Maintaining a diet that reduces inflammation can meaningfully lower the risk of developing dementia, even when brain changes that lead to dementia have already begun, according to a new study. The preventive effect was confirmed even in older adults who showed warning signs of dementia, such as the accumulation of Alzheimer's-related proteins or nerve cell damage, drawing renewed attention to the importance of managing dietary habits.
On Wednesday, a joint research team from Sweden's Karolinska Institute and Slovenia's University of Ljubljana announced that after long-term tracking of 1,865 older adults aged 60 and over without dementia, those who maintained a healthy diet that triggers less inflammation were less likely to develop dementia. The findings were published in JAMA Network Open, an international journal under the American Medical Association (JAMA).
The study was conducted over an average of 8.4 years and up to about 16 years, during which 240 of the participants were diagnosed with dementia. The researchers analyzed participants' dietary habits along with biomarkers related to Alzheimer's disease through blood tests, and then compared subsequent dementia incidence.
In particular, the researchers divided participants into risk groups for analysis using biomarkers that reflect Alzheimer's disease progression, nerve cell damage and brain inflammation, including phosphorylated tau217 (p-tau217), neurofilament light chain (NFL) and glial fibrillary acidic protein (GFAP) in the blood.
The dietary assessment used an index that comprehensively reflected the degree of adherence to the Mediterranean diet, the overall healthiness of the diet, and how much the food triggers inflammation in the body. Among these, the most pronounced preventive effect appeared in people who consistently followed a diet with a low potential to trigger inflammation.
According to the findings, even those already at high risk of dementia saw their risk of developing the disease reduced by about 20 to 30 percent when they maintained an anti-inflammatory diet. In the high-risk group with high levels of phosphorylated tau217, the risk fell by 29 percent. The risk dropped by 21 percent for those with high NFL levels, which indicate nerve cell damage, and by 27 percent for those with high GFAP levels, which reflect brain inflammation.
Alzheimer's disease is a representative degenerative disorder that progresses as amyloid beta and tau proteins accumulate in the brain over a long period. However, having such pathological changes does not necessarily lead to dementia, and various factors such as lifestyle, genetic factors and cardiovascular health are known to determine the timing and degree of risk of onset.
The researchers explained that while there have been many studies showing that a healthy diet helps prevent dementia in the general population, it was unclear whether the same effect applies to people in whom pathological changes have already begun in the brain. They assessed that this study is significant in that it showed the potential for dietary management to be used as a disease prevention strategy even in older adults at high risk of dementia.
The researchers said the findings are consistent with previous studies indicating that chronic inflammation promotes neuroinflammation and neurodegeneration, affecting the progression of Alzheimer's disease. This suggests that dietary habits that reduce inflammation may have contributed in part to slowing the progression of brain damage.
They also advised that dietary habits of increasing the intake of plant-based foods such as vegetables, fruits, nuts, legumes and whole grains, while reducing the consumption of processed meat, red meat, sugary beverages and ultra-processed foods, can help maintain brain health.
However, as this study is an observational study, it cannot be concluded that dietary habits directly lower the risk of dementia. The researchers said further research is needed on which food groups or nutrients drive this preventive effect, and how much actual cognitive decline can be delayed.
