In a recent study posted to the medRxiv preprint* server, researchers in the US investigated whether higher Dietary Inflammatory Index (DII) scores were related to an increased incidence of dementia resulting from Alzheimer’s disease (AD) or some other cause.

Dementia is one among the world’s most vital health and social care issues. The DII was created primarily to judge the inflammatory contents of the eating regimen. Several studies have found a link between DII and neurodegenerative disease outcomes. Nevertheless, evidence is scarce on the involvement of DII-evaluated diet-induced inflammation in new-onset AD or some other reason behind dementia.

Study: Association between dietary inflammatory index rating and incident dementia: results from the Framingham heart Study offspring cohort. Image Credit: Burdun Iliya / Shutterstock

*Necessary notice: medRxiv publishes preliminary scientific reports that usually are not peer-reviewed and, subsequently, mustn’t be considered conclusive, guide clinical practice/health-related behavior, or treated as established information.

In regards to the study

In the current observational longitudinal study, researchers determined the association between Dietary Inflammatory Index scores and dementia risk resulting from AD or some 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 on 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 final result was new-onset AD or some other reason behind dementia. The study exposure was the cumulative Dietary Inflammatory Index rating, derived based on prior studies that linked individual diet-related aspects to inflammatory biomarkers equivalent to 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 rating was obtained by taking a median 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 exertion, total calorie intake, total cholesterol (TC) to high-density lipoprotein-cholesterol (HDL-C) ratio, and lipid-lowering drug use.

Within the secondary analyses, the team determined the associations between the Dietary Inflammatory Index scores and kind 2 diabetes, hypertension, gender, apolipoprotein ε4 status, heart problems, and hypertension individually. Dementia was diagnosed by neuropsychologists and neurologists using neurologic examination findings, neuropsychological evaluations, neuroimaging reports, hospital/outpatient clinic/nursing home records, member of the family interviews, and autopsy reports (at any time when 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 many 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 greater than 13 FFQ components were excluded from the evaluation. As well as, those with other neurological disorders or abnormal total calorie intake (lower than 600.0 or greater than 3,999.0 kcal for females and lower than 600.0 or greater than 4,199.0 kcal for males) were excluded.

Results and discussion

In total, 1,487 individuals were included, amongst 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 rating 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, heart problems, and hypertension related to 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 capability can all result from the production of those cytokines.

One other possibility is that beta-amyloid-induced brain damage promotes cytokine production. Cytokines within the brain result in a rise in beta-amyloid plaque production, which is a characteristic of Alzheimer’s disease. Dietary pro-inflammatory components, equivalent to 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 the next risk of new-onset dementia resulting from AD or some other cause, corroborating the outcomes of previous studies. Diets correlated with low Dietary Inflammatory Index scores might prevent dementia development in later life, and individuals would profit from incorporating dietary interventions into population-level health preventive strategies for dementia. Nevertheless, further research, including longitudinal studies determining the associations amongst diverse populations, is required to validate the findings.

*Necessary notice: medRxiv publishes preliminary scientific reports that usually are not peer-reviewed and, subsequently, mustn’t be considered conclusive, guide clinical practice/health-related behavior, or treated as established information.