Recently, a study conducted by the journal Respiratory Research found that vitamin D deficiency accelerates and intensifies specific disease features of COPD in mice.
Chronic obstructive pulmonary disease (COPD) is a condition characterized by chronic inflammation of the airways. Individuals with COPD experience a progressive restriction in their expiratory airflow, resulting in shortness of breath, coughing and mucus production.
The majority of COPD cases result from long-term exposure to cigarette smoke causing damage to the airways and a gradual decrease in lung function. Disease flare-ups are more common in those with a more severe progression of COPD, and are typically triggered by bacterial and viral infections. These flare ups may result in hospitalization, reduced quality of life and death.
Due to the anti-microbial and anti-inflammatory properties of vitamin D, researchers have hypothesized that vitamin D plays a role in COPD. However, epidemiological research has produced conflicting results. Furthermore, the specific involvement of vitamin D deficiency in COPD disease onset and progression has not been thoroughly assessed.
In the current study, researchers evaluated the combined effect of cigarette smoke and vitamin D deficiency on the development of COPD like symptoms in mice. Half of the mice were vitamin D deficient, while the vitamin D sufficient mice served as the control group. All mice were randomly divided into two groups: those exposed to cigarette smoke and those that who received ambient air for a period of 6 weeks (sub-acute) or 23 weeks (chronic).
An in depth analysis was performed on the composition and function of the lungs. The scientists also conducted a test tube assessment of the phagocytic and oxidative burst capacity of alveolar macrophages in the mice. A lower phagocytic and oxidative burst capacity indicates a decreased ability of the cells lining the lungs to fight off infection.
Here is what the researchers found:
- The vitamin D deficient mice exhibited an accelerated decline in lung function following exposure to cigarette smoke when compared to controls.
- Early signs of emphysema were also observed only in the cigarette smoke exposed mice.
- The vitamin D deficient mice showed an increased presence of the inflammatory cells in the airways after both sub-acute and chronic smoke exposure compared to vitamin D sufficient mice.
- The vitamin D deficient mice also had elevated levels of common pro inflammatory cytokines and chemokines in the lungs compared to control mice.
- All mice exposed to cigarette smoke experienced a significant decrease in test tube phagocytic and oxidative burst function of alveolar macrophages, regardless of their vitamin D status (p < 0.05).
The authors stated,
“In conclusion, we have shown that vitamin D deficiency accelerates and aggravates the development of COPD like characteristics (lung function changes, emphysema and pulmonary inflammation) in the lungs following cigarette smoke exposure, suggesting an important role for the vitamin D pathway in COPD pathogenesis and progression.”
This is the first study to experimentally demonstrate the structural and functional airway alterations occurring in vitamin D deficient mice with cigarette smoke induced COPD. However, because this is an animal study, the results can’t be directly translated to human populations.
The researchers call for preventative trials evaluating the specific role of vitamin D supplementation on COPD onset in order to provide a more definitive connection between vitamin D deficiency and COPD development. However, how could such trials ever be done ethically? How can scientists ethically identify a vitamin D deficient control group and not treat them?
Sturges, M. & Cannell, JJ. Closer look: vitamin D deficiency may worsen COPD. The Vitamin D Council blog/newsletter, September 30, 2015.