Diseases related to blood pressure — including stroke, coronary heart disease, heart failure and kidney disease are leading causes of morbidity and mortality in the United States. Even slightly-elevated BP levels can lead to increased risk in cardiovascular diseases or stroke.

And a major culprit in these diseases is sodium.

According to a Centers for Disease Control and Prevention (CDC) report, nearly all Americans, regardless of age, race, gender or hypertension, consume more sodium than is recommended for a healthy diet. Recent findings show that more than 90 percent of children and 89 percent of adults ages 19 and older eat too much salt that is, more than the recommended limits in the 2015-2020 Dietary Guidelines for Americans, not including salt added at the table.

The 2020 goal of the American Heart Association is to improve the cardiovascular heath of all Americans by 20 percent while continuing to reduce deaths from cardiovascular disease and stroke by 20 percent. The AHA recommends a BP of 120/80 mm Hg and sodium consumption of 1,500 mg or less per day.

A national effort that reduces sodium intake to around 1,200 mg per day should result in 60,000 to 120,000 fewer coronary heart disease events, 32,000 to 66,000 fewer strokes, 54,000 to 99,000 fewer myocardial infarctions and 44,000 to 92,000 fewer deaths.

Although a diet rich in salt is linked to an increased risk of cerebrovascular diseases, it remains unclear how dietary salt harms the brain. In a recent study, Costantino Ladecola, from Weill Cornell Medicine in New York City, and colleagues 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, the researchers noted endothelial dysfunction and a reduction in the blood flow to the brain in the mice. Although behavioral tests revealed cognitive decline in the rodents, their BP remained unchanged.

The researchers also discovered an increase in the gut's TH17 white blood cells, which led to an increase in the levels of a pro-inflammatory molecule, plasma interleukin-17 (IL-17). They also identified the molecular pathway through which higher levels of IL-17 in the blood led to the negative cognitive and cerebrovascular effects.

To replicate their findings in human cells, the researchers treated human endothelial cells with IL-17 and obtained similar results. This supports a new gut-brain axis linking dietary habits to cognitive impairment through a gut-initiated adaptive immune response that compromises brain function via circulating IL-17.

Fortunately, the negative effects of the high-salt diet seem to be reversible, and the harmful effects of a high-salt diet were reversed by returning the mice to a normal diet after 12 weeks, suggesting that reducing dietary salt can reverse vascular dysfunction and cognitive impairment.