Too much salt can cause cognitive deficits, according to a new study published in the journal Nature Neuroscience. Luckily, these negative effects may be reversed, and the new study shows how.
It’s a well-known fact that too much salt in our diet raises the risk of cardiovascular disease and high blood pressure.
But it is less known that brain-related problems, such as cerebrovascular disease, stroke, and cognitive impairment, have all been linked to dietary salt.
As the authors of the new research explain, it was suggested that one possible mechanism behind these negative effects involves the so-called endothelial cells inside the cerebral blood vessels.
Endothelial cells line our blood vessels and are responsible for regulating the vascular tone — but a high dietary intake of salt has been associated with dysfunction of these cells.
Although it is known that epithelial dysfunction can bring a plethora of chronic illnesses, it remains unclear exactly how salt-induced endothelial dysfunction may affect the brain in the long run.
This is particularly important given that the brain is heavily reliant on a steady and smooth flow of oxygen to function properly, explain the study authors, who were led in their research efforts by Costantino Iadecola, from Weill Cornell Medicine in New York City, NY.
In their paper, Iadecola and colleagues show how excessive dietary salt affects our gut, immune system, and, ultimately, our brain.
How excessive salt affects the gut-brain axis
Iadecola and team fed a group of mice the equivalent of a human diet high in salt for a period of 12 weeks.
After the first few weeks, endothelial dysfunction, as well as a reduction in the blood flow to the brain, could be noticed in the mice. Additionally, behavioral tests revealed cognitive decline in the rodents.
Their blood pressure, however, remained unchanged.
An important discovery was the increase in the gut’s so-called TH17 white blood cells. In turn, the high number of TH17 cells led to an increase in the levels of a proinflammatory molecule called plasma interleukin-17 (IL-17).
The researchers were also able to identify the molecular pathway through which higher levels of IL-17 in the blood led to the negative cognitive and cerebrovascular effects.
The researchers wanted to see whether or not their findings would replicate in human cells. So, they treated human endothelial cells with IL-17 and obtained similar results.
As Iadecola and his colleagues explain:
“The findings unveil a gut-brain axis by which environmental factors linked to the diet lead to an adaptive immune response in the gut, promoting […] neurovascular dysregulation and cognitive impairment.”