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Sleep Initiation and Maintenance Disorders: HELP
Articles by Max A. Little
Based on 2 articles published since 2009
(Why 2 articles?)
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Between 2009 and 2019, Max A. Little wrote the following 2 articles about Sleep Initiation and Maintenance Disorders.
 
+ Citations + Abstracts
1 Article Biological and clinical insights from genetics of insomnia symptoms. 2019

Lane, Jacqueline M / Jones, Samuel E / Dashti, Hassan S / Wood, Andrew R / Aragam, Krishna G / van Hees, Vincent T / Strand, Linn B / Winsvold, Bendik S / Wang, Heming / Bowden, Jack / Song, Yanwei / Patel, Krunal / Anderson, Simon G / Beaumont, Robin N / Bechtold, David A / Cade, Brian E / Haas, Mary / Kathiresan, Sekar / Little, Max A / Luik, Annemarie I / Loudon, Andrew S / Purcell, Shaun / Richmond, Rebecca C / Scheer, Frank A J L / Schormair, Barbara / Tyrrell, Jessica / Winkelman, John W / Winkelmann, Juliane / Anonymous1871412 / Hveem, Kristian / Zhao, Chen / Nielsen, Jonas B / Willer, Cristen J / Redline, Susan / Spiegelhalder, Kai / Kyle, Simon D / Ray, David W / Zwart, John-Anker / Brumpton, Ben / Frayling, Timothy M / Lawlor, Deborah A / Rutter, Martin K / Weedon, Michael N / Saxena, Richa. ·Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. · Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. · Broad Institute, Cambridge, MA, USA. · Genetics of Complex Traits, University of Exeter Medical School, Exeter, UK. · Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. · Cardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA. · Netherlands eScience Center, Amsterdam, the Netherlands. · K.G. Jebsen Centre for Genetic Epidemiology, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. · FORMI and Department of Neurology, Oslo University Hospital, Oslo, Norway. · Division of Clinical Neuroscience, Oslo University Hospital and University of Oslo, Oslo, Norway. · Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, MA, USA. · Division of Sleep Medicine, Department of Medicine, Harvard Medical School, Boston, MA, USA. · MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK. · Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK. · College of Science, Northeastern University, Boston, MA, USA. · Division of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK. · Farr Institute of Health Informatics Research, University College London, London, UK. · Division of Endocrinology, Diabetes & Gastroenterology, School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK. · Department of Mathematics, Aston University, Birmingham, UK. · Media Lab, Massachusetts Institute of Technology, Cambridge, MA, USA. · Sleep and Circadian Neuroscience Institute, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK. · Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, the Netherlands. · Department of Psychiatry, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA. · School of Social and Community Medicine, University of Bristol, Bristol, UK. · Medical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK. · Institute of Neurogenomics, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany. · Departments of Psychiatry and Neurology, Massachusetts General Hospital, Boston, MA, USA. · Cluster for Systems Neurology (SyNergy), Munich, Germany. · Institute of Human Genetics, Technische Universität München, Munich, Germany. · Neurogenetics, Technische Universität München, Munich, Germany. · Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA. · Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA. · Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, MI, USA. · Departments of Medicine, Brigham and Women's Hospital and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. · Clinic for Psychiatry and Psychotherapy, Medical Centre-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany. · Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, OX37LE/NIHR Oxford Biomedical Research Centre, John Radcliffe Hospital, Oxford, UK. · Department of Thoracic and Occupational Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. · Manchester Diabetes Centre, Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. · Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA. rsaxena@partners.org. · Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. rsaxena@partners.org. · Broad Institute, Cambridge, MA, USA. rsaxena@partners.org. ·Nat Genet · Pubmed #30804566.

ABSTRACT: Insomnia is a common disorder linked with adverse long-term medical and psychiatric outcomes. The underlying pathophysiological processes and causal relationships of insomnia with disease are poorly understood. Here we identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Our results suggest enrichment of genes involved in ubiquitin-mediated proteolysis and of genes expressed in multiple brain regions, skeletal muscle, and adrenal glands. Evidence of shared genetic factors was found between frequent insomnia symptoms and restless legs syndrome, aging, and cardiometabolic, behavioral, psychiatric, and reproductive traits. Evidence was found for a possible causal link between insomnia symptoms and coronary artery disease, depressive symptoms, and subjective well-being.

2 Article Sleep and cognitive performance: cross-sectional associations in the UK Biobank. 2017

Kyle, Simon D / Sexton, Claire E / Feige, Bernd / Luik, Annemarie I / Lane, Jacqueline / Saxena, Richa / Anderson, Simon G / Bechtold, David A / Dixon, William / Little, Max A / Ray, David / Riemann, Dieter / Espie, Colin A / Rutter, Martin K / Spiegelhalder, Kai. ·Sleep and Circadian Neuroscience Institute (SCNi), Nuffield Department of Clinical Neurosciences, University of Oxford, UK. Electronic address: simon.kyle@ndcn.ox.ac.uk. · FMRIB Centre, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, UK. · Clinic for Psychiatry and Psychotherapy, Medical Centre - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany. · Sleep and Circadian Neuroscience Institute (SCNi), Nuffield Department of Clinical Neurosciences, University of Oxford, UK. · Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA; Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, USA. · Center for Human Genetic Research, Massachusetts General Hospital, Boston, MA, USA; Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, USA; Department of Anesthesia, Division of Sleep and Circadian Disorders, Brigham and Women's Hospital, Boston, MA, USA. · Cardiovascular Research Group, Institute of Cardiovascular Sciences, The University of Manchester, Manchester, UK. · Faculty of Life Sciences, University of Manchester, Manchester, UK. · Centre for Musculoskeletal Research, Institute of Inflammation and Repair, The University of Manchester, Manchester, UK. · Engineering and Applied Science, Aston University, Birmingham, UK; Media Lab, Massachusetts Institute of Technology, Cambridge, MA, USA. · Centre for Endocrinology and Diabetes, Institute of Human Development, University of Manchester, UK. · Centre for Endocrinology and Diabetes, Institute of Human Development, University of Manchester, UK; Manchester Diabetes Centre, Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. ·Sleep Med · Pubmed #29031762.

ABSTRACT: OBJECTIVE: The relationship between insomnia symptoms and cognitive performance is unclear, particularly at the population level. We conducted the largest examination of this association to date through analysis of the UK Biobank, a large population-based sample of adults aged 40-69 years. We also sought to determine associations between cognitive performance and self-reported chronotype, sleep medication use and sleep duration. METHODS: This cross-sectional, population-based study involved 477,529 participants, comprising 133,314 patients with frequent insomnia symptoms (age: 57.4 ± 7.7 years; 62.1% female) and 344,215 controls without insomnia symptoms (age: 56.1 ± 8.2 years; 52.0% female). Cognitive performance was assessed by a touchscreen test battery probing reasoning, basic reaction time, numeric memory, visual memory, and prospective memory. Adjusted models included relevant demographic, clinical, and sleep variables. RESULTS: Frequent insomnia symptoms were associated with cognitive impairment in unadjusted models; however, these effects were reversed after full adjustment, leaving those with frequent insomnia symptoms showing statistically better cognitive performance over those without. Relative to intermediate chronotype, evening chronotype was associated with superior task performance, while morning chronotype was associated with the poorest performance. Sleep medication use and both long (>9 h) and short (<7 h) sleep durations were associated with impaired performance. CONCLUSIONS: Our results suggest that after adjustment for potential confounding variables, frequent insomnia symptoms may be associated with a small statistical advantage, which is unlikely to be clinically meaningful, on simple neurocognitive tasks. Further work is required to examine the mechanistic underpinnings of an apparent evening chronotype advantage in cognitive performance and the impairment associated with morning chronotype, sleep medication use, and sleep duration extremes.