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Sleep Initiation and Maintenance Disorders: HELP
Articles by Judith E. Carroll
Based on 4 articles published since 2008
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Between 2008 and 2019, Judith E. Carroll wrote the following 4 articles about Sleep Initiation and Maintenance Disorders.
 
+ Citations + Abstracts
1 Article Epigenetic Aging and Immune Senescence in Women With Insomnia Symptoms: Findings From the Women's Health Initiative Study. 2017

Carroll, Judith E / Irwin, Michael R / Levine, Morgan / Seeman, Teresa E / Absher, Devin / Assimes, Themistocles / Horvath, Steve. ·Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles. Electronic address: jcarroll@mednet.ucla.edu. · Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles. · Department of Human Genetics, Los Angeles. · Department of Geriatrics, David Geffen School of Medicine, Los Angeles. · HudsonAlpha Institute for Biotechnology, Huntsville, Alabama. · Department of Medicine, Stanford University, Palo Alto, California. · Department of Human Genetics, Los Angeles; Department of Biostatistics, Fielding School of Public Health, University of California, Los Angeles, Los Angeles. ·Biol Psychiatry · Pubmed #27702440.

ABSTRACT: BACKGROUND: Insomnia symptoms are associated with vulnerability to age-related morbidity and mortality. Cross-sectional data suggest that accelerated biological aging may be a mechanism through which sleep influences risk. A novel method for determining age acceleration using epigenetic methylation to DNA has demonstrated predictive utility as an epigenetic clock and prognostic of age-related morbidity and mortality. METHODS: We examined the association of epigenetic age and immune cell aging with sleep in the Women's Health Initiative study (N = 2078; mean 64.5 ± 7.1 years of age) with assessment of insomnia symptoms (restlessness, difficulty falling asleep, waking at night, trouble getting back to sleep, and early awakenings), sleep duration (short sleep 5 hours or less; long sleep greater than 8 hours), epigenetic age, naive T cell (CD8+CD45RA+CCR7+), and late differentiated T cells (CD8+CD28-CD45RA-). RESULTS: Insomnia symptoms were related to advanced epigenetic age (β ± SE = 1.02 ± 0.37, p = .005) after adjustments for covariates. Insomnia symptoms were also associated with more late differentiated T cells (β ± SE = 0.59 ± 0.21, p = .006), but not with naive T cells. Self-reported short and long sleep duration were unrelated to epigenetic age. Short sleep, but not long sleep, was associated with fewer naive T cells (p < .005) and neither was related to late differentiated T cells. CONCLUSIONS: Symptoms of insomnia were associated with increased epigenetic age of blood tissue and were associated with higher counts of late differentiated CD8+ T cells. Short sleep was unrelated to epigenetic age and late differentiated cell counts, but was related to a decline in naive T cells. In this large population-based study of women in the United States, insomnia symptoms are implicated in accelerated aging.

2 Article Insomnia and Telomere Length in Older Adults. 2016

Carroll, Judith E / Esquivel, Stephanie / Goldberg, Alyssa / Seeman, Teresa E / Effros, Rita B / Dock, Jeffrey / Olmstead, Richard / Breen, Elizabeth C / Irwin, Michael R. ·University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA. · Children's National Medical Center, Department of Pediatrics, Washington, DC. · University of California, Los Angeles, Department of Medicine, Division of Geriatrics, David Geffen School of Medicine, Los Angeles, CA. · University of California, Los Angeles, Department of Pathology and Laboratory Medicine, Los Angeles, CA. ·Sleep · Pubmed #26715231.

ABSTRACT: STUDY OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

3 Article Improved sleep quality in older adults with insomnia reduces biomarkers of disease risk: pilot results from a randomized controlled comparative efficacy trial. 2015

Carroll, Judith E / Seeman, Teresa E / Olmstead, Richard / Melendez, Gerson / Sadakane, Ryan / Bootzin, Richard / Nicassio, Perry / Irwin, Michael R. ·University of California, Los Angeles-Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA; University of California, Los Angeles, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, Los Angeles, CA, USA. Electronic address: jcarroll@mednet.ucla.edu. · University of California, Los Angeles, Division of Geriatrics, David Geffen School of Medicine, Los Angeles, CA, USA. · University of California, Los Angeles-Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA; University of California, Los Angeles, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, Los Angeles, CA, USA. · University of Arizona, Department of Psychology, Tucson, AZ, USA. · University of California, Los Angeles-Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA. · University of California, Los Angeles-Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, USA; University of California, Los Angeles, Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, Los Angeles, CA, USA. Electronic address: mirwin1@ucla.edu. ·Psychoneuroendocrinology · Pubmed #25770704.

ABSTRACT: IMPORTANCE: Sleep disturbances have been linked to increased morbidity and mortality, yet it is unknown whether improving sleep quality in older adult patients with insomnia alters biomarkers of diabetes and cardiovascular disease risk. OBJECTIVE: Determine the comparative efficacy of cognitive behavioral therapy (CBT), tai chi chih (TCC), and a sleep seminar control (SS) to reduce multisystem biomarkers of disease risk in older adults with insomnia. DESIGN: Randomized controlled comparative efficacy trial. SETTING: Los Angeles community. PARTICIPANTS: A population-based sample of 109 older adults with chronic and primary insomnia. INTERVENTION: Random assignment to CBT, TCC, or SS for 2-h group sessions weekly over 4 months with a 16-month evaluation (1 year after follow-up). MAIN OUTCOME(S) AND MEASURE(S): Multisystem biological risk comprised of 8 biomarkers: high-density lipoprotein, low-density lipoprotein, triglycerides, hemoglobinA1c, glucose, insulin, C-reactive protein, and fibrinogen. Using clinical laboratory cutoffs defined as abnormal, a multisystem risk score was computed representing a sum of the deviation around the cutoffs across the 8 biomarkers. In addition, high risk grouping was classified if subjects exhibited 4 or more biomarkers in the abnormal laboratory range. RESULTS: An interaction of time-by-treatment-by-high risk group was found (F(4, 197.2)=3.14, p=.02) in which both TCC (p=.04) and CBT (p=.001) showed significantly lower risk scores as compared to SS at 16-months. CBT reduced risk of being in the high risk group at 4-months (odds ratio [OR]=.21 [95% CI, .03-1.47], p<.10) and at 16-months (OR=.06 [95% CI, .005-.669]; p<.01). TCC reduced the risk at 16-months (OR=.10 [95% CI, .008-1.29]; p<.05) but not at 4 months. Of participants who were classified in the high risk category at baseline, improvements in sleep quality, as defined by a clinical severity threshold, reduced the likelihood of being in the high risk group at 16-months, OR=.08 (95% CI, .008-.78); p=.01. CONCLUSIONS AND RELEVANCE: Participants classified as having high multisystem biological risk at entry and assigned to CBT or TCC show improvements in risk scores after one year follow-up. Given that these clinical biomarkers are associated with cardiovascular, metabolic, and inflammatory disease risk, improving sleep quality has the potential to reduce the risk of chronic disease in older adults with insomnia. Clinical Trial Registration # and name—ClinicalTrials.gov: NCT00280020, Behavioral Treatment of Insomnia in Aging

4 Article Cognitive behavioral therapy vs. Tai Chi for late life insomnia and inflammatory risk: a randomized controlled comparative efficacy trial. 2014

Irwin, Michael R / Olmstead, Richard / Carrillo, Carmen / Sadeghi, Nina / Breen, Elizabeth C / Witarama, Tuff / Yokomizo, Megumi / Lavretsky, Helen / Carroll, Judith E / Motivala, Sarosh J / Bootzin, Richard / Nicassio, Perry. · ·Sleep · Pubmed #25142571.

ABSTRACT: STUDY OBJECTIVES: To investigate the comparative efficacy of cognitive behavioral therapy (CBT), Tai Chi Chih (TCC), and sleep seminar education control (SS) on the primary outcome of insomnia diagnosis, and secondary outcomes of sleep quality, fatigue, depressive symptoms, and inflammation in older adults with insomnia. DESIGN: Randomized controlled, comparative efficacy trial. SETTING: Los Angeles community. PATIENTS: 123 older adults with chronic and primary insomnia. INTERVENTIONS: Random assignment to CBT, TCC, or SS for 2-hour group sessions weekly over 4 months with follow-up at 7 and 16 months. MEASUREMENTS: Insomnia diagnosis, patient-reported outcomes, polysomnography (PSG), and high-sensitivity C-reactive protein (CRP) levels. RESULTS: CBT performed better than TCC and SS in remission of clinical insomnia as ascertained by a clinician (P < 0.01), and also showed greater and more sustained improvement in sleep quality, sleep parameters, fatigue, and depressive symptoms than TCC and SS (all P values < 0.01). As compared to SS, CBT was associated with a reduced risk of high CRP levels (> 3.0 mg/L) at 16 months (odds ratio [OR], 0.26 [95% CI, 0.07-0.97] P < 0.05). Remission of insomnia was associated with lower levels of CRP (P < 0.05) at 16 months. TCC was associated with improvements in sleep quality, fatigue, and depressive symptoms as compared to SS (all P's < 0.05), but not insomnia remission. PSG measures did not change. CONCLUSIONS: Treatment of late-life insomnia is better achieved and sustained by cognitive behavioral therapies. Insomnia treatment and remission reduces a marker of inflammatory risk, which has implications for cardiovascular morbidity and diabetes observed with sleep disturbance in epidemiologic surveys.