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Cardiometabolic diseases are the leading cause of death worldwide and are strongly linked to both genetic and nutritional factors. The field of nutrigenomics encompasses multiple approaches aimed at understanding the effects of diet on health or disease development, including nutrigenetic studies investigating the relationship between genetic variants and diet in modulating cardiometabolic risk, as well as the effects of dietary components on multiple "omic" measures, including transcriptomics, metabolomics, proteomics, lipidomics, epigenetic modifications, and the microbiome. Here, we describe the current state of the field of nutrigenomics with respect to cardiometabolic disease research and outline a direction for the integration of multiple omics techniques in future nutrigenomic studies aimed at understanding mechanisms and developing new therapeutic options for cardiometabolic disease treatment and prevention.
© 2016 American Heart Association, Inc.
OBJECTIVE - Despite patent vein bypass grafts, some patients with critical limb ischemia (CLI) receive major amputations. We analyzed the predictive factors leading to major amputation in the presence of patent lower extremity bypass (LEB) grafts.
METHODS - Data from the Project of Ex-Vivo vein graft Engineering via Transfection III (PREVENT III), a large prospective randomized trial of 1404 patients who underwent LEB with vein graft for CLI, were queried for outcomes. The primary outcome was major amputation with patent (PMA) LEB compared with patients with patent LEB who achieved limb salvage (PLS). The population excluded those who received amputation for occluded grafts. A Cox proportional hazard model identified independent predictors.
RESULTS - Of 1404 LEB patients, 162 (11.5%) had major amputation: 89 (6.3%) with patent and 73 (5.2%) with occluded LEB. For PMA, 21 of 89 (23.6%) developed critical stenosis and 11 of 21 (52.4%) were revised. For PLS, 460 of 1242 (37.0%) developed critical stenosis and 351 of 460 (76.3%) were revised. Predictive patient factors included having preoperative gangrene (vs rest pain; hazard ratio [HR], 3.504; 95% confidence interval [CI], 1.533-8.007; P = .0029), diabetes (HR, 1.800; 95% CI, 1.006-3.219; P = .0477), black (vs white) race (HR, 1.779; 95% CI, 1.051-3.011; P = .0321), baseline creatinine clearance <25 mL/min (vs >65 mL/min; HR, 1.759; 95% CI, 1.016-3.048; P = .0439), prior history of coronary artery bypass grafting (HR, 1.702; 95% CI, 1.080-2.683; P = .0221), and lower baseline activity quality of life score (HR, 1.401; 95% CI, 1.105-1.778; P = .0054). Postoperative wound factors included gangrenous changes (HR, 5.830; 95% CI, 1.647-20.635; P = .0063), surgical wound necrosis (HR, 5.319; 95% CI, 1.478-19.146; P = .0105), deep (vs superficial) wound infection (HR, 3.815; 95% CI, 1.220-11.927; P = .0213), and wound healing abnormally (HR, 3.754; 95% CI, 1.061-13.278; P = .0402). Associated postoperative consequences leading to PMA included having recurrent CLI symptoms (HR, 2.915; 95% CI, 1.816-4.681; P < .0001), a severe (vs mild) adverse event (HR, 2.751; 95% CI, 1.391-5.443; P = .0036), fewer percutaneous revisions (HR, 2.425; 95% CI, 1.573-3.740; P < .0001), discharge on low-molecular-weight heparin (HR, 2.087; 95% CI, 1.309-3.326; P = .0020), and decreasing days to critical stenosis/occlusion/revision/amputation (HR, 1.010; 95% CI, 1.007-1.012; P < .0001).
CONCLUSIONS - Whereas a patent vein graft is important to all vascular surgeons, additional factors should be considered in trying to attain limb salvage for patients with CLI. These factors include intervening surgically before CLI has progressed to a state of gangrene or limited activity and optimizing nutrition, diabetes control, cardiac conditions, and activity level. Revision offers hope for clinical improvement but may be delayed when there is no graft lesion identified. The absence of a graft lesion to revise may also portend amputation despite a patent graft because of nongraft-related factors such as infection. Finally, the experience of a severe (vs mild) adverse event may also result in limb loss despite a patent graft. Systematic efforts to reduce severe adverse events among patients may also lead to increased limb salvage.
Copyright © 2016 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Although much is known about magnesium, its interactions with calcium and vitamin D are less well studied. Magnesium intake is low in populations who consume modern processed-food diets. Low magnesium intake is associated with chronic diseases of global concern [e.g., cardiovascular disease (CVD), type 2 diabetes, metabolic syndrome, and skeletal disorders], as is low vitamin D status. No simple, reliable biomarker for whole-body magnesium status is currently available, which makes clinical assessment and interpretation of human magnesium research difficult. Between 1977 and 2012, US calcium intakes increased at a rate 2-2.5 times that of magnesium intakes, resulting in a dietary calcium to magnesium intake ratio of >3.0. Calcium to magnesium ratios <1.7 and >2.8 can be detrimental, and optimal ratios may be ∼2.0. Background calcium to magnesium ratios can affect studies of either mineral alone. For example, US studies (background Ca:Mg >3.0) showed benefits of high dietary or supplemental magnesium for CVD, whereas similar Chinese studies (background Ca:Mg <1.7) showed increased risks of CVD. Oral vitamin D is widely recommended in US age-sex groups with low dietary magnesium. Magnesium is a cofactor for vitamin D biosynthesis, transport, and activation; and vitamin D and magnesium studies both showed associations with several of the same chronic diseases. Research on possible magnesium and vitamin D interactions in these human diseases is currently rare. Increasing calcium to magnesium intake ratios, coupled with calcium and vitamin D supplementation coincident with suboptimal magnesium intakes, may have unknown health implications. Interactions of low magnesium status with calcium and vitamin D, especially during supplementation, require further study.
© 2016 American Society for Nutrition.
The annual mortality rate for patients undergoing maintenance hemodialysis (MHD) treatment in the United States is 20%, a rate higher than most other countries in the world. Poor nutrition status in MHD patients contributes to this adverse outcome as well as poor quality of life. Providing oral nutrition to MHD patients, especially during hemodialysis (HD) treatment has many potential benefits including improvements in nutrition status and attenuating HD-related muscle wasting. However, this practice is generally restricted in the United States presumably because of concerns that include worsening hemodynamic instability, reductions in treatment efficiency, and increased gastrointestinal symptoms. Despite widespread restrictions, few studies have adequately examined the effect of eating during HD on these outcomes, leaving many questions unanswered. This review outlines the current evidence regarding the effects of feeding during HD and provides potential future directions to outline the best practices in this controversial area.
Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
OBJECTIVES - Postnatal infant weight curves are used to assess fluid management and evaluate postnatal nutrition and growth. Traditionally, postnatal weight curves are based on birth weight and do not incorporate postnatal clinical information. The aim of the present study was to compare the accuracy of birth weight-based weight curves with weight curves created from individual patient records, including electronic records, using 2 predictive modeling methods, linear regression (LR) and an artificial neural network (NN), which apply mathematical relations between predictor and outcome variables.
METHODS - Perinatal demographic and postnatal nutrition data were collected for extremely-low-birth-weight (ELBW; birth weight <1000 g) infants. Static weight curves were generated using published algorithms. The postnatal predictive models were created using the demographic and nutrition dataset.
RESULTS - Birth weight (861 ± 83 g, mean ± 1 standard deviation [SD]), gestational age (26.2 ± 1.4 weeks), and the first month of nutrition data were collected from individual health records for 92 ELBW infants. The absolute residual (
) for weight was 84.8 ± 74.4 g for the static weight curves, 60.9 ± 49.1 g for the LR model, and 12.9 ± 9.2 g for the NN model, analysis of variance: both LR and NN P<0.01 versus static curve. NPO (nothing by mouth) infants had greater weight curve discrepancies.
CONCLUSIONS - Compared with birth weight-based and logistic regression-generated weight curves, NN-generated weight curves more closely approximated ELBW infant weight curves, and, using the present electronic health record systems, may produce weight curves better reflective of the patient's status.
OBJECTIVE - Sustained low efficiency dialysis (SLED) involves the use of standard dialysis machines for prolonged intermittent renal replacement therapy in critically ill patients. In this study we aimed to quantify dialysate amino acid (AA) and albumin losses in 5 patients who underwent successful SLED treatment.
DESIGN - This was a prospective observational study.
SETTING - The study was performed in a general intensive care unit.
SUBJECTS - The study was performed in critically ill patients with acute kidney injury undergoing SLED using low-flux hemodialyzers.
INTERVENTION - We performed total dialysate collection and measured dialysate AA profiles by reverse phase high-pressure liquid chromatography using an automated AA analyser.
MAIN OUTCOME MEASURE - Individual and total amino acid losses.
RESULTS - Albumin was undetectable in dialysate. The median (mean ± SD) total amino acid loss was 15.7 (23.4 ± 19.2) g/treatment, or 122.1 (180.6 ± 148.5) mmol/treatment. Two patients were receiving intravenous nutrition. One patient had severe hepatic failure with encephalopathy, and had high dialysate AA levels with a total loss of 57 g/treatment.
CONCLUSIONS - During SLED with low-flux hemodialyzers, albumin losses are negligible but AA losses to dialysate are comparable to those during continuous renal replacement therapy. Patients' nutritional protein prescriptions should be augmented to account for this.
PURPOSE OF REVIEW - This review examines recent advances in understanding of how clinical outcomes for hemodialysis patients may be improved by achieving longer or more frequent treatment times, lower ultrafiltration rates (UFRs), improving nutritional status, and individualizing dialysate composition. This review also discusses the controversy related to timing of dialysis initiation.
RECENT FINDINGS - Many observational studies and several randomized controlled trials indicate longer dialysis treatment times, particularly nocturnal dialysis, and/or more frequent dialysis improve morbidity and mortality. Recent evidence also suggests that lower UFR and more consistent achievement of 'dry weight' may help minimize the damage from myocardial stunning and chronic volume overload that occurs in the majority of patients who receive conventional hemodialysis during the day with a standard schedule of 3-5 h, 3 times a week. Other aspects of the dialysis procedure such as appropriate estimated glomerular filtration rate for dialysis initiation and individualizing dialysate composition may also minimize cardiovascular risk. Finally, several studies have highlighted the benefits of oral nutritional supplementation (ONS) during dialysis.
SUMMARY - Greater treatment times per week with slower UFR, consistent attainment of 'dry weight', individualized dialysate prescriptions, and administration of ONS to malnourished patients are likely to reduce hospitalizations and improve survival in this high-risk population of end-stage renal disease patients.
Protein energy wasting is common in patients with CKD and ESRD and is associated with adverse clinical outcomes, such as increased rates of hospitalization and death, in these patients. A multitude of factors can affect the nutritional and metabolic status of patients with CKD, including decreased dietary nutrient intake, catabolic effects of renal replacement therapy, systemic inflammation, metabolic and hormonal derangements, and comorbid conditions (such as diabetes and depression). Unique aspects of CKD also confound reliable assessment of nutritional status, further complicating management of this comorbid condition. In patients in whom preventive measures and oral dietary intake from regular meals cannot help them maintain adequate nutritional status, nutritional supplementation, administered orally, enterally, or parenterally, is effective in replenishing protein and energy stores. The advantages of oral nutritional supplements include proven efficacy, safety, and compliance. Anabolic steroids and exercise, with nutritional supplementation or alone, improve protein stores and represent potential additional approaches for the treatment of PEW. There are several emerging novel therapies, such as appetite stimulants, anti-inflammatory interventions, and anabolic agents.