Does Body Mass Index Impact The Choice Of Lipid Lowering Treatment?

2016 ◽  
Vol 10 (3) ◽  
pp. 694-697
Author(s):  
Dominik Lautsch ◽  
Anselm Gitt ◽  
Jean Ferrieres ◽  
Martin Horack ◽  
Philippe Brudi ◽  
...  
2018 ◽  
Vol 20 (11) ◽  
pp. 2670-2674 ◽  
Author(s):  
Jean Ferrières ◽  
Dominik Lautsch ◽  
Anselm K. Gitt ◽  
Gaetano De Ferrari ◽  
Hermann Toplak ◽  
...  

2019 ◽  
Vol 8 (10) ◽  
pp. 1725 ◽  
Author(s):  
Yinkun Yan ◽  
Lydia A. Bazzano ◽  
Markus Juonala ◽  
Olli T. Raitakari ◽  
Jorma S. A. Viikari ◽  
...  

Background: Data are limited regarding the association of cumulative burden and trajectory of body mass index (BMI) from early life with adult lipid disorders. Methods: The study cohort consisted of 5195 adults who had BMI repeatedly measured 4 to 21 times from childhood and had blood lipid measurements of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) and information on lipid-lowering medications in the last adult survey. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI. Results: Participants with dyslipidemia, high LDL-C, low HDL-C and high TG had consistently and significantly higher BMI levels from childhood to adulthood compared to those with normal lipid levels. After adjusting for age, race, sex, and cohort, increased risk of adult dyslipidemia was significantly associated with higher values of childhood BMI, adulthood BMI, total AUC and incremental AUC, with odds ratio (95% confidence interval) = 1.22 (1.15–1.29), 1.85 (1.74–1.97), 1.61 (1.52–1.71), and 1.59 (1.50–1.69), respectively, and p < 0.001 for all. The association patterns were similar in most race–sex subgroups. Conclusions: Adults with dyslipidemia versus normal lipid levels have consistently higher levels and distinct life-course trajectories of BMI, suggesting that the impact of excessive body weight on dyslipidemia originates in early life.


2007 ◽  
Vol 53 (6) ◽  
pp. 1144-1152 ◽  
Author(s):  
Dolores Corella ◽  
Donna K Arnett ◽  
Michael Y Tsai ◽  
Edmond K Kabagambe ◽  
James M Peacock ◽  
...  

Abstract Background: Apolipoprotein A-II (APOA2) plays an ambiguous role in lipid metabolism, obesity, and atherosclerosis. Methods: We studied the association between a functional APOA2 promoter polymorphism (−265T&gt;C) and plasma lipids (fasting and postprandial), anthropometric variables, and food intake in 514 men and 564 women who participated in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study. We obtained fasting and postprandial (after consuming a high-fat meal) measures. We measured lipoprotein particle concentrations by proton nuclear magnetic resonance spectroscopy and estimated dietary intake by use of a validated questionnaire. Results: We observed recessive effects for this polymorphism that were homogeneous by sex. Individuals homozygous for the −265C allele had statistically higher body mass index (BMI) than did carriers of the T allele. Consistently, after multivariate adjustment, the odds ratio for obesity in CC individuals compared with T allele carriers was 1.70 (95% CI 1.02–2.80, P = 0.039). Interestingly, total energy intake in CC individuals was statistically higher [mean (SE) 9371 (497) vs 8456 (413) kJ/d, P = 0.005] than in T allele carriers. Likewise, total fat and protein intakes (expressed in grams per day) were statistically higher in CC individuals (P = 0.002 and P = 0.005, respectively). After adjustment for energy, percentage of carbohydrate intake was statistically lower in CC individuals. These associations remained statistically significant even after adjustment for BMI. We found no associations with fasting lipids and only some associations with HDL subfraction distribution in the postprandial state. Conclusions: The −265T&gt;C polymorphism is consistently associated with food consumption and obesity, suggesting a new role for APOA2 in regulating dietary intake.


2013 ◽  
Vol 110 (09) ◽  
pp. 593-597 ◽  
Author(s):  
Claire De Moreuil ◽  
Hélène Kerspern ◽  
Emmanuelle Le Moigne ◽  
Dominique Mottier ◽  
Cécile Tromeur ◽  
...  

SummaryShared risk factors help explain the association between venous thromboembolism (VTE) and atherothrombosis. The potential association between insulin resistance and VTE has been poorly evaluated. Thus, we aimed to assess the association between insulin resistance and VTE in the EDITH hospital-based case-control study. Between May 2000 and December 2004, 677 patients with unprovoked VTE and their age- and sex-matched controls were included. Fasting glycaemia and insulinaemia were measured and insulin resistance was estimated with the homeostasis model assessment of insulin resistance (HOMAIR) equation. The association between HOMA-IR and VTE was determined in non-diabetic patients in a quintile-based analysis. A total of 590 non-diabetic cases (median age 73.0 years, 255 men) and 581 non-diabetic controls (median age 72.0 years, 247 men) were analysed. There was a trend for a higher median level of HOMA-IR index in cases than in controls (1.21 [interquartile range 0.84-2.10] vs 1.19 [interquartile range 0.72-2.02], p=0.08). The unadjusted analysis showed an increased risk of unprovoked VTE associated with increasing HOMA-IR (odds ratio [OR] 1.53; 95% confidence interval [CI] 1.00-2.34 for the highest quintile of HOMA-IR compared with the first quintile). Adjustment for lipid lowering drugs and antiplatelet agents use slightly modified the association (OR 1.51; 95% CI 0.97-2.34). When body mass index was added in the adjusted model, HOMA-IR was no longer associated with VTE (OR 1.08; 95% CI 0.67-1.73). Our results highlight the role of body mass index in the association between cardiovascular risk factors and VTE.


2007 ◽  
Vol 177 (4S) ◽  
pp. 64-64
Author(s):  
Murugesan Manoharan ◽  
Martha A. Reyes ◽  
Alan M. Nieder ◽  
Bruce R. Kava ◽  
MarkS Soloway

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