Bruce M. Psaty works in General / Preventive / Lipids affiliated with University of Washington.
Bruce M. Psaty, MD, PhD, MPH is a Professor of Medicine, Epidemiology, and Health Services at the University of Washington and Emeritus Co-Director of the Cardiovascular Health Research Unit. He is an investigator at Kaiser Permanente Washington Health Research Institute and a general internist at Harborview Medical Center. His research focuses on cardiovascular epidemiology, epidemiological methods, drug safety, pharmacoepidemiology, genetics, genomics, and pharmacogenetics.
1,864 pubs · 175,248 cites · h-index 207
MD
Indiana University School of Medicine
1981
PhD
Indiana University, Bloomington
1979
MPH
University of Washington
1986
Professor of Medicine, Epidemiology, and Health Services
University of Washington
Emeritus Co-Director, Cardiovascular Health Research Unit
University of Washington
Investigator
Kaiser Permanente Washington Health Research Institute
General Internist
Harborview Medical Center
Introduction Genetic variants that determine the vitamin D binding protein isoform (GC) are consistently associated with total serum 25(OH)D concentration in cross-sectional genome-wide association studies. Previous studies suggest GC isoforms may influence the increment of total 25(OH)D in response to vitamin D supplementation. The free serum 25(OH)D concentration may better reflect vitamin D status, but whether GC isoforms modify the effect of supplementation on free 25(OH)D requires further study. Objectives This study aimed to determine the associations between GC isoforms and the increments of total and free 25(OH)D 3 in response to vitamin D 3 supplementation among older adults. Methods Data were derived from the Multi-Ethnic Study of Atherosclerosis Individualized Response to Vitamin D Treatment (MESA INVITe) Study (NCT02925195). Participants (n = 666) were randomized 3:1 to 16 weeks of 2,000 IU of vitamin D 3 or placebo daily. Complete data from 559 participants (414 vitamin D 3 ; 145 placebo) were used for analysis. Total serum 25(OH)D 3 concentration, GC isoforms, and serum VDBP concentration were determined by LC-MS/MS. Free serum 25(OH)D 3 was measured by LC-MS/MS following sample preparation by size-exclusion separation. Additionally, an established prediction equation was used to estimate free 25(OH)D 3 from common biochemical measurements. The associations of GC isoforms with baseline, endpoint, and 16-week changes in total and free 25(OH)D 3 were modeled with linear regression. Models were adjusted for sex, age, season, body mass index, estimated glomerular filtration rate, and genetic ancestry. Results Mean age (SD) of the participants was 72 (8) y; 53% were females, 36% White, 33% Black, 18% Hispanic/Latino, and 13% Chinese. In each treatment group at both baseline and endpoint, total 25(OH)D 3 was lower among individuals carrying GC2 isoform (3 to 6 ng/mL lower per GC2 allele), whereas free 25(OH)D 3 , whether measured or calculated, did not vary according to GC isoform. Supplementation significantly increased total and free 25(OH)D 3 , but the increments of total and free 25(OH)D 3 were independent of GC isoform. Discussion At baseline and endpoint, total serum 25(OH)D 3 concentration, but not free 25(OH)D 3 , was lower among individuals with GC2 isoform. However, neither the total nor free 25(OH)D 3 response to vitamin D 3 supplementation varied according to GC isoform.
Background Omega‐6 polyunsaturated fatty acids (PUFAs) have previously been associated with several peripheral artery disease (PAD) risk factors. We studied the association between individual omega‐6 PUFAs and incident PAD in a multicohort analysis. Methods This study was conducted among participants from 9 cohorts (N=137 704; PAD cases=2014) in the FORCE (Fatty Acids and Outcomes Research Consortium) who were free of clinical PAD at baseline. Omega‐6 PUFAs were measured at baseline and with a median follow‐up of 14 years. Cox proportional hazards regression analyses were conducted in individual cohorts to evaluate associations of omega‐6 PUFAs (continuous cohort‐standardized interquintile ranges [difference between the medians of the 10th and 90th omega‐6 PUFAs percentiles] and cohort‐specific quintiles) with incident clinical PAD adjusting for prespecified covariates. Inverse‐variance weighted meta‐analysis was used to calculate the combined hazard ratios (HRs) and 95% CIs. Results Linoleic acid (LA) was measured in all 9 cohorts, arachidonic acid in 8 (N=33 541; PAD cases=1766), dihomo‐γ‐LA and γ‐LA in 7 (N=29 861; PAD cases=1686), and eicosadienoic acid in 6 (N=27 538; PAD cases=1435). Only LA was associated with a lower risk of incident PAD (quintile 5 versus quintile 1: HR, 0.75 [95% CI, 0.64–0.89]; P =0.0009). Results did not differ in a statistically significant manner by age, sex, diabetes status, or smoking status. Conclusions Results suggest that the omega‐6 PUFA LA may be protective against PAD, and other omega‐6 PUFAs are not associated with PAD incidence. This is further evidence that omega‐6 PUFA—disease relationships should be evaluated by individual fatty acids rather than grouped as total omega‐6 PUFAs.
This study identifies putative causal DNA methylation markers for AAA, highlighting the role of inflammatory pathways and blood lipids in aneurysm formation.
Cohort study reveals clinical risk factors predict disease progression in calcific aortic-valve disease, indicating localized injury rather than systemic inflammation.
Coronary artery calcium (CAC) score provides the most significant, though modest, improvement in ASCVD risk discrimination when added to the Pooled Cohort Equations compared to other nontraditional risk markers.
Chair of Preventive Medicine, Northwestern University
Yes, high cholesterol is worse for you than low cholesterol, but high cholesterol that's related to one of these single-gene disorders is particularly risky and even riskier than the polygenic variety.
CirculationZhang et al.
Prospective cohort study observes increased chronic kidney disease risk with high ultra-processed food intake in older adults, suggesting food processing negates plant-based benefits.
Cohort study reveals pre-pandemic depressive symptoms increase severe COVID-19 risk in women, highlighting depression as an underlying risk factor for viral complications.
Professor of medicine, Sanford School of Medicine · Sanford School of Medicine, University of South Dakota
The health benefits or harms that may come from the consumption of omega-6 fatty acids--especially LA, which constitutes 99% of the omega-6 fatty acids in the diet--are controversial. These two studies indicate that consuming more LA will likely lower risk for diabetes and CVD. This means that LA is good for us, not bad.
CirculationMarklund et al.
Systematic recalibration of widely used CVD risk algorithms equalizes their performance and improves the targeting of preventive statin therapy.
Although FH mutations are identified in <2% of individuals with severe hypercholesterolemia, mutation carriers face a substantially higher risk of CAD compared to non-carriers with similar LDL cholesterol levels.
May refine MACE risk stratification in type 2 diabetes; leaves open whether scores should guide GLP-1 RA selection.
Hypothesis-generating for inflammation in incident HF; leaves open whether targeting IL-6 or TNF-α alters risk in older adults.
Associate professor, internal medicine, UT Southwestern · University of Texas Southwestern Medical Center
We consistently found an association between physical activity, BMI and overall heart failure risk. This was not unexpected, however the impact of these lifestyle factors on heart failure subtypes was quite different.
Journal of the American College of CardiologyPandey et al.
Director of clinical research, UCSF Division of Cardiology · University of California, San Francisco
We cannot exclude the possibility that PVCs are an 'epiphenomenon' or some marker of future heart failure. However, as everyone in our study had no previous history of heart failure and had a normal left ventricle by an ultrasound of the heart, our data would appear to be quite convincing that PVCs represent an important predictor of the disease, causal or not. If indeed there is a causal relationship, this could represent a new approach to preventing heart failure from occurring in the first place.
Journal of the American College of CardiologyDukes et al.
Clonal hematopoiesis of indeterminate potential (CHIP), particularly mutations in ASXL1, TET2, and JAK2, is independently associated with an increased risk of incident heart failure.
Reassures clinicians on dietary omega-3 safety regarding AF; leaves open causal effects of high-dose supplementation.
Supports expanded serial Q-wave criteria in silent MI research; leaves open standardized ECG definitions for clinical prognosis.
Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. To identify potential biomarkers and therapeutic targets, we applied Mendelian randomization to examine over 2,500 proteins measured in plasma and, uniquely, cerebrospinal fluid, in relation to magnetic resonance imaging (MRI) markers of cSVD in more than 40,000 individuals. Here we show that 49 proteins are associated with MRI markers of cSVD, most prominently in cerebrospinal fluid. We highlight associations that are consistent across platforms and ancestries, and supported by complementary observational analyses, and we explore differences between fluids. The proteins are enriched in pathways related to the extracellular matrix, immune response and microglial activity. Many also associate with stroke and dementia, and several correspond to existing drug targets. Together, these findings reveal a robust biological fingerprint of cSVD and highlight opportunities for biomarker and drug discovery and repositioning.
