Izquierdo Andrea G, Lorenzo Paula M, Costa-Fraga Nicolás, Primo-Martin David, Rodriguez-Carnero Gemma, Nicoletti Carolina F, Martínez J Alfredo, Casanueva Felipe F, de Luis Daniel, Diaz-Lagares Angel, Crujeiras Ana B
Epigenomics in Endocrinology and Nutrition Group, Epigenomics Unit, Instituto de Investigacion Sanitaria de Santiago de Compostela (IDIS), Complejo Hospitalario Universitario de Santiago de Compostela (CHUS/SERGAS), 15706 Santiago de Compostela, Spain.
CIBER Fisiopatologia de La Obesidad y Nutricion (CIBERobn), 28029 Madrid, Spain.
Nutrients. 2025 Mar 18;17(6):1060. doi: 10.3390/nu17061060.
: Epigenetic clocks have emerged as a tool to quantify biological age, providing a more accurate estimate of an individual's health status than chronological age, helping to identify risk factors for accelerated aging and evaluating the reversibility of therapeutic strategies. This study aimed to evaluate the potential association between epigenetic acceleration of biological age and obesity, as well as to determine whether nutritional interventions for body weight loss could slow down this acceleration. : Biological age was estimated using three epigenetic clocks (Horvath (Hv), Hannum (Hn), and Levine (Lv)) based on the leukocyte methylome analysis of individuals with normal weight (n = 20), obesity (n = 24), and patients with obesity following a VLCKD (n = 10). We analyzed differences in biological age estimates, the relationship between age acceleration and obesity, and the impact of VLCKD. Correlations were assessed between age acceleration, BMI, and various metabolic parameters. : Analysis of the epigenetic clocks revealed an acceleration of biological age in individuals with obesity (Hv = +3.4(2.5), Hn = +5.7(3.2), Lv = +3.9(2.7)) compared to a slight deceleration in individuals with normal weight. This epigenetic acceleration correlated with BMI ( < 0.0001). Interestingly, patients with obesity following a VLCKD showed a deceleration in estimated biological age, both in nutritional ketosis (Hv = -3.3(4.0), Hn = -6.3(5.3), Lv = -8.8(4.5)) and at endpoint (Hv = -1.1(4.3), Hn = -7.4(5.6), Lv = -8.2(5.3)). Relevantly, this slowdown in age is associated with BMI ( < 0.0001), ketonemia ( ≤ 0.001), and metabolic parameters ( < 0.05). : Our findings highlight the applicability of epigenetic clocks to monitor obesity-related biological aging in precision medicine and show the potential efficacy of the VLCKD in slowing obesity-related epigenetic aging.
表观遗传时钟已成为一种量化生物年龄的工具，与实际年龄相比，它能更准确地估计个体的健康状况，有助于识别加速衰老的风险因素并评估治疗策略的可逆性。本研究旨在评估生物年龄的表观遗传加速与肥胖之间的潜在关联，并确定体重减轻的营养干预措施是否能减缓这种加速。：基于对体重正常者（n = 20）、肥胖者（n = 24）以及极低热量生酮饮食（VLCKD）后的肥胖患者（n = 10）的白细胞甲基化组分析，使用三种表观遗传时钟（霍瓦斯（Hv）、汉纳姆（Hn）和莱文（Lv））估计生物年龄。我们分析了生物年龄估计值的差异、年龄加速与肥胖之间的关系以及VLCKD的影响。评估了年龄加速、体重指数（BMI）与各种代谢参数之间的相关性。：对表观遗传时钟的分析显示，与体重正常者的轻微减速相比，肥胖者的生物年龄加速（Hv = +3.4(2.5)，Hn = +5.7(3.2)，Lv = +3.9(2.7)）。这种表观遗传加速与BMI相关（< 0.0001）。有趣的是，VLCKD后的肥胖患者在营养性酮症阶段（Hv = -3.3(4.0)，Hn = -6.3(5.3)，Lv = -8.8(4.5)）和终点时（Hv = -1.1(4.3)，Hn = -7.4(5.6)，Lv = -8.2(5.3)）估计的生物年龄出现减速。相关的是，这种年龄减缓与BMI（< 0.0001）、酮血症（≤ 0.001）和代谢参数（< 0.05）有关。：我们的研究结果突出了表观遗传时钟在精准医学中监测肥胖相关生物衰老的适用性，并显示了VLCKD在减缓肥胖相关表观遗传衰老方面的潜在疗效。
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