Eat-Lancet Planetary Diet shows no risk of dementia, may protect against Alzheimer's

Eat-Lancet Planetary Diet shows no risk of dementia, may protect against Alzheimer's

Could a planet-friendly diet also protect your brain? New study links eating Lancet eating patterns to a lower risk of dementia, but only if your genes cooperate.

In a recent study inThe Journal of Prevention of Alzheimer's DiseaseThe researchers used a large Swedish cohort (n = 25,898, age = 45-73 years) to elucidate any relationships between Eat-Lancet diet and dementia incidence. The effects of covariates, including Apoe ε4 status, were also estimated. The study results showed that the Eat-Lancet diet does not worsen dementia but may reduce incident dementia in non-carriers of the ApoE ε4 gene.

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The red meat-free participants scored lower on some metrics, challenging assumptions about "all-or-nothing" approaches to planetary health diets.

Advances in medical research and clinical interventions are allowing humans to live longer than ever before. Although the benefits of these advances cannot be understated, they have resulted in more of the global population surviving beyond reproductive age and increased the incidence of non-communicable age-related diseases such as cancer and dementia.

To combat the burden of these diseases, several past and ongoing scientific studies aim to unravel the risk factors associated with these diseases and thereby provide public health authorities with the knowledge necessary to limit their incidence. Using this research, the Lancet Commission on Dementia Prevention identified several (n=14) modifiable factors that may worsen dementia risks, including physical inactivity, smoking, alcohol consumption, and obesity.

While diet was not explicitly listed, previous research has confirmed its association with neurodegenerative outcomes. Some “healthy” diets such as the Mediterranean Diet (MEDI) have been found to reduce the risk of dementia, while unhealthy diets such as the Western Diet (WD) make it worse. Surprisingly, the Eat-Lancet Planetary Health Diet (2019) dementia risk associations remain untested. The diet is primarily plant-based, leading some experts to believe it can reduce mortality risk, while others argue it can negatively impact brain health through nutrient deficiencies.

About the study

The study followed participants for an average of 18 years and offers insights into the ways midlife eating habits could influence brain health much later.

The present study aims to validate the neurodegenerative safety of the ecologically sustainable planetary nutrition diet by examining its risk associations with dementia incidence. Study data were obtained from the Swedish Malmö Study and Cancer Study (MDCS), a long-term, large (n = 68,905) cohort investigation of Swedish individuals initiated between 1991 and 1996.

The present analyzes included individuals aged 45 to 73 years with complete dementia and nutritional data. Study data collected included nutritional assessment, dementia assessment, genetic risk determination, amyloid-β accumulation assessments, and sociodemographic information.

Comprehensive dietary assessment included participants' dietary history recorded using validated 7-day food diaries, participant-completed 168-item food frequency questionnaires (FFQ), and seven Eat-Lancet adherence scores. Scores were obtained from previous publications and categorized into “proportional scores” (n = 4), “binary scores” (n = 2), and “ordinal scale scores” (n = 1). The assessments were subjected to statistical transformations to enable comparisons between different methods.

The Swedish National Patient Register (NPR) established dementia and dementia subtype (all-cause, vascular dementia [VaD] and Alzheimer's disease [AD]) diagnoses. Dementia was classified using the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) and the International Classification of Diseases (ICD-9 and ICD-10).

Genetic predisposition to dementia risk was assessed using apolipoprotein E (APOE) levels as proxies, with APOE ε4 status (carrier/non-carrier) serving as a binary analysis variable. Participants' Aβ42 levels (CSF) measured via innotest ELISA were used for Aβ analyses. Sociodemographic information, specifically body mass index (BMI), physical activity (17 activities), alcohol consumption, education level, and smoking status, was used for potential confounding factor analyses.

Study results

There was no association between following the Eat-Lancet diet and amyloid-β pathology, a hallmark of Alzheimer's that suggests other possible ways diet might protect the brain.

Of the 68,905 MDCs participants, 30,446 met the present study criteria and 25,898 completed dementia and nutrition information. Of these, 6.9% (all-cause = 1,783, VAD = 426, AD = 1,040) were reported to develop dementia by 2014 (follow-up time = 18 years), and 11.5% (n = 2,976) by 2020.

Analysis by the Diet Dementia Association showed that five of the seven scores assessed suggested that dietary adherence to the diet of the meal reduced the risk of developing dementia (overall). After adjusting for education as a potential confounder, three items remained statistically significant, and after fully adjusting for all confounders (including age, gender, season, education, smoking, alcohol, physical activity, BMI, and energy intake), only one score (the Kesse-Guyot score) showed a significant association with reduced all-cause dementia risk.

When assessing AD risk, a score suggested that dietary dietary availability was positively associated with reduced AD risk. Again, this significant association remained only for the Kesse-Guyot score after full adjustment for all confounders.

None of the models (with or without covariate corrections) suggest that food dietary availability increases the risk of dementia and validates its safety.

It is important to note that the direction of effect was similar in most assessments, but the strength and statistical significance of the associations varied depending on the assessment method used to measure adherence to the Eat-Lancet diet. This highlights the importance of how dietary adherence is assessed in such research.

When adjusting for participants' ApoE-ε4 status, logistic regression analyzes revealed an interplay between diet and genetic predisposition to dementia, particularly for non-carriers. Carrier participants showed no changes in their risk, but non-carriers were observed to significantly reduce their overall risk (three scores) and AD risk (five scores) after Eat-Lancet Noidary adherence. VAD risks showed no such associations with genetic status.

No associations were found between nutrition recipient and amyloid-β (Aβ42) pathology measured in the subsample with available CSF data.

The authors also conducted a series of sensitivity analyses, e.g. B. excluding participants with diabetes or those who developed dementia within five years of baseline, they found similar patterns in the results, supporting the robustness of their main findings.

Conclusions

Except for people with diabetes or those who developed dementia shortly after entering the study, the key findings did not change and added confidence to the conclusions.

The present study highlights the neurodegenerative safety of the Eat-Lancet diet, showing that it does not increase the risk of dementia across all assessment metrics. Instead, the diet can significantly reduce the risk of dementia (total and AD), particularly in ApoE ε4 non-carriers.

However, because this was an observational study, the results cannot prove causality, and limitations include the possibility of residual confounding, possible misreporting of dietary intake and dietary changes during the long follow-up period.

“While intervention studies are needed to further clarify the effects of the Eat Lancet diet on dementia incidence, the results of this study demonstrate that environmental sustainability in dietary guidelines can be translated into dementia prevention strategies.”

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