High salt intake could increase dementia and Alzheimer’s Disease risk, study flags
30 May 2023 --- As warnings against high salt consumption – especially of table salt – have been given by the World Health Organization (WHO), several non-governmental health-related organizations and numerous health-promoting entities, a new study shows that high salt-induced hypertension can also be correlated with emotional and cognitive impairment.
The WHO advises limiting salt intake to less than 5 g per day and the reasons for these often revolve around salt’s effects on the cardiovascular system, obesity and non-communicable diseases.
However, researchers in Japan have now concluded that high salt intake can also lead to an increase in a key biomarker associated with Alzheimer’s disease and other biomarkers associated with the symptoms of dementia.
The study shows that excessive table salt intake can increase several biomarkers for dementia and Alzheimer’s disease.“This study is of particular social and economic importance because the annual social cost of dementia treatment in Japan is surging like never before,” Dr. Akihiro Mouri, a professor and researcher at Fujita Health University in Toyoake, Japan, and secondary author of the study.
“Therefore, developing preventive and therapeutic drugs for dementia seems critical for Japan’s rapidly aging population.”
Increased biomarkers
Though some studies have linked diets, such as the Mediterranean and DASH (dietary approaches to stop hypertension) diets, to lowering the Alzheimer’s disease-specific biomarker called the tau protein, this study seems to show that high salt consumption contributes to the phosphates that form tau tangles – clusters of tau proteins – in the brain.
The researchers used a mouse model and fed the mice a high salt solution consisting of 2% sodium chloride in drinking water for 12 weeks and monitored their blood pressure during that time.
The brains of the mice were then analyzed and were found to have undergone biochemical alterations such as the increase in phosphates attached to taus and a decrease in CaMKII – a key enzyme involved in signaling in the brain. Additionally, the levels of the protein PSD95 which aids in the functioning of brain synapses were also noted.
The researchers then looked for changes in angiotensin II (Ang II) and its receptor AT1 and the lipid molecule prostaglandin E2 (PGE2) and its receptor EP1. The hormone Ang II plays a vital role in fluid balance and the regulation of blood pressure, while PGE2 is associated with hypertension and neurotoxicity.
The researchers used a mouse model to understand the extent of salt’s effects on the brain.
The results show that high salt consumption interplayed with all of these factors. Salt-induced hypertension in conjunction with a “crosstalk” between Ang II-AT1 and PGE2-EP1 caused emotional and cognitive dysfunction while promoting the Alzheimer’s-related tau protein biomarker.
Rapidly aging populations
According to the study, published in the British Journal of Pharmacology, the importance of these findings in light of several countries which are now experiencing what the researchers call “rapidly aging societies,” wherein the number of those aging into retirement and beyond supersedes the birth rate.
The study also stresses that Japan has one of the largest aging societies in the world and a high prevalence of dementia. Moreover, the study highlights that there are no treatments, pharmacological or otherwise, that can cure or satisfactorily treat the disease. Therefore, novel interventions and preventive measures should be researched and instituted, such as lowering salt intake.
“Excessive salt intake is considered a risk factor for hypertension, cognitive dysfunction, and dementia,” says Dr. Hisayoshi Kubota, lead author of the study. “However, studies focusing on the interaction between the peripheral and central nervous system have not sufficiently investigated this association.”
In related news, recent studies have found that increasing omega 3 and magnesium intake could also lower the risk of developing dementia.
Edited by William Bradford Nichols
