Bernhard Haring

Dr. Bernhard Haring


Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
29 August 2025 in European Heart Journal
Verified
Journal Article
Closed access
JBJulie De Backer
Julie De Backer
Kristina Hermann HaugaaKristina Hermann Haugaa
Kristina Hermann Haugaa
NHNina Eide Hasselberg
Nina Eide Hasselberg
MHMichèle de Hosson
Michèle de Hosson
MBMargarita Brida
Margarita Brida
FZFeruza Zakirova
Feruza Zakirova

1 July 2017 in Journal of Renal Nutrition
Verified
Journal Article
Closed access
PDF file
BHBernhard Haring
Bernhard Haring
ESElizabeth Selvin
Elizabeth Selvin
MLMenglu Liang
Menglu Liang
JCJosef Coresh
Josef Coresh
MGMorgan E. Grams
Morgan E. Grams
CRCasey M. Rebholz
Casey M. Rebholz

1 May 2016 in JAMA Internal Medicine
Verified
Journal Article
Open access
PDF file
BHBernhard Haring
Bernhard Haring
CCCarolyn J. Crandall
Carolyn J. Crandall
CWChunyuan Wu
Chunyuan Wu
ELErin S. LeBlanc
Erin S. LeBlanc
JSJames M. Shikany
James M. Shikany
SWSylvia Wassertheil-Smoller
Sylvia Wassertheil-Smoller
Osteoporotic fractures constitute a major burden for health care systems in aging societies. Although considerable research1-6 has examined whether intake of nutrients involved in bone metabolism, such as protein, calcium, or unsaturated fat, can prevent fracture events, the findings are not consistent. However, suboptimal single nutrient intake does not occur in isolation but rather reflects a poor-quality diet.7

1 June 2016 in Journal of the Academy of Nutrition and Dietetics
Verified
Journal Article
Closed access
BHBernhard Haring
Bernhard Haring
CWChunyuan Wu
Chunyuan Wu
YMYasmin Mossavar-Rahmani
Yasmin Mossavar-Rahmani
LSLinda Snetselaar
Linda Snetselaar
RBRobert Brunner
Robert Brunner
SWSylvia Wassertheil-Smoller
Sylvia Wassertheil-Smoller

2 March 2021 in Journal of the American Heart Association
Verified
Journal Article
Open access
PDF file
BHBernhard Haring
Bernhard Haring
ARAlexander P. Reiner
Alexander P. Reiner
JLJingmin Liu
Jingmin Liu
DTDeirdre K. Tobias
Deirdre K. Tobias
EWEric Whitsel
Eric Whitsel
JMJoAnn E. Manson
JoAnn E. Manson
Background: Presence of clonal hematopoiesis of indeterminate potential (CHIP) is associated with a higher risk of atherosclerotic cardiovascular disease, cancer, and mortality. The relationship between a healthy lifestyle and CHIP is unknown. Methods and Results: This analysis included 8709 postmenopausal women (mean age, 66.5 years) enrolled in the WHI (Women's Health Initiative), free of cancer or cardiovascular disease, with deep‐coverage whole genome sequencing data available. Information on lifestyle factors (body mass index, smoking, physical activity, and diet quality) was obtained, and a healthy lifestyle score was created on the basis of healthy criteria met (0 point [least healthy] to 4 points [most healthy]). CHIP was derived on the basis of a prespecified list of leukemogenic driver mutations. The prevalence of CHIP was 8.6%. A higher healthy lifestyle score was not associated with CHIP (multivariable‐adjusted odds ratio [OR] [95% CI], 0.99 [0.80–1.23] and 1.13 [0.93–1.37]) for the upper (3 or 4 points) and middle category (2 points), respectively, versus referent (0 or 1 point). Across score components, a normal and overweight body mass index compared with obese was significantly associated with a lower odds for CHIP (OR, 0.71 [95% CI, 0.57–0.88] and 0.83 [95% CI, 0.68–1.01], respectively; P ‐trend 0.0015). Having never smoked compared with being a current smoker tended to be associated with lower odds for CHIP. Conclusions: A healthy lifestyle, based on a composite score, was not related to CHIP among postmenopausal women. However, across individual lifestyle factors, having a normal body mass index was strongly associated with a lower prevalence of CHIP. These findings support the idea that certain healthy lifestyle factors are associated with a lower frequency of CHIP.

10 October 2014 in PLOS ONE
Verified
Journal Article
Open access
PDF file
BHBernhard Haring
Bernhard Haring
NGNoelle Gronroos
Noelle Gronroos
JNJennifer A Nettleton
Jennifer A Nettleton
MBMoritz C Wyler Von Ballmoos
Moritz C Wyler Von Ballmoos
ESElizabeth Selvin
Elizabeth Selvin
AAAlvaro Alonso
Alvaro Alonso
Prospective data examining the relationship between dietary protein intake and incident coronary heart disease (CHD) are inconclusive. Most evidence is derived from homogenous populations such as health professionals. Large community-based analyses in more diverse samples are lacking. We studied the association of protein type and major dietary protein sources and risk for incident CHD in 12,066 middle-aged adults (aged 45–64 at baseline, 1987–1989) from four U.S. communities enrolled in the Atherosclerosis Risk in Communities (ARIC) Study who were free of diabetes mellitus and cardiovascular disease at baseline. Dietary protein intake was assessed at baseline and after 6 years of follow-up by food frequency questionnaire. Our primary outcome was adjudicated coronary heart disease events or deaths with following up through December 31, 2010. Cox proportional hazard models with multivariable adjustment were used for statistical analyses. During a median follow-up of 22 years, there were 1,147 CHD events. In multivariable analyses total, animal and vegetable protein were not associated with an increased risk for CHD before or after adjustment. In food group analyses of major dietary protein sources, protein intake from red and processed meat, dairy products, fish, nuts, eggs, and legumes were not significantly associated with CHD risk. The hazard ratios [with 95% confidence intervals] for risk of CHD across quintiles of protein from poultry were 1.00 [ref], 0.83 [0.70–0.99], 0.93 [0.75–1.15], 0.88 [0.73–1.06], 0.79 [0.64–0.98], P for trend = 0.16). Replacement analyses evaluating the association of substituting one source of dietary protein for another or of decreasing protein intake at the expense of carbohydrates or total fats did not show any statistically significant association with CHD risk. Based on a large community cohort we found no overall relationship between protein type and major dietary protein sources and risk for CHD.