Insomnia and Telomere Length in Older Adults

Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age t...

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Vydáno v:Sleep (New York, N.Y.) Ročník 39; číslo 3; s. 559
Hlavní autoři: Carroll, Judith E, Esquivel, Stephanie, Goldberg, Alyssa, Seeman, Teresa E, Effros, Rita B, Dock, Jeffrey, Olmstead, Richard, Breen, Elizabeth C, Irwin, Michael R
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.03.2016
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ISSN:1550-9109, 1550-9109
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Abstract Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age to increase cellular aging. A total of 126 males and females (60-88 y) were assessed for insomnia using the Diagnostic and Statistical Manual IV criterion for primary insomnia and the International Classification of Sleep Disorders, Second Edition for general insomnia (45 insomnia cases; 81 controls). Telomere length in peripheral blood mononuclear cells (PBMC) was determined using real-time quantitative polymerase chain reaction (qPCR) methodology. In the analysis of covariance model adjusting for body mass index and sex, age (60-69 y versus 70-88 y) and insomnia diagnosis interacted to predict shorter PBMC telomere length (P = 0.04). In the oldest age group (70-88 y), PBMC telomere length was significantly shorter in those with insomnia, mean (standard deviation) M(SD) = 0.59(0.2) compared to controls with no insomnia M(SD) = 0.78(0.4), P = 0.04. In the adults aged 60-69 y, PBMC telomere length was not different between insomnia cases and controls, P = 0.44. Insomnia is associated with shorter PBMC telomere length in adults aged 70-88 y, but not in those younger than 70 y, suggesting that clinically severe sleep disturbances may increase cellular aging, especially in the later years of life. These findings highlight insomnia as a vulnerability factor in later life, with implications for risk for diseases of aging.
AbstractList Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age to increase cellular aging. A total of 126 males and females (60-88 y) were assessed for insomnia using the Diagnostic and Statistical Manual IV criterion for primary insomnia and the International Classification of Sleep Disorders, Second Edition for general insomnia (45 insomnia cases; 81 controls). Telomere length in peripheral blood mononuclear cells (PBMC) was determined using real-time quantitative polymerase chain reaction (qPCR) methodology. In the analysis of covariance model adjusting for body mass index and sex, age (60-69 y versus 70-88 y) and insomnia diagnosis interacted to predict shorter PBMC telomere length (P = 0.04). In the oldest age group (70-88 y), PBMC telomere length was significantly shorter in those with insomnia, mean (standard deviation) M(SD) = 0.59(0.2) compared to controls with no insomnia M(SD) = 0.78(0.4), P = 0.04. In the adults aged 60-69 y, PBMC telomere length was not different between insomnia cases and controls, P = 0.44. Insomnia is associated with shorter PBMC telomere length in adults aged 70-88 y, but not in those younger than 70 y, suggesting that clinically severe sleep disturbances may increase cellular aging, especially in the later years of life. These findings highlight insomnia as a vulnerability factor in later life, with implications for risk for diseases of aging.
Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age to increase cellular aging.STUDY OBJECTIVESInsomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study examines the effects of insomnia on telomere length, a measure of cellular aging, and tests whether insomnia interacts with chronological age to increase cellular aging.A total of 126 males and females (60-88 y) were assessed for insomnia using the Diagnostic and Statistical Manual IV criterion for primary insomnia and the International Classification of Sleep Disorders, Second Edition for general insomnia (45 insomnia cases; 81 controls). Telomere length in peripheral blood mononuclear cells (PBMC) was determined using real-time quantitative polymerase chain reaction (qPCR) methodology.METHODSA total of 126 males and females (60-88 y) were assessed for insomnia using the Diagnostic and Statistical Manual IV criterion for primary insomnia and the International Classification of Sleep Disorders, Second Edition for general insomnia (45 insomnia cases; 81 controls). Telomere length in peripheral blood mononuclear cells (PBMC) was determined using real-time quantitative polymerase chain reaction (qPCR) methodology.In the analysis of covariance model adjusting for body mass index and sex, age (60-69 y versus 70-88 y) and insomnia diagnosis interacted to predict shorter PBMC telomere length (P = 0.04). In the oldest age group (70-88 y), PBMC telomere length was significantly shorter in those with insomnia, mean (standard deviation) M(SD) = 0.59(0.2) compared to controls with no insomnia M(SD) = 0.78(0.4), P = 0.04. In the adults aged 60-69 y, PBMC telomere length was not different between insomnia cases and controls, P = 0.44.RESULTSIn the analysis of covariance model adjusting for body mass index and sex, age (60-69 y versus 70-88 y) and insomnia diagnosis interacted to predict shorter PBMC telomere length (P = 0.04). In the oldest age group (70-88 y), PBMC telomere length was significantly shorter in those with insomnia, mean (standard deviation) M(SD) = 0.59(0.2) compared to controls with no insomnia M(SD) = 0.78(0.4), P = 0.04. In the adults aged 60-69 y, PBMC telomere length was not different between insomnia cases and controls, P = 0.44.Insomnia is associated with shorter PBMC telomere length in adults aged 70-88 y, but not in those younger than 70 y, suggesting that clinically severe sleep disturbances may increase cellular aging, especially in the later years of life. These findings highlight insomnia as a vulnerability factor in later life, with implications for risk for diseases of aging.CONCLUSIONSInsomnia is associated with shorter PBMC telomere length in adults aged 70-88 y, but not in those younger than 70 y, suggesting that clinically severe sleep disturbances may increase cellular aging, especially in the later years of life. These findings highlight insomnia as a vulnerability factor in later life, with implications for risk for diseases of aging.
Author Dock, Jeffrey
Breen, Elizabeth C
Olmstead, Richard
Esquivel, Stephanie
Effros, Rita B
Irwin, Michael R
Carroll, Judith E
Goldberg, Alyssa
Seeman, Teresa E
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  surname: Carroll
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  organization: University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA
– sequence: 2
  givenname: Stephanie
  surname: Esquivel
  fullname: Esquivel, Stephanie
  organization: University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA
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  givenname: Alyssa
  surname: Goldberg
  fullname: Goldberg, Alyssa
  organization: Children's National Medical Center, Department of Pediatrics, Washington, DC
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  givenname: Teresa E
  surname: Seeman
  fullname: Seeman, Teresa E
  organization: University of California, Los Angeles, Department of Medicine, Division of Geriatrics, David Geffen School of Medicine, Los Angeles, CA
– sequence: 5
  givenname: Rita B
  surname: Effros
  fullname: Effros, Rita B
  organization: University of California, Los Angeles, Department of Pathology and Laboratory Medicine, Los Angeles, CA
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  surname: Dock
  fullname: Dock, Jeffrey
  organization: University of California, Los Angeles, Department of Pathology and Laboratory Medicine, Los Angeles, CA
– sequence: 7
  givenname: Richard
  surname: Olmstead
  fullname: Olmstead, Richard
  organization: University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA
– sequence: 8
  givenname: Elizabeth C
  surname: Breen
  fullname: Breen, Elizabeth C
  organization: University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA
– sequence: 9
  givenname: Michael R
  surname: Irwin
  fullname: Irwin, Michael R
  organization: University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA
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Keywords sleep
late life
telomere
cellular aging
older adults
aging
insomnia
Language English
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Snippet Insomnia, particularly in later life, may raise the risk for chronic diseases of aging and mortality through its effect on cellular aging. The current study...
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SubjectTerms Aged
Aged, 80 and over
Aging - genetics
Aging - pathology
Case-Control Studies
Cellular Senescence - genetics
Chronic Disease
Female
Humans
Leukocytes, Mononuclear - metabolism
Male
Middle Aged
Real-Time Polymerase Chain Reaction
Risk
Sleep Initiation and Maintenance Disorders - diagnosis
Sleep Initiation and Maintenance Disorders - genetics
Sleep Initiation and Maintenance Disorders - pathology
Telomere - genetics
Telomere - metabolism
Title Insomnia and Telomere Length in Older Adults
URI https://www.ncbi.nlm.nih.gov/pubmed/26715231
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Volume 39
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