How unhealthy diets may increase stroke risk with gut microbiome imbalance
- Stroke risk is associated with lower intake of fiber, fruits, and vegetables but higher intake of sugary beverages.
- Stroke patients have higher leaky gut symptoms and higher abundance of inflammatory gut microbiota.
- Higher abundance of “good” microbes of the patients predict better functional recovery.
Every year in the United States, more than 795,000 people suffer from strokes, which are serious medical emergencies that occur when the blood supply to the brain is disrupted or reduced. These strokes can cause brain damage and lead to difficulties with language and motor skills. While medical advancements have focused on reducing mortality rates associated with strokes, survivors often face significant physical challenges. This has created an urgent need to find new ways to enhance brain plasticity, which refers to the brain’s ability to adapt and change its structure and functions. Brain plasticity is crucial for recovering from strokes and other brain injuries.
Recent studies suggest that the gut microbiome, which consists of various microorganisms aiding in digestion, can influence brain plasticity and play a role in stroke recovery. The gut and the brain have a bidirectional communication system, allowing them to interact. Researchers believe that by modifying the gut microbiome through factors like diet and exercise, we could potentially improve stroke recovery.
In a recent study, we investigated the relationship between changes in the gut microbiome and the recovery of individuals affected by strokes. By comparing stroke survivors to healthy individuals, we found notable differences in the levels of gut microbes. Specifically, stroke survivors tended to consume less fiber, fruits, and vegetables while increasing their intake of sugary beverages. These dietary factors were associated with changes in the gut microbiome. We also discovered that stroke survivors had higher levels of a marker for a “leaky gut” called alpha-1-antitrypsin in their stool compared to the control group. Additionally, we found negative correlations between alpha-1-antitrypsin and certain types of bacteria, including Roseburia species, which are known to produce beneficial substances like butyrate.
To assess recovery after stroke, we evaluated participants’ brain function and their ability to perform daily activities such as eating, brushing teeth, bathing, dressing, and putting on shoes. Our findings revealed a strong connection between the levels of gut microbes and their performance in these activities.
Furthermore, we observed that stroke survivors scored lower on memory tests compared to the control group. However, those with higher levels of Roseburia bacteria performed better on tasks involving picture vocabulary, while increased levels of Bacteroides uniformis (a butyrate-producing bacterium) and decreased levels of Escherichia coli (a pro-inflammatory bacterium) were associated with higher self-efficacy.
Overall, our study suggests that stroke survivors have higher levels of pro-inflammatory bacteria and lower levels of beneficial bacteria, such as butyrate producers and secondary bile acid producers, in their gut microbiome. These altered microbial communities are linked to poorer functional performance. Future research should investigate whether manipulating the gut microbiome can optimize rehabilitation and accelerate recovery after strokes.
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