In a recent study posted to the medRxiv preprint* server, researchers in the United States investigated whether higher Dietary Inflammatory Index (DII) scores were related to an increased incidence of dementia due to Alzheimer's disease (AD) or any other cause.
Dementia is one of the world's most significant health and social care issues. The DII was created primarily to evaluate the inflammatory contents of the diet. Several studies have found a link between DII and neurodegenerative disease outcomes. However, evidence is scarce on the involvement of DII-evaluated diet-induced inflammation in new-onset AD or any other cause of dementia.
Study: Association between dietary inflammatory index score and incident dementia: results from the Framingham heart Study offspring cohort. Image Credit: Burdun Iliya / Shutterstock
*Important notice: medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
About the study
In the present observational longitudinal study, researchers determined the association between Dietary Inflammatory Index scores and dementia risk due to AD or any other cause.
Dementia surveillance was carried out until 2020. The Framingham Heart Study (FHS) cohort data were evaluated between December 2020 and June 2022. Individuals filled out the 126.0-component food frequency questionnaire (FFQ), administered at the community-based examination cycles 7.0 (between 1998 and 2001) and 5.0 (between 1991 and 1995) or 6.0 (between 1995 and 1998).
The study outcome was new-onset AD or any other cause of dementia. The study exposure was the cumulative Dietary Inflammatory Index score, derived based on prior studies that linked individual diet-related factors to inflammatory biomarkers such as tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), and interleukins (ILs)-1β, 4, 6, and 10. The Dietary Inflammatory Index was calculated using the validated 131.0-component Harvard semi-quantitative food frequency questionnaire.
The cumulative Dietary Inflammatory Index score was obtained by taking an average of the Dietary Inflammatory Index scores across cycles 7.0 and 5.0 or 6.0. Cox proportional hazard modeling was performed to calculate the hazard ratios (HRs), adjusting for age, sex, body mass index, educational attainment, apolipoprotein ε4 (APOE ε4) status, smoking habits, physical exercise, total calorie intake, total cholesterol (TC) to high-density lipoprotein-cholesterol (HDL-C) ratio, and lipid-lowering drug use.
In the secondary analyses, the team determined the associations between the Dietary Inflammatory Index scores and type 2 diabetes, hypertension, gender, apolipoprotein ε4 status, cardiovascular disease, and hypertension individually. Dementia was diagnosed by neuropsychologists and neurologists using neurologic examination findings, neuropsychological evaluations, neuroimaging reports, hospital/outpatient clinic/nursing home records, family member interviews, and autopsy reports (whenever available).
The team used the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) criteria to diagnose any-cause dementia, whereas the National Institute of Neurological and Communicative Disorders and Stroke and the AD and Related Disorders Association (NINCDS-ADRDA) criteria to diagnose AD dementia.
Among the enrolled individuals, 1,326 individuals aged below 60 years, 10 with prevalent dementia, 73 with no follow-up for dementia, and 643 with missing information on more than 13 FFQ components were excluded from the analysis. In addition, those with other neurological disorders or abnormal total calorie intake (less than 600.0 or more than 3,999.0 kcal for females and less than 600.0 or more than 4,199.0 kcal for males) were excluded.
Results and discussion
In total, 1,487 individuals were included, among whom the mean age was 69 years, 53% were female, 32% were college graduates, and 246 individuals developed any-cause dementia (inclusive of 187 AD patients) over 22 years of follow-up (median: 13 years). The mean Dietary Inflammatory Index score was -0·3, indicating that the sample population consumed anti-inflammatory diets.
Higher or pro-inflammatory Dietary Inflammatory Index scores were linked to increases in any-cause and AD dementia incidences, adjusting for participants' gender and age (HR, 1.2), and the associations remained unaltered after additional adjustments for clinical, lifestyle, and demographic variables (HR, 1.2). The secondary analyses showed non-significant associations between the Dietary Inflammatory Index scores and apolipoprotein ε4, sex, type 2 diabetes, cardiovascular disease, and hypertension associated with new-onset Alzheimer's or any-cause dementia.
Studies have reported that systemic inflammation contributes to dementia. Inflammaging, which stimulates microglial macrophages to create pro-inflammatory cytokines, is a driving force in systemic inflammation. Neuronal loss, cerebral small artery disease, neurodegeneration, and diminished brain capacity can all result from the production of these cytokines.
Another possibility is that beta-amyloid-induced brain damage promotes cytokine production. Cytokines in the brain lead to an increase in beta-amyloid plaque production, which is a characteristic of Alzheimer's disease. Dietary pro-inflammatory components, such as saturated fatty acids, trans-fatty acids, and overall calorie consumption, are linked to chronic systemic inflammation.
Overall, the study findings showed that higher Dietary Inflammatory Index scores were linked to a higher risk of new-onset dementia due to AD or any other cause, corroborating the results of previous studies. Diets correlated with low Dietary Inflammatory Index scores might prevent dementia development in later life, and individuals would benefit from incorporating dietary interventions into population-level health preventive strategies for dementia. However, further research, including longitudinal studies determining the associations among diverse populations, is required to validate the findings.
*Important notice: medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
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