Other physiological roles of vitamin D in maintaining health are now recognised. Vitamin D deficiency is associated with increased risk of cardiovascular disease (Chowdhury et al. 2014), some cancers (Chowdhury et al. 2014), type 2 diabetes (Mitri et al. 2011) and multiple sclerosis (Mokry et al. 2015). There is also some evidence that low levels are associated with increased risk of all cause mortality (Garland et al. 2014; Afzal et al. 2014). Most of the evidence relating low vitamin D with higher mortality is derived from observational studies and it is not clear if the association represents a causal relationship. A recent large meta-analysis found an association between genes involved in the vitamin D pathway and cancer survival, supporting a causal link (Vaughan-Shaw et al. 2017). But it has also been suggested that, as vitamin D levels are reduced by disease processes, low levels may be the result rather than the cause of various illnesses (Autier et al, 2013).   It is also possible that the relationship is mediated through the association of vitamin D deficiency with other risk factors, such as lack of physical activity and obesity.

Rickets, the most obvious manifestation of vitamin D deficiency in children, was in the past common in Scotland but its incidence declined rapidly over the 20th century such that it is now uncommon. The majority of cases seen recently in Scotland have been in individuals of Asian or African ethnicity (Ahmed et al. 2011). Vitamin D production is in part dependent on skin pigmentation with paler-skinned individuals able to synthesise vitamin D more efficiently under UV exposure; therefore, darker-skinned individuals who move to a region experiencing low sunlight are at particular risk of deficiency.

It has been suggested that vitamin D deficiency, resulting from low sunlight exposure, may be in part responsible for the excess mortality seen in Scotland, and particularly in Glasgow, compared to other parts of the UK. However, the excess mortality in Scotland is most marked in younger age groups, i.e. those under 65 years. A systematic review and meta-analysis investigating the association between vitamin D deficiency and premature mortality concluded that although a significant increase in mortality risk was seen with low compared to high concentrations of vitamin D, the risk was lower in the studies that contained younger participants and there was potential for substantial residual confounding. It seems unlikely, therefore, that vitamin D deficiency plays a major role in Scotland’s ‘excess’ levels of mortality.

The effect of having higher than average vitamin D is unclear, with one meta-analysis of observational studies suggesting that pancreatic cancer is more common in individuals with the highest levels (Stolzenberg-Solomon et al. 2010). Some of the available observational evidence suggests that all-cause mortality is higher in individuals with both the lowest and highest levels of vitamin D and that health benefits are greatest at more moderate concentrations (Durup et al, 2012).

There have been few well-conducted randomised controlled trials (RCTs) of vitamin D supplementation in healthy adults and those that have been performed have not shown clear evidence of a benefit from taking supplements (Autier and Gandini, 2007; Chung et al. 2011). In a 2019 meta-analysis of 50 RCTs with a total of 74,655 participants Zhang et al. found that vitamin D supplementation significantly reduced risks of cancer mortality, but not of all-cause or cardiovascular mortality. The potential risks of excessive sun exposure must also be considered in the context of attempts to increase vitamin D levels. 

Since the onset of the COVID-19 pandemic in 2020 there has been interest in whether vitamin D could reduce the risk of contracting COVID-19, based on evidence that vitamin D can reduce inflammation, increase the body’s antiviral immune response, and reduce the risk of acute respiratory infections (Martineau et al. 2017; Torjesen 2020). A few observational studies have associated low vitamin D status with adverse COVID-19 outcomes, but the possibility for reverse causation (i.e., the disease causing the vitamin deficiency) cannot be ruled out in these studies (Jolliffe et al. 2020; Autier et al. 2013).