Population-based studies have shown both beneficial and neutral associations between dairy consumption and kidney function outcomes. We investigated the association between dairy products and kidney ...function decline in drug-treated post-myocardial infarction (MI) patients.
We analysed data of 2169 post–MI patients (aged 60–80 years, 81% male) of the Alpha Omega Cohort. Dietary data were collected at baseline (2002–2006) using a validated 203-item food frequency questionnaire. The 2021 Chronic Kidney Disease Epidemiology (CKD-EPI) equation was used to estimate 40-months change in creatinine-cystatin C based glomerular filtration rate (eGFRcr-cysC, mL/min per 1.73 m2). Beta coefficients and 95% confidence intervals (CIs) for dairy products in relation to annual eGFRcr-cysC change were obtained from multivariable linear regression, adjusted for age, sex, energy intake, and other lifestyle and dietary factors.
Baseline energy-adjusted median intakes were 64 g/day for total milk, 20 g/day for hard cheeses, 18 g/day for plain yogurt, and 70 g/day for dairy desserts. Mean ± SD eGFRcr-cysC was 84 ± 20 (13% with CKD), and annual eGFRcr-cysC change was −1.71 ± 3.85. In multivariable models, high vs. low intakes of total milk, cheese, and dairy desserts were not associated with annual eGFRcr-cysC change (βtotal milk: −0.21 −0.60; 0.19, βcheese: −0.08 −0.52; 0.36, βdairy desserts: −0.24 −0.72; 0.24). High vs. low intake of yogurt was adversely associated with annual eGFRcr-cysC change (βtotal yogurt: −0.50 −0.91;-0.09), but subsequent spline analyses showed no clear dose–response association.
Intakes of milk, cheese or dairy desserts were not associated with a delayed kidney function decline after MI. The observed adverse association for yogurt should be interpreted with caution. Our findings require confirmation in other cohorts of coronary heart disease patients.
Purpose
We examined the relation between diet quality, its components and kidney function decline in post-myocardial infarction (MI) patients, and we explored differences by genetic risk of chronic ...kidney disease (CKD).
Methods
We analysed 2169 patients from the Alpha Omega Cohort (aged 60–80 years, 81% male). Dietary intake was assessed at baseline (2002–2006) using a validated food-frequency questionnaire and diet quality was defined using the Dutch Healthy Diet Cardiovascular Disease (DHD-CVD) index. We calculated 40-months change in estimated glomerular filtration rate (eGFR, mL/min per 1.73m
2
). We constructed a weighted genetic risk score (GRS) for CKD using 88 single nucleotide polymorphisms previously linked to CKD. Betas with 95%-confidence intervals (CIs) were obtained using multivariable linear regression models for the association between DHD-CVD index and its components and eGFR change, by GRS.
Results
The average DHD-CVD index was 79 (SD 15) points and annual eGFR decline was 1.71 (SD 3.86) mL/min per 1.73 m
2
. The DHD-CVD index was not associated with annual eGFR change (per 1-SD increment in adherence score: -0.09 95% CI -0.26,0.08). Results for adherence to guidelines for red meat showed less annual eGFR decline (per 1-SD: 0.21 0.04,0.38), whereas more annual eGFR decline was found for legumes and dairy (per 1-SD: -0.20
legumes
-0.37,-0.04 and − 0.18
dairy
-0.34,-0.01). Generally similar results were obtained in strata of GRS.
Conclusion
The DHD-CVD index for overall adherence to Dutch dietary guidelines for CVD patients was not associated with kidney function decline after MI, irrespective of genetic CKD risk. The preferred dietary pattern for CKD prevention in CVD patients warrants further research.
Population-based studies have suggested a protective effect of coffee against development of chronic kidney disease (CKD), possibly through coffee's anti-inflammatory and antioxidant compounds. ...Studies on coffee and kidney function decline in the general population are scarce. We studied associations of habitual coffee consumption with repeated assessments of estimated glomerular filtration rate (eGFR) and urinary albumin-to-creatinine ratio (ACR).
We used data from 7,914 participants of the population-based Rotterdam Study. Baseline coffee consumption data (cups/day) were obtained from home interviews and validated food frequency questionnaires (1997–2008). Repeated assessments of eGFR (ml/min per 1.73 m2, 1997–2014) were calculated according to the creatinine-based CKD Epidemiology Collaboration equation of 2012. Repeated assessments of urinary albumin and creatinine were used to estimate ACR (mg/g, 2006–2014). Data were analyzed by applying linear mixed models, adjusted for sociodemographic, lifestyle and dietary factors, and cardiovascular disease risk factors. Predefined subgroup analyses were performed stratified by CKD risk factors.
Participants’ mean (SD) baseline age was 66 (10) years, 57% were women and median IQR coffee consumption was 3.0 2.0, 5.0 cups/day. Those drinking more coffee were more likely to smoke, and to have type 2 diabetes (T2D) and obesity. Mean eGFR was 79 (15) ml/min per 1.73 m2. In the total study population, coffee was not associated with longitudinal eGFR during a median of 5.4 years of follow-up (β = 0.04 ml/min per 1.73 m2 per one cup/day 95% CI: −0.10,0.18). However, among those aged >70 years, one additional coffee cup/day was associated with on average 0.84 (0.51,1.18) ml/min per 1.73 m2 higher longitudinal eGFR. Among obese participants this estimate was 0.32 (0.01,0.63). A protective trend was also observed among former smokers (0.17 −0.03,0.39) and those with T2D (0.42 −0.05,0.88). Coffee was not associated with longitudinal ACR (0.01 mg/ml −0.01,0.02).
While coffee was not associated with eGFR and ACR in the total population, more coffee consumption was associated with higher longitudinal eGFR among those at higher risk for CKD, i.e., among those aged 70+ and obese participants. These findings require confirmation in other prospective cohort studies.
Aims
To investigate the association between circulating lipoprotein(a) (Lp(a)) and risk of all-cause and cause-specific mortality in the general population and in patients with chronic diseases, and ...to elucidate the dose-response relations.
Methods and results
We searched literature to find prospective studies reporting adjusted risk estimates on the association of Lp(a) and mortality outcomes. Forty-three publications, reporting on 75 studies (957,253 participants), were included. The hazard ratios (HRs) and 95% confidence intervals (95%CI ) for the top versus bottom tertile of Lp(a) levels and risk of all-cause mortality were 1.09 (95%CI: 1.01–1.18, I
2
: 75.34%, n = 19) in the general population and 1.18 (95%CI: 1.04–1.34, I
2
: 52.5%, n = 12) in patients with cardiovascular diseases (CVD). The HRs for CVD mortality were 1.33 (95%CI: 1.11–1.58, I
2
: 82.8%, n = 31) in the general population, 1.25 (95%CI: 1.10–1.43, I
2
: 54.3%, n = 17) in patients with CVD and 2.53 (95%CI: 1.13–5.64, I
2
: 66%, n = 4) in patients with diabetes mellitus. Linear dose-response analyses revealed that each 50 mg/dL increase in Lp(a) levels was associated with 31% and 15% greater risk of CVD death in the general population and in patients with CVD. No non-linear dose-response association was observed between Lp(a) levels and risk of all-cause or CVD mortality in the general population or in patients with CVD (P
nonlinearity
> 0.05).
Conclusion
This study provides further evidence that higher Lp(a) levels are associated with higher risk of all-cause mortality and CVD-death in the general population and in patients with CVD. These findings support the ESC/EAS Guidelines that recommend Lp(a) should be measured at least once in each adult person’s lifetime, since our study suggests those with higher Lp(a) might also have higher risk of mortality.
•This systematic review summarizes current evidence about the effects of whole-diet interventions on cardiovascular risk factors among postmenopausal women.•Due to the large heterogeneity in ...intervention diets, comparison groups, intervention durations, and population characteristics in the limited number of studies that are currently available, overall findings are inconclusive.•Fat-modified diets are the most studied dietary interventions, and may improve concentrations of total and low-density lipoprotein cholesterol, systolic blood pressure, fasting blood sugar, and apolipoprotein A in comparison with the control diets.•Some adverse effects of fat-modified diets on other lipid profile markers and insignificant effects on glycemic indices and blood pressure were also observed.•Further well-designed clinical trials to find optimal diets for cardiovascular disease prevention in postmenopausal women are urgently needed.
Menopause is accompanied by many metabolic changes, increasing the risk of cardiometabolic diseases. The impact of diet, as a modifiable lifestyle factor, on cardiovascular health in general populations has been well established. The purpose of this systematic review is to summarize the evidence on the effects of whole diet on lipid profile, glycemic indices, and blood pressure in postmenopausal women.
Embase, Medline, Cochrane Central Register of Controlled Trials, and Google Scholar were searched from inception to February 2021. We included controlled clinical trials in postmenopausal women that assessed the effect of a whole-diet intervention on lipid profile, glycemic indices, and/or blood pressure. The risk of bias in individual studies was assessed using RoB 2 and ROBINS-I tools.
Among 2,134 references, 21 trials met all eligibility criteria. Overall, results were heterogenuous and inconsistent. Compared to control diets, some studies showed that participants experienced improvements in total cholesterol (TC), low-density lipoprotein cholesterol (LDL), systolic blood pressure (SBP), fasting blood sugar (FBS), and apolipoprotein A (Apo-A) after following fat-modified diets, but some adverse effects on triglycerides (TG), very low-density lipoprotein cholesterol (VLDL), lipoprotein(a) (Lp(a)), and high-density lipoprotein cholesterol (HDL) concentrations were also observed. A limited number of trials found some effects of the Paleolithic, weight-loss, plant-based, or energy-restricted diets, or of following American Heart Association recommendations on TG, TC, HDL, insulin, FBS, or insulin resistance.
Current evidence suggests that diet may affect levels of some lipid profile markers, glycemic indices, and blood pressure among postmenopausal women. However, due to the large heterogeneity in intervention diets, comparison groups, intervention durations, and population characteristics, findings are inconclusive. Further well-designed clinical trials are needed on dietary interventions to reduce cardiovascular risk in postmenopausal women.
Whether coffee consumption is associated with changes in estimated glomerular filtration rate (eGFR) is unknown. We investigated the relationship between coffee consumption and annual eGFR change in ...a large Dutch population-based study.
This study was performed in 78,346 participants without chronic kidney disease (CKD) in the population-based Lifelines Cohort Study. Coffee consumption was assessed at baseline using food frequency questionnaires. Outcomes were annual eGFR change and a composite kidney outcome (defined as eGFR <60 mL/min per 1.73 m2 or >20 % eGFR decline). Multivariable linear and logistic regression analyses were used to evaluate the associations of coffee consumption (categories and cups/day) with kidney outcomes. Overall, 90 % of the participants drank coffee daily and 36 % drank >2–4 cups/day. Unadjusted mean ± SD annual eGFR change ranged from −2.86 ± 2.96 (for non-coffee drinkers) to −2.35 ± 2.62 (for participants consuming >6 cups/day) mL/min per 1.73 m2. During 3.6 ± 0.9 years follow-up, 11.1 % of participants reached the composite kidney outcome. As compared to non-coffee drinkers, higher coffee consumption was associated with less annual eGFR decline in multivariable models (β 95 % CIs ranged from 0.15 0.07, 0.22 for >0–2 cups/day to 0.29 0.20, 0.38 for >6 cups/day, P-trend <0.001). Consumption of one more cup of coffee per day was associated with a 3 % lower risk of the composite kidney outcome (OR 95%CI, 0.97 0.96, 0.99). The inverse association was more pronounced in a subgroup of individuals with diabetes.
Coffee consumption was inversely associated with annual eGFR change and CKD risk in a large Dutch population-based cohort.
•In a general Dutch population, coffee drinkers experienced a slower kidney function decline over time, compared to non-coffee drinkers.•Coffee was related to a lower risk of chronic kidney disease in a dose-dependent manner, especially in individuals with diabetes.•Filtered, unsweetened coffee may be considered as a healthy beverage in a kidney-friendly diet.•Beneficial effects of coffee on the kidneys warrant confirmation in randomised controlled trials.
Age-related kidney function decline is accelerated in patients with coronary heart disease (CHD). CHD and chronic kidney disease may share common etiologies. We examined plasma fatty acids (FAs) as ...novel biomarkers of kidney function decline after myocardial infarction (MI).
The analysis included 2329 Dutch post–MI patients aged 60-80y (Alpha Omega Cohort) most receiving state-of-the-art medications. Plasma FAs (% total FAs) in cholesteryl esters were assessed at baseline (2002–2006), and ∼40 months change in creatinine-cystatin C based glomerular filtration rate was estimated (eGFR, in ml/min per 1.73 m2). Beta coefficients for annual eGFR change in relation to plasma linoleic acid (LA; 50.1% of total FAs in CE), omega-3 FAs (EPA + DHA; 1.7%), odd-chain FAs (C15:0 and C17:0; 0.2%), and C14:0 (0.7%) were obtained from linear regression analyses adjusted for age, sex, smoking, and alcohol intake. Mean baseline eGFR ±SD was 78.5 ± 18.7, which declined by 4.7 ± 13.1 during follow-up, or 1.4 ± 3.9 per year. The annual decline in eGFR was less in patients with higher plasma LA (adjusted beta: 0.40 for LA >47 vs ≤ 47%, 95% CI: 0.01; 0.78; p = 0.046). Associations of plasma LA with annual eGFR decline were stronger in 437 patients with diabetes (1.21, 0.24; 2.19) and in 402 patients with CKD (eGFR<60; 0.90, −0.09; 1.89). Weaker, non-significant associations with kidney function decline were observed for the other plasma FAs.
Higher plasma LA may be a good predictor of less kidney function decline after MI, particularly in patients with diabetes.
The Alpha Omega Cohort is registered with clinicaltrials.gov, NCT03192410.
•Post-myocardial infarction patients have accelerated kidney function decline.•Plasma fatty acids have been related to cardiometabolic diseases.•Plasma linoleic acid predicted less kidney function loss, especially in diabetics.•Plasma n-3 fatty acids in cholesteryl esters did not predict kidney function loss.•Plasma odd-chain fatty acids did not predict kidney function loss.
To assess the prospective associations of circulating levels of omega 3 polyunsaturated fatty acid (n-3 PUFA) biomarkers (including plant derived α linolenic acid and seafood derived eicosapentaenoic ...acid, docosapentaenoic acid, and docosahexaenoic acid) with incident chronic kidney disease (CKD).
Pooled analysis.
A consortium of 19 studies from 12 countries identified up to May 2020.
Prospective studies with measured n-3 PUFA biomarker data and incident CKD based on estimated glomerular filtration rate.
Each participating cohort conducted de novo analysis with prespecified and consistent exposures, outcomes, covariates, and models. The results were pooled across cohorts using inverse variance weighted meta-analysis.
Primary outcome of incident CKD was defined as new onset estimated glomerular filtration rate <60 mL/min/1.73 m
. In a sensitivity analysis, incident CKD was defined as new onset estimated glomerular filtration rate <60 mL/min/1.73 m
and <75% of baseline rate.
25 570 participants were included in the primary outcome analysis and 4944 (19.3%) developed incident CKD during follow-up (weighted median 11.3 years). In multivariable adjusted models, higher levels of total seafood n-3 PUFAs were associated with a lower incident CKD risk (relative risk per interquintile range 0.92, 95% confidence interval 0.86 to 0.98; P=0.009, I
=9.9%). In categorical analyses, participants with total seafood n-3 PUFA level in the highest fifth had 13% lower risk of incident CKD compared with those in the lowest fifth (0.87, 0.80 to 0.96; P=0.005, I
=0.0%). Plant derived α linolenic acid levels were not associated with incident CKD (1.00, 0.94 to 1.06; P=0.94, I
=5.8%). Similar results were obtained in the sensitivity analysis. The association appeared consistent across subgroups by age (≥60
<60 years), estimated glomerular filtration rate (60-89
≥90 mL/min/1.73 m
), hypertension, diabetes, and coronary heart disease at baseline.
Higher seafood derived n-3 PUFA levels were associated with lower risk of incident CKD, although this association was not found for plant derived n-3 PUFAs. These results support a favourable role for seafood derived n-3 PUFAs in preventing CKD.
It is unknown whether dietary intake of polyunsaturated fatty acids (PUFA) modifies the cardiovascular disease (CVD) risk associated with a family history of CVD. We assessed interactions between ...biomarkers of low PUFA intake and a family history in relation to long-term CVD risk in a large consortium.
Blood and tissue PUFA data from 40 885 CVD-free adults were assessed. PUFA levels ≤25th percentile were considered to reflect low intake of linoleic, alpha-linolenic, and eicosapentaenoic/docosahexaenoic acids (EPA/DHA). Family history was defined as having ≥1 first-degree relative who experienced a CVD event. Relative risks with 95% CI of CVD were estimated using Cox regression and meta-analyzed. Interactions were assessed by analyzing product terms and calculating relative excess risk due to interaction.
After multivariable adjustments, a significant interaction between low EPA/DHA and family history was observed (product term pooled RR, 1.09 95% CI, 1.02-1.16;
=0.01). The pooled relative risk of CVD associated with the combined exposure to low EPA/DHA, and family history was 1.41 (95% CI, 1.30-1.54), whereas it was 1.25 (95% CI, 1.16-1.33) for family history alone and 1.06 (95% CI, 0.98-1.14) for EPA/DHA alone, compared with those with neither exposure. The relative excess risk due to interaction results indicated no interactions.
A significant interaction between biomarkers of low EPA/DHA intake, but not the other PUFA, and a family history was observed. This novel finding might suggest a need to emphasize the benefit of consuming oily fish for individuals with a family history of CVD.
Background Observational studies have shown that women with an early menopause are at higher risk of stroke compared with women with a later menopause. However, associations with stroke subtypes are ...inconsistent, and the causality is unclear. Methods and Results We analyzed data of the UK Biobank and EPIC-CVD (European Prospective Investigation Into Cancer and Nutrition-Cardiovascular Diseases) study. A total of 204 244 postmenopausal women without a history of stroke at baseline were included (7883 from EPIC-CVD 5292 from the subcohort, 196 361 from the UK Biobank). Pooled mean baseline age was 58.9 years (SD, 5.8), and pooled mean age at menopause was 47.8 years (SD, 6.2). Over a median follow-up of 12.6 years (interquartile range, 11.8-13.3), 6770 women experienced a stroke (5155 ischemic strokes, 1615 hemorrhagic strokes, 976 intracerebral hemorrhages, and 639 subarachnoid hemorrhages). In multivariable adjusted observational Cox regression analyses, the pooled hazard ratios per 5 years younger age at menopause were 1.09 (95% CI, 1.07-1.12) for stroke, 1.09 (95% CI, 1.06-1.13) for ischemic stroke, 1.10 (95% CI, 1.04-1.16) for hemorrhagic stroke, 1.14 (95% CI, 1.08-1.20) for intracerebral hemorrhage, and 1.00 (95% CI, 0.84-1.20) for subarachnoid hemorrhage. When using 2-sample Mendelian randomization analysis, we found no statistically significant association between genetically proxied age at menopause and risk of any type of stroke. Conclusions In our study, earlier age at menopause was related to a higher risk of stroke. We found no statistically significant association between genetically proxied age at menopause and risk of stroke, suggesting no causal relationship.
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