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Journal ArticleDOI: 10.1016/J.PNPBP.2020.110158

Biological rhythms and chronotherapeutics in depression.

02 Mar 2021-Progress in Neuro-psychopharmacology & Biological Psychiatry (Elsevier)-Vol. 106, pp 110158-110158
Abstract: Depressive syndromes are frequent and heterogeneous brain conditions with more than 90% of patients suffering from sleep complaints. Better characterizing this "sleep" domain may allow to both better treat acute episodes with existing chronotherapeutics, but also to prevent the manifestation or recurrences of mood disorders. This work aims to i) review theoretical and fundamental data of chronotherapeutics, and ii) provide practical recommendations. Light therapy (LT) can be used as a first-line monotherapy of moderate to severe depression of all subtypes. LT can be also used as a combination with antidepressant to maximize patients' response rates, which has a clear superiority to antidepressant alone. Sleep deprivation (SD) is a rapid and powerful chronotherapeutic with antidepressant responses within hours in 45-60% of patients with unipolar or bipolar depression. Different strategies should be combined to stabilize the SD antidepressant effect, including concomitant medications, repeated SD, combination with sleep phase advance and/or LT (triple chronotherapy). Melatonin treatment is of interest in remitted patients with mood disorder to prevent relapses or recurrences, if a complaint of insomnia, poor sleep quality or phase delay syndrome is associated. During the acute phase, melatonin could be used as an adjuvant treatment for symptoms of insomnia associated with depression. The cognitive behavioral therapy for insomnia (CBT-I) can be recommend to treat insomnia during euthymic phases. The Interpersonal and social rhythm therapy (IPSRT) is indicated for the acute treatment of bipolar depression and for the prevention of mood episodes. Chronotherapeutics should always be associated with behavioral measures for healthy sleep.

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10 results found


Open access
01 Jan 2007-
Abstract: PART I CLINICAL DESCRIPTION AND DIAGNOSIS 1. Conceptualizing Manic-Depressive Illness: The Bipolar-Unipolar Distinction and the Development of the Manic-Depressive Spectrum 2. Clinical Description 3. Diagnosis PART II CLINICAL STUDIES 4. Course and Outcome 5. Epidemiology 6. Children and Adolescents 7. Comorbidity 8. Suicide PART III PSYCHOLOGICAL STUDIES 9. Neuropsychology 10. Personality, Personality Disorders, and Interpersonal Functioning 11. Assessment 12. Creativity PART IV PATHOPHYSIOLOGY 13. Genetics 14. Neurobiology 15. Neuroanatomy and Neuroimaging 16. Sleep and Circadian Rhythms PART V TREATMENT 17. Fundamentals of Treatment 18. Medical Treatment of Hypomania, Mania, and Mixed States 19. Medical Treatment of Depression 20. Maintenance Medical Treatment 21. Medication Adherence 22. Psychotherapy 23. Treatment of Children and Adolescents 24. Treatment of Comorbidity 25. Clinical Management of Suicide Risk

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12 Citations


Open accessJournal ArticleDOI: 10.3389/FPSYT.2021.688890
Laura Palagini1, Raffaele Manni, Eugenio Aguglia2, Mario Amore  +20 moreInstitutions (9)
Abstract: Introduction: Insomnia and circadian rhythm disorders, such as the delayed sleep phase syndrome, are frequent in psychiatric disorders and their evaluation and management in early stages should be a priority. The aim of this paper was to express recommendations on the use of exogenous melatonin, which exhibits both chronobiotic and sleep-promoting actions, for the treatment of these sleep disturbances in psychiatric disorders. Methods: To this aim, we conducted a systematic review according to PRISMA on the use of melatonin for the treatment of insomnia and circadian sleep disorders in neuropsychiatry. We expressed recommendations for the use of melatonin in psychiatric clinical practice for each disorder using the RAND/UCLA appropriateness method. Results: We selected 41 studies, which included mood disorders, schizophrenia, substance use disorders, attention deficit hyperactivity disorders, autism spectrum disorders, neurocognitive disorders, and delirium; no studies were found for both anxiety and eating disorders. Conclusion: The administration of prolonged release melatonin at 2-10 mg, 1-2 h before bedtime, might be used in the treatment of insomnia symptoms or comorbid insomnia in mood disorders, schizophrenia, in adults with autism spectrum disorders, neurocognitive disorders and during sedative-hypnotics discontinuation. Immediate release melatonin at <1 mg might be useful in the treatment of circadian sleep disturbances of neuropsychiatric disorders.

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Topics: Delayed sleep phase (63%), Mood disorders (61%), Melatonin (56%) ... read more

4 Citations


Open access
24 Nov 2017-
Abstract: Abstract Objective: Bipolar disorders (BD) are characterized by sleep disturbances and emotional dysregulation both during acute episodes and remission periods. We hypothesized that sleep quality (SQ) and emotional reactivity (ER) defined clusters of patients with no or abnormal SQ and ER and we studied the association with functioning. Method: We performed a bi-dimensional cluster analysis using SQ and ER measures in a sample of 533 outpatients patients with BD (in remission or with subsyndromal mood symptoms). Clusters were compared for mood symptoms, sleep profile and functioning. Results: We identified three clusters of patients: C1 (normal ER and SQ, 54%), C2 (hypo-ER and low SQ, 22%) and C3 (hyper-ER and low SQ, 24%). C1 was characterized by minimal mood symptoms, better sleep profile and higher functioning than other clusters. Although highly different for ER, C2 and C3 had similar levels of subsyndromal mood symptoms as assessed using classical mood scales. When exploring sleep domains, C2 showed poor sleep efficiency and a trend for longer sleep latency as compared to C3. Interestingly, alterations in functioning were similar in C2 and C3, with no difference in any of the sub-domains. Conclusion: Abnormalities in ER and SQ delineated three clusters of patients with BD and significantly impacted on functioning.

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1 Citations


Open accessJournal ArticleDOI: 10.1038/S41386-021-01241-W
Shogo Sato1, Shogo Sato2, Blynn G. Bunney2, Lucia Mendoza-Viveros3  +4 moreInstitutions (3)
Abstract: A growing number of epidemiological and experimental studies has established that circadian disruption is strongly associated with psychiatric disorders, including major depressive disorder (MDD). This association is becoming increasingly relevant considering that modern lifestyles, social zeitgebers (time cues) and genetic variants contribute to disrupting circadian rhythms that may lead to psychiatric disorders. Circadian abnormalities associated with MDD include dysregulated rhythms of sleep, temperature, hormonal secretions, and mood which are modulated by the molecular clock. Rapid-acting antidepressants such as subanesthetic ketamine and sleep deprivation therapy can improve symptoms within 24 h in a subset of depressed patients, in striking contrast to conventional treatments, which generally require weeks for a full clinical response. Importantly, animal data show that sleep deprivation and ketamine have overlapping effects on clock gene expression. Furthermore, emerging data implicate the circadian system as a critical component involved in rapid antidepressant responses via several intracellular signaling pathways such as GSK3β, mTOR, MAPK, and NOTCH to initiate synaptic plasticity. Future research on the relationship between depression and the circadian clock may contribute to the development of novel therapeutic strategies for depression-like symptoms. In this review we summarize recent evidence describing: (1) how the circadian clock is implicated in depression, (2) how clock genes may contribute to fast-acting antidepressants, and (3) the mechanistic links between the clock genes driving circadian rhythms and neuroplasticity.

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Topics: Circadian clock (65%), CLOCK (65%), Circadian rhythm (60%) ... read more

Journal ArticleDOI: 10.1007/S00406-021-01266-8
Hinuga Sandahl1, Lone Baandrup2, Lone Baandrup1, Erik Vindbjerg1  +3 moreInstitutions (3)
Abstract: The relation of aspects of rest–activity patterns, i.e., social zeitgebers, physical activity and circadian rhythm, to the severity of PTSD and depressive symptoms has not previously been studied. Doing so could provide valuable insight into possible targets for treatment. Our study explored these links in a population of 219 trauma-affected refugees diagnosed with PTSD who were seeking treatment. Data regarding social zeitgebers, such as affiliation with the labor market and contact with social network, and symptoms of PTSD and depression were collected from them. Furthermore, their levels of physical activity and circadian rest–activity parameters were calculated from actigraphy data. Bivariate correlation analyses and multiple linear regression analyses were performed to examine various aspects of rest–activity regarding relation to severity of PTSD and depressive symptoms. Several social zeitgebers were associated with severity of PTSD and depressive symptoms. The level of physical activity was unrelated to symptom severity, whereas a rest–activity pattern, with early onset of the most active 10 h, was associated with severity of PTSD, and a circadian rhythm with a large difference between periods of rest and activity was associated with severity of depression. Social zeitgebers, levels of physical activity and circadian rhythm parameters were all associated with each other. Social zeitgebers and circadian rhythm parameters were significantly related to the severity of PTSD and depressive symptoms—a relationship indicating that interventions targeting regularity of daily routines have a potential role in treating PTSD and depression in trauma-affected refugees. Trial registration: ClinicalTrials.gov, ID: NCT02761161, April 27, 2016.

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Topics: Actigraphy (53%), Population (51%), Circadian rhythm (50%)

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194 results found


Open accessJournal ArticleDOI: 10.1001/ARCHPSYC.62.6.593
Ronald C. Kessler1, Patricia A. Berglund1, Olga Demler1, Robert Jin1  +2 moreInstitutions (1)
Abstract: Context Little is known about lifetime prevalence or age of onset of DSM-IV disorders. Objective To estimate lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the recently completed National Comorbidity Survey Replication. Design and Setting Nationally representative face-to-face household survey conducted between February 2001 and April 2003 using the fully structured World Health Organization World Mental Health Survey version of the Composite International Diagnostic Interview. Participants Nine thousand two hundred eighty-two English-speaking respondents aged 18 years and older. Main Outcome Measures Lifetime DSM-IV anxiety, mood, impulse-control, and substance use disorders. Results Lifetime prevalence estimates are as follows: anxiety disorders, 28.8%; mood disorders, 20.8%; impulse-control disorders, 24.8%; substance use disorders, 14.6%; any disorder, 46.4%. Median age of onset is much earlier for anxiety (11 years) and impulse-control (11 years) disorders than for substance use (20 years) and mood (30 years) disorders. Half of all lifetime cases start by age 14 years and three fourths by age 24 years. Later onsets are mostly of comorbid conditions, with estimated lifetime risk of any disorder at age 75 years (50.8%) only slightly higher than observed lifetime prevalence (46.4%). Lifetime prevalence estimates are higher in recent cohorts than in earlier cohorts and have fairly stable intercohort differences across the life course that vary in substantively plausible ways among sociodemographic subgroups. Conclusions About half of Americans will meet the criteria for a DSM-IV disorder sometime in their life, with first onset usually in childhood or adolescence. Interventions aimed at prevention or early treatment need to focus on youth.

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Topics: National Comorbidity Survey (65%), Mood disorders (57%), Comorbidity (56%) ... read more

15,369 Citations


Open accessJournal ArticleDOI: 10.1016/S0140-6736(17)32154-2
16 Sep 2017-The Lancet
Abstract: Summary Background As mortality rates decline, life expectancy increases, and populations age, non-fatal outcomes of diseases and injuries are becoming a larger component of the global burden of disease. The Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) provides a comprehensive assessment of prevalence, incidence, and years lived with disability (YLDs) for 328 causes in 195 countries and territories from 1990 to 2016. Methods We estimated prevalence and incidence for 328 diseases and injuries and 2982 sequelae, their non-fatal consequences. We used DisMod-MR 2.1, a Bayesian meta-regression tool, as the main method of estimation, ensuring consistency between incidence, prevalence, remission, and cause of death rates for each condition. For some causes, we used alternative modelling strategies if incidence or prevalence needed to be derived from other data. YLDs were estimated as the product of prevalence and a disability weight for all mutually exclusive sequelae, corrected for comorbidity and aggregated to cause level. We updated the Socio-demographic Index (SDI), a summary indicator of income per capita, years of schooling, and total fertility rate. GBD 2016 complies with the Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, low back pain, migraine, age-related and other hearing loss, iron-deficiency anaemia, and major depressive disorder were the five leading causes of YLDs in 2016, contributing 57·6 million (95% uncertainty interval [UI] 40·8–75·9 million [7·2%, 6·0–8·3]), 45·1 million (29·0–62·8 million [5·6%, 4·0–7·2]), 36·3 million (25·3–50·9 million [4·5%, 3·8–5·3]), 34·7 million (23·0–49·6 million [4·3%, 3·5–5·2]), and 34·1 million (23·5–46·0 million [4·2%, 3·2–5·3]) of total YLDs, respectively. Age-standardised rates of YLDs for all causes combined decreased between 1990 and 2016 by 2·7% (95% UI 2·3–3·1). Despite mostly stagnant age-standardised rates, the absolute number of YLDs from non-communicable diseases has been growing rapidly across all SDI quintiles, partly because of population growth, but also the ageing of populations. The largest absolute increases in total numbers of YLDs globally were between the ages of 40 and 69 years. Age-standardised YLD rates for all conditions combined were 10·4% (95% UI 9·0–11·8) higher in women than in men. Iron-deficiency anaemia, migraine, Alzheimer's disease and other dementias, major depressive disorder, anxiety, and all musculoskeletal disorders apart from gout were the main conditions contributing to higher YLD rates in women. Men had higher age-standardised rates of substance use disorders, diabetes, cardiovascular diseases, cancers, and all injuries apart from sexual violence. Globally, we noted much less geographical variation in disability than has been documented for premature mortality. In 2016, there was a less than two times difference in age-standardised YLD rates for all causes between the location with the lowest rate (China, 9201 YLDs per 100 000, 95% UI 6862–11943) and highest rate (Yemen, 14 774 YLDs per 100 000, 11 018–19 228). Interpretation The decrease in death rates since 1990 for most causes has not been matched by a similar decline in age-standardised YLD rates. For many large causes, YLD rates have either been stagnant or have increased for some causes, such as diabetes. As populations are ageing, and the prevalence of disabling disease generally increases steeply with age, health systems will face increasing demand for services that are generally costlier than the interventions that have led to declines in mortality in childhood or for the major causes of mortality in adults. Up-to-date information about the trends of disease and how this varies between countries is essential to plan for an adequate health-system response. Funding Bill & Melinda Gates Foundation, and the National Institute on Aging and the National Institute of Mental Health of the National Institutes of Health.

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Topics: Mortality rate (55%)

8,768 Citations


Open accessJournal ArticleDOI: 10.1215/23289252-2399740
01 May 2014-
Abstract: Background—Although stroke and ischemic heart disease (IHD) have several well-established risk factors in common, the extent of global variation in the relative burdens of these forms of vascular disease and reasons for any observed variation are poorly understood. Methods and Results—We analyzed mortality and disability-adjusted life-year loss rates from stroke and IHD, as well as national estimates of vascular risk factors that have been developed by the World Health Organization Burden of Disease Program. National income data were derived from World Bank estimates. We used linear regression for univariable analysis and the Cuzick test for trends. Among 192 World Health Organization member countries, stroke mortality rates exceeded IHD rates in 74 countries (39%), and stroke disability-adjusted life-year loss rates exceeded IHD rates in 62 countries (32%). Stroke mortality ranged from 12.7% higher to 27.2% lower than IHD, and stroke disability-adjusted life-year loss rates ranged from 6.2% higher to 10.2% lower than IHD. Stroke burden was disproportionately higher in China, Africa, and South America, whereas IHD burden was higher in the Middle East, North America, Australia, and much of Europe. Lower national income was associated with higher relative mortality (P 0.001) and burden of disease (P 0.001) from stroke. Diabetes mellitus prevalence and mean serum cholesterol were each associated with greater relative burdens from IHD even after adjustment for national income. Conclusions—There is substantial global variation in the relative burden of stroke compared with IHD. The disproportionate burden from stroke for many lower-income countries suggests that distinct interventions may be required. (Circulation. 2011; 124:314-323.)

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6,287 Citations


Open accessJournal ArticleDOI: 10.1016/S0140-6736(18)32279-7
Gbd Disease, Injury Incidence, Lorenzo Monasta1, Luca Ronfani1  +8 moreInstitutions (1)
10 Nov 2018-The Lancet
Abstract: Research reported in this publication was supported by the Bill & Melinda Gates Foundation, the University of Melbourne, Public Health England, the Norwegian Institute of Public Health, St Jude Children’s Research Hospital, the National Institute on Ageing of the National Institutes of Health (award P30AG047845), and the National Institute of Mental Health of the National Institutes of Health (award R01MH110163).

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Topics: Public health (63%), Mental health (53%)

3,736 Citations


Open accessBook
01 Dec 2013-
Abstract: Part I: What Is Motivational Interviewing? Conversations about Change. The Spirit of Motivational Interviewing. The Method of Motivational Interviewing. Part II: Engaging: The Relational Foundation. Engagement and Disengagement. Listening: Understanding the Person's Dilemma. Core Interviewing Skills: OARS. Exploring Values and Goals. Part III: Focusing: The Strategic Direction. Why Focus? Finding the Horizon. When Goals Differ. Exchanging Information. Part IV: Evoking: Preparation for Change. Evoking the Person's Own Motivation. Responding to Change Talk. Responding to Sustain Talk and Discord. Evoking Hope and Confidence. Counseling with Neutrality. Developing Discrepancy. Part V: Planning: The Bridge to Change. Developing a Change Plan. Strengthening Commitment. Supporting Change. Part VI: Motivational Interviewing in Everyday Practice. Experiencing Motivational Interviewing. Applying Motivational Interviewing. Integrating Motivational Interviewing. Part VII: Evaluating Motivational Interviewing. Research Evidence and the Evolution of Motivational Interviewing. Evaluating Motivational Conversations. Appendix A: Glossary of Motivational Interviewing Terms. McLouth, Appendix B: A Bibliography of Motivational Interviewing.

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2,158 Citations


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