Should vitamin D supplements be recommended to prevent chronic diseases?BMJ 2015; 350 doi: https://doi.org/10.1136/bmj.h321 (Published 29 January 2015) Cite this as: BMJ 2015;350:h321
All rapid responses
I have a special interest - I am ancient, and suffer from Eczema of recent onset.
1.Could the authors, or indeed anyone else, please explain the mechanism through which “Vitamin D,” helps in any of the chronic diseases other than those of bone metabolism?
2. It is lost in the mists of time, but I seem to recall thst Vit A and Vit D were reportedly antagonistic.
Is it now considered to be false? And if it is true, how does the human body cope with it?
3. Given that the melanin concentration of the Caucasian population of Norway, and the Eskimo population of the same country evolved separately, with perhaps differing mechanisms of vitamin absorption and vitamin D production in the skin, are there different ways in which these people cope with the same poor level of ultraviolet light?
Dr JK Anand
Competing interests: Please see the text
Vitamin D deficiency-An epidemic ignored unfortunately. Re: Should vitamin D supplements be recommended to prevent chronic diseases?
Historically, vitamin D has been shown to be associated with the regulation of bone metabolism and related musculo-skeletal disorders, However, the insightful opinion of the author that currently vitamin D has gained much attention in research and clinical practice as a possible preventive factor for a wide array of chronic diseases , has been applauded by several physicians and researchers worldwide. Vitamin D deficiency is now recognised as an epidemic in the United States .
A circulating level of 25-hydroxyvitamin D of >75 nmol/L, or 30 ng/mL, is required to maximise vitamin D's beneficial effects for health while in the absence of adequate sun exposure, at least 800-1000 IU vitamin D3/d may be needed to achieve this in children and adults .
In recent years several clinical research studies demonstrated the significance of vitamin D deficiency in various disorders including neuropathy , malignancy , infertility , cardiovascular diseases [6, ], kidney diseases , glucose metabolism , and immunological dysfunctions .
Moreover, in vitro studies showed that vitamin D inhibits pro-inflammatory activity of CD4+ Th1 cells and their production of cytokines such as IL-2, interferon (IFN)-γ, and tumor necrosis factor-α . 1,25(OH)2D exerts an inhibitory effect on T cell proliferation, the expression of IL-2  and IFN-γ mRNA and protein in T cells .
In addition, vitamin D receptor regulates transcription factors in immune cell lineages, including Th1, Th17, Th2, regulatory T, and natural killer T cells; and (13) the prevalence of vitamin D insufficiency/deficiency in patients with multiple sclerosis, type 1 diabetes mellitus, and systemic lupus erythematosus.
Low level of Vitamin D is now thought to be a risk factor for psychosis [8, 9]. There are systematic review and meta-analysis which are indicative of an association between depression and low Vitamin D levels. 
Conclusion: The major cause of vitamin D deficiency is the lack of appreciation that sun exposure in moderation is the major source of vitamin D. Deliberate avoidance of sun exposure is currently a common practice in Jamaica to prevent darker skin pigmentation. Nowadays many schools are no longer promoting outdoor physical education, while most vehicles have tinted window screens to avoid sunlight. If 'bleachers' are taken into account, vitamin D deficiency may reveal its serious impact on immunity, mental health, cancer incidence, arthritic incidences, hormone levels, etc.
In this connection, it is important to mention that we are disappointed because instead of emphasising that large scale studies are urgently needed to substantiate the role of vitamin-D in various extra-skeletal chronic diseases including cancers, the authors unfortunately chose to emphasise the absence of adequate evidence in support of supplementation of vitamin-D for preventing chronic diseases . Absence of sufficient evidence should not be used to misguide the general public and thus we should not ignore the alarm raised about the epidemic of vitamin-D deficiency .
1. Meyer HE, Holvik K, Lips P. Should Vitamin D Supplements be Recommended to Prevent Chronic Diseases? BMJ 2015; 350: h321.
2. Holick MF1, Chen TC. Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008 Apr;87 (4):1080S-6S
3. Agmon-Levin N, Kivity S, Tzioufas AG, et al. Low levels of vitamin-D are associated with neuropathy and lymphoma among patients with Sjogren’s syndrome. J Autoimmun. 2012;39:234–239. [PubMed]
4. Giovannucci E. Vitamin D and cancer incidence in the Harvard cohorts. Ann Epidemiol. 2009;19:84–88. [PubMed]
5. Twig G, Shina A, Amital H, Shoenfeld Y. Pathogenesis of infertility and recurrent pregnancy loss in thyroid autoimmunity. J Autoimmun. 2012;38:J275–J281. [PubMed]
6. Anderson JL, May HT, Horne BD, et al. Relation of vitamin D deficiency to cardiovascular risk factors, disease status, and incident events in a general healthcare population. Am J Cardiol. 2010;106:963–968. [PubMed]
7. Qazi RA, Martin KJ. Vitamin D in kidney disease: pathophysiology and the utility of treatment. Rheum Dis Clin N Am. 2012;38:115–123. [PubMed]
8. Pittas AG, Dawson-Hughes B. Vitamin D and diabetes. J Steroid Biochem Mol Biol. 2010;121:425–429. [PMC free article] [PubMed]
9. Cantorna MT, Mahon BD. D-hormone and the immune system. J Rheumatol Suppl. 2005;76:11–20. [PubMed]
10. Alroy I, Towers TL, Freedman LP. Transcriptional repression of the interleukin-2 gene by vitamin D3: direct inhibition of NFATp/AP-1 complex formation by a nuclear hormone receptor. Mol Cell Biol. 1995;15:5789–5799. [PMC free article] [PubMed]
11. Rigby WF, Stacy T, Fanger MW. Inhibition of T lymphocyte mitogenesis by 1,25-dihydroxyvitamin D3 (calcitriol) J Clin Invest. 1984;74:1451–1455. [PMC free article] [PubMed]
12. Reichel H, Koeffler HP, Tobler A, Norman AW. 1 alpha,25-Dihydroxyvitamin D3 inhibits gamma-interferon synthesis by normal human peripheral blood lymphocytes. Proc Natl Acad Sci U S A. 1987;84:3385–3389. [PMC free article] [PubMed]
13. Boonstra A, Barrat FJ, Crain C, Heath VL, Savelkoul HF, O’Garra A. 1Alpha,25-dihydroxyvitamin d3 has a direct effect on naive CD4(+) T cells to enhance the development of Th2 cells. J Immunol. 2001;167:4974–4980. [PubMed]
14. Anglin RES, Samaan Z, Walter SD, McDonald SD. Vitamin D Deficiency and Depression in Adults: Systematic Review and Meta-analysis. British Journal of Psychiatry 2013; 202(2): 100-107.
Competing interests: No competing interests
We agree with dr. Adamidou and dr. Udo that mental illnesses constitute a very important group of diseases and that there are indications that vitamin D might play a protective role. However, in line with the conclusion regarding other types of chronic diseases reported in our review, there is currently no clear evidence for recommending vitamin D supplementation to prevent these diseases.
This is not to say that vitamin D should be ignored, and prevention and treatment of vitamin D deficiency is of importance in these patients as in the rest of the population.
Competing interests: No competing interests
Severe, enduring mental illnesses are also chronic diseases. In Meyer HE et al’s paper, they have considered evidence in reaching the recommendation that vitamin D supplementation is not recommended for the prevention of chronic disease.  This evidence pertained to cancer, cardiovascular diseases, myocardial infarction, cerebrovascular disorder, fractures, respiratory tract diseases, diabetes mellitus, and multiple sclerosis. However, evidence for the role of vitamin D in mental illness does exist but was not considered by this paper. These mental health conditions such as depression may be comorbid with the considered conditions  and are associated with poorer prognoses.  Consideration or acknowledgment of these may have conveyed the full ramifications and implications of Vitamin D deficiency and possibly affected their recommendations.
The World Health Organisation estimates that by 2020, mental illness, in particular depression would outstrip most other chronic diseases to become the second leading cause of Disability Adjusted Life Years (DALYs) lost. “Worldwide it will be second only to ischaemic heart disease for DALYs lost for both sexes. In the developed regions, depression will then be the highest ranking cause of burden of disease.”  Approximately 25% of prevalent depression is thought to be chronic in nature.  In the 2000 Global Burden of Disease study, Schizophrenia accounted for 1.1% of the total DALYs and 2.8% of Years Lived with Disability (YLDs).  Hence any associations of Vitamin D with mental disorders, where existent needs to be factored into public health recommendations.
Anglin et al’s systematic review and meta-analysis was indicative of an association between depression and low Vitamin D levels.  However, supplementation with Vitamin D did not significantly improve depression [6, 7]; but these studies had low numbers of participants. Low level of Vitamin D is now thought to be a risk factor for psychosis [8, 9].
We appreciate that limited resources ought to be well managed. However, we were disappointed that instead of stressing that bigger studies are urgently needed to clarify these associations, the authors chose to emphasize the absence of evidence for supplementation. Absence of evidence does not necessarily mean the non-existence of causality or association.
1. Meyer HE, Holvik K, Lips P. Should Vitamin D Supplements be Recommended to Prevent Chronic Diseases? BMJ 2015;350: h321.
2. Moussavi S, Chatterji S, Verdes E, Tandon A, Patel V, Ustun B. Depression, Chronic Diseases, and Decrements in Health: Results from the World Health Surveys. The Lancet 2007;370(9590): 851-858.
3. Wells KB, Stewart A, Hays RD, Burnam MA, Rogers W, Daniels M, Berry S, Greenfield S, Ware J. The Functioning and Well-being of Depressed Patients. Results from the Medical Outcomes Study. JAMA. 1989;262(7): 914-919.
4. World Health Organisation. The World Health Report 2001 Mental Health: New Understanding, New Hope. Geneva: World Health Organisation; 2001.
5. Rubio, JM, Markowitz JC, Alegría A, Pérez-Fuentes G, Liu S-M, Lin K-H, Blanco C. Epidemiology of Chronic and Nonchronic Major Depressive Disorder: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Depression and Anxiety 2011;28: 622–631. doi: 10.1002/da.20864. (accessed 25 July 2015).
6. Murray CJL, Lopez AD, eds. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability from Diseases, Injuries and Risk Factors in 1990 and Projected to 2020. Cambridge, Massachussets: Harvard School of Public Health on behalf of the World Health Organization and the World Bank; 1996.
7. Anglin RES, Samaan Z, Walter SD, McDonald SD. Vitamin D Deficiency and Depression in Adults: Systematic Review and Meta-analysis. British Journal of Psychiatry 2013;202(2): 100-107.
8. Kjærgaard M, Waterloo K, Wang CEA, Almås B, Figenschau Y, Hutchinson MS, Svartberg J, Jorde R. Effect of Vitamin D Supplement on Depression Scores in People with Low Levels of Serum 25-Hydroxyvitamin D: Nested Case–control Study and Randomised Clinical Trial. British Journal of Psychiatry 2012;201(5): 360-368.
9. Sanders KM, Stuart AL, Williamson EJ, Jacka FN, Dodd S, Nicholson G, Berk M. Annual High-dose Vitamin D3 and Mental Well-being: Randomised Controlled Trial. British Journal of Psychiatry 2011; 198(5): 357-364.
10. Cieslak K, Feingold J, Antonius D, Walsh-Messinger J, Dracxler R, Rosendale M, Aujero N, Keefe D, Goetz D, Goetz R, Malaspina D. Low Vitamin D Levels Predict Clinical Features of Schizophrenia. Schizophrenia Research 2014;59: 543-545.
11. Crews M, Lally J, Gardner-Sood P, Howes O, Bonaccorso S, Smith S, Murray RM, Forti MD, Gaughran F. Vitamin D Deficiency in First Episode Psychosis: A Case-control Study. Schizophrenia Research 2013;150: 533-537.
Competing interests: No competing interests
As pointed out by Meyer et al (1) people with the lowest 25(OH)D values (below 50 nmol/l) might have the most to gain by increasing concentrations in respect to total mortality and disease outcomes such as cardio-vascular disease and cancer. This concerns the people who live in Scotland: their serum average 25(OH)D concentration is 37 nmol/l and in half of the people in the lowest social class this level is below 25 nmol/l. (2)
Could the devolved Scottish health department please listen?
1. Meyer H.E, Holvic K, Lips P. Uncertainties: Should vitamin D supplements be recommended to prevent chronic diseases? BMJ 2015;350:h321
2. Food Standards Agency in Scotland. Vitamin D status of Scottish adults: Results from the 2010 & 2011 Scottish Health Surveys . Purdon G, Comrie F, Rutherford L, Marcinkiewicz A. September 2013
Competing interests: No competing interests
We highly appreciate the response provided by Professor Meyer et al to our previous comment (1). However, in our opinion this new explanation doesn’t focus on the most relevant issue: is there good-quality evidence that vitamin D plus calcium reduce sound outcomes for the general elderly population?
Among the several references cited by the authors on nutritional recommendations, 2011 IOM guideline is probably the most significant (2). Its recommendation (600-800 IU of vitamin D) is based mainly on bone health criteria, a concept that comes from the 2007 Evidence Report on vitamin D published by the American Agency for Healthcare Research and Quality. In the conclusion of this report (3) it can be read that “There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). However, the evidence for an association was inconsistent for other outcomes (e.g., BMC in infants and fractures in adults)”. Therefore, even if the recommendation of vitamin D supplements was carefully followed, a decrease in overall fractures cannot be taken for granted (and especially if we consider the outcomes on the main target, that is, hip fractures).
On the other hand, “a modestly decreased risk of all-cause mortality (from 11.4% to 11.0%; RR 0.94, 95% CI 0.91-0.98)” is claimed based on the Bjelakovic et al Cochrane review (4). However, we should not miss out the authors’ remarks on the quality of evidence of this statement: “We found evidence suggesting that vitamin D3 may significantly benefit survival of elderly ambulatory participants living in institutional care who were likely to be vitamin D deficient with significant risk of falls and fractures, when we disregard the risks of attrition bias and outcome reporting bias. However, if these bias risks are considered, we do not yet know whether vitamin D3 affects mortality”.
Thus, according to the above-mentioned considerations, we maintain our suggestion of thinking twice before recommending a vitamin D plus calcium supplement to healthy people.
(2) Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab2011;96:53-8.
(3) Cranney A, Horsley T, O'Donnell S, Weiler H, Puil L, Ooi D, et al. 2007 Effectiveness and safety of vitamin D in relation to bone health. Evidence Report/Technology Assessment no. 158 (prepared by the University of Ottawa Evidence-based Practice Center. AHRQ Publication no. 07-E013. Rockville, MD: Agency for Healthcare Research and Quality.
(4) Bjelakovic G, Gluud LL, Nikolova D, Whitfield K, Wetterslev J, Simonetti RG, et al. Vitamin D supplementation for prevention of mortality in adults. Cochrane Database Syst Rev 2014;1:CD007470.
Competing interests: No competing interests
We welcome the response from Dr. Grant et al to our paper (04 February 2015). They argue that new trials should include persons with low initial 25-hydroxyvitamin D (25(OH)D) concentrations. This is in line with our recommendations for further research (see box in article). The lower initial 25(OH)D concentration, the more potential benefit would be expected, and trials predominantly including persons with higher 25(OH)D could fail to demonstrate an effect. Under these circumstances we assume that they also would agree that smaller increases in 25(OH)D concentrations have beneficial health potentials even if their proposed target of 75 nmol/l is not reached. Although 75 nmol/l has been recommended as a target level by the Endocrine Society task force, the evidence is not clear as discussed by the Institute of Medicine and others who advocate a target of 50 nmol/l. As noted in our article, this discussion is also complicated by the large variations between laboratories in the determination of 25(OH)D. For example, in a Swedish study, the mean concentration of 25(OH)D varied between 85 nmol/l, 70 nmol/l and 60 nmol/l when identical samples from 204 individual were analysed at three different laboratories. This implies that at worst, 75 nmol/l in one laboratory could correspond to 50 nmol/l in another. Even though there are current efforts to improve standardisation between laboratories, this is a major limitation when interpreting 25(OH)D concentration in the literature.
Grant el al also point to a large body of evidence supporting that chronic disease risk can be reduced by higher 25(OH)D. We are well aware of this literature, and it is both biologically plausible and supported by observational studies that vitamin D might help prevent some chronic diseases. However, the question posed in our review is whether vitamin D supplements should be recommended to prevent chronic diseases, and our major message is that such an intervention has not been proven effective thus far, since evidence from clinical trials is lacking. In a situation of widespread use of high dose vitamin D supplementation, potential harms by high intakes should not be ignored, as emphasised by Dr. Schwarz in his response to our manuscript (08 February 2015). In this respect, 75 nmol/l would not pose a safety issue in individuals, but if this is a general minimum target concentration in a population, many individuals would potentially reach much higher concentrations, which often will stay undetected, as a close monitoring would be very resource consuming and unrealistic in most settings.
We agree with Dr. Saiz et al (05 February 2015) that most benefit of vitamin D plus calcium supplements would be expected in high risk populations with poor vitamin D status and low calcium intake. However, the recommendation of vitamin D supplements in doses of 600-800 IU (15-20 µg) per day combined with calcium (0-1000 mg/day, depending on current dairy intake) is in accordance with nutritional recommendations in the general elderly population. As outlined, it has also been related to a modestly decreased risk of all-cause mortality.
1. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2011; 96:1911-30.
2. Rosen CJ, Abrams SA, Aloia JF, Brannon PM, Clinton SK, Durazo-Arvizu RA, et al. IOM committee members respond to Endocrine Society vitamin D guideline. J Clin Endocrinol Metab 2012; 97:1146-52.
3. Bouillon R, Van Schoor NM, Gielen E, Boonen S, Mathieu C, Vanderschueren D, et al. Optimal vitamin D status: a critical analysis on the basis of evidence-based medicine. J Clin Endocrinol Metab 2013;98(8):E1283-304.
4. Snellman G, Melhus H, Gedeborg R, Byberg L, Berglund L, Wernroth L, et al. Determining vitamin D status: a comparison between commercially available assays. PloS One 2010;5:e11555
Competing interests: HEM and PL have none. KH received payment for performing independent food safety assessments concerning vitamin D as a member of the Norwegian Scientific Committee for Food Safety’s panel on nutrition, dietetic products, novel food and allergy. She also received an honorarium from Renapharma for a lecture in an educational symposium for general practitioners in November 2012. The funding company had no influence on the content of the lecture.
Professor Meyer state that we need a balanced view on vitamin D, with not too little and not too much and because clear evidence of benefit over harm for vitamin D has not been proved, we should not recommend
vitamin D supplements for prevention of chronic diseases (such
as cardiovascular disease, cancer, chronic obstructive lung
disease, or diabetes) until more definitive further research
evidence is available. I do agree in full. However, our knowledge about potential harms if we recommend to much vitamin D are increasing. The CopD-study (1) and the recalculations on the NHANES data (2)confirm the potential harm i.e. increased mortality for 25(OH)D3 >100 nmol/L.
I do agree, vitamin D deficiency (25(OH)D3 <30 nmol/L) should of course be treated to prevent skeletal complications, falls and fractures.
1. Durup D, Jorgensen HL, Christensen J, Schwarz P, Heegaard AM, Lind B. A reverse J-shaped association of all-cause mortality with serum 25-hydroxyvitamin D in general practice: the CopD study. J Clin Endocrinol Metab 2012;97:2644-2652.
2. Sempos CT, Durazo-Arvizu RA, Dawson-Hughes B et al. Is there a reverse J-shaped association between 25-hydroxyvitamin D and all-cause mortality? Results from the U.S. nationally representative NHANES. J Clin Endocrinol Metab 2013;98:3001-3009.
Competing interests: No competing interests
Dr. Haakon E. Meyer and colleagues state firmly in their article that “vitamin D supplementation (…) combined with calcium may be recommended to prevent fractures in elderly people, according to evidence from a Cochrane review and updated nutritional recommendations for vitamin D intake in the general population” (1). However, in our opinion benefits and harms of combined supplements for an overall community-dwelling people are not so clearly in favour of pharmacological treatment.
This is because the main outcome to have in mind should not be a decrease in non-vertebral fractures or any type of fracture, as the invoked Cochrane review claims (2) (DIPART study (3) was later included in this review). Instead, hip fracture should be underlined as the most relevant endpoint in terms of morbi-mortality and population quality of life (4). Taking this into account, even if a small reduction in hip fracture risk has been shown in the overall population with calcium and vitamin D combination, it must be recognised that most of benefits were due to the results in the high-risk population subgroup (9 fewer hip fractures per 100 older adults-year (95% CI, 2 to 14) (2). Thus, high-risk population could be expected to benefit from vitamin D plus calcium supplements to some extent, in terms of fewer hip fractures, while the risk-benefit ratio in healthy low-risk population is uncertain and overtreatment might occur. We all need to be aware of these data in order to properly address drug therapy to the right target.
1. Meyer HE, Holvik K, Lips P. Should vitamin D supplements be recommended to prevent chronic diseases? BMJ 2015;350:h321.
2. Avenell A, Mak JCS, O’Connell D. Vitamin D and vitamin D analogues for preventing fractures in post-menopausal women and older men. Cochrane Database of Systematic Reviews 2014, Issue 4. Art. No.: CD000227. DOI:10.1002/14651858.CD000227.pub4.
3. DIPART (Vitamin D Individual Patient Analysis of Randomized Trials) Group. Patient level pooled analysis of 68 500 patients from seven major vitamin D fracture trials in US and Europe. BMJ 2010;340:b5463.
4. National Clinical Guideline Centre, (2011) [The Management of Hip Fracture in Adults]. London: National Clinical Guideline Centre. Available from: www.ncgc.ac.uk
Competing interests: No competing interests
Vitamin D supplements and reasonable solar UVB should be recommended to prevent escalating incidence of chronic diseases
There is strong evidence from observational studies that 25-hydroxyvitamin D [25(OH)D] concentrations above 75 nmol/L (30 ng/mL) are associated with better outcomes for chronic diseases [1-3]. In addition, for African-Americans, there is evidence that the poor survival rates after diagnosis of cancer in this community is linked to lower 25(OH)D concentrations independent of socioeconomic status, stage at diagnosis and treatment .
Unfortunately, most vitamin D randomized controlled trials (RCTs) conducted to date, as well as the major ones currently underway that are listed in Meyer et al , have not been designed to answer the question of the relationship of serum25(OH)D to intended health outcomes. Therefore, if studies are not conducted in vitamin D deficient or insufficient populations, one would not expect a positive outcome .
In fact, most published vitamin D RCTs were based on the guidelines for pharmaceutical agents, assuming that the trial agent is the only source of intervention and there is a linear dose-response relation; however, this is not the case. Neither assumption is satisfied for vitamin D. Heaney recently outline guidelines that are applicable for RCTs designed to assess the impact of nutrient supplementation . The main steps for conducting vitamin D RCTs should include, (A) start with an understanding of the 25(OH)D concentration-health outcome relation; (B) measure 25(OH)D concentrations prior to the clinical study in all prospective participants and only include those with concentrations below the optimal threshold; (C) supplement with adequate vitamin D3 to raise (and titrate) serum 25(OH)D concentrations to near the upper end of the expected relation; (D) measure 25(OH)D concentrations following enrollment to the trial to assure the right serum concentrations have been achieved; and (E) optimize co-nutrients in all participants.
In this regard, we refer to the recent paper by Meyer and colleagues who concluded that vitamin D supplementation for preventing chronic diseases is not recommended due to ‘lack’ of supporting evidence . However, their paper overlooked a large body of evidence that supports higher 25(OH)D concentrations in reducing risk of chronic diseases [7, 8]. There are only three ways that 25(OH)D concentrations can be raised: by UVB exposure, diet, and supplements. This commentary intended to presents some of that missing and important evidence that supports why supplementing with vitamin D is imperative in reducing the escalating incidence of chronic disease, worldwide.
First, inflammation is a risk factor for many types of chronic disease  and adequate levels of vitamin D have the potential to reduce inflammation . A meta-analysis of vitamin D RCTs found that those studies using vitamin D3 in subjects with mean baseline 25(OH)D concentrations below 48 nmol/L had a 49% chance of finding reduced biomarkers of inflammation but only 27% of those with higher 25(OH)D concentrations did . Raising 25(OH)D concentrations to the range 35-82 nmol/L resulted in 55% beneficial reduction in inflammation. This study and many other studies, support a value of 75 nmol/L as more protective against chronic disease than 50 nmol/L.
Another approach is to use sensible and adequate exposure to solar UVB radiation to improve the human’s well-being. There are many new findings in the recent literature supporting exposure to solar UVB radiation B reducing risk for many chronic diseases including multiple sclerosis, type 1 diabetes and many types of cancer . Moreover, solar UVB, UVA and visible light exposure has beneficial effects independent of vitamin D production [13-15].
A mouse model of UVB exposure found that UVB exposure raising 25(OH)D concentrations the same amount as oral vitamin D intake decreased the progression of intestinal tumors more than oral vitamin D . This finding could further explain why geographical and ecological studies reporting strong evidence of inverse correlation of solar UVB doses with the incidence and mortality rates of many types of cancers . In addition, outdoor occupation has been shown to inversely correlate with incidence rates of many types of cancer in Nordic countries .
There are many other benefits of appropriate exposure to solar and artificial UVB and UVA, including lowering blood pressure, increasing beta endorphin concentrations, improving wound healing and many other benefits . However, incidental short exposures are inadequate to generate appreciable amounts of vitamin D in the skin, especially during non-summer months. A study found an increased risk of MS for young people who spent less time in the sun in summer in Norway and during the wintertime in Italy . Another study in Sweden found that those who avoided sun exposure had significantly higher all-cause mortality rates .
It should be noted that the understanding of the mechanisms whereby solar UVB exposure reduces risk of chronic diseases independent of vitamin D production is limited at present . In addition, some people are concerned about the risk of skin cancer and melanoma from UV exposure, but data suggest that sun-exposure is only applicable and specific to squamous cell carcinoma of the skin . In fact most melanomas occur on the least sun exposed areas, and occupational sun exposure in fact, reduces risk for this deadly skin cancer .
It is well documented not only in the United States but worldwide that it is not possible to obtain even the minimum 600 IUs daily of vitamin D that is recommended by the Institute of Medicine for most children and adults from dietary sources.
Thus, without adequate sun exposure most of the world population is vitamin D deficient. The only way to guarantee sufficiency is to recommend a three-part strategy to improve everyone’s vitamin D status. This includes (A): Encouraging consuming more foods that naturally contain vitamin D including oily fish such as salmon and foods fortified with vitamin D. There needs to be an evaluation by health regulatory agencies for regulations to promote vitamin D fortification of local foods. (B): The World Health Organization and local health regulatory agencies should provide guidelines for sensible sun exposure which would improve the world’s vitamin D status while minimizing risk for skin cancer. And (C): Because vitamin D deficiency is pandemic all children and adults who were unable to obtain adequate vitamin D from dietary, food fortification, and solar sources should be encouraged to take a vitamin D supplement to satisfy their vitamin D requirement.
Based on the evidence to date from ecological and observational studies and RCTs, serum 25(OH)D concentrations should be above 75 nmol/L (30 ng/mL) for optimal health through a combination of UVB exposure, diet, and supplements. Available results to date support that this would cost-effectively decrease the escalating incidences of chronic non-communicable disease worldwide.
Disclosure and conflicts of interests:
WBG receives funding from Bio-Tech Pharmacal (Fayetteville, AR),MediSun Technology (Highland Park, IL), and the Vitamin D Council (San Luis Obispo, CA). MFH and SJW have no conflicts of interests.
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Competing interests: WBG receives funding from Bio-Tech Pharmacal (Fayetteville, AR),MediSun Technology (Highland Park, IL), and the Vitamin D Council (San Luis Obispo, CA). MFH and SJW have no conflicts of interests.