An Integrative Chronobiological-Cognitive Approach to Seasonal Affective Disorder Jennifer Nicole Rough University of Vermont

Total Page:16

File Type:pdf, Size:1020Kb

An Integrative Chronobiological-Cognitive Approach to Seasonal Affective Disorder Jennifer Nicole Rough University of Vermont University of Vermont ScholarWorks @ UVM Graduate College Dissertations and Theses Dissertations and Theses 2016 An integrative chronobiological-cognitive approach to seasonal affective disorder Jennifer Nicole Rough University of Vermont Follow this and additional works at: https://scholarworks.uvm.edu/graddis Part of the Clinical Psychology Commons Recommended Citation Rough, Jennifer Nicole, "An integrative chronobiological-cognitive approach to seasonal affective disorder" (2016). Graduate College Dissertations and Theses. 483. https://scholarworks.uvm.edu/graddis/483 This Dissertation is brought to you for free and open access by the Dissertations and Theses at ScholarWorks @ UVM. It has been accepted for inclusion in Graduate College Dissertations and Theses by an authorized administrator of ScholarWorks @ UVM. For more information, please contact [email protected]. AN INTEGRATIVE CHRONOBIOLOGICAL-COGNITIVE APPROACH TO SEASONAL AFFECTIVE DISORDER A Dissertation Presented by Jennifer Nicole Rough to the Faculty of the Graduate College of the University of Vermont In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Specializing in Clinical Psychology January, 2016 Defense Date: September, 17, 2015 Dissertation Examination Committee: Kelly Rohan, Ph.D., Advisor Terry Rabinowitz, M.D., Chairperson Timothy Stickle, Ph.D. Mark Bouton, Ph.D. Donna Toufexis, Ph.D. Cynthia J. Forehand, Ph.D., Dean of the Graduate College ABSTRACT Seasonal affective disorder (SAD) is characterized by annual recurrence of clinical depression in the fall and winter months. The importance of SAD as a public health problem is underscored by its high prevalence (an estimated 5%) and by the large amount of time individuals with SAD are impaired (on average, 5 months each year). The specific cause of SAD remains unknown; however, researchers have identified possible chronobiological and psychological vulnerabilities to SAD. The study aimed to clarify psychological and chronobiological correlates of SAD in the first test of an integrative model of SAD. The project used a longitudinal design to test the respective contributions of the chronobiological and cognitive vulnerabilities on winter depression severity in 31 SAD patients and 33 never-depressed controls at sites in Burlington, VT and Pittsburgh, PA. The measures selected for the cognitive vulnerability were established measures of vulnerability to nonseasonal depression with empirical support for their relevance to SAD: brooding rumination, dysfunctional attitudes, cognitive reactivity to an induced sad mood, and season-specific cognitions. The chronobiological vulnerability was measured as Phase Angle Difference (PAD) and deviation from PAD of 6 hours. All measures were completed once in the summer, when the SAD patients were remitted, and once in the winter, when patients were clinically depressed. Patients were distinguished from controls on most cognitive vulnerability measures (brooding, as well as rumination, dysfunctional attitudes, and seasonal beliefs). SAD patients exhibited shorter PAD than controls, but did not exhibit greater deviation from PAD-6. Results provide further support for specific cognitive, but not chronobiological, vulnerabilities in prediction of SAD. Limitations of the current sample are discussed. Results hold implications for future SAD research bridging the chronobiological and psychological disciplines with the ultimate aim of improved understanding, assessment, treatment, and prevention of SAD. ACKNOWLEDGEMENTS I would like to thank my committee members, Drs. Terry Rabinowitz, Tim Stickle, Mark Bouton, and Donna Toufexis, for their support of this project and guidance throughout my graduate training. I am honored to have you as part of my capstone graduate experience. I would like to express my deepest gratitude to my mentor, Dr. Kelly Rohan, for her incredible support, guidance, caring, and dedication to my graduate training. Her enthusiasm for my research and continued support of my career has made this a wonderful experience. My sincerest thanks to Dr. Al Lewy for his support of my research career from square one: my research assistantship through the fellowship funding this project. Without that first step, I may not have come this far. I am indebted to Dr. Kathryn Roecklein of the University of Pittsburgh for her collaboration and consultation on this project, with a special thanks to her research assistant, Lewis Schneider, for his assistance in data preparation. My wonderful lab mates – Yael Nillni, Lilya Sitnikov, Maggie Evans, Sheau-Yan Ho, and Jonah Meyerhoff – have made the past 7 years extraordinary. A special thanks to Dr. Yael Nillni for her mentorship in my initial years of graduate study. She set a wonderful example. ii I could not have completed the project without the help of my undergraduate research assistants: Ashley Deeb, Benjamin Cornell, Dan Cheney, and Craig Pastel, who generously volunteered their time to assist in data management. I am grateful to the University of Vermont Center of Biomedical Research Excellence for providing support for immunoassay, with a special thanks to Thomm Buttolph for his light-hearted approach to immunoassay training. A special thanks to Alan Howard and Dr. Marketa Krenek for their statistical consultation. I would like to acknowledge the National Institute of Mental Health for funding my graduate fellowship training (1F31MH094046-01A1) and making this project possible. I am extremely grateful to the Department of Psychological Science at the University of Vermont for providing supplementary research funding and continued support of my research. Lastly, I would like to thank my loving friends and family who have been by my side throughout this journey. I am especially grateful to Ben Mahon for his support in my pursuit of graduate study. And, to my Mom, who continues to inspire me through her love, spirit, and aspiration to make a true difference. It is to all of you that I owe this accomplishment. Thank you. iii TABLE OF CONTENTS ACKNOWLEDGMENTS ........................................................................................ ii LIST OF TABLES ................................................................................................... vi LIST OF FIGURES ................................................................................................... viii CHAPTER 1: Seasonal Affective Disorder (SAD) .................................................... 1 Prevalence Across Latitude ............................................................................. 2 Environmental Triggers of SAD ..................................................................... 3 Chronobiological Vulnerability to SAD ......................................................... 4 Mechanisms Linking Photoperiod to Circadian Rhythmicity ........................ 22 Psychological Vulnerability to SAD .............................................................. 26 Integrative Models of SAD ............................................................................ 32 Limitations of SAD Research ........................................................................ 33 CHAPTER 2: The Current Project ............................................................................ 35 Study Aims and Hypotheses ............................................................................ 35 CHAPTER 3: Method .............................................................................................. 38 Participants ...................................................................................................... 38 Procedure ......................................................................................................... 39 Measures ........................................................................................................ 43 Data Analytic Method .................................................................................... 48 CHAPTER 4: Results ............................................................................................... 54 Participant Flow ............................................................................................... 54 Aim 1 ............................................................................................................... 58 Aim 2 ............................................................................................................... 74 iv CHAPTER 5: Discussion ........................................................................................... 87 Aim 1 .............................................................................................................. 88 Aim 2 .............................................................................................................. 97 Study Limitations ........................................................................................... 102 Future Directions ........................................................................................... 105 Conclusions ................................................................................................... 108 REFERENCES .......................................................................................................... 111 APPENDIX A ............................................................................................................ 126 APPENDIX B ............................................................................................................ 127 APPENDIX C ...........................................................................................................
Recommended publications
  • No Evidence for a Phase Delay in Human Circadian Rhythms After a Single Morning Melatonin Administration
    J. Pineal Res. 2002; 32:1±5 Copyright ã Munksgaard, 2002 Journal of Pineal Research ISSN 0742-3098 No evidence for a phase delay in human circadian rhythms after a single morning melatonin administration Wirz-Justice A, Werth E, Renz C, MuÈ ller S, KraÈ uchi K. No evidence for a Anna Wirz-Justice, Esther Werth, phase delay in human circadian rhythms after a single morning melatonin Claudia Renz, Simon MuÈ ller and administration. J. Pineal Res. 2002; 32: 1±5. ã Munksgaard, 2002 Kurt KraÈuchi Abstract: Although there is good consensus that a single administration of Centre for Chronobiology, Psychiatric University Clinic, Basel, Switzerland melatonin in the early evening can phase advance human circadian rhythms, the evidence for phase delay shifts to a single melatonin stimulus given in the early morning is sparse. We therefore carried out a double-blind randomized- order placebo-controlled study under modi®ed constant routine (CR) conditions (58 hr bedrest under 8 lux with sleep 23:00±07:00 hr) in nine healthy young men. A single (pharmacological) dose of melatonin (5 mg p.o.) or a placebo was administered at 07:00 hr on the ®rst morning. Core body temperature (CBT) and heart rate (HR) were continuously recorded, and saliva was collected half-hourly for assay of melatonin. Neither the timing of the mid-range crossing times of temperature (MRCT) and HR rhythms, nor dim light melatonin onset (DLMOn) or oset (DLMO) were phase shifted the day after melatonin administration compared with placebo. Key words: human circadian rhythms, morning The only change was an altered wave form of the CBT rhythm: longer melatonin, phase delay duration of higher-than-average temperature after melatonin administration.
    [Show full text]
  • Differentiating External Zeitgeber Impact on Peripheral Circadian
    www.nature.com/scientificreports OPEN Diferentiating external zeitgeber impact on peripheral circadian clock resetting Isabel Heyde & Henrik Oster * Circadian clocks regulate physiological functions, including energy metabolism, along the 24-hour day cycle. The mammalian clock system is organized in a hierarchical manner with a coordinating pacemaker residing in the hypothalamic suprachiasmatic nucleus (SCN). The SCN clock is reset primarily by the external light-dark cycle while other zeitgebers such as the timing of food intake are potent synchronizers of many peripheral tissue clocks. Under conficting zeitgeber conditions, e.g. during shift work, phase synchrony across the clock network is disrupted promoting the development of metabolic disorders. We established a zeitgeber desynchrony (ZD) paradigm to quantify the diferential contributions of the two main zeitgebers, light and food, to the resetting of specifc tissue clocks and the efect on metabolic homeostasis in mice. Under 28-hour light-dark and 24-hour feeding-fasting conditions SCN and peripheral clock, as well as activity and hormonal rhythms showed specifc periodicities aligning in-between those of the two zeitgebers. During ZD, metabolic homeostasis was cyclic with mice gaining weight under synchronous and losing weight under conficting zeitgeber conditions. In summary, our study establishes an experimental paradigm to compare zeitgeber input in vivo and study the physiological consequences of chronodisruption. In most species, endogenous circadian clocks have evolved adjusting behaviour and physiology to anticipate daily recurring events, thus increasing the organism’s chance of survival. In mammals, ubiquitously expressed cellular clocks are organized in a hierarchical network1 coordinated by a central pacemaker residing in the hypo- thalamic suprachiasmatic nucleus (SCN)2.
    [Show full text]
  • Normal and Delayed Sleep Phases
    1 Overview • Introduction • Circadian Rhythm Sleep Disorders – DSPS – Non-24 • Diagnosis • Treatment • Research Issues • Circadian Sleep Disorders Network © 2014 Circadian Sleep Disorders Network 2 Circadian Rhythms • 24 hours 10 minutes on average • Entrained to 24 hours (zeitgebers) • Suprachiasmatic nucleus (SCN) – the master clock • ipRGC cells (intrinsically photosensitive Retinal Ganglion Cells) © 2014 Circadian Sleep Disorders Network 3 Circadian Rhythm Sleep Disorders • Definition – A circadian rhythm sleep disorder is an abnormality of the body’s internal clock, in which a person is unable to fall asleep at a normal evening bedtime, although he is able to sleep reasonably well at other times dictated by his internal rhythm. • Complaints – Insomnia – Excessive daytime sleepiness • Inflexibility • Coordination with other circadian rhythms © 2014 Circadian Sleep Disorders Network 4 Circadian Sleep Disorder Subtypes* • Delayed Sleep-Phase Syndrome (G47.21**) • Non-24-Hour Sleep-Wake Disorder (G47.24) • Advanced Sleep-Phase Syndrome (G47.22) • Irregular Sleep-Wake Pattern (G47.23) • Shift Work Sleep Disorder (G47.26) • Jet Lag Syndrome * From The International Classification of Sleep Disorders, Revised (ICSD-R) ** ICD-10-CM diagnostic codes in parentheses © 2014 Circadian Sleep Disorders Network 5 Definition of DSPS from The International Classification of Sleep Disorders, Revised (ICSD-R): • Sleep-onset and wake times that are intractably later than desired • Actual sleep-onset times at nearly the same daily clock hour • Little or no reported difficulty in maintaining sleep once sleep has begun • Extreme difficulty awakening at the desired time in the morning, and • A relatively severe to absolute inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake times.
    [Show full text]
  • Chronobiology and the Design of Marine Biology Experiments Audrey M
    Chronobiology and the design of marine biology experiments Audrey M. Mat To cite this version: Audrey M. Mat. Chronobiology and the design of marine biology experiments. ICES Journal of Marine Science, Oxford University Press (OUP), 2019, 76 (1), pp.60-65. 10.1093/icesjms/fsy131. hal-02873899 HAL Id: hal-02873899 https://hal.archives-ouvertes.fr/hal-02873899 Submitted on 18 Jun 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. ICES Journal of Marine Science (2019), 76(1), 60–65. doi:10.1093/icesjms/fsy131 Food for Thought Chronobiology and the design of marine biology experiments Downloaded from https://academic.oup.com/icesjms/article-abstract/76/1/60/5116189 by guest on 18 June 2020 Audrey M. Mat 1,2,* 1LEMAR, Universite´ de Bretagne Occidentale UMR 6539 CNRS/UBO/IRD/Ifremer, IUEM, Rue Dumont D’Urville, 29280 Plouzane´, France 2Ifremer, Centre de Bretagne, REM/EEP, Laboratoire Environnement Profond, ZI de la Pointe du Diable, CS 10070, 29280 Plouzane´, France *Corresponding author: tel: þ33 (0)2 98 22 43 04; e-mail: [email protected]. Mat, A. M. Chronobiology and the design of marine biology experiments.
    [Show full text]
  • The Use of Bright Light in the Treatment of Insomnia
    Chapter e39 The Use of Bright Light in the Treatment of Insomnia Leon Lack and Helen Wright Department of Psychology, Flinders University, Adelaide, South Australia PROTOCOL NAME The use of bright light in the treatment of insomnia. GROSS INDICATION Certain types of insomnia that are associated with abnormal timing of circa- dian rhythms may be treated with bright light therapy. SPECIFIC INDICATION Some individuals with sleep onset insomnia experience difficulty falling asleep at a “normal time” but no difficulty maintaining sleep once it is initi- ated. Individuals with this type of insomnia may have a delayed or later timed circadian rhythm. Bright light therapy timed in the morning after arising can advance or time circadian rhythms earlier and thus would be indicated for sleep onset or initial insomnia. Morning bright light therapy is also indicated for the related problem of delayed sleep phase disorder. Individuals experiencing early morning awakening insomnia have no diffi- culty initiating sleep but their predominant difficulty is waking before intended and not being able to resume sleep. These individuals may have an advanced or early timed circadian rhythm. Bright light therapy in the evening before sleep would be indicated for this type of insomnia as well as for the more extreme version, advanced sleep phase disorder. CONTRAINDICATIONS Bright light therapy would not be recommended in the following cases: ● Insomnia in which there is no indication of abnormal timing of circadian rhythms (e.g. combined problem initiating and maintaining sleep, having no strong morning or evening activity preferences) Behavioral Treatments for Sleep Disorders. DOI: 10.1016/B978-0-12-381522-4.00053-5 © 2011 Elsevier Inc.
    [Show full text]
  • Circadian Rhythms and Depression Sleep-Wake Cycle Is out of Phase with the Day- in the Day, While Bright Light Applied in the with Remission in Spring and Summer)
    CLINICAL Circadian rhythms Philip Boyce Erin Barriball and depression However, current treatments have been developed Background on the basis of a causal model for depression. Depression is a common disorder in primary care. Disruptions to the circadian rhythms Focused psychological treatments target those associated with depression have received little attention yet offer new and exciting depressions that arise from psychosocial approaches to treatment. difficulties. Examples include: Objective • cognitive behavioural therapy (CBT), which This article discusses circadian rhythms and the disruption to them associated with corrects maladaptive thinking patterns depression, and reviews nonpharmaceutical and pharmaceutical interventions to shift • behavioural treatments that aim to overcome circadian rhythms. ‘depressogenic’ behaviours such as avoiding Discussion pleasurable activities, and Features of depression suggestive of a disturbance to circadian rhythms include early • lifestyle modifications, particularly work-life morning waking, diurnal mood changes, changes in sleep architecture, changes in balance, diet and exercise and sleep-wake timing of the temperature nadir, and peak cortisol levels. Interpersonal social rhythm cycle management.5 therapy involves learning to manage interpersonal relationships more effectively Antidepressant medications target the and stabilisation of social cues, such as including sleep and wake times, meal times, neurotransmitter disturbances (serotonin or and timing of social contact. Bright light therapy is used to treat seasonal affective noradrenaline) considered to underlie biological disorders. Agomelatine is an antidepressant that works in a novel way by targeting depression. While the focus of biological melatonergic receptors. aspects of depression has centred on changes in Keywords: circadian rhythm, depression neurotransmitters, there has been relatively little attention paid to the changes in circadian rhythms associated with depression that offer new and rational treatment options for depression.
    [Show full text]
  • Circadian Phase Sleep and Mood Disorders (PDF)
    129 CIRCADIAN PHASE SLEEP AND MOOD DISORDERS ALFRED J. LEWY CIRCADIAN ANATOMY AND PHYSIOLOGY SCN Efferent Pathways Anatomy Not much is known about how the SCN entrains overt circadian rhythms. We know that the SCN is the master The Suprachiasmatic Nucleus: Locus of the pacemaker, but regarding its regulation of the rest/activity Biological Clock cycle, core body temperature rhythm and cortisol rhythm, Much is known about the neuroanatomic connections of among others, it is not clear if there is a humoral factor or the circadian system. In vertebrates, the locus of the biologi- neural connection that transmits the SCN’s efferent signal; cal clock (the endogenous circadian pacemaker, or ECP) however, a great deal is known about the efferent neural pathway between the SCN and pineal gland. that drives all circadian rhythms is in the hypothalamus, specifically, the suprachiasmatic nucleus (SCN)(1,2).This paired structure derives its name because it lies just above The Pineal Gland the optic chiasm. It contains about 10,000 neurons. The In mammals, the pineal gland is located in the center of molecular mechanisms of the SCN are an active area of the brain; however, it lies outside the blood–brain barrier. research. There is also a great deal of interest in clock genes Postganglionic sympathetic nerves (called the nervi conarii) and clock components of cells in general, not just in the from the superior cervical ganglion innervate the pineal (4). SCN. The journal Science designated clock genes as the The preganglionic neurons originate in the spinal cord, spe- second most important breakthrough for the recent year; cifically in the thoracic intermediolateral column.
    [Show full text]
  • Non-24-Hour Sleep-Wake Disorder Revisited – a Case Study
    CASE REPORT published: 29 February 2016 doi: 10.3389/fneur.2016.00017 Non-24-Hour Sleep-Wake Disorder Revisited – a Case study Corrado Garbazza1,2† , Vivien Bromundt3† , Anne Eckert2,4 , Daniel P. Brunner5 , Fides Meier2,4 , Sandra Hackethal6 and Christian Cajochen1,2* 1 Centre for Chronobiology, Psychiatric Hospital of the University of Basel, Basel, Switzerland, 2 Transfaculty Research Platform Molecular and Cognitive Neurosciences, University of Basel, Basel, Switzerland, 3 Sleep-Wake-Epilepsy-Centre, Department of Neurology, Inselspital, Bern University Hospital, Bern, Switzerland, 4 Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric Hospital of the University of Basel, Basel, Switzerland, 5 Center for Sleep Medicine, Hirslanden Clinic Zurich, Zurich, Switzerland, 6 Charité – Universitaetsmedizin Berlin, Berlin, Germany The human sleep-wake cycle is governed by two major factors: a homeostatic hourglass process (process S), which rises linearly during the day, and a circadian process C, which determines the timing of sleep in a ~24-h rhythm in accordance to the external Edited by: Ahmed S. BaHammam, light–dark (LD) cycle. While both individual processes are fairly well characterized, the King Saud University, Saudi Arabia exact nature of their interaction remains unclear. The circadian rhythm is generated by Reviewed by: the suprachiasmatic nucleus (“master clock”) of the anterior hypothalamus, through Axel Steiger, cell-autonomous feedback loops of DNA transcription and translation. While the phase Max Planck Institute of Psychiatry, Germany length (tau) of the cycle is relatively stable and genetically determined, the phase of Timo Partonen, the clock is reset by external stimuli (“zeitgebers”), the most important being the LD National Institute for Health and Welfare, Finland cycle.
    [Show full text]
  • SAD Presentation Copy
    Winter Is Coming How to Recognize and Treat Seasonal Affective Disorder Karl Lanocha, MD November 8, 2017 Objectives • Clinical presentation, epidemiology, and pathophysiology of seasonal affective disorder (SAD), winter type • Light therapy as treatment for SAD • Mechanism of action of light therapy • Optimum dosing and timing based on chronotype and circadian rhythm • Recognize and limit side effects Definition • Depression that occurs during a specific season, usually winter • At least two episodes of seasonal mood disorder • Seasonal episodes outnumber non-seasonal episodes • Unclear if a discreet diagnostic entity Clinical Features • Sadness, irritability, mood reactivity • Lethargy, increased sleep • Social withdrawal • Carbohydrate craving, weight gain • Cognitive problems, psychomotor slowing Epidemiology • Female > Male (4:1) • Incidence correlates with latitude Tropic of Cancer 30° N Lat No SAD Tropic of Capricorn 30° S Lat Scientific American Mind, Vol 16, Nr 3, 2005 NH 10% Portland 10% NY 7% 45° N Lat Halfway Between Equator and North Pole MD 5% San Francisco 5% 38° N Lat San Diego 2% FL 1% 30° N Lat AK >10% HI 0% 54-71° N Lat 18-28° N Lat 52bc835a15d22daeadf44fd316dd2a25.jpg 800×720 pixels 10/28/17, 1)18 PM Vitamin D synthesis https://i.pinimg.com/originals/52/bc/83/52bc835a15d22daeadf44fd316dd2a25.jpg Page 1 of 1 Etiology • Neurotransmitters • Genetic polymorphisms • Hormonal factors • Psychological factors • Circadian rhythm dysregulation Neurotransmitter Factors • Serotonin turnover decreases during winter • Light therapy
    [Show full text]
  • A Three Pulse Phase Response Curve to Three Milligrams of Melatonin in Humans
    J Physiol 586.2 (2008) pp 639–647 639 A three pulse phase response curve to three milligrams of melatonin in humans Helen J. Burgess1,VictoriaL.Revell2 and Charmane I. Eastman1 1Biological Rhythms Research Laboratory, Department of Behavioural Sciences, Rush University Medical Center, Chicago, IL, USA 2Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK Exogenousmelatoninisincreasinglyusedforitsphaseshiftingandsoporificeffects.Wegenerated a three pulse phase response curve (PRC) to exogenous melatonin (3 mg) by administering it to free-running subjects. Young healthy subjects (n = 27) participated in two 5 day laboratory sessions,eachprecededbyatleastaweekofhabitual,butfixedsleep.Each5 daylaboratorysession started and ended with a phase assessment to measure the circadian rhythm of endogenous melatonin in dim light using 30 min saliva samples. In between were three days in an ultradian dim light (< 150 lux)–dark cycle (LD 2.5 : 1.5) during which each subject took one pill per day at the same clock time (3 mg melatonin or placebo, double blind, counterbalanced). Each individual’s phase shift to exogenous melatonin was corrected by subtracting their phase shift to placebo (a free-run). The resulting PRC has a phase advance portion peaking about 5 h before the dim light melatonin onset, in the afternoon. The phase delay portion peaks about 11 h after the dim light melatonin onset, shortly after the usual time of morning awakening. A dead zone of minimal phase shifts occurred around the first half of habitual sleep. The fitted maximum advance and delay shifts were 1.8 h and 1.3 h, respectively. This new PRC will aid in determining the optimal time to administer exogenous melatonin to achieve desired phase shifts and demonstrates that using exogenous melatonin as a sleep aid at night has minimal phase shifting effects.
    [Show full text]
  • Circadian Rhythm Phase Shifts Caused by Timed Exercise Vary with Chronotype
    Circadian rhythm phase shifts caused by timed exercise vary with chronotype J. Matthew Thomas, … , Jody L. Clasey, Julie S. Pendergast JCI Insight. 2020. https://doi.org/10.1172/jci.insight.134270. Clinical Medicine In-Press Preview Clinical trials Graphical abstract Find the latest version: https://jci.me/134270/pdf Circadian rhythm phase shifts caused by timed exercise vary with chronotype J. Matthew Thomas1,2, Philip A. Kern2,3,4, Heather M. Bush2,5, Kristen J. McQuerry5, W. Scott Black6, Jody L. Clasey1,2,4, Julie S. Pendergast2,4,7,8 1Department of Kinesiology and Health Promotion, University of Kentucky, Lexington, Kentucky, USA 2Center for Clinical and Translational Science, University of Kentucky, Lexington, Kentucky, USA 3The Department of Internal Medicine, Division of Endocrinology, University of Kentucky, Lexington, Kentucky, USA 4Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, Kentucky, USA 5Department of Biostatistics, University of Kentucky, Lexington, Kentucky, USA 6Department of Clinical Sciences, University of Kentucky, Lexington, Kentucky, USA 7Department of Biology, University of Kentucky, Lexington, Kentucky, USA 8Saha Cardiovascular Research Center, University of Kentucky, Lexington, Kentucky, USA JL Clasey and JS Pendergast contributed equally to this work. Address for Correspondence: Julie S. Pendergast 316 Thomas Hunt Morgan Building Department of Biology University of Kentucky Lexington, KY 40502 (859) 218-6770 [email protected] The authors have declared that no conflict of interest exists. Submission Category: Clinical Medicine 1 ABSTRACT BACKGROUND. The circadian system entrains behavioral and physiological rhythms to environmental cycles and modern lifestyles disrupt this entrainment. We investigated a timed exercise intervention to phase shift the internal circadian rhythm.
    [Show full text]
  • Circadian Misalignment and Metabolic Disorders: a Story of Twisted Clocks
    biology Review Circadian Misalignment and Metabolic Disorders: A Story of Twisted Clocks Aurore Woller 1 and Didier Gonze 2,* 1 Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel; [email protected] 2 Unité de Chronobiologie Théorique, Faculté des Sciences CP 231, Université Libre de Bruxelles, Bvd du Triomphe, 1050 Bruxelles, Belgium * Correspondence: [email protected] Simple Summary: In mammals, many physiological processes follow a 24 h rhythmic pattern. These rhythms are governed by a complex network of circadian clocks, which perceives external time cues (notably light and nutrients) and adjusts the timing of metabolic and physiological functions to allow a proper adaptation of the organism to the daily changes in the environmental conditions. Circadian rhythms originate at the cellular level through a transcriptional–translational regulatory network involving a handful of clock genes. In this review, we show how adverse effects caused by ill-timed feeding or jet lag can lead to a dysregulation of this genetic clockwork, which in turn results in altered metabolic regulation and possibly in diseases. We also show how computational modeling can complement experimental observations to understand the design of the clockwork and the onset of metabolic disorders. Abstract: Biological clocks are cell-autonomous oscillators that can be entrained by periodic envi- ronmental cues. This allows organisms to anticipate predictable daily environmental changes and, thereby, to partition physiological processes into appropriate phases with respect to these changing Citation: Woller, A.; Gonze, D. Circadian Misalignment and external conditions. Nowadays our 24/7 society challenges this delicate equilibrium. Indeed, many Metabolic Disorders: A Story of studies suggest that perturbations such as chronic jet lag, ill-timed eating patterns, or shift work in- Twisted Clocks.
    [Show full text]