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The study itself (abstract and introduction pasted below; worth a full read at the source, linked below):

Diet’s Role in Modifying Risk of Alzheimer’s Disease: History and Present Understanding

Authors: Grant, William B.a; * | Blake, Steven M.b

https://content.iospress.com/articles/journal-of-alzheimers-disease/jad230418

Abstract
Diet is an important nonpharmacological risk-modifying factor for Alzheimer’s disease (AD). The approaches used here to assess diet’s role in the risk of AD include multi-country ecological studies, prospective and cross-sectional observational studies, and laboratory studies. Ecological studies have identified fat, meat, and obesity from high-energy diets as important risk factors for AD and reported that AD rates peak about 15–20 years after national dietary changes. Observational studies have compared the Western dietary pattern with those of the Dietary Approaches to Stop Hypertension (DASH), Mediterranean (MedDi), and Mediterranean–DASH Intervention for Neurodegenerative Delay (MIND) diets. Those studies identified AD risk factors including higher consumption of saturated and total fats, meat, and ultraprocessed foods and a lower risk of AD with higher consumption of fruits, legumes, nuts, omega-3 fatty acids, vegetables, and whole grains. Diet-induced factors associated with a significant risk of AD include inflammation, insulin resistance, oxidative stress, elevated homocysteine, dietary advanced glycation end products, and trimethylamine N-oxide. The molecular mechanisms by which dietary bioactive components and specific foods affect risk of AD are discussed. Given most countries’ entrenched food supply systems, the upward trends of AD rates would be hard to reverse. However, for people willing and able, a low–animal product diet with plenty of anti-inflammatory, low–glycemic load foods may be helpful.

INTRODUCTION
Alzheimer’s disease (AD) is the most common cause of dementia characterized by accumulation of tau protein tangles and amyloid-β (Aβ) plaque, progressive loss of neurons, and deterioration of normal brain function.

According to a 2023 review, the global number of people with AD, prodromal AD, and preclinical AD were estimated at 32 million, 69 million, and 315 million, respectively. Together they constituted 416 million across the AD continuum, or 22% of all people aged 50 or older [1]. Thus, AD is a serious health risk. A 2022 article identified 75 genetic risk foci, of which 42 were newly discovered [2]. However, people with genetic risk factors such as apolipoprotein E ɛ4 can modify their risk of developing AD by taking measures to reduce dietary risk factors.

A 2015 meta-analysis of modifiable risk factors for AD identified a healthful dietary pattern as the most important factor with a risk ratio (RR)/odds ratio (OR) of 0.45 (95% confidence interval [CI], 0.23–0.61) with grade II-A level of evidence [3]. The RR/OR values for specific dietary consumption were high folate intake, 0.49 (95% CI, 0.28–0.74), grade I; fish consumption, 0.68 (95% CI, 0.46–0.95), grade II-A; high vitamin E intake, 0.74 (95% CI, 0.63–0.83), grade I; and high vitamin C intake, 0.75 (95% CI, 0.57–0.02), grade I.

A 2020 review outlined the modifiable risk factors for AD throughout the lifespan [4]. In early life, more schooling reduces risk. Starting after age 45 years, many other modifiable risk factors become important. The review identified 10 factors with level A evidence (lack of cognitive activity, hyperhomocysteinemia, increased body mass index (BMI) in late life, depression, stress, diabetes, head trauma, hypertension in midlife, orthostatic hypotension, and education) and 9 factors with level B evidence (obesity in midlife, weight loss in late life, lack of physical exercise, smoking, poor sleep, cardiovascular disease ( CVD), frailty, atrial fibrillation, and lack of vitamin C). Levels of evidence were summarized to represent the quality of scientific evidence on the basis of directness of outcome for AD, credibility of meta-analyses, and consistency of evidence from clinical trials and/or observational studies: level A > level B > level C (based on the evidence level). Several of those factors, identified in boldface, are related to diet, yet diet was not included as a factor. However, a 2021 review did include diet as a modifiable risk factor [5]. That review cited the article by Morris and colleagues in 2015 [6] reporting that the Mediterranean diet (MedDi; hazard ratio [HR] = 0.46; 95% CI, 0.26–0.79), the Dietary Approaches to Stop Hypertension (DASH) diet (Hazard ratio [HR] = 0.61 [95%, CI 0.38–0.97]), and the Mediterranean–DASH Intervention for Neurodegenerative Delay (MIND) diet (HR = 0.47 [95% CI, 0.26–0.76]) were all inversely associated with the risk of AD. The protective effects of those dietary patterns on cognition might be attributed to antioxidant, anti-inflammatory, protective plant polyphenols, antidiabetic effects, and a higher ratio of mono- or polyunsaturated fats to saturated fatty acids (SFAs) [7].

Several ways exist to determine how diet affects risk of AD and to assess their relative influence. Ecological studies compare AD prevalence rates by country or time with respect to dietary supply values of macronutrients several years before the prevalence [8]. Cross-sectional studies compare prevalence of AD with respect to dietary factors [9]. Prospective studies enroll participants, obtain data for many factors, and use a food-frequency questionnaire to determine dietary factors, and then monitor participants for several years and compare dietary patterns for incidence of AD [10]. Such prospective studies also can be used to examine the role of specific foods and food groups in risk of AD [11]. Clinical trials also can be conducted in which diets are modified and changes in bioparameters associated with AD are sought [12]. In addition, once the general risk factors for AD are known, such as inflammation and insulin resistance (IR), the foods that affect those factors can be identified. Each approach can contribute to the understanding of how diet and dietary factors affect risk of AD.

The outline of this review is as follows:

1. A brief history of ecological and observational studies regarding dietary patterns and risk of AD is presented.

2. The mechanisms by which inflammation, IR, and oxidative stress affect risk of AD are discussed, followed by the roles of obesity, advanced glycation end products (AGEs), homocysteine, lipopolysaccharides, arachidonic acid (AA), and trimethylamine N-oxide (TMAO).

3. The effects of various food factors that reduce risk of AD are discussed along with the mechanisms by which they affect risk of AD.