Two recent papers have recommended that public health recommendations regarding sun avoidance be changed to encourage greater sun exposure. The authors of one paper argue that the health benefits of adequate sun exposure – distinct from vitamin D supplementation – outweigh the risks of skin cancers, and that insufficient sun exposure has become a major public health problem (Hoel et al. Dermatoendocrinol 2016;8:e1248325).

In the second paper, Canadian researchers recommend public health promotion of safe sun exposure, use of vitamin D supplements and vitamin D-fortified foods (Grant et al. Dermato-Endocrinology 2016;8:e1248324). Low vitamin D levels have been linked to numerous diseases, including cancers, cardiovascular disease, and neurological diseases. They authors estimate that increasing serum vitamin D concentrations in the Canadian population would reduce annual premature deaths by 23,000, and lower the economic burden of disease by $12.5 billion per year.

In the Canadian Health Measures survey, 6% of the population had severe vitamin D deficiency, defined as serum 25(OH)D levels < 30 nmol/L [<12 ng/mL]; that number increased to 15% during the winter months (Statistics Canada; chart available at www.statcan.gc.ca/pub/82-624-x/2013001/article/chart/11727-01-chart3-eng.htm). A high proportion (25% in summer; 40% in winter) had vitamin D insufficiency, defined as serum 25(OH)D levels < 50 nmol/L [<20 ng/mL]. Similar prevalences of vitamin D deficiency (8%) and insufficiency (32%) have been reported in the U.S. (Looker et al. NCHS Data Brief, No. 59, March 2011). These definitions of vitamin D status may underrepresent the problem: many groups now define vitamin D insufficiency as < 75 nmol/L [30 ng/mL], with 100-150 nmol/L [40–60 ng/mL] recommended for optimal health (Holick et al. J Clin Endocrinol Metab 2011;96:1911-1930).

Sun avoidance and the use of sun blocks have long been advocated due to the risk of melanoma. Commercial sunscreens were first marketed in 1928 (Shaath NA. In Lowe & Shaath. New York: Dekker, 1990). However, Hoel and colleagues note that chronic non-burning sun exposure is associated with minimal risk of melanoma; melanocytes are normally indolent cells that only replicate following damage due to sunburn (Hoel 2016). Moreover, chronic non-burning sun exposure has been shown to be associated with a decreased risk of melanoma (Gandini et al. Eur J Cancer 2005;41:45-60). This effect has been attributed to increased serum levels of 25(OH)D, which are associated with enhanced DNA repair mechanisms (Gordon-Thomson et al. Adv Exp Med Biol 2014; 810:303-328).

Inadequate sun exposure is increasingly recognized as an important health risk. A meta-analysis of randomized controlled trials and cohort studies (n=880,000) reported that the relative risk of all-cause mortality was 1.35 for individuals in the bottom tertile of serum 25(OH)D levels (Chowdhury et al. Br Med J 2014;348:g1903). Other meta-analyses have reported risk ratios of 1.6 and 1.9 for the lowest versus highest serum vitamin D levels (Schottker et al. Br Med J 2014; 348:g3656; Garland et al. Am J Pub Health 2014;104:e43-50). A recent 20-year cohort study of Swedish women found that the health risk associated with low sun exposure was similar to that of smoking, a finding that the group described as “novel”; life expectancy was reduced 0.6 to 2.1 years in sun avoiders (Lindqvist et al. J Intern Med 2016;280:375-387).

Sun avoidance has also been associated with a range of neurological and psychiatric conditions. Perhaps the most studied is multiple sclerosis.  Low sun exposure has been linked to an increased risk of MS, both in epidemiological studies of the latitude effect, and in studies of patient self-reported sun exposure. Low serum 25(OH)D levels, which are considered to be equivalent to low sun exposure, are associated with an increased risk of conversion from clinically isolated syndrome to clinically-definite MS (Martinelli et al. Mult Scler 2014;20:147-155); increased disease activity and more rapid progression (Ascherio et al. JAMA Neurol 2014;71:306-314); and increased disability (Thouvenot et al. Eur J Neurol 2015;22:564-569).

That said, randomized, controlled studies of vitamin D supplementation have generally produced disappointing results in MS (Kampman et al. Mult Scler 2012;18:1144-1151; Stein et al. Neurology 2011;77:1611-1618). The best evidence is for vitamin D add-on therapy in patients treated with interferon-beta, which has been shown to reduce MRI disease activity (Loken-Amsrud et al. Neurology 2012;79:267-273; Soilu-Hanninen et al. J Neurol Neurosurg Psychiatry 2012;83:565-571; Smolders et al. ECTRIMS 2016; abstract 166).

One possible explanation for the modest benefits of vitamin D supplementation is that vitamin D and sun exposure exert different effects on MS pathophysiology. Indeed, it has been suggested that the benefits of sun exposure occur in part through non-vitamin D-mediated pathways (reviewed in Lucas et al. Neurodegener Dis Manag 2015;5:413-424; free full text at www.futuremedicine.com/doi/pdf/10.2217/nmt.15.33).  For example, vitamin D deficiency has been shown to prevent the development of experimental autoimmune encephalomyelitis (EAE), and vitamin D receptor knock-out mice do not develop EAE (reviewed in DeLuca & Plum. Photochem Photobiol Sci 2016; epublished December 2, 2016). In addition, an Australian case-control study found that sun exposure and vitamin D status were independent risk factors for CNS demyelination (Lucas et al. Neurology 2011;76:540-548). Recent data suggest that the reduction in demyelination with sun exposure may be mediated in part by B cells; ultraviolet light exposure was shown not to be protective in B cell-depleted EAE mice (Kok et al. J Autoimmun 2016;73:10-23). One possible implication is that the benefits of sun exposure/vitamin D may be mitigated by B cell-depleting therapies.

In Alzheimer’s disease, a large, prospective study of adults aged >65 years with serum 25(OH)D levels < 10 ng/mL had an increased risk of developing Alzheimer’s disease (HR 2.2) compared to those with serum levels >20 ng/mL over a six-year follow-up period (Littlejohns et al. Neurology 2014;83:920-928). In addition, numerous studies have linked low serum vitamin D levels with cognitive decline (Annweiler et al. J Alzheimers Dis 2013;37:147-171; Balion et al. Neurology 2012;79:1397-1405; Slinen et al. J Gerontol A Biol Sci Med Sci 2012;67:1092-1098; Llewellyn et al. J Gerontol A Biol Sci Med Sci 2011;66:59-65).

It has been suggested that sun exposure can affect brain serotonin levels (Lambert et al. Lancet 2002;360:1840-1842), which may have implications for a range of psychiatric disorders. Light therapy has long been used for seasonal affective disorder (Lam et al. J Affect Disord 1992;24:237-243), but few studies of the possible benefits of increased sun exposure have been conducted in other mood disorders.

Trials of high-dose vitamin D supplementation have generally reported no benefit with respect to depression prophylaxis, depressive symptoms or mental well-being (Kjaergaard et al. Br J Psychiatry 2012;201:360-368; (Sanders et al. Br J Psychiatry 2011;198:357-364). One study reported a benefit with vitamin D add-on therapy in patients with major depressive disorder treated with fluoxetine (Khoraminya et al. Aust N Z J Psychiatry 2013;47:271-275). A recent publication found that vitamin D add-on therapy improved evening symptoms of attention deficit-hyperactivity disorder in patients receiving methylphenidate (Mohammadpour et al. Nutr Neurosci 2016; epublished December 7, 2016).

Vitamin D insufficiency has been proposed as an explanation for the excess of winter births in schizophrenia (Dealberto MJ. Med Hypotheses 2007;68:259-267). Bioavailable serum vitamin D levels have been reported to be lower in subjects with first-episode psychosis; lower vitamin D levels have been linked to negative symptoms in schizophrenia (Yee et al. Psychiatry Res 2016;243:390-394). A separate study has also reported that serum 25(OH)D levels are lower in patients with schizophrenia during an acute episode compared to patients in remission or healthy controls (Yuksel et al. Ther Adv Psychopharmacol 2014;4:268-275). However, this finding requires validation from larger studies.