Leverage Sunlight To Help Improve Your Health and Chronic Pain

The Sun has it's risk - we know - but did you know that will also improve your health? If the answer is no then give me 10 minutes to convince you of the benefits to why getting safe sun exposure could change your health (and pain) for the better!

Professor Richard Weller, a consultant physician in dermatology and researcher has dedicated a large portion of his career to elucidating this risk-to-benefit ratio of sun exposure and health. His recent co-authored paper with lead author Gu Jiayue, conducted a risk analysis of sun exposure using the UK biobank data (a collection of UK residents' data) analysing some 419 007 people (Jiayue et al., 2026).

Their findings?

Higher exposure to sunlight using the Sun-BEEM composite, which stratified people into low, medium and high UV-exposure, found a dose-response relationship between increasing sun exposure and reduced risk in mortality of 16%, 23% and 11% for all-cause, cardiovascular and cancer respectively. For Melanoma, mortality did not appear to increase with low versus high sun exposure but did show an increase in the low versus medium sun exposure group with a hazard ratio of 1.22 (1.00 - 1.49) but the confidence intervals are fairly wide and the lower bound (of 1) implies no increased risk at all; the authors labelled this as a 'borderline increased risk' as shown in Figure 2A.

Unsurprisingly, the incidence of skin cancer (including melanoma and non-melanoma types) did appear to show increased incidence in the low-vs-medium but not low-vs-high group for Melanoma, and the low-vs-medium and low-vs-high group for other skin cancers, for the latter there was a 14% and 19% increased risk of developing these other skin cancers but the mortality analysis did not find any increased risk of death from these cancers. However, the authors stress that due to the very small number of deaths from these other skin cancers (60 out of 419 007 people) there is imprecision in the data set.

The authors go on to show the modelled scenario of lives saved versus lives lost when you put the entire cohort in low and high sun exposures and it shows some really interesting results. The crux of this seminal paper is that whilst there is an increased risk of skin cancers and a possible increased risk of death from them, there is a large reduction in risk of other health conditions and death from those conditions with what appears to be a dose-response! I would urge anyone interested in sun exposure and the risk-to-benefit ratio to read this paper!

Similar dose-responses have been observed in type 2 diabetes in the Southern Sweden Cohort study, whereby people with the lowest sun exposure were 147% more likely to have diabetes than those who ranked in the highest quartile for sun exposure (Lindqvist et al., 2025).

Hopefully by now you have an appreciation that sun exposure has benefits (which you probably already intuitively knew!) but shares with this, the possibility of increased risk of Melanoma and other skin cancers. I believe that safe sun exposure plays an important role in helping to effectively manage symptoms of persistent musculoskeletal pain but the evidence looking at relationships around this is sparse, and there seems to be little interest in the area. So here are my thoughts on the different (possible) mechanisms by which regular, safe sun exposure could help manage and reduce persistent pain symptoms.

Splitting skin deep mechanisms of improving health with sunlight into Vitamin D dependent and independent pathways

Vitamin D dependent

Multiple cohort studies link vitamin D levels to a lower symptom burden in people with persistent musculoskeletal pain conditions including neuropathic pain, chronic low back pain and fibromyalgia (Abrego-Guandique et al., 2025). Vitamin D is synthesised by photons in the UVB wavelengths being absorbed by 7-dehydrocholesterol in the epidermis that forms previtamin D3, this is then converted into Vitamin D over an 8 hour period (Wacker & Hollick, 2013).

The possible benefits of vitamin D mediated actions most likely occur through immune modulatory pathways. Components of the adaptive immune system, specifically T and B cells express vitamin D receptors (VDR) and current reviews suggest a modulatory role of vitamin D in T cell function. This may occur through increasing expression of Th2 or Treg phenotypes and reducing Th1/Th17 phenotype, consequently having a net immunosuppressive effect on immune function rather than a net inflammatory response (Cantorna et al., 2012). In human cell culture studies, the addition of vitamin D resulted in a largely net anti-inflammatory effect with consistent decreases in interleukins 6, 8, 10, TNF-a and MCP-1 expressed by monocytes and macrophages (Calton et al., 2015). The authors also found strong evidence of modulation of T cell activity, again pointing to an adaptive immune system being involved in downstream effects of vitamin D which is unsurprising given the VDR described above.

Large trials looking at the effects of vitamin d supplementation on health impacts have found conflicting results. The VITAL trial, a randomized, double-blind, placebo-controlled trial involving found no reduction in cancer incidence, cardiovascular disease incidence or all-cause mortality (Manson et al., 2020) and this is echoed in other large vitamin D randomised trials in a recent critical appraisal of the literature, with inconsistencies possibly being due to methodological confounders (Pilz et al., 2022). Earlier reviews have pointed to the wider small and often inconsistent effects of vitamin D supplementation on hypertension, cerebrovascular disease, type 2 diabetes mellitus (T2DM), chronic kidney disease and multiple sclerosis (Weller et al., 2024). So whilst many cells express a multitude of vitamin D receptors across the neuroimmune system, oral supplementation does not appear to have the same potent impact as vitamin D derived from sunlight-mediated mechanisms.

It should come as no surprise that inconsistencies continue for persistent pain states. A recent review highlighted possible benefits of vitamin D supplementation on self-reported questionnaires in people with fibromyalgia but omitted any data around confounding variables relating to sun exposure between treatment groups (Ilari et al., 2025). Another recent meta-analysis of vitamin D supplementation for persistent low back pain found no impact on pain outcomes in any form of vitamin D used but again, there is no mention in the analysis of stratifying for sun exposure (Lee et al., 2024). The trend of not accounting for sun exposure in sensitivity analysis (or even in primary studies) continues in meta-analysis' of vitamin D supplementation in people with rheumatoid arthritis, and whilst showing improvements in disease activity failed to show significant effects on patient-reported pain via VAS (Ranjbar et al., 2025).

I feel here we have fallen foul of the well known idiom: "Not seeing the forest for the trees". The over emphasis on vitamin D supplementation as opposed to vitamin D derived from sunlight exposure, likely because of demonisation of the sun, it missing a great opportunity. This is even more important given we now spend up to 90% of our time indoors in the UK... (Bun et al., 2023).

Supplementation may not be the answer to our sunlight-deprived lives we were looking for (but this could change with increasing research!) and the paper by Jiayue discussed in the opening of the article challenges the notion that sunlight is entirely negative with no benefits. The ailing ability of vitamin D to impact health via supplementation is not evidence of its failure but rather an incorrect assumption we can do a better job than natures billion year long experiment of evolving complex life under direct full spectrum sunlight.

I believe that there are likely beneficial effects of vitamin-dependent mechanisms on health, immune function and by association, musculoskeletal pain but we are yet to look through the correct lens to see this. The other emphasis on vitamin D forgoes the impact of wider non-vitamin D pathways that are activated by sun exposure that have profound impacts on human health and quality of life. Those that I feel have great relevance to persistent musculoskeletal pain will be discussed below.

Non-dependent Vitamin D pathways

Numerous immune factors show potent changes in response to different wavelengths of light. Ultraviolet B (UVB) are wavelengths in the 280-320nm range. Human trials involving UVB light panels localised to body parts, or whole body irradiation, show decreased inflammatory cytokines (IL-10 and TNF-a) following treatment (Hart, 2021). Both cytokines' are known to mediate pain intensity and severity across a spectrum of persistent pain conditions and UVB-dependent changes in IL-10 have been previously shown to occur independent of the Vitamin D pathway associated with UVB exposure (Xu, et al., 2012). Other studies have shown reduced adhesion ability of neutrophils following ultraviolet radiation (UVR) and such characteristics of neutrophils allows them to bind to the endothelial walls of blood vessels (Hart, 2021) contributing to the inflammatory-mediated aspect of pain. It is well known that neutrophil adhesion and infiltration is elevated in people with persistent pain phenotypes - if you reduce the adhesion capacity then you limit the neutrophils' ability to linger in the injured tissues (via the nerve blood vessels) for extended periods of time and further inflammation-mediated responses.

In people with clinically isolated syndrome, the earliest detectable form of multiple sclerosis, narrowband-UVB therapy given over 8 weeks showed changes in B-cell and monocyte concentrations, specifically naïve B cells (Trend, 2019). This has been further confirmed in a recent expert panel review and conference report attesting to the ability of UVB radiation to modulate T and B cell concentrations via skin-photon interactions through cytokine, neuropeptide and hormone changes (Reidman, 2025). Research groups have concluded that adaptive immune system modulation via UVB wavelengths occurs through vitamin D independent and dependent pathways (Hart & Gorman, 2013) and that significant challenges still lie in establishing how much contribution from each occurs.

Linking back to persistent pain, autoimmune antibodies in B cells and T cells and differentiate into T helper cells, which accumulate at the site of injury and activate glial cells that in turn are heavily involved in the transition to chronicity of pain (Li et al., 2025). It may be that changes in B and T cell concentrations and subgroup expression following irradiation with the full solar spectrum (including UVB wavelengths), causes a shift in the expression of the cells toward a normal (pre-chronicity) stage. Interestingly, low naïve B cells at baseline are predictors of transition to chronic pain states (Brezic et al., 2026) with Trend et al., (2019) reporting increases in naive B cell concentrations following UVB therapy, highlighting the possible mechanisms for action.

In rodents, mice reared under conditions that created lumbar degenerative disc disease had UVB therapy 3 x weekly for 2 or 4 minutes each. Following the trial, there was reduce nociceptive sensitisation and improved disc characteristics in the treatment versus control group; disc height was maintained, there was reduced endplate ossification, increased extracellular metabolism and reduced markers of apoptosis (Zhang et al., 2025). Unsurprisingly, the treatment group had a 50% reduction in circulating levels (in the lumbar material) of TNF-a, IL-B and IL-6. As a side note, the structural differences between groups could be due to improved mitochondrial function, given the mitochondria's role in serving as a gatekeeper for apoptosis and cytoskeletal integrity of the cell, something that will be discussed later in the context of infra-red wavelengths.

Discussed extensively in existing reviews on neuroimmune signalling and chronic pain (Brezic et al., 2026) the pro-inflammatory cytokines including TNF-a and interleukins are mediators in pain chronicity, thus it provides further evidence for the direct pain-dampening effects of sunlight exposure via reducing classical cytokine levels. This is further supported by human observational studies showing seasonal variations in CRP levels being higher in winter, where photon pressure is lowest, than spring or summer (Liu et al., 2015; Chiriboga et al., 2009) with pro-inflammatory cytokines TNF-a and interleukins 8, MCP-1 also showing significant increases in winter months (Spath et al., 2017).

Nitric oxide is a signalling molecule in the body that plays a number of important roles including vasodilator, immune modulator, neurotransmitter and mitochondrial enhancer. In the human dermis, nitrate is reduced to nitrite then nitric oxide in the presence of ultraviolet A wavelengths or infra-red wave lengths, so naturally this also happens during irradiation via sunlight. This process occurs independently of vitamin D synthesis (Weller, 2016). Linking to persistent MSK pain, NO is expressed in large quantities in the injured sciatic nerve in the dorsal root ganglion, the axon and the vasa nervorum (the small blood vessels inside the nerve itself) around the injury site (Gonzalez-Hernandez, 1999). Because of its vasodilation properties, NO can increase O2 and respiratory substrate delivery to the mitochondria, and acts directly on cytochrome c oxidase to regulate respiration (Poderoso et al., 2019). NO appears to have a biphasic capacity when it comes to cytokine regulation, narrative reviews point to both augmentation or suppression of pro-inflammatory cytokines including TNF-a, MCP-1, and IL-8 (Kobayashi, 2010).

Recent reviews highlight mitochondrial dysfunction as a central tenet of pain chronicity. This is characterised by impaired mitochondrial redox balance, oxidative stress and hyperactivity (Hanneke, 2023). Increase endogenous NO levels in the body could provide viable contributions to improved mitochondrial dynamics in tissues associated with persistent pain. The caveat!? NO has a short half life of < 2 seconds in the body, its effects are likely localised to the region exposed to UVB wavelengths, so it would require the person to a large surface area to the sun for extended periods of time over the day, on a daily basis (similar to our hunter-gatherer ancestors!).

Another possible molecule that could be involved in pain modulation via sunlight is proopiomelanocortin (POMC). This is produced when UVB wavelengths strike keratinocytes, triggers the p53 tumour suppressor protein which produces POMC. Interestingly, although this is produced as a precursor involved in the tanning process, POMC also has a number of other immune-modulating effects. Some POMC-derived peptides activate pathways that directly alter macrophage activity and supress pro-inflammatory cytokine release in rodent models (Getting et al., 1999) and B-endorphin, another peptide, plays a central role on pain analgesia with it being up to 33 times more potent than morphine (Hartwig, 1999). It has been recently suggested in a meta-analysis as a surrogate marker of successful treatment of chronic low back pain, explaining up to 80% of the variance in pain between treatment and control groups (Choi et al., 2019). Ultimately, this suggests a possible broad-spectrum anti-inflammatory function of POMC and POMC-derived peptides in the peripheral skin organ in relation to people with persistent musculoskeletal pain.

The wonders of near infra-red light and the direct tissue effects of light on pain

Certain wavelengths of light in the solar spectrum have the capacity to penetrate deep into the body through to the cartilage, bone and muscle.

These are in the near-infrared wavelengths ranging from 700 - 800nm to 1 millimetre and in natural daylight, NIR photon pressure is highest during early morning (< 2 hours after sunrise) and during early evening just before sunset. In people with persistent pain, NIR lamps have shown improvements in symptoms in people with knee OA, carpal tunnel syndrome, lumbar disc herniation, patellofemoral pain syndrome and subacromial shoulder pain (de la Barra Ortiz et al., 2026; Pereira et al., 2025). However, the quality rating of outcomes (using GRADE) was very low due to inconsistencies in methods across studies. Interestingly, one consistency across both analysis' was the primary outcome (pain) improved to a greater extent under NIR plus exercise than NIR alone, emphasising the need for a multidimensional approach.

Photons in the NIR range are absorbed by certain tissues as they pass through the body; metal-ion containing molecules have the highest capacity but DNA and water are also high absorbers (Henderson et al., 2015). In the cells of the tissues, the mitochondria, specifically cytochrome c oxidase, when it absorbs NIR photons, initiates photobiomodulation. Irradiation of this enzyme in complex IV speeds up the entire electron transport chain, increases endogenous NO production (benefits discussed previously) and increases O2 consumption (Henderson et al., 2015). Complex IV has a high absorption capacity because it contains a copper centre and water. Moreover, NIR therapy also increases gene expression for antioxidants and reactive oxygen species inhibitors (Henderson et al., 2015).

Linking into persistent pain, studies consistently show NIR photons achieving depths of up to 5mm in cartilage (Padalkar et al., 2015) suggesting the capacity to target certain painful tissues directly like the knee, ankle, hands, upper extremities and the spine. Previously touched upon, mitochondrial function impacts cytoskeletal integrity and appears to be a bidirectional relationship; the microtubules provide a rail road within the cells that allows mitochondria to track along it (Anesti et al., 2006). In Bovine intervertebral disc samples, the three cytoskeleton elements  β-actin, β-tubulin and vimentin showed regional specificity likely related to the types of forces (compression or tension) that the discs are exposed to (Duance et al., 2008). Substantial evidence shows that impaired ATP production due to mitochondrial dysfunction results in impaired actin dynamics in the cytoskeleton and increased mitochondrial ROS (mROS) thus impacting cytoskeleton function (Yadav et al., 2022). This change in cytoskeleton structure and function may be involved in the causal pain pathway in load bearing joints such as the spinal vertebrae or knee joints.

In dysfunctional mitochondria in the knee, spine or other peripheral tissues with little overlying tissues, near infrared photons could exert their benefits by directly regulating ATP synthesis and mROS as complex IV is a direct absorber of NIR photons thereby normalising cytoskeletal dynamics and cell function. To my knowledge, I have been unable to find any studies in humans either in vivo or vitro looking specifically at whether this wavelength of light exerts such effects mitochondrial-cytoskeletal dynamics.

To wrap it up, I believe there are substantial benefits to managing persistent musculoskeletal pain via consistent and safe sun exposure largely through the neuroimmune mediated pathways. Ancedotally, this is something I have seen during my clinical practise in the NHS where patients with symptomatic knee osteoarthritis have ventured to sunny locations and report consistent improvements in their pain. Now obviously I have no way of controlling for the myriad of other confounding variables but... based on my current understanding of the literature, I would wager the sun exposure would be having a big impact!

Remember, this is an educational post only. I have no considered your individual risk profile or circumstances and I am not advocating you lay in the sun and cook yourself red raw! For a nuanced discussion around the risks and benefits you should consult your GP or family physician for any advice.

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