https://nutritionj.biomedcentral.com/ar ... 24-00966-w
only N=19 ApoE carriers, but the data pointed to benefits of a Mediterranean diet. more data exists in the supplementary tables 4 and 5. I only skimmed the material, someone else can look at it further if they want.
Effect of APOE genotype APOE differences in cognition
At baseline, there were no differences in cognitive performance based on APOE genotype (Supplementary Table 4). After 1 year of MedDiet intervention, both APOE-ε4 carriers and noncarriers exhibited improvements in global cognition and memory (p < 0.05), with no significant differences between groups (Supplementary Table 5). However, the Cohen’s d effect size of differences ranged 0.30 to 0.57, favoring APOE-ε4 carriers. After 3 years, global cognition and executive functioning composites improved in APOE-ε4 noncarriers but, on average, there was no significant change in these composites in APOE-ε4 carriers. However, although the Cohen’s d effect size of differences in cognitive change was moderate (-0.52 for global cognition and − 0.46 for memory), multivariable-adjusted models showed no significant differences between groups, except for the specific domain of visuoconstructive praxis and attention favoring APOE-ε4 noncarriers (Cohen’s d of -0.74, p = 0.010).
APOE differences in eCBs and NAEs
At baseline, the concentrations of eCBs and NAEs did not differ according to APOE genotype (Supplementary Table 6). After 6 months of MedDiet intervention, 2-AG, AEA, and several NAEs (OEA, PEA, DHEA, DGLEA, LEA, POEA, and SEA) decreased in APOE-ε4 noncarriers but remained unchanged in APOE-ε4 carriers (Supplementary Table 7). Larger differences between groups were observed for OEA (Cohen’s d = 1.08, p = 0.009) and PEA (Cohen’s d = 1.09, p = 0.009), and smaller differences were detected for AEA (Cohen’s d = 0.34, p = 0.003), LEA (Cohen’s d = 0.38, p = 0.007) and DEA (Cohen’s d = 0.14, p = 0.006) and DGLEA (Cohen’s d = 0.10, p = 0.048). After 1 year, APOE-ε4 noncarriers exhibited greater increases in the PEA/AEA ratio (Cohen’s d=-1.02, p = 0.031). Similarly, APOE-ε4 noncarriers showed greater increases in the DHEA/AEA ratio after 1 year (Cohen’s d=-0.36, p = 0.083) and 3 years (Cohen’s d=-0.30, p = 0.015).
APOE differences in cardiovascular and lifestyle risk factors
At baseline, cardiovascular and lifestyle risk factors did not differ according to APOE genotype (Supplementary Table 8). Between-group differences in changes in these factors were detected in terms of diastolic blood pressure and total cholesterol (Supplementary Table 9). Accordingly, after 6 months, APOE-ε4 carriers showed greater reductions in diastolic blood pressure than noncarriers (mean change of -8.0 vs. -3.6 mmHg, Cohen’s d= -1.64, p = 0.053). Similarly, after 1 year, APOE-ε4 carriers experienced greater reductions in total cholesterol than noncarriers (mean change of -9.0 vs. 3.7 mg/dL, Cohen’s d= -2.09, p = 0.045).
Association between eCBs and cognition by APOE genotype
As shown in Fig. 4A-B, within-subject changes in 2-AG concentrations after 1 year were negatively associated with changes in global cognition (β = -0.02, 95%CI -0.04, 0.00; pGAM = 0.012) and executive functions (β = -0.03, 95%CI -0.06, 0.00; pGAM =0.043) among APOE-ε4 carriers. In turn, within-subject change in the OEA/AEA ratio after 3 years was positively associated with change in executive function among APOE-ε4 noncarriers (Fig. 4C), and this relationship was linear (β = 0.05, 95%CI 0.00, 0.10; pGAM = 0.010).
