“We are what we eat:” Diet, gut and stroke

Author: Dr. Xabier Urra, Functional Unit of Cerebrovascular Diseases, Hospital Clínic, Barcelona

There are increasing pieces of evidence supporting that the old saying “we are what we eat”, is true, and it may be particularly true in patients with cerebrovascular disease. Poor dietary habits cause a great proportion of cardiovascular deaths, also to cerebrovascular disease (Kumar et al. 2010). A few years ago, the PREDIMED study demonstrated that a Mediterranean diet supplemented with extra virgin olive oil or nuts could reduce the incidence of cardiovascular events by 30% compared to a low-fat diet in people who had vascular risk factors (Estruch et al. 2013). The protection was largest for stroke (hazard ratio of 61%), and in addition to reducing acute cardiovascular events, the intervention also improved cognitive function.

The relevance of diet in cerebrovascular disease may seem surprising because neurons consume almost exclusively glucose. However, the brain is not just a bunch of neurons, but a complex organ composed of different cell types in which blood vessels are in a close relationship with the surrounding cells. It is therefore not surprising that any factor influencing blood vessels may have a huge impact on the health of the whole brain. On top of that, the brain is not an isolated organ, it is interconnected with the rest of our body, and systemic conditions, such as inflammatory diseases in distant organs, can affect it. One of the most interesting connections occurs between the brain and the gut, and stroke may impair the relationship between both of them. It’s been known for long that after stroke, gastrointestinal motility is disturbed, probably due to an excess of inhibitory sympathetic signaling. However, recent experimental studies suggest that cerebral ischemia also has a broader impact on the gastrointestinal tract. In humans, the gastrointestinal tract is the main site for microbiota, with several trillion microbial cells living there. The quantity and diversity of the gut microbiome are influenced by many factors, including diet, and acute lesions like stroke are a cause of imbalances in the composition and function of the intestinal microbes (microbiota dysbiosis). Intestinal dysbiosis, in turn, alters immune homeostasis resulting in the increase of inflammatory lymphocyte subsets that can reach the brain and enhance deleterious inflammatory responses in the ischemic tissue, potentially hampering recovery (Benakis et al. 2016).

The good news is that the gut microbiota can be rapidly modulated with dietary interventions, even in a few days (David et al. 2014), and a high adherence to a Mediterranean diet has been associated with a favorable microbiome-related metabolomic profile (De Filippis et al. 2015). Whether an early adoption of such a diet after stroke provides benefits has not been specifically studied yet. However, given its great efficacy in the primary prevention of cardiovascular disease, it is possible that the benefits of a Mediterranean diet supplemented with olive oil or nuts are even more significant in the secondary prevention of ischemic events.

Overall, considering the complex relationships between diet, microbiome, and cardiovascular health, it is worth spending a few minutes with the patients not only reviewing their medication list but also discussing eating habits. Healthy diet recommendations do not necessarily mean a long list of forbidden foods. In fact, I’ve had quite many patients leaving the clinic with a smile on their face after knowing that keeping on taking their loved toast with a generous amount of fresh extra virgin olive oil for breakfast could be a good way of avoiding in the future a surgical procedure for their moderate carotid disease.

Kumar, S., et al. Lancet Neurology 9, 105–18 (2010).
Estruch, R. et al. N Engl J Med 368, 1279–90 (2013).
Benakis, C. et al. Nat Med 22, 516–23 (2016).
David, L.A. et al. Nature 505, 559–63 (2014).
De Filippis, F. et al. Gut 65, 1812–21 (2015).