Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Mikras Asias 75, Goudi, 11527, Athens, Greece.
Second Department of Critical Care, Attikon General University Hospital, Medical School, National and Kapodistrian University of Athens, 1 Rimini St, Haidari, 12462, Athens, Greece.
Curr Obes Rep. 2021 Sep;10(3):214-243. doi: 10.1007/s13679-021-00436-y. Epub 2021 Apr 28.
A growing body of evidence suggests that obesity and increased visceral adiposity are strongly and independently linked to adverse outcomes and death due to COVID-19. This review summarizes current epidemiologic data, highlights pathogenetic mechanisms on the association between excess body weight and COVID-19, compares data from previous pandemics, discusses why COVID-19 challenges the "obesity paradox," and presents implications in prevention and treatment as well as future perspectives.
Data from meta-analyses based on recent observational studies have indicated that obesity increases the risks of infection from SARS-CoV-2, severe infection and hospitalization, admission to the ICU and need of invasive mechanical ventilation (IMV), and the risk of mortality, particularly in severe obesity. The risks of IMV and mortality associated with obesity are accentuated in younger individuals (age ≤ 50 years old). The meta-inflammation in obesity intersects with and exacerbates underlying pathogenetic mechanisms in COVID-19 through the following mechanisms and factors: (i) impaired innate and adaptive immune responses; (ii) chronic inflammation and oxidative stress; (iii) endothelial dysfunction, hypercoagulability, and aberrant activation of the complement; (iv) overactivation of the renin-angiotensin-aldosterone system; (v) overexpression of the angiotensin-converting enzyme 2 receptor in the adipose tissue; (vi) associated cardiometabolic comorbidities; (vii) vitamin D deficiency; (viii) gut dysbiosis; and (ix) mechanical and psychological issues. Mechanistic and large epidemiologic studies using big data sources with omics data exploring genetic determinants of risk and disease severity as well as large randomized controlled trials (RCTs) are necessary to shed light on the pathways connecting chronic subclinical inflammation/meta-inflammation with adverse COVID-19 outcomes and establish the ideal preventive and therapeutic approaches for patients with obesity.
越来越多的证据表明，肥胖和内脏脂肪增加与 COVID-19 的不良结局和死亡密切相关且独立相关。本文综述了目前的流行病学数据，强调了体重过度与 COVID-19 之间关联的发病机制，比较了以往大流行的数据，讨论了 COVID-19 为何对“肥胖悖论”构成挑战，并提出了预防和治疗方面的意义以及未来展望。
基于最近观察性研究的荟萃分析数据表明，肥胖增加了感染 SARS-CoV-2、严重感染和住院、入住 ICU 和需要有创机械通气（IMV）以及死亡率的风险，尤其是在严重肥胖的情况下。肥胖与 IMV 和死亡率相关的风险在年轻个体（年龄 ≤ 50 岁）中更为突出。肥胖中的代谢炎症与 COVID-19 的潜在发病机制相交错，并通过以下机制和因素加重其发病机制：（i）先天和适应性免疫反应受损；（ii）慢性炎症和氧化应激；（iii）内皮功能障碍、高凝状态和补体异常激活；（iv）肾素-血管紧张素-醛固酮系统过度激活；（v）脂肪组织中血管紧张素转换酶 2 受体过度表达；（vi）相关的心血管代谢合并症；（vii）维生素 D 缺乏；（viii）肠道菌群失调；（ix）机械和心理问题。利用大型流行病学研究和大数据来源进行机制研究以及探索风险和疾病严重程度的遗传决定因素的大型随机对照试验（RCT）对于阐明将慢性亚临床炎症/代谢炎症与不良 COVID-19 结局联系起来的途径以及为肥胖患者建立理想的预防和治疗方法是必要的。
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