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Lifestyle intervention in elderly (ID 1404)
Is there a role for diet in secondary prevention? (ID 1405)
O055 - MEDITERRANEAN DIET PRESERVES KIDNEY FUNCTION IN PATIENTS WITH TYPE 2 DIABETES AND OBESITY: FROM THE CORDIOPREV STUDY. (ID 356)
Abstract
Background and Aims
Type 2 diabetes mellitus (T2DM) is considered an independent risk factor for chronic kidney disease (CKD); however, the distinctive contribution of obesity remains controversial. Our main aim was to establish an accurate contribution of obesity, with T2DM or not, to kidney function in patients with coronary heart disease (CHD), highly predisposed to renal complications, to assign the most appropriate dietary strategy.
Methods
1002 CHD patients from the CORDIOPREV study (Spain) were classified into four groups: Non-Obese/Non-T2DM, Obese/Non-T2DM, Non-Obese/T2DM and Obese/T2DM. Kidney function was assessed by estimated glomerular filtration rate (eGFR) after 5-years of dietary intervention with a low-fat or a Mediterranean diet. Generalized linear model (GLM) analysis were performed to determine the contribution of obesity and T2DM to changes in eGFR.
Results
Obese/T2DM patients showed lower baseline eGFR compared to those without T2DM (p < 0.001). After dietary intervention, the Mediterranean diet produced a lower decline of eGFR only in patients with concomitant T2DM and obesity, compared to low-fat diet (p = 0.014). GLM analysis showed that Obese/T2DM and Non-obese/T2DM patients (95% CI -4.966 to -1.080 and 95% CI -5.386 to -1.117, respectively, compared to Non-obese/Non-T2DM patients) and consumption of a low-fat diet determined more likelihood of declining eGFR.
Conclusions
The presence of obesity provided an additive effect to T2DM determining a greater impairment of kidney function in CHD patients. Long-term consumption of a Mediterranean diet, compared to low-fat diet, may preserve kidney function, providing a dietary strategy for the reduction of CKD complications in the context of secondary prevention of cardiovascular disease.
O056 - METHYLOMIC SIGNATURES MEDIATE THE EFFECT OF PSYCHOSOCIAL STRESS ON CORONARY HEART DISEASE (ID 438)
Abstract
Background and Aims
Elevated psychosocial stress has been repeatedly associated with altered immune function and increased coronary heart disease (CHD) risk, but the mechanisms underlying these associations are unclear. DNA methylation, a critical epigenetic process in humans, has emerged as a key link between environmental exposures and human health. Our aim was to examine whether methylomic changes mediate the effect of psychosocial stress on incident CHD.
Methods
Analyses included 3584 participants of the Women's Health Initiative (WHI). Stressful life events (SLEs) were measured with a self-administered questionnaire. Incident CHD was ascertained by certified personnel following standardized protocols. Genome-wide DNA (CpG) methylation was measured with the Illumina 450K array. Regression models identified stress-associated CpG sites and tested if their methylation levels statistically mediate the SLEs-CHD relationship. All models controlled for socioeconomic factors, lifestyle parameters, technical batch variables, and methylation-estimated blood cell proportions.
Results
In adjusted analyses, greater stress burden predicted higher incident CHD (HR=1.22, p=0.013) and was associated with methylome-wide differences at 872 CpG sites at false discovery rate (FDR)-adjusted p<0.05, 100 CpGs at FDR p<0.01, and 14 CpGs at the Bonferroni-adjusted p. Methylation risk scores (MRS) derived from the stress-associated CpGs predicted incident CHD (all p<0.008). Moreover, the effect of SLEs on CHD was significantly mediated by MRS100 and MRS14 (p<0.05).
Conclusions
Our findings suggest that methylomic changes mediate the effect of stress burden on incident CHD. These findings are now being replicated in independent human cohorts affiliated with the Trans-Omics for Precision Medicine (TOPMed) program and are further mechanistically dissected in immune cell model of stress.
O057 - NEW EVIDENCE OF MODIFIABLE RISK FACTORS FOR ALZHEIMER’S DISEASE (ID 520)
Abstract
Background and Aims
Forty percent of dementia is potentially preventable by modifying 12 risk factors throughout the life course. Robust evidence for most of these risk factors is however lacking. We therefore aimed to comprehensively disentangle the causal associations between 12 modifiable risk factors and risk of Alzheimer’s disease (AD).
Methods
We performed two-sample univariable and multivariable Mendelian randomization. Independent genetic variants associated with modifiable risk factors were selected as instrumental variables from large genome-wide association studies. We obtained outcome data for AD from the European Alzheimer’s & Dementia Biobank (EADB) including 39,106 clinically diagnosed cases, 46,828 proxy-AD cases and 401,577 controls. Main analyses were conducted using the EADB clinically diagnosed endpoint data.
Results
Genetically determined high HDL cholesterol concentrations were associated with increased risk of AD [odds ratio (OR) 1.10 (95% CI: 1.05-1.16)] per one-SD increase. Genetically determined per 10-mmHg increase of systolic blood pressure was associated with increased risk of AD after adjusting for diastolic blood pressure [OR (95% CI): 1.22 (1.02-1.46)]. To minimize bias due to sample overlap, we both excluded the entire UK Biobank from the EADB consortium and used cross-trait linkage disequilibrium-score regression to account for sample overlap, and the estimates remained similar. No robust genetic associations with AD were identified for other lipid traits, smoking, alcohol consumption, body mass index, and type 2 diabetes.
Conclusions
The results supported novel causal associations between high HDL cholesterol concentrations and high systolic blood with high risk of AD. These findings may inspire new drug targeting and improved prevention implementation.