Kian Parsapour Moghadam * , Alessia David , Shahenaz Walji , Lucy Barton , Jaimini Cegla , Ben Jones
{"title":"Real-world efficacy and side effect profile of bempedoic acid in a tertiary centre lipid clinic","authors":"Kian Parsapour Moghadam * , Alessia David , Shahenaz Walji , Lucy Barton , Jaimini Cegla , Ben Jones","doi":"10.1016/j.athplu.2024.08.008","DOIUrl":"10.1016/j.athplu.2024.08.008","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 9"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Valaiyapathi ∗ , N. Rao , R. Chandra , R.P. Vincent , R. Ranasinghe
{"title":"Ketogenic Diet – a culinary delight but is there a cautionary tale?","authors":"R. Valaiyapathi ∗ , N. Rao , R. Chandra , R.P. Vincent , R. Ranasinghe","doi":"10.1016/j.athplu.2024.08.011","DOIUrl":"10.1016/j.athplu.2024.08.011","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 10"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Martin Bird , Antoine Rimbert , Alan M. Pittman , Steve E. Humphries , Marta Futema ∗
{"title":"Variants in LPA are associated with mutation-negative Familial Hypercholesterolaemia: whole genome sequencing analysis in the 100,000 Genomes Project","authors":"Martin Bird , Antoine Rimbert , Alan M. Pittman , Steve E. Humphries , Marta Futema ∗","doi":"10.1016/j.athplu.2024.08.015","DOIUrl":"10.1016/j.athplu.2024.08.015","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Page 2"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142423456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N.W.P. Cantley ∗ , S. Tapley , K. Antwi , P. Downie , E. Willis
{"title":"A tale of 2 pregnancies: the biochemical trends, medical management, and outcomes of hypertriglyceridemia in pregnancy secondary to multi-factorial chylomicronaemia syndrome (MCS) and extreme ketogenic/carnivorous diet","authors":"N.W.P. Cantley ∗ , S. Tapley , K. Antwi , P. Downie , E. Willis","doi":"10.1016/j.athplu.2024.08.003","DOIUrl":"10.1016/j.athplu.2024.08.003","url":null,"abstract":"","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 6-7"},"PeriodicalIF":1.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142416450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ingo Kennerknecht , Johannes M. Hämmerle , Manfred Fobker , Jerzy-Roch Nofer
{"title":"Extreme founder effect associated with hyperglycemia and hyperlipidemia on the island of NIAS/Indonesia","authors":"Ingo Kennerknecht , Johannes M. Hämmerle , Manfred Fobker , Jerzy-Roch Nofer","doi":"10.1016/j.athplu.2024.07.002","DOIUrl":"10.1016/j.athplu.2024.07.002","url":null,"abstract":"<div><p>The island of Nias/Indonesia shows an extremely reduced genetic diversity indicating a strong founder effect. As a consequence, the prevalence of some disease genes should significantly differ among populations depending on the gene pool passed on to the founder population and their successive expansion as it has already been documented for several monogenic diseases. Results of the current study based on routine laboratory blood examination give rise to the notion that this might also hold true for polygenic disorders. We observed very high prevalence of hyperglycemia (non-fasting glucose above 200 mg/dL in 14 % Nias population compared to 1.5 % in the population of the neighboring island of Sumatra) accompanied by hypertriglyceridemia, high non-HDL-cholesterol, and low HDL-cholesterol levels. These findings suggest that the Nias population may be disproportionally affected by prediabetes and type 2 diabetes mellitus. By contrast, laboratory parameters potentially indicative of other polygenic disorders such as total plasma cholesterol, electrolytes, creatinine, urea, and uric acid were comparable between the inhabitants of Nias and Sumatra islands. To our knowledge this is the first study suggesting that the extremely strong genetic bottleneck seen in the Nias population translates into the widespread metabolic disease with potentially deleterious influence on public health.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 26-29"},"PeriodicalIF":1.4,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000178/pdfft?md5=308d0b8c2f1c0734c601c409bf9639ac&pid=1-s2.0-S2667089524000178-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141846605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ming Wai Yeung , M. Abdullah Said , Yordi J. van de Vegte , Niek Verweij , Robin P.F. Dullaart , Pim van der Harst
{"title":"Associations of very low Lipoprotein(a) levels with risks of new-onset diabetes and non-alcoholic liver disease","authors":"Ming Wai Yeung , M. Abdullah Said , Yordi J. van de Vegte , Niek Verweij , Robin P.F. Dullaart , Pim van der Harst","doi":"10.1016/j.athplu.2024.07.001","DOIUrl":"https://doi.org/10.1016/j.athplu.2024.07.001","url":null,"abstract":"<div><h3>Background and aims</h3><p>We aimed to study the association of very low serum Lipoprotein(a) [Lp(a)] concentrations with new-onset type 2 diabetes (T2D) and non-alcoholic liver disease (NAFLD) in the context of statin usage in the UK Biobank, a large prospective population cohort.</p></div><div><h3>Methods</h3><p>Using an extended biomarker dataset, we identified 47,362 participants with very low Lp(a) concentrations (<3.8 nmol/L) from a total of 451,479 participants. With a median follow-up of 12.3 years, we assessed the risk of new-onset cardiometabolic diseases in participants stratified by statin usage with Cox proportional hazards models. We performed two-sample Mendelian randomization MR analyses to test causal relationship between genetically predicted Lp(a) and T2D and NAFLD.</p></div><div><h3>Results</h3><p>Taking the participants with Lp(a) within reportable range as the reference group, the hazard ratios (HR) for T2D were 1.07 (95 % confidence interval, CI 1.01–1.13) and for NAFLD 1.30 (95 % CI 1.20–1.41) respectively for participants with very low Lp(a) (<3.8 nmol/L). The risk for new-onset T2D was higher in participants using statins (adjusted HR 1.15; 95 % CI 1.05–1.27). The risk estimates for new-onset NAFLD were comparable in the analysis stratified by statin use. There was no evidence for causal links between genetically predicted Lp(a) and T2D nor NAFLD in two-sample MR analyses.</p></div><div><h3>Conclusions</h3><p>Very low Lp(a) was associated with higher risks of T2D and NAFLD in a prospective analysis of the UK Biobank. The association with T2D was influenced by lipid lowering medication usage. MR analyses did not support causality for these inverse associations.</p></div>","PeriodicalId":72324,"journal":{"name":"Atherosclerosis plus","volume":"57 ","pages":"Pages 19-25"},"PeriodicalIF":1.4,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667089524000166/pdfft?md5=c3a6777b13986ebec4c5e9321f64810d&pid=1-s2.0-S2667089524000166-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141607836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}