Pub Date : 2025-01-14DOI: 10.1016/s2213-8587(24)00316-4
Francesco Rubino, David E Cummings, Robert H Eckel, Ricardo V Cohen, John P H Wilding, Wendy A Brown, Fatima Cody Stanford, Rachel L Batterham, I Sadaf Farooqi, Nathalie J Farpour-Lambert, Carel W le Roux, Naveed Sattar, Louise A Baur, Katherine M Morrison, Anoop Misra, Takashi Kadowaki, Kwang Wei Tham, Priya Sumithran, W Timothy Garvey, John P Kirwan, Geltrude Mingrone
<h2>Section snippets</h2><section><section><h2>Executive summary</h2>Current BMI-based measures of obesity can both underestimate and overestimate adiposity and provide inadequate information about health at the individual level, which undermines medically-sound approaches to health care and policy. This Commission sought to define clinical obesity as a condition of illness that, akin to the notion of chronic disease in other medical specialties, directly results from the effect of excess adiposity on the function of organs and tissues. The specific aim of the</section></section><section><section><section><h2>Conception of the Commission</h2>The idea and general plan to convene a global expert group for the definition of diagnostic criteria of chronic illness in obesity (clinical obesity) was conceived by FR, and discussed with editors of <em>The Lancet Diabetes & Endocrinology</em> journal for consideration as a <em>Lancet</em> Commission. The Commission on clinical obesity was organised in partnership with the Institute of Diabetes, Endocrinology and Obesity at Kings Health Partners. Additional scientific input about the programme of the</section></section></section><section><section><section><h2>General principles</h2>Although the notion of disease might seem obvious, a clear definition of disease does not exist. One comprehensive approach to the definition of disease was proposed by Stanley Heshka and David Allison:<sup>27</sup> (A) a condition of the body, its parts, organs, or systems, or an alteration thereof; (B) resulting from infection, parasites, nutritional, dietary, environmental, genetic, or other causes; (C) having a characteristic, identifiable, marked group of symptoms or signs; and (D) deviation from</section></section></section><section><section><h2>Commissioners' views on obesity as a disease</h2>The idea of obesity as a disease was a controversial subject also within this Commission. Initial opinions diverged substantially, clearly indicating that a consensus would not be reached on a blanket definition of obesity as a disease, at least as currently defined. A specific pre-Delphi survey on the question of whether obesity is a disease showed that more than half of the commissioners rejected the all-or-nothing scenario implied in the question, but supported the view that obesity is a</section></section><section><section><section><h2>Conceptual and practical issues in the current definition of obesity</h2>Obesity is currently conceived and defined as a condition of excess adiposity that presents a “risk to health”.<sup>34</sup> The current diagnosis of obesity worldwide is based on BMI, calculated as weight in kilograms divided by height in metres squared. According to WHO, an adult with a BMI of 30 kg/m<sup>2</sup> or higher is considered to have obesity.This definition has been widely adopted and used in epidemiological studies, clinical practice, and public health policy.<sup>35</sup> However, several studies have shown t
当前基于bmi的肥胖测量既可能低估肥胖，也可能高估肥胖，而且提供的个人健康信息不足，这破坏了医疗保健和政策的医学上合理的方法。该委员会试图将临床肥胖定义为一种疾病，这种疾病与其他医学专业中的慢性病概念类似，是过度肥胖对器官和组织功能的影响直接导致的。委员会构想的具体目的是召集一个全球专家组来定义肥胖慢性疾病（临床肥胖）诊断标准的构想和总体计划，由FR构想，并与《柳叶刀糖尿病》的编辑进行了讨论；作为柳叶刀委员会考虑的内分泌学杂志。临床肥胖委员会是与国王健康伙伴的糖尿病、内分泌学和肥胖研究所合作组织的。关于《一般原则》计划的额外科学投入尽管疾病的概念似乎很明显，但并不存在对疾病的明确定义。斯坦利·赫什卡（Stanley Heshka）和大卫·艾利森（David Allison）提出了一种关于疾病定义的综合方法：27 (A)身体、身体各部分、器官或系统的状况，或其变化；(B)由感染、寄生虫、营养、饮食、环境、遗传或其他原因引起的；(C)具有特征性的、可识别的、明显的一组症状或体征；(D)委员们对肥胖作为一种疾病的看法的偏差。肥胖作为一种疾病的观点在委员会内部也是一个有争议的话题。最初的意见分歧很大，清楚地表明，不可能就肥胖作为一种疾病的笼统定义达成共识，至少不可能像目前的定义那样。34 .针对肥胖是否是一种疾病这一问题，在德尔菲前进行了一项具体的调查，结果显示，半数以上的委员拒绝接受问题中暗示的“要么全有，要么全无”的观点，但支持这样一种观点，即肥胖在目前对肥胖的定义中是一个概念上和实际上的问题目前世界范围内对肥胖的诊断是基于身体质量指数，计算方法是体重（公斤）除以身高（米）的平方。根据世界卫生组织，成年人的身体质量指数为30 kg/m2或更高被认为是肥胖。这一定义已被广泛采用，并用于流行病学研究、临床实践和公共卫生政策然而，一些研究表明，患者、卫生保健专业人员和政策制定者对肥胖的看法和态度围绕肥胖作为一种疾病的观点的辩论引发了两极分化，往往是基于非医学考虑的情绪反应。支持这一想法的人经常引用这样一个事实，即这样做可以最大限度地减少基于体重的耻辱和歧视，因为它转移了人们对个人的指责。这一结果似乎是合理的，而且确实是可取的，但这并不是一种医疗状况应该被视为疾病的理由。对这一观点持批评态度的人担心，重新定义肥胖及其临床特征肥胖可能会增加患其他疾病和过早死亡的风险，或者本身就会引发疾病，或者两者兼而有之。因此，有必要对肥胖的病因、病理生理和临床特征进行更好的描述。虽然替代的人体测量和生物标志物已被建议作为BMI的诊断工具或治疗决策的可能替代品，但它们尚未被用作个体患者健康的衡量标准，并且作为持续疾病的衡量标准的诊断准确性不足。在其他医学领域，疾病的诊断通常是基于对器官或整个机体功能障碍引起的体征和症状的检测（见肥胖的原因）肥胖的原因是多因素的，而且尚未完全了解。2,5,80遗传、环境、心理、营养和代谢因素可诱导维持脂肪组织正常质量、分布和功能的生物学机制发生改变，从而导致肥胖。身体脂肪的积累是正能量平衡的一个功能，即大量营养素的出现速度超过消失速度。成人肥胖直接引起器官功能障碍的临床表现肥胖可通过多种病理生理机制直接引起器官功能障碍，包括脂肪组织质量增加的物理效应、组织和器官内异位脂肪的存在、代谢效应、炎症机制和心理后果（图3）。 器官功能障碍和肥胖并发症的发展，无论是心脏代谢还是生物力学，都可能在不同的个体中出现不同程度的肥胖。此外，儿童和青少年肥胖的严重程度已经成为世界范围内一个主要的健康、社会和经济负担在5-19岁的儿童和青少年中，超重和肥胖的患病率大幅上升，从1975年的4%上升到2016年的18%以上。在这一年龄组中，全球肥胖患病率从1975年的1%上升到2016年的7%（女孩占6%，男孩占8%），有超过1.24亿儿童和青少年患有这一疾病。肥胖可早发：2019年《儿童青少年肥胖直接导致的器官功能障碍临床表现》本节综述了儿童青少年临床肥胖的主要表现，描述了过度肥胖如何影响主要器官、组织和身体系统，导致健康不良。然而，与成年人一样，肥胖也会促进肥胖相关疾病或失调的发展，从而增加儿童和成年时期发病率、死亡率和生活质量的风险，如果肥胖得不到治疗的话。委员会建议：临床肥胖的定义和诊断标准委员会的结论和建议是通过对证据和观点的广泛讨论得出的，加上一个正式的共识发展过程，以产生专家组中最多数人支持的建议。所有的定义、建议和诊断标准都是由专家组内一致或近乎一致的共识达成的。所有基于共识的结论和建议，每个结论和建议都有其相关的委员会的优势和局限性。我们承认本委员会工作中的一些局限性。委员们采用了一种类似德尔菲的方法来得出共同的结论。德尔菲技术的迭代特性具有内在的局限性，并可能导致群体思维，其中参与者可能符合群体的主导意见，这可能影响客观性然而，广泛使用现场和离线的德尔菲前调查，并在较小的小组（小组委员会）内进行讨论，得出结论：肥胖作为一种疾病的观点是现代医学中最具争议和两极分化的辩论之一，对受影响的人群和整个社会具有广泛而深远的影响。肥胖的最初定义是“对健康构成风险的状况”，与之一致的是，肥胖被认为是其他疾病的先兆，并被广泛研究。然而，肥胖作为一种疾病的表现还没有得到充分的描述。缺乏临床利益声明fr宣布从Ethicon (Johnson &；强生)、诺和诺德和美敦力；Morphic Medical的咨询费；美敦力、Ethicon、诺和诺德、礼来和安进公司致词；曾担任Keyron科学顾问委员会成员（无薪），GI Metabolic Solutions数据安全和监测委员会成员；是代谢健康研究所（非营利）的主席；也是国际代谢健康协会和伦敦代谢协会的唯一主任。临床肥胖内分泌委员会是由King's Health Partners的糖尿病、内分泌和肥胖研究所合作组织的。King's Health Partners为组织在线会议、内部沟通和达成共识进程提供后勤和行政支持。我们要感谢King's Health Partners的糖尿病、内分泌和肥胖研究所提供的宝贵支持。在
{"title":"Definition and diagnostic criteria of clinical obesity","authors":"Francesco Rubino, David E Cummings, Robert H Eckel, Ricardo V Cohen, John P H Wilding, Wendy A Brown, Fatima Cody Stanford, Rachel L Batterham, I Sadaf Farooqi, Nathalie J Farpour-Lambert, Carel W le Roux, Naveed Sattar, Louise A Baur, Katherine M Morrison, Anoop Misra, Takashi Kadowaki, Kwang Wei Tham, Priya Sumithran, W Timothy Garvey, John P Kirwan, Geltrude Mingrone","doi":"10.1016/s2213-8587(24)00316-4","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00316-4","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Executive summary</h2>Current BMI-based measures of obesity can both underestimate and overestimate adiposity and provide inadequate information about health at the individual level, which undermines medically-sound approaches to health care and policy. This Commission sought to define clinical obesity as a condition of illness that, akin to the notion of chronic disease in other medical specialties, directly results from the effect of excess adiposity on the function of organs and tissues. The specific aim of the</section></section><section><section><section><h2>Conception of the Commission</h2>The idea and general plan to convene a global expert group for the definition of diagnostic criteria of chronic illness in obesity (clinical obesity) was conceived by FR, and discussed with editors of <em>The Lancet Diabetes & Endocrinology</em> journal for consideration as a <em>Lancet</em> Commission. The Commission on clinical obesity was organised in partnership with the Institute of Diabetes, Endocrinology and Obesity at Kings Health Partners. Additional scientific input about the programme of the</section></section></section><section><section><section><h2>General principles</h2>Although the notion of disease might seem obvious, a clear definition of disease does not exist. One comprehensive approach to the definition of disease was proposed by Stanley Heshka and David Allison:<sup>27</sup> (A) a condition of the body, its parts, organs, or systems, or an alteration thereof; (B) resulting from infection, parasites, nutritional, dietary, environmental, genetic, or other causes; (C) having a characteristic, identifiable, marked group of symptoms or signs; and (D) deviation from</section></section></section><section><section><h2>Commissioners' views on obesity as a disease</h2>The idea of obesity as a disease was a controversial subject also within this Commission. Initial opinions diverged substantially, clearly indicating that a consensus would not be reached on a blanket definition of obesity as a disease, at least as currently defined. A specific pre-Delphi survey on the question of whether obesity is a disease showed that more than half of the commissioners rejected the all-or-nothing scenario implied in the question, but supported the view that obesity is a</section></section><section><section><section><h2>Conceptual and practical issues in the current definition of obesity</h2>Obesity is currently conceived and defined as a condition of excess adiposity that presents a “risk to health”.<sup>34</sup> The current diagnosis of obesity worldwide is based on BMI, calculated as weight in kilograms divided by height in metres squared. According to WHO, an adult with a BMI of 30 kg/m<sup>2</sup> or higher is considered to have obesity.This definition has been widely adopted and used in epidemiological studies, clinical practice, and public health policy.<sup>35</sup> However, several studies have shown t","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"31 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-14DOI: 10.1016/s2213-8587(24)00344-9
Olivier Steichen
No Abstract
没有抽象的
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Pub Date : 2025-01-14DOI: 10.1016/s2213-8587(24)00308-5
Jun Yang, Jacopo Burrello, Jessica Goi, Martin Reincke, Christian Adolf, Evelyn Asbach, Denise Brűdgam, Qifu Li, Yi Song, Jinbo Hu, Shumin Yang, Fumitoshi Satoh, Yoshikiyo Ono, Renata Libianto, Michael Stowasser, Nanfang Li, Qing Zhu, Namki Hong, Drishya Nayak, Troy H Puar, Peter J Fuller
Background
Primary aldosteronism can be treated medically but there is no standardised method to evaluate treatment outcomes. We aimed to develop criteria for assessing the outcomes of targeted medical treatment of primary aldosteronism, analyse outcomes across an international cohort, and identify factors associated with a complete treatment response.
Methods
An international panel of 31 primary aldosteronism experts used the Delphi method to reach consensus on the definition of complete, partial, or absent biochemical and clinical outcomes of medical treatment of primary aldosteronism. Clinical data at baseline and 6–12 months post-treatment were collected from patients with primary aldosteronism who started targeted medical treatment between 2016 and 2021 at 28 participating centres.
Findings
Consensus was reached for defining complete, partial, or absent biochemical or clinical response. Of 1258 patients (with a mean age of 52 years [SD 11·5] and of whom 610 [48·5%] were female and 648 [51·5%] were male), 1057 (84·0%) had biochemical outcome data (559 [52·9%] had a complete biochemical response). The median daily dose of spironolactone was significantly higher for those with a complete biochemical response than for those without (40 mg [IQR 25−50] vs 25 mg [20−50]; p=0·011). Of the 1248 patients with clinical outcome data, 228 [18·3%] had a complete clinical response whereas 227 (18·2%) had an absent response. Patients with a complete clinical response were more likely than those with partial or absent clinical response to be women (OR 2·099, 95% CI 1·485–2·968; p<0·001), require lower doses of antihypertensive drugs at baseline (0·687, 0·603–0·782; p<0·001), and were less likely to have microalbuminuria or left ventricular hypertrophy (0·584, 0·391–0·873; p=0·009).
Interpretation
The Primary Aldosteronism Medical Treatment Outcome (PAMO) criteria represent an internationally developed outcome standard that can guide clinical practice and research into primary aldosteronism. Efforts to optimise treatment intensity and minimise factors associated with an absent treatment response are needed to improve patient outcomes.
Funding
None.
Translations
For the Chinese (simple), Chinese (complex), Japanese, Korean, German, French, Spanish, Dutch, Swedish, Slovenian, Polish, Italian and Russian translations of the abstract see Supplementary Materials section.
{"title":"Outcomes after medical treatment for primary aldosteronism: an international consensus and analysis of treatment response in an international cohort","authors":"Jun Yang, Jacopo Burrello, Jessica Goi, Martin Reincke, Christian Adolf, Evelyn Asbach, Denise Brűdgam, Qifu Li, Yi Song, Jinbo Hu, Shumin Yang, Fumitoshi Satoh, Yoshikiyo Ono, Renata Libianto, Michael Stowasser, Nanfang Li, Qing Zhu, Namki Hong, Drishya Nayak, Troy H Puar, Peter J Fuller","doi":"10.1016/s2213-8587(24)00308-5","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00308-5","url":null,"abstract":"<h3>Background</h3>Primary aldosteronism can be treated medically but there is no standardised method to evaluate treatment outcomes. We aimed to develop criteria for assessing the outcomes of targeted medical treatment of primary aldosteronism, analyse outcomes across an international cohort, and identify factors associated with a complete treatment response.<h3>Methods</h3>An international panel of 31 primary aldosteronism experts used the Delphi method to reach consensus on the definition of complete, partial, or absent biochemical and clinical outcomes of medical treatment of primary aldosteronism. Clinical data at baseline and 6–12 months post-treatment were collected from patients with primary aldosteronism who started targeted medical treatment between 2016 and 2021 at 28 participating centres.<h3>Findings</h3>Consensus was reached for defining complete, partial, or absent biochemical or clinical response. Of 1258 patients (with a mean age of 52 years [SD 11·5] and of whom 610 [48·5%] were female and 648 [51·5%] were male), 1057 (84·0%) had biochemical outcome data (559 [52·9%] had a complete biochemical response). The median daily dose of spironolactone was significantly higher for those with a complete biochemical response than for those without (40 mg [IQR 25−50] <em>vs</em> 25 mg [20−50]; p=0·011). Of the 1248 patients with clinical outcome data, 228 [18·3%] had a complete clinical response whereas 227 (18·2%) had an absent response. Patients with a complete clinical response were more likely than those with partial or absent clinical response to be women (OR 2·099, 95% CI 1·485–2·968; p<0·001), require lower doses of antihypertensive drugs at baseline (0·687, 0·603–0·782; p<0·001), and were less likely to have microalbuminuria or left ventricular hypertrophy (0·584, 0·391–0·873; p=0·009).<h3>Interpretation</h3>The Primary Aldosteronism Medical Treatment Outcome (PAMO) criteria represent an internationally developed outcome standard that can guide clinical practice and research into primary aldosteronism. Efforts to optimise treatment intensity and minimise factors associated with an absent treatment response are needed to improve patient outcomes.<h3>Funding</h3>None.<h3>Translations</h3>For the Chinese (simple), Chinese (complex), Japanese, Korean, German, French, Spanish, Dutch, Swedish, Slovenian, Polish, Italian and Russian translations of the abstract see Supplementary Materials section.","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"17 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-13DOI: 10.1016/s2213-8587(24)00309-7
Jawad H Butt, Pardeep S Jhund, Alasdair D Henderson, Brian L Claggett, Akshay S Desai, Prabhakar Viswanathan, Peter Kolkhof, Patrick Schloemer, Flaviana Amarante, Carolyn S P Lam, Michele Senni, Sanjiv J Shah, Adriaan A Voors, Faiez Zannad, Bertram Pitt, Muthiah Vaduganathan, Scott D Solomon, John J V McMurray
<h3>Background</h3>Data on the effect of mineralocorticoid receptor antagonist therapy on HbA<sub>1c</sub> levels and new-onset diabetes are conflicting. We aimed to examine the effect of oral finerenone, compared with placebo, on incident diabetes in the Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients with Heart Failure (FINEARTS-HF) trial.<h3>Methods</h3>In this randomised, double-blind, placebo-controlled trial, 6001 participants with heart failure with New York Heart Association functional class II–IV, left ventricular ejection fraction 40% or higher, evidence of structural heart disease, and elevated N-terminal pro-B-type natriuretic peptide levels were randomly assigned to finerenone or placebo, administered orally. Randomisation was performed with concealed allocation. The primary outcome of the trial was the composite of cardiovascular death and total (first and recurrent) heart failure events (ie, heart failure hospitalisation or urgent heart failure visit). In the present analysis, participants with diabetes at baseline (investigator-reported history of diabetes or baseline HbA<sub>1c</sub> ≥6·5%) were excluded. New-onset diabetes was defined as a HbA<sub>1c</sub> measurement of 6·5% or higher on two consecutive follow-up visits or new initiation of glucose-lowering therapy. The full-analysis set comprised all participants randomly assigned to study treatment, analysed according to their treatment assignment irrespective of the treatment received (ie, intention to treat). The safety analysis set comprised participants randomly assigned to study treatment who took at least one dose of the investigational product, analysed according to the treatment actually received. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>, <span><span>NCT04435626</span><svg aria-label="Opens in new window" focusable="false" height="20" viewbox="0 0 8 8"><path d="M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z"></path></svg></span>, and is closed to new participants.<h3>Findings</h3>Between Sept 14, 2020, and Jan 10, 2023, 6001 participants were recruited and randomly assigned to finerenone or placebo. 3222 (53·7%) participants did not have diabetes at baseline and comprised the study population. During a median duration of follow-up of 31·3 months (IQR 21·5–36·3), 115 (7·2%) participants in the finerenone group and 147 (9·1%) in the placebo group developed new-onset diabetes, corresponding to a rate of 3·0 events per 100 person-years (95% CI 2·5–3·6) in the finerenone group and 3·9 events per 100 person-years (3·3–4·6) in the placebo group. Compared with placebo, finerenone significantly reduced the hazard of new-onset diabetes by 24% (hazard ratio [HR] 0·76 [95% CI
{"title":"Finerenone and new-onset diabetes in heart failure: a prespecified analysis of the FINEARTS-HF trial","authors":"Jawad H Butt, Pardeep S Jhund, Alasdair D Henderson, Brian L Claggett, Akshay S Desai, Prabhakar Viswanathan, Peter Kolkhof, Patrick Schloemer, Flaviana Amarante, Carolyn S P Lam, Michele Senni, Sanjiv J Shah, Adriaan A Voors, Faiez Zannad, Bertram Pitt, Muthiah Vaduganathan, Scott D Solomon, John J V McMurray","doi":"10.1016/s2213-8587(24)00309-7","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00309-7","url":null,"abstract":"<h3>Background</h3>Data on the effect of mineralocorticoid receptor antagonist therapy on HbA<sub>1c</sub> levels and new-onset diabetes are conflicting. We aimed to examine the effect of oral finerenone, compared with placebo, on incident diabetes in the Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients with Heart Failure (FINEARTS-HF) trial.<h3>Methods</h3>In this randomised, double-blind, placebo-controlled trial, 6001 participants with heart failure with New York Heart Association functional class II–IV, left ventricular ejection fraction 40% or higher, evidence of structural heart disease, and elevated N-terminal pro-B-type natriuretic peptide levels were randomly assigned to finerenone or placebo, administered orally. Randomisation was performed with concealed allocation. The primary outcome of the trial was the composite of cardiovascular death and total (first and recurrent) heart failure events (ie, heart failure hospitalisation or urgent heart failure visit). In the present analysis, participants with diabetes at baseline (investigator-reported history of diabetes or baseline HbA<sub>1c</sub> ≥6·5%) were excluded. New-onset diabetes was defined as a HbA<sub>1c</sub> measurement of 6·5% or higher on two consecutive follow-up visits or new initiation of glucose-lowering therapy. The full-analysis set comprised all participants randomly assigned to study treatment, analysed according to their treatment assignment irrespective of the treatment received (ie, intention to treat). The safety analysis set comprised participants randomly assigned to study treatment who took at least one dose of the investigational product, analysed according to the treatment actually received. This trial is registered with <span><span>ClinicalTrials.gov</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>, <span><span>NCT04435626</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>, and is closed to new participants.<h3>Findings</h3>Between Sept 14, 2020, and Jan 10, 2023, 6001 participants were recruited and randomly assigned to finerenone or placebo. 3222 (53·7%) participants did not have diabetes at baseline and comprised the study population. During a median duration of follow-up of 31·3 months (IQR 21·5–36·3), 115 (7·2%) participants in the finerenone group and 147 (9·1%) in the placebo group developed new-onset diabetes, corresponding to a rate of 3·0 events per 100 person-years (95% CI 2·5–3·6) in the finerenone group and 3·9 events per 100 person-years (3·3–4·6) in the placebo group. Compared with placebo, finerenone significantly reduced the hazard of new-onset diabetes by 24% (hazard ratio [HR] 0·76 [95% CI","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"75 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142974794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-13DOI: 10.1016/s2213-8587(24)00339-5
Amélie Bonnefond, Jose C Florez, Ruth J F Loos, Philippe Froguel
Diabetes is a leading cause of global mortality and disability, and its economic burden is substantial. This Review focuses on type 2 diabetes, which makes up 90–95% of all diabetes cases. Type 2 diabetes involves a progressive loss of insulin secretion often alongside insulin resistance and metabolic syndrome. Although obesity and a sedentary lifestyle are considerable contributors, research over the last 25 years has shown that type 2 diabetes develops on a predisposing genetic background, with family and twin studies indicating considerable heritability (ie, 31–72%). This Review explores type 2 diabetes from a genetic perspective, highlighting insights into its pathophysiology and the implications for precision medicine. More specifically, the traditional understanding of type 2 diabetes genetics has focused on a dichotomy between monogenic and polygenic forms. However, emerging evidence suggests a continuum that includes monogenic, oligogenic, and polygenic contributions, revealing their complementary roles in type 2 diabetes pathophysiology. Recent genetic studies provide deeper insights into disease mechanisms and pave the way for precision medicine approaches that could transform type 2 diabetes management. Additionally, the effect of environmental factors on type 2 diabetes, particularly from epigenetic modifications, adds another layer of complexity to understanding and addressing this multifaceted disease.
{"title":"Dissection of type 2 diabetes: a genetic perspective","authors":"Amélie Bonnefond, Jose C Florez, Ruth J F Loos, Philippe Froguel","doi":"10.1016/s2213-8587(24)00339-5","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00339-5","url":null,"abstract":"Diabetes is a leading cause of global mortality and disability, and its economic burden is substantial. This Review focuses on type 2 diabetes, which makes up 90–95% of all diabetes cases. Type 2 diabetes involves a progressive loss of insulin secretion often alongside insulin resistance and metabolic syndrome. Although obesity and a sedentary lifestyle are considerable contributors, research over the last 25 years has shown that type 2 diabetes develops on a predisposing genetic background, with family and twin studies indicating considerable heritability (ie, 31–72%). This Review explores type 2 diabetes from a genetic perspective, highlighting insights into its pathophysiology and the implications for precision medicine. More specifically, the traditional understanding of type 2 diabetes genetics has focused on a dichotomy between monogenic and polygenic forms. However, emerging evidence suggests a continuum that includes monogenic, oligogenic, and polygenic contributions, revealing their complementary roles in type 2 diabetes pathophysiology. Recent genetic studies provide deeper insights into disease mechanisms and pave the way for precision medicine approaches that could transform type 2 diabetes management. Additionally, the effect of environmental factors on type 2 diabetes, particularly from epigenetic modifications, adds another layer of complexity to understanding and addressing this multifaceted disease.","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"8 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142974790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-13DOI: 10.1016/s2213-8587(25)00002-6
Li C, Bishop TRP, Imamura F, et al. Meat consumption and incident type 2 diabetes: an individual-participant federated meta-analysis of 1·97 million adults with 100 000 incident cases from 31 cohorts in 20 countries. Lancet Diabetes Endocrinol 2024; 12: 619–30—In the Table of this Article, the number of participants in the UKB cohort should have read “457 239”; the proportion of women and men in the MVP cohort should have read “10·0%, 90·0%”; the processed meat consumption for the UKB cohort should have read “39 (0–80)”; the number of events for both primary and secondary outcomes should have read “17 043” for the CKB cohort, “274” for the SUN cohort, and “16 643” for the UKB cohort; and the footnote text “Meat consumption for the HPFS, NHS I, and NHS II cohorts was reported as mean (min, max)” has been added. In figure 2, the number of cases for the SUN cohort should have read “274” and the line showing the 95% CI for the MVP cohort was not displayed correctly. In the final sentence of the Results section, the point estimate and 95% CI should have read “0·98 (0·90–1·07)”. The appendix has been corrected. These corrections have been made to the online version as of Jan 13, 2025.
{"title":"Correction to Lancet Diabetes Endocrinol 2024; 12: 619–30","authors":"","doi":"10.1016/s2213-8587(25)00002-6","DOIUrl":"https://doi.org/10.1016/s2213-8587(25)00002-6","url":null,"abstract":"<em>Li C, Bishop TRP, Imamura F, et al. Meat consumption and incident type 2 diabetes: an individual-participant federated meta-analysis of 1·97 million adults with 100 000 incident cases from 31 cohorts in 20 countries.</em> Lancet Diabetes Endocrinol <em>2024;</em> 12: <em>619–30</em>—In the Table of this Article, the number of participants in the UKB cohort should have read “457 239”; the proportion of women and men in the MVP cohort should have read “10·0%, 90·0%”; the processed meat consumption for the UKB cohort should have read “39 (0–80)”; the number of events for both primary and secondary outcomes should have read “17 043” for the CKB cohort, “274” for the SUN cohort, and “16 643” for the UKB cohort; and the footnote text “Meat consumption for the HPFS, NHS I, and NHS II cohorts was reported as mean (min, max)” has been added. In figure 2, the number of cases for the SUN cohort should have read “274” and the line showing the 95% CI for the MVP cohort was not displayed correctly. In the final sentence of the Results section, the point estimate and 95% CI should have read “0·98 (0·90–1·07)”. The appendix has been corrected. These corrections have been made to the online version as of Jan 13, 2025.","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"88 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142974791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-23DOI: 10.1016/s2213-8587(24)00366-8
Kim R Quimby
No Abstract
没有抽象的
{"title":"Evaluation of a type 2 diabetes remission programme","authors":"Kim R Quimby","doi":"10.1016/s2213-8587(24)00366-8","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00366-8","url":null,"abstract":"No Abstract","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"58 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142879643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-23DOI: 10.1016/s2213-8587(24)00367-x
Jiashu Han, Dan Shan
No Abstract
没有抽象的
{"title":"Evaluation of a type 2 diabetes remission programme","authors":"Jiashu Han, Dan Shan","doi":"10.1016/s2213-8587(24)00367-x","DOIUrl":"https://doi.org/10.1016/s2213-8587(24)00367-x","url":null,"abstract":"No Abstract","PeriodicalId":48790,"journal":{"name":"The Lancet Diabetes & Endocrinology","volume":"85 1","pages":""},"PeriodicalIF":44.5,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142879642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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