Yonghwan Kim1,2, Hee-Taik Kang1,3, Duk-Chul Lee4. 1. Department of Family Medicine, Chungbuk National University Hospital, Cheongju 28644, Korea. 2. Department of Medicine, Graduate School, Yonsei University College of Medicine, Seoul 03722, Korea. 3. Department of Family Medicine, Chungbuk National University College of Medicine, Cheongju 28644, Korea. 4. Department of Family Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Korea.
Abstract
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. METHODS: 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. RESULTS:Sleep quality index using PSQI was improved in the melatonin group from a score of 11 to 8 (p = 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 (p = 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. CONCLUSIONS: 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.
RCT Entities:
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. METHODS: 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. RESULTS: Sleep quality index using PSQI was improved in the melatonin group from a score of 11 to 8 (p = 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 (p = 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. CONCLUSIONS: 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.
Entities:
Keywords:
arterial stiffness; insomnia; melatonin; mitochondrial DNA
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