J, Płudowski P, Jones G. Vitamin D Toxicity-A Clinical Perspective. Front Endocrinol (Lausanne). 2018;9:550. doi:10.3389/fendo.2018.00550
20. Blank S, Scanlon KS, Sinks TH, Lett S, Falk H. An outbreak of hypervitaminosis D associated with the overfortification of milk from a home-delivery dairy. Am J Public Health. 1995;85(5):656-659. doi:10.2105/AJPH.85.5.656
21. Garg S, Sabri D, Kanji J, et al. Evaluation of vitamin D medicines and dietary supplements and the physicochemical analysis of selected formulations. J Nutr Health Aging. 2013;17(2):158-161. doi:10.1007/s12603-012-0090-4
22. LeBlanc ES, Perrin N, Johnson JD, Ballatore A, Hillier T. Over-the-Counter and Compounded Vitamin D: Is Potency What We Expect? JAMA Intern Med. 2013;173(7):585. doi:10.1001/jamainternmed.2013.3812
23. Taylor PN, Davies JS. A review of the growing risk of vitamin D toxicity from inappropriate practice. Br J Clin Pharmacol. 2018;84(6):1121-1127. doi:10.1111/bcp.13573
24. Mangin M, Sinha R, Fincher K. Inflammation and vitamin D: the infection connection. Inflamm Res. 2014;63(10):803-819. doi:10.1007/s00011-014-0755-z
25. Holick MF, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008;87(4):1080S-1086S. doi:10.1093/ajcn/87.4.1080S
26. Autier P, Boniol M, Pizot C, Mullie P. Vitamin D: chasing a myth? Lancet Diabetes Endocrinol. 2014;2(1). doi:10.1016/S2213-8587(13)70164-5
27. Noordam R, de Craen AJM, Pedram P, et al. Levels of 25-hydroxyvitamin D in familial longevity: the Leiden Longevity Study. Can Med Assoc J. 2012;184(18):E963-E968. doi:10.1503/cmaj.120233
28. Autier P, Boniol M, Pizot C, Mullie P. Vitamin D status and ill health: a systematic review. Lancet Diabetes Endocrinol. 2014;2(1):76-89. doi:10.1016/S2213-8587(13)70165-7
29. Albert PJ, Proal AD, Marshall TG. Vitamin D: The alternative hypothesis. Autoimmun Rev. 2009;8(8):639-644. doi:10.1016/j.autrev.2009.02.011
30. Sangkhae V, Nemeth E. Regulation of the Iron Homeostatic Hormone Hepcidin. Adv Nutr An Int Rev J. 2017;8(1):126-136. doi:10.3945/an.116.013961
31. Gallagher J, Sai A. Dose Response to Vitamin D Supplementation in Postmenopausal Women A Randomized Trial. Ann Intern Med. 2012;156(6):425-437.
32. Overweight & Obesity. Australian Institute of Health and Welfare. https://www.aihw.gov.au/reports-data/behaviours-risk-factors/overweight-obesity/overview. Published 2020. Accessed September 17, 2020.
33. Bilinski KL, Boyages SC. The rising cost of vitamin D testing in Australia: time to establish guidelines for testing. Med J Aust. 2012;197(2):90-90. doi:10.5694/mja12.10561
34. Gordon L, Waterhouse M, Reid IR, Neale RE. The vitamin D testing rate is again rising, despite new <scp>MBS</scp> testing criteria. Med J Aust. 2020;213(4):155. doi:10.5694/mja2.50619
35. Cancer Council Annual Report 2011 - 2012. https://www.canceraustralia.gov.au/sites/default/files/publications/canceraust-ar-201112_50909b2d90533.pdf.
36. Graham D. Accuracy of 25-Hydroxyvitamin D Assays: Confronting the Issues. Curr Drug Targets. 2011;12(1):19-28.
37. Holmes E. Two new vitamin D blood tests are often highly inaccurate. Endocrine Society. www.sciencedaily.com/releases/2012/06/120625152310.htm. Published 2012. Accessed September 16, 2020.
38. Lucas R, Neale R. What is the optimal level of vitamin D? Aust Fam Physician. 2014;43(3):119-122.
39. Vidal M, Thibodaux RJ, Neira LFV, Messina OD. Osteoporosis: a clinical and pharmacological update. Clin Rheumatol. 2019;38(2):385-395. doi:10.1007/s10067-018-4370-1
40. Reid IR, Bolland MJ, Grey A. Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis. Lancet. 2014;383(9912):146-155. doi:10.1016/S0140-6736(13)61647-5
41. Tai V, Leung W, Grey A, Reid IR, Bolland MJ. Calcium intake and bone mineral density: systematic review and meta-analysis. BMJ. 2015;351. doi:10.1136/bmj.h4183
42. Yao P, Bennett D, Mafham M, et al. Vitamin D and Calcium for the Prevention of Fracture. JAMA Netw Open. 2019;2(12):e1917789. doi:10.1001/jamanetworkopen.2019.17789
43. Bolland MJ, Grey A, Avenell A. Effects of vitamin D supplementation on musculoskeletal health: a systematic review, meta-analysis, and trial sequential analysis. Lancet Diabetes Endocrinol. 2018;6(11):847-858. doi:10.1016/S2213-8587(18)30265-1
44. Zhao J-G, Zeng X-T, Wang J, Liu L. Association Between Calcium or Vitamin D Supplementation and Fracture Incidence in Community-Dwelling Older Adults. JAMA. 2017;318(24):2466. doi:10.1001/jama.2017.19344
45. Chakhtoura M, Chamoun N, Rahme M, Fuleihan GE-H. Impact of vitamin D supplementation on falls and fractures—A critical appraisal of the quality of the evidence and an overview of the available guidelines. Bone. 2020;131:115112. doi:10.1016/j.bone.2019.115112
46. Mateussi MV, Latorraca C de OC, Daou JP, et al. What do Cochrane systematic reviews say about interventions for vitamin D supplementation? Sao Paulo Med J. 2017;135(5):497-507. doi:10.1590/1516-3180.2017.0230150817
47. Burt LA, Billington EO, Rose MS, Kremer R, Hanley DA, Boyd SK. Adverse Effects of High‐Dose Vitamin D Supplementation on Volumetric Bone Density Are Greater in Females than Males. J Bone Miner Res. September 2020. doi:10.1002/jbmr.4152