Hebrew University-Hadassah School of Public Health and Community Medicine, Ein Kerem, Jerusalem, Israel.
Am J Clin Nutr. 2012 Feb;95(2):479-87. doi: 10.3945/ajcn.111.024521. Epub 2012 Jan 11.
Dietary energy restriction in mammals, particularly at a young age, extends the life span. Leukocyte telomere length (LTL) is thought to be a bioindicator of aging in humans. High n-6 (omega-6) PUFA intake may accelerate LTL attrition.
We determined whether lower energy and higher PUFA intakes in young adulthood are associated with shorter LTL in cross-sectional and longitudinal analyses.
In a longitudinal observational study (405 men, 204 women), diet was determined at baseline by a semiquantitative food-frequency questionnaire, and LTL was determined by Southern blots at mean ages of 30.1 y (baseline) and 43.2 y (follow-up). Spearman correlations and multivariable linear regression were used.
Baseline energy intake was inversely associated with follow-up LTL in men (standardized β = -0.171, P = 0.0005) but not in women (P = 0.039 for sex interaction). The difference in men between the highest and lowest quintiles of energy was 244 base pairs (bp) (95% CI: 59, 429 bp) and between extreme quintiles of LTL was 440 kcal (95% CI: 180, 700 kcal). Multivariable adjustment modestly attenuated the association (β = -0.157, P = 0.002). Inverse associations, which were noted for all macronutrients, were strongest for the unsaturated fatty acids. In multivariable models including energy and the macronutrients (as percentage of energy), the significant inverse energy-LTL association (but not the PUFA-LTL association) persisted. The energy-LTL association was restricted to never smokers (standardized β = -0.259, P = 0.0008; P = 0.050 for the smoking × calorie interaction).
The inverse calorie intake-LTL association is consistent with trial data showing beneficial effects of calorie restriction on aging biomarkers. Further exploration of energy intake and LTL dynamics in the young is needed.
在哺乳动物中,特别是在年轻时限制饮食能量可以延长寿命。白细胞端粒长度(LTL)被认为是人类衰老的生物标志物。高 n-6(ω-6)多不饱和脂肪酸(PUFA)摄入可能会加速 LTL 的损耗。
我们通过横断面和纵向分析来确定年轻时较低的能量和较高的 PUFA 摄入量是否与 LTL 缩短有关。
在一项纵向观察性研究(405 名男性,204 名女性)中,通过半定量食物频率问卷在基线时确定饮食,在平均年龄为 30.1 岁(基线)和 43.2 岁(随访)时通过 Southern 印迹法确定 LTL。使用 Spearman 相关和多变量线性回归。
男性基线时的能量摄入量与随访时的 LTL 呈负相关(标准化β=-0.171,P=0.0005),但在女性中无相关性(性别交互作用 P=0.039)。男性能量最高和最低五分位组之间的差异为 244 个碱基对(95%置信区间:59,429 个碱基对),LTL 极值五分位组之间的差异为 440 卡路里(95%置信区间:180,700 卡路里)。多变量调整略微减弱了这种关联(β=-0.157,P=0.002)。所有宏量营养素都存在负相关,其中不饱和脂肪酸的相关性最强。在包括能量和宏量营养素(以能量百分比表示)的多变量模型中,与能量相关的负相关与 LTL 显著相关(但与 PUFA 与 LTL 之间的关联不相关)。能量与 LTL 的关联仅限于从不吸烟者(标准化β=-0.259,P=0.0008;吸烟与卡路里交互作用 P=0.050)。
摄入卡路里与 LTL 之间的反比关系与试验数据一致,表明卡路里限制对衰老生物标志物有益。需要进一步探索年轻人的能量摄入和 LTL 动态。