Kim Yonghwan, Kang Hee-Taik, Lee Duk-Chul
Department of Family Medicine, Chungbuk National University Hospital, Cheongju 28644, Korea.
Department of Medicine, Graduate School, Yonsei University College of Medicine, Seoul 03722, Korea.
Int J Environ Res Public Health. 2021 Mar 4;18(5):2561. doi: 10.3390/ijerph18052561.
Melatonin is a hormone produced in the pineal gland that controls sleep and circadian rhythm. Some studies have reported antioxidant and anti-inflammatory effects of melatonin that could benefit cardiometabolic function; however, there is a lack of evidence to support these assertions. The aim of this study was to investigate whether melatonin has beneficial effects on arterial stiffness and mitochondrial deoxyribonucleic acid (DNA) in humans.
This study was designed as a double-blind randomized controlled study. Thirty-eight healthy women aged 55 years and older were enrolled. All had insomnia (Pittsburgh Sleep Quality Index (PSQI) ≥ 5), not treated with any medications, for at least three months before enrollment. Subjects were divided into a melatonin and a placebo group according to melatonin supplementation. The melatonin group took 2 mg melatonin every night for six weeks. The cardio-ankle vascular index (CAVI) was used as an indicator of arterial stiffness. After six weeks, CAVI, mitochondrial DNA (mtDNA) copy number in white blood cells (WBCs), and other metabolic indices, such as homeostasis model assessment of insulin resistance (HOMA-IR), were checked.
Sleep quality index using PSQI was improved in the melatonin group from a score of 11 to 8 ( = 0.01), but did not change significantly in the control group. However, there was no significant intergroup difference in PSQI. Systolic blood pressure (SBP) decreased in the melatonin group from 135 to 128 mmHg ( = 0.015), while remaining stable in the placebo group. Right CAVI, mitochondrial DNA copy number, and HOMA-IR were not altered in either group. There were no intergroup differences in CAVI, mtDNA, HOMA-IR, or SBP between baseline and week six.
We found no evidence that melatonin supplementation improved cardiometabolic parameters like arterial stiffness, mtDNA, or insulin resistance compared to the placebo between baseline and week six. Sleep quality was improved in the melatonin group. Further research, including longer-term studies with higher doses of melatonin, is warranted.
褪黑素是一种由松果体分泌的激素，可控制睡眠和昼夜节律。一些研究报告了褪黑素的抗氧化和抗炎作用，这些作用可能有益于心脏代谢功能；然而，缺乏证据支持这些说法。本研究的目的是调查褪黑素对人体动脉僵硬度和线粒体脱氧核糖核酸（DNA）是否有有益影响。
本研究设计为双盲随机对照研究。招募了38名55岁及以上的健康女性。所有受试者在入组前至少三个月患有失眠（匹兹堡睡眠质量指数（PSQI）≥5），且未接受任何药物治疗。根据褪黑素补充情况，将受试者分为褪黑素组和安慰剂组。褪黑素组每晚服用2毫克褪黑素，持续六周。使用心踝血管指数（CAVI）作为动脉僵硬度的指标。六周后，检查CAVI、白细胞（WBC）中线粒体DNA（mtDNA）拷贝数以及其他代谢指标，如胰岛素抵抗稳态模型评估（HOMA-IR）。
褪黑素组使用PSQI的睡眠质量指数从11分提高到8分（=0.01），而对照组无显著变化。然而，PSQI组间差异无统计学意义。褪黑素组收缩压（SBP）从135 mmHg降至128 mmHg（=0.015），而安慰剂组保持稳定。两组的右侧CAVI、线粒体DNA拷贝数和HOMA-IR均未改变。基线和第六周之间，CAVI、mtDNA、HOMA-IR或SBP组间无差异。
我们没有发现证据表明，与安慰剂相比，在基线和第六周之间，补充褪黑素能改善动脉僵硬度、mtDNA或胰岛素抵抗等心脏代谢参数。褪黑素组的睡眠质量得到改善。有必要进行进一步的研究，包括更高剂量褪黑素的长期研究。
