Correcting vitamin D deficiency nearly halves the risk of potentially fatal lung attacks in patients with chronic obstructive pulmonary disease (COPD), our latest study has found.
COPD describes several lung conditions, including emphysema and chronic bronchitis, where a person’s airways become inflamed, making it harder to breathe. Almost all COPD deaths are due to lung attacks (termed “exacerbations”) in which symptoms worsen sharply. These are often triggered by viral upper respiratory infections – the type that cause the common cold.
Vitamin D – “the sunshine vitamin” – is best known for its effects on bone, but it also boosts immunity to viral infections. Our previous research at Queen Mary, University of London, has shown that vitamin D supplements protect against asthma attacks and acute respiratory infections, such as colds and flu, in people who have low vitamin D levels to start with.
A number of clinical trials have tested whether vitamin D supplementation might have a role in reducing the risk of COPD attacks, but they have yielded conflicting results. Some show a benefit, others do not.
One way to get a handle on the reason for their different findings is to pool the data from the various studies into a single database and then run analyses to determine whether vitamin D might have stronger protective effects against lung attacks in certain groups of COPD patients compared with others. This approach is known as “individual participant data meta-analysis”.
Our latest study, published in the journal Thorax, reports the findings of such an analysis. We pooled data from 469 patients who took part in one of three clinical trials of vitamin D that were conducted in the UK, Belgium and the Netherlands.
We found that giving vitamin D supplements led to a 45% reduction in the rate of lung attacks in COPD patients with low vitamin D levels (less than 25 nanomoles per litre of blood or 10 nanograms per millilitre of blood, which is the standard cut-off used by the UK Department of Health to define vitamin D deficiency). We didn’t observe any benefit in patients with higher vitamin D levels.
Doses of vitamin D investigated in the original trials ranged from 30 micrograms daily to 2,500 micrograms, monthly. For comparison, Public Health England and the Scientific Advisory Committee on Nutrition advise a daily intake of 10 micrograms of vitamin D. Supplementation at the higher doses given in the clinical trials did not influence the proportion of participants experiencing serious side effects, indicating that they were safe.
Given this excellent safety profile, and the fact that vitamin D supplements cost just a few pence per year, offering them to patients with COPD is a potentially highly cost-effective treatment that could be targeted at those who have low vitamin D levels following routine testing.
Around one-fifth of COPD patients in the UK – about 240,000 people – have low levels of vitamin D. Reducing risk of attacks in such a large group would have major benefits for patients and for health services, since many attacks require costly hospital admission. (COPD costs the NHS £800m per year.)
Our study provides the strongest evidence yet of a benefit of giving vitamin D supplements to patients with COPD who have low vitamin D levels. But it is important to recognise that the data contributing to this analysis come from a relatively small number of trials, so our findings should be interpreted with caution.
Another clinical trial of vitamin D, focused just on COPD patients with low baseline vitamin D levels, is underway in the Netherlands. Results are expected in 2020.