1.
Causal effects of relative fat, protein, and carbohydrate intake on chronic kidney disease: a Mendelian randomization study.
Park, S, Lee, S, Kim, Y, Lee, Y, Kang, MW, Kim, K, Kim, YC, Han, SS, Lee, H, Lee, JP, et al
The American journal of clinical nutrition. 2021;(4):1023-1031
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Abstract
BACKGROUND The effects of specific macronutrients on kidney function independent of total calorie intake have rarely been studied, although the composition of macronutrient intake has been reported to affect health outcomes. OBJECTIVES We aimed to investigate the effects of macronutrient intake ratios on the risk of chronic kidney disease (CKD) by Mendelian randomization (MR) analysis. METHODS The study was an observational cohort study mainly based on the UK Biobank and including MR analysis. First, we evaluated the relative baseline macronutrient composition-that is, the number of calories from each macronutrient divided by total calorie intake-of the diets of UK Biobank participants, and we used Cox regression to assess the incidence of end-stage kidney disease (ESKD) in 65,164 participants with normal kidney function [estimated glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2]. We implemented a genetic instrument for relative fat, protein, and carbohydrate intake developed by a previous genome-wide association study (GWAS) and performed MR analysis. Two-sample MR was performed with the summary statistics from independent CKDGen GWAS for kidney function traits (n = 567,460), including CKD (eGFR <60 mL/min/1.73 m2) and log-transformed eGFR. RESULTS The median relative macronutrient intake composition at baseline was 35% fats, 15% protein, and 50% carbohydrates. Higher relative protein intake in subjects with normal kidney function was significantly associated with a lower risk of incident ESKD (HR: 0.54; 95% CI: 0.30, 0.95) in the observational investigation. Two-sample MR indicated that increased relative fat intake causally increased the risk of kidney function impairment [CKD (OR: 1.94; 95% CI: 1.39, 2.71); log eGFR (β: -0.036; 95% CI: -0.048, -0.024)] and that higher relative protein intake was causally linked to a lower CKD risk [CKD (OR: 0.50; 95% CI: 0.35, 0.72); log eGFR (β: 0.044; 95% CI: 0.030, 0.058)]. CONCLUSIONS A desirable macronutrient composition, including high relative protein intake and low relative fat intake, may causally reduce the risk of CKD in the general population.
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Association between dietary fat intake and mortality from all-causes, cardiovascular disease, and cancer: A systematic review and meta-analysis of prospective cohort studies.
Kim, Y, Je, Y, Giovannucci, EL
Clinical nutrition (Edinburgh, Scotland). 2021;(3):1060-1070
Abstract
BACKGROUND & AIMS The association between dietary fat and mortality remains inconsistent, and recent results for the association between dietary saturated fat and chronic disease are controversial. To quantitatively assess this association, we conducted a meta-analysis of prospective cohort studies. METHODS The PubMed and Web of Science were searched up to February 2020. A random effects model was used. RESULTS Nineteen studies including 1,013,273participants and 195,515deaths were identified. Significant inverse associations between all-cause mortality and a 5% energy increment in intakes of total (RR = 0.99; 95% CI:0.98-1.00), monounsaturated (RR = 0.98; 95% CI:0.97-0.99), and polyunsaturated fat (RR = 0.93; 95% CI:0.89-0.97) were found. A 5% increase in energy from polyunsaturated fat was associated with 5% (RR = 0.95; 95% CI:0.91-0.98) and 4% (RR = 0.96; 95% CI:0.94-0.99) lower mortality from CVD and cancer, respectively. A 1% energy increment in dietary trans-fat was associated with 6% higher risk of mortality from all-causes (RR = 1.06; 95% CI:1.01-1.10) and CVD (RR = 1.06; 95% CI:1.02-1.11). We found a non-linear association between dietary saturated fat and all-cause mortality showing a significant increased risk up to 11% of energy from saturated fat intake. The risk of cancer mortality increased by 4% for every 5% increase in energy from saturated fat (RR = 1.04; 95% CI:1.02-1.06). CONCLUSIONS Diets high in saturated fat were associated with higher mortality from all-causes, CVD, and cancer, whereas diets high in polyunsaturated fat were associated with lower mortality from all-causes, CVD, and cancer. Diets high in trans-fat were associated with higher mortality from all-causes and CVD. Diets high in monounsaturated fat were associated with lower all-cause mortality.
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Antioxidant enzymes induced by repeated intake of excess energy in the form of high-fat, high-carbohydrate meals are not sufficient to block oxidative stress in healthy lean individuals.
Lim, S, Won, H, Kim, Y, Jang, M, Jyothi, KR, Kim, Y, Dandona, P, Ha, J, Kim, SS
The British journal of nutrition. 2011;(10):1544-51
Abstract
It has been reported that high-fat, high-carbohydrate (HFHC) meals increase oxidative stress and inflammation. We examined whether repeated intake of excess energy in the form of HFHC meals alters reactive oxygen species (ROS) generation and the expression levels of antioxidant enzymes and mitochondrial proteins in mononuclear cells, and to determine whether this is associated with insulin resistance. We recruited healthy lean individuals (n 10). The individuals were divided into two groups: one group (n 5) ingested 10878·4 kJ/d (2600 kcal/d; 55-70 % carbohydrate, 9·5-16 % fat, 7-20 % protein) recommended by the Dietary Reference Intake for Koreans for 4 d and the other group (n 5) ingested a HFHC meal containing 14 644 kJ/d (3500 kcal/d). Then, measurements of blood insulin and glucose levels, together with suppressor of cytokine signalling-3 (SOCS-3) expression levels, were performed in both groups. Also, cellular and mitochondrial ROS levels as well as malondialdehyde (MDA) levels were measured. Expression levels of cytosolic and mitochondrial antioxidant enzymes, and mitochondrial complex proteins were analysed. Repeated intake of HFHC meals induced an increase in homeostasis model of assessment-insulin resistance (HOMA-IR), together with an increase in SOCS-3 expression levels. While a single intake of the HFHC meal increased cytosolic and mitochondrial ROS, repeated intake of HFHC meals reduced them and increased the levels of MDA, cytosolic and mitochondrial antioxidant enzymes, and several mitochondrial complex proteins. Repeated intake of HFHC meals induced cellular antioxidant mechanisms, which in turn increased lipid peroxidation (MDA) and SOCS-3 expression levels, induced hyperinsulinaemia and increased HOMA-IR, an index of insulin resistance. In conclusion, excess energy added to a diet can generate detrimental effects in a short period.