Eating Too Much Salt Can Cause Dementia

Eating Too Much Salt Can Cause Dementia

The western diet contains too much salt, which increases blood pressure and elevates the risk of suffering from cardiovascular diseases and strokes, although new research has suggested that eating too much salt can also cause dementia.

The recommended level of salt intake is 2300 mg per day, yet 90% of people in the United States consume more than the recommended maximum amount. In many cases, salt intake is well in excess of the recommended maximum.

The potentially harmful effects of a high salt diet have been well documented. The findings of research have led many health organizations to recommend reducing salt intake and adopting low-sodium diets.

Many of the negative effects of a high salt diet are linked to a rise in blood pressure. Some studies have also linked a high salt diet with cognitive impairment, although such deleterious effects on cognition have been attributed to the increase in blood pressure.

The latest study, conducted by researchers at Weill Cornell Medicine, shows not all harm from excess salt intake is due to a rise in blood pressure. The study suggests cognitive impairment as a result of a high salt diet occurs even in the absence of elevated blood pressure. Excessive salt intake therefore results in other bodily changes that have an impact in the brain.

The study examined how a high salt diet causes cognitive impairment as little was known about the mechanism involved. The new study is the first to determine how cognitive function is impaired by excessive salt in the diet.

Rather than negative effects from high blood pressure, cognitive impairment is caused by changes in the gut related to a high salt intake.

For the study, mice were fed a diet containing either 4% or 8% salt –eight and sixteen times the normal level. These excessive levels of salt intake are comparable to diets at the upper end of the scale in humans.

The studies showed that after eight weeks on the diet, cerebral resting blood flow had decreased by 28%, while blood flow in the hippocampus decreased by 25%. Both of these areas of the brain are involved in learning. Further, the ability of the body to increase blood flow in the brain was hampered.

Endothelial cells produce nitric oxide to relax blood vessels and increase blood flow, yet their ability to do so was reduced as a result of the high salt diet. The researchers note that endothelial cell dysfunction was not the result of an inflammatory response.

Blood flow in the brain is essential for normal cognitive functioning, and the reduction in blood flow causes cognitive impairment and dementia. Mice on the high salt diets were found to perform worse in maze and object recognition tests, and displayed reduced nest building ability. Returning the mice to a normal diet saw the harmful effects of the high salt diet reverse in four weeks.

The researchers point to a study that shows that a high salt diet causes immune system changes in the gut. “A diet rich in salt induces the accumulation in the gut of T-helper lymphocytes producing the proinflammatory cytokine interleukin-17 (TH17).” The pathways involved suppress the anti-inflammatory function of regulatory T cells.”

Further investigations showed that the high salt diet caused an adaptive immune response in the gut with elevated levels of TH17 cells and higher levels of IL-17 production. IL-17 regulates immune and inflammatory responses. When mice were administered with IL-17 antibodies, they did not develop the cognitive impairment caused by the high salt diet.

“We have demonstrated that HSD induces a TH17 response in the gut that leads to increases in circulating IL-17, which, in turn, acts on cerebral endothelial cells to suppress endothelial NO production, leading to reductions in cerebral perfusion and cognitive dysfunction,” the researchers wrote in the paper.

The researchers point out “Our findings suggest that the IL-17–ROCK pathway is a putative therapeutic target to counteract the deleterious cerebrovascular and cognitive effects of HSD and of other conditions associated with TH17 polarization. Activation of the TH17 cell–IL-17 pathway is observed in a number of diseases associated with cerebrovascular dysfunction, including, for example, multiple sclerosis, rheumatoid arthritis, psoriasis and inflammatory bowel disease. Counteracting the deleterious effects of IL-17–ROCK on the cerebral endothelium would be beneficial to reduce cardiovascular risk in these conditions.”

The study – Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response – was recently published in Nature Neuroscience.

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