首頁(yè) 資訊大腦與心臟代謝健康：需要精準(zhǔn)生活方式醫(yī)學(xué)方法的微妙平衡。

大腦與心臟代謝健康：需要精準(zhǔn)生活方式醫(yī)學(xué)方法的微妙平衡。

來(lái)源：泰然健康網(wǎng) 時(shí)間：2025年05月07日 05:16

大腦與心臟代謝健康：需要精準(zhǔn)生活方式醫(yī)學(xué)方法的微妙平衡。

IF 4.2 2區(qū) 醫(yī)學(xué) Q1 ENDOCRINOLOGY & METABOLISM

摘要

抑郁癥是發(fā)病的一個(gè)主要原因，對(duì)生活質(zhì)量有重大影響，同時(shí)還會(huì)影響缺勤率、工作效率和醫(yī)療成本[(1)]。2023 年，24% 的成年女性和 11% 的成年男性因抑郁癥狀而接受治療[(2)]。此外，三十多年來(lái)的心臟代謝成像（計(jì)算機(jī)斷層掃描 [CT] 或磁共振成像 [MRI]）研究也提供了大量證據(jù)，證明在相同體重指數(shù)（BMI）下，個(gè)體的身體成分和區(qū)域脂肪組織分布存在很大差異[(4)]。例如，內(nèi)臟脂肪組織（VAT）是與胰島素抵抗和增加 2 型糖尿病和心血管疾病風(fēng)險(xiǎn)的代謝綜合征特征最密切相關(guān)的身體脂肪區(qū)，這一點(diǎn)現(xiàn)已得到公認(rèn)[(5)]。我們還了解到，過(guò)多的腹腔脂肪是皮下脂肪組織相對(duì)無(wú)法膨脹并充當(dāng)代謝匯的標(biāo)志，導(dǎo)致脂肪不僅沉積在腹腔，而且還沉積在心臟、肝臟、腎臟、胰腺和骨骼肌等通常較瘦的組織中，這種現(xiàn)象被稱為異位脂肪沉積。安德森（Andersson）等人利用獲得英國(guó)生物庫(kù)（UK Biobank）成像數(shù)據(jù)（n = 40,174）的機(jī)會(huì)，回顧性地研究了AD（選擇性5-羥色胺再攝取抑制劑和三環(huán)類抗抑郁藥）使用者與性別、年齡和體重指數(shù)匹配的非使用者相比，是否會(huì)在體內(nèi)脂肪分布和肌肉組成方面出現(xiàn)差異[(6)]。作者在報(bào)告中指出，與對(duì)照組相比，選擇性 5-羥色胺再攝取抑制劑使用者的增值脂肪水平較高，肌肉體積較小，脂肪浸潤(rùn)較多。隨著時(shí)間的推移，在體重指數(shù)的增加方面也發(fā)現(xiàn)了性別差異（女性和男性）。雖然發(fā)現(xiàn)三環(huán)類抗抑郁藥使用者罹患心血管疾?。行裕┖?2 型糖尿病的風(fēng)險(xiǎn)增加，但無(wú)法確定肌肉成分的變化對(duì)這種風(fēng)險(xiǎn)增加的具體影響。Andersson 等人的論文探討了一個(gè)重要的話題，因?yàn)閾?jù)報(bào)道，一些抗抑郁藥物會(huì)誘發(fā)體重增加，不同類別和特定分子的藥物之間存在差異。該論文還很好地證明了體重的變化（或無(wú)變化）有時(shí)可能會(huì)誤導(dǎo)追蹤對(duì)心臟代謝健康有重大影響的身體成分的臨床相關(guān)變化。該論文提供了來(lái)自幾項(xiàng)相關(guān)探索性分析的大量數(shù)據(jù)，進(jìn)一步證明了長(zhǎng)期監(jiān)測(cè)體重不足以監(jiān)測(cè)心臟代謝健康的變化，尤其是在接受這些藥物治療的患者中。然而，一些研究的局限性也應(yīng)得到強(qiáng)調(diào)。與其他在英國(guó)生物庫(kù)隊(duì)列中進(jìn)行的子分析相反，作者無(wú)法使用加速度測(cè)量數(shù)據(jù)來(lái)更好地評(píng)估各組的體力活動(dòng)水平。另一個(gè)限制因素是無(wú)法檢查整體飲食質(zhì)量和熱量攝入的潛在變化。最后，由于沒(méi)有心血管代謝健康的中間指標(biāo)，作者假設(shè)與某些藥物相關(guān)的肌肉質(zhì)量下降和脂肪浸潤(rùn)增加有助于增加心血管代謝健康是推測(cè)性的。盡管肌少癥顯然對(duì)肥胖患者不利，但在控制了內(nèi)臟脂肪（以及肝臟和心臟脂肪增加）后，這一現(xiàn)象在多大程度上獨(dú)立地增加了該隊(duì)列中的心臟代謝風(fēng)險(xiǎn)，這是作者無(wú)法妥善解決的問(wèn)題。有一點(diǎn)是肯定的：在當(dāng)今時(shí)代，由于許多藥物并不是體重中性的，我們顯然需要比 BMI 更好的工具來(lái)評(píng)估臨床實(shí)踐中的脂肪表型，尤其是評(píng)估對(duì)哪種治療的反應(yīng)。此外，由于已知行為會(huì)調(diào)節(jié)與任何特定脂肪表型（無(wú)論是否由藥物引起）相關(guān)的風(fēng)險(xiǎn)[(4)]，因此應(yīng)在所有患者中獲取 "生活方式生命體征"，如整體飲食質(zhì)量、體力活動(dòng)水平、睡眠質(zhì)量、心肺功能和腹部脂肪的人體測(cè)量指標(biāo)[(7, 8)]。Andersson等人的這一有趣分析應(yīng)為在這一需要改善心血管代謝健康、心理健康和生活質(zhì)量的高發(fā)人群中進(jìn)一步開(kāi)展精準(zhǔn)生活方式醫(yī)學(xué)研究鋪平道路。

本文章由計(jì)算機(jī)程序翻譯，如有差異，請(qǐng)以英文原文為準(zhǔn)。

Brain versus cardiometabolic health: a delicate balance in need of precision lifestyle medicine approaches

Depression is a major cause of morbidity and has major consequences on quality of life, impacting absenteeism, productivity at work, and health care costs [(1)]. In 2023, 24% of adult women and 11% of adult men were treated for depressive symptoms [(2)]. Because some antidepressants (AD) are known to have an impact on body weight [(3)], the balance between managing mental health versus limiting adiposity-related cardiometabolic risk remains an important dilemma in clinical practice.

Furthermore, we have substantial evidence from more than three decades of cardiometabolic imaging (computed tomography [CT] or magnetic resonance imaging [MRI]) studies demonstrating that, for the same body mass index (BMI), there are considerable individual differences in body composition and regional adipose tissue distribution [(4)]. For instance, it is now well established that visceral adipose tissue (VAT) is the body fat compartment most closely associated with insulin resistance and features of the metabolic syndrome that increase risk of type 2 diabetes and cardiovascular disease [(5)]. We also understand that excess VAT is a marker of the relative inability of subcutaneous adipose tissue to expand and act as a metabolic sink, leading to deposition of fat not only in the abdominal cavity but also in usually lean tissues such as the heart, liver, kidney, pancreas, and skeletal muscle, a phenomenon referred to as ectopic fat deposition.

Andersson et al. took the opportunity of having access to the now-famous UK Biobank imaging data (n?=?40,174) to retrospectively examine whether AD (selective serotonin reuptake inhibitors and tricyclic antidepressants) users would display differences in body fat distribution and muscle composition compared with sex-, age-, and BMI-matched nonusers [(6)]. The authors report that selective serotonin reuptake inhibitor users had higher levels of VAT and less muscle volume combined with greater fat infiltration than control individuals. Sex differences were also found in BMI gained over time (women?> men). Although an increased risk of cardiovascular disease (men) and type 2 diabetes was found among tricyclic antidepressant users, the specific contribution of changes in muscle composition to such increased risks could not be determined with certainty.

The paper by Andersson et al. addresses an important topic because some AD medications have been reported to induce weight gain, with differences observed among classes and specific molecules. The paper also nicely demonstrates that changes (or lack of changes) in body weight could sometimes be misleading in order to track clinically relevant variations in body composition with significant consequences on cardiometabolic health.

This paper presents a large amount of data from several relevant exploratory analyses providing additional evidence that monitoring body weight over time is not sufficient to monitor changes in cardiometabolic health, especially among patients treated with these drugs. However, some study limitations should be highlighted. Contrary to other subanalyses conducted in the UK Biobank cohort, the authors could not use accelerometry data to better evaluate the level of physical activity across the groups. Another limitation is the inability to examine potential changes in overall diet quality and caloric intake. Finally, because intermediate markers of cardiometabolic health were not available, the assumption made by the authors that the decreased muscle mass and increased fat infiltration associated with some of these drugs contributed to increasing cardiometabolic health is speculative. Although sarcopenia is clearly detrimental to people living with obesity, to what extent this phenomenon independently contributed to cardiometabolic risk in this cohort after control for visceral adiposity (and increased liver and heart fat) is a question that could not be properly addressed by the authors.

One thing is certain: in this day and age, because many pharmacological agents are not weight-neutral, we are clearly in need of better tools than BMI to assess adiposity phenotypes in clinical practice, particularly to evaluate the response to whichever treatment. Furthermore, because behaviors are known to modulate the risk associated with any given adiposity phenotype (drug-induced or not) [(4)], “l(fā)ifestyle vital signs” such as overall diet quality, level of physical activity, quality of sleep, cardiorespiratory fitness, and anthropometric markers of abdominal adiposity should be obtained in all patients [(7, 8)]. This interesting analysis by Andersson et al. should pave the way to further precision lifestyle medicine studies conducted in this prevalent patient population in need of solutions to improve not only their cardiometabolic health but also their mental health and quality of life.

The authors declared no conflict of interest.

來(lái)源期刊

Obesity

期刊介紹： Obesity is the official journal of The Obesity Society and is the premier source of information for increasing knowledge, fostering translational research from basic to population science, and promoting better treatment for people with obesity. Obesity publishes important peer-reviewed research and cutting-edge reviews, commentaries, and public health and medical developments.

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