Growing scientific evidence suggests that lack of sunlight exposure, and consequently low levels of vitamin D, may increase susceptibility to a range of chronic and autoimmune diseases, including multiple sclerosis (MS), Crohn’s disease, systemic lupus erythematosus (lupus), rheumatoid arthritis, as well as certain cancers such as leukaemia and colorectal cancer. While sunlight has historically been viewed primarily in relation to bone health, modern genomic and epidemiological research highlights its broader implications for immune regulation, gene expression and long-term disease risk.
This article examines the scientific basis linking lack of sun exposure to chronic illness, drawing upon textbooks, peer-reviewed journal articles and reputable public health organisations, using the Harvard referencing system and British spelling.
1.0 Vitamin D: Production and Biological Function
Vitamin D is a fat-soluble secosteroid hormone synthesised in the skin following exposure to ultraviolet B (UVB) radiation from sunlight. Approximately 80–90 per cent of vitamin D is produced cutaneously, with the remainder obtained through diet (Holick, 2007). After synthesis, vitamin D undergoes conversion in the liver and kidneys to its biologically active form, 1,25-dihydroxyvitamin D, which binds to the vitamin D receptor (VDR) present in numerous tissues.
According to Holick (2007), vitamin D regulates calcium homeostasis, bone metabolism and immune modulation. However, recent genomic studies demonstrate that vitamin D influences far more than skeletal health.
2.0 Vitamin D and Gene Regulation
A landmark genomic study published in Genome Research demonstrated that vitamin D interacts directly with DNA at numerous sites, influencing the expression of over 200 genes, many implicated in immune and inflammatory pathways (Ramagopalan et al., 2010). Using high-throughput sequencing technologies, researchers identified vitamin D receptor binding sites across the human genome.
The study found that several genes associated with autoimmune conditions, including multiple sclerosis, Crohn’s disease and lupus, are regulated by vitamin D signalling (Ramagopalan et al., 2010). This supports the hypothesis that vitamin D plays a crucial role in immune tolerance and inflammatory control.
As Dr Andreas Heger from the MRC Functional Genomics Unit stated, vitamin D exerts a “wide-ranging influence” over health, affecting both innate and adaptive immunity.
3.0 Vitamin D Deficiency and Autoimmune Disease
Autoimmune diseases occur when the immune system mistakenly attacks healthy tissue. Vitamin D is known to regulate T-cell differentiation and cytokine production, mechanisms central to immune balance (Aranow, 2011).
3.1 Multiple Sclerosis (MS)
Multiple sclerosis is more prevalent in regions with lower sunlight exposure, particularly at higher latitudes. Epidemiological data demonstrate a strong inverse relationship between UV exposure and MS incidence (Ascherio et al., 2010). Vitamin D is thought to reduce inflammatory responses implicated in demyelination.
For example, individuals living in Northern Europe, where winter sunlight is limited, show higher MS prevalence compared with equatorial populations.
3.2 Crohn’s Disease
Crohn’s disease, a chronic inflammatory bowel disorder, has also been associated with vitamin D deficiency. Ananthakrishnan et al. (2013) reported that low vitamin D levels correlate with increased disease activity and higher relapse rates.
Vitamin D’s immunomodulatory properties may help regulate gut inflammation, suggesting that deficiency could exacerbate intestinal immune dysregulation.
3.3 Lupus and Rheumatoid Arthritis
Vitamin D deficiency has been observed in patients with systemic lupus erythematosus and rheumatoid arthritis. Aranow (2011) notes that inadequate vitamin D may contribute to immune hyperactivity and autoantibody production.
4.0 Vitamin D and Cancer Risk
Beyond autoimmune disorders, vitamin D deficiency has been linked to certain malignancies. Garland et al. (2006) proposed that adequate vitamin D levels reduce risk of colorectal cancer, potentially by regulating cell proliferation and apoptosis.
Similarly, observational studies have suggested associations between low vitamin D and increased risk of haematological cancers, including leukaemia, though causal pathways require further investigation.
Vitamin D influences genes involved in cell growth regulation and tumour suppression, providing biological plausibility for these associations (Ramagopalan et al., 2010).
5.0 Global Prevalence of Vitamin D Deficiency
It is estimated that approximately one billion people worldwide are vitamin D deficient (Holick, 2007). Causes include:
- Limited sun exposure
- Indoor lifestyles
- Use of sunscreen
- Darker skin pigmentation
- Obesity
- Poor dietary intake
The NHS (2023) advises that individuals in the UK are at particular risk during autumn and winter months when UVB radiation is insufficient for adequate synthesis.
6.0 Public Health Implications
Some countries have implemented routine supplementation policies, particularly for pregnant women and young children. France, for example, has incorporated vitamin D supplementation into maternal and infant health programmes (Ramagopalan et al., 2010).
The UK Government recommends vitamin D supplementation during winter months, particularly for:
- Pregnant and breastfeeding women
- Infants and young children
- Older adults
- Individuals with limited sun exposure
Adequate levels during pregnancy may influence immune development and potentially reduce future disease susceptibility.
7.0 Safe Sun Exposure and Alternative Sources
While sunlight is the primary source of vitamin D, excessive UV exposure increases skin cancer risk. Therefore, balanced and sensible sun exposure is essential.
Holick (2007) suggests that short periods (approximately 15–30 minutes) of midday sun exposure to arms and legs several times per week during summer may be sufficient for many individuals, depending on skin type and geographical location.
Dietary sources include:
- Oily fish (salmon, mackerel)
- Liver
- Egg yolks
- Fortified milk and cereals
- Butter
However, dietary intake alone is often insufficient to meet recommended levels.
8.0 Limitations and Ongoing Debate
Although strong associations exist between vitamin D deficiency and chronic illness, causality remains complex. Some researchers argue that low vitamin D may be a consequence rather than a cause of chronic disease (Autier et al., 2014). Randomised controlled trials have produced mixed results regarding supplementation and disease prevention.
Thus, while maintaining adequate vitamin D is important for overall health, supplementation should follow evidence-based guidelines rather than excessive dosing.
Emerging genomic and epidemiological research highlights the significant role of sunlight-derived vitamin D in immune regulation, gene expression and chronic disease susceptibility. Deficiency has been associated with increased risk of multiple sclerosis, Crohn’s disease, lupus, rheumatoid arthritis and certain cancers.
Vitamin D interacts with hundreds of genes involved in immune function, providing biological plausibility for these associations. However, balanced interpretation is necessary, as ongoing research continues to refine our understanding of causality.
Ensuring safe sun exposure, appropriate supplementation and dietary intake represents a practical public health strategy to reduce widespread deficiency and potentially lower chronic disease risk.
References
Ananthakrishnan, A.N., Khalili, H., Higuchi, L.M. et al. (2013) ‘Higher predicted vitamin D status is associated with reduced risk of Crohn’s disease’, Gastroenterology, 142(3), pp. 482–489.
Aranow, C. (2011) ‘Vitamin D and the immune system’, Journal of Investigative Medicine, 59(6), pp. 881–886.
Ascherio, A., Munger, K.L. and Simon, K.C. (2010) ‘Vitamin D and multiple sclerosis’, The Lancet Neurology, 9(6), pp. 599–612.
Autier, P., Boniol, M. and Pizot, C. (2014) ‘Vitamin D status and ill health: A systematic review’, The Lancet Diabetes & Endocrinology, 2(1), pp. 76–89.
Garland, C.F., Gorham, E.D., Mohr, S.B. and Garland, F.C. (2006) ‘Vitamin D and prevention of colorectal cancer’, Journal of Steroid Biochemistry and Molecular Biology, 97(1–2), pp. 179–194.
Holick, M.F. (2007) ‘Vitamin D deficiency’, New England Journal of Medicine, 357(3), pp. 266–281.
NHS (2023) Vitamin D. Available at: https://www.nhs.uk/conditions/vitamins-and-minerals/vitamin-d/ (Accessed: 17 February 2026).
Ramagopalan, S.V., Heger, A., Berlanga, A.J. et al. (2010) ‘A ChIP-seq defined genome-wide map of vitamin D receptor binding’, Genome Research, 20(10), pp. 1352–1360.
