Eveningness increases risks for depressive and anxiety symptoms and hospital treatments mediated by insufficient sleep in a population-based study of 18,039 adults

cited By 0Background Epidemiological data show that having the eveningness associates with poor mental health. For preventive measures it is important to know which underlying factors mediate these associations and the burden posed to public health. This study examines at a population-based level, whether (1) circadian type and the sleep-wake behavior-based phase entrainment similarly associate with mental health problems, (2) there are differences in hospital treatments due to mental disorders between chronotypes, and (3) the association of chronotype with mental health is mediated by insufficient sleep. Methods The study sample (N = 18,039) consisted of population-based sample of Finnish adults, aged 25-74 years, with information on their circadian type and sleep patterns, mental health symptoms, and diagnosis as reported in a health examination survey, as well as hospital treatments as recorded on the national Hospital Discharge Register. Results All the mental health symptoms, diagnoses and hospital treatments were more pronounced among Evening-types, especially when assessed by circadian type. Insufficient sleep mediated most but not all of the associations between eveningness and mental health. Conclusions Eveningness does not increase mental health risks only on symptom or diagnosis level, but also on hospital admission level. A higher prevalence of insufficient sleep among the Evening-types elevates the risk and severity for many of the mental health outcomes. Improving the sleep among Evening-types could help to improve their mental health prospective and ease the health care burden.Peer reviewe

Increase in eveningness and insufficient sleep among adults in population-based cross-sections from 2007 to 2017

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Ecological interactions in the evolution of virulence and in disease dynamics among opportunistic pathogens

Many pathogens are able to survive and reproduce in the environment outside of host for instance by saprotrophic lifestyle. These kinds of pathogens are called opportunistic as compared to obligatory pathogens that cannot interact or reproduce in the environment outside of host. Opportunistic pathogens are subject to strong selection forces in the environment outside of host for instance while they compete for resources they share with other microbes. Ecological interactions in the environment outside of host can therefore influence on the disease dynamics and evolution of virulence of an opportunistic pathogen. No proper theoretical model that would acknowledge opportunistic reproduction and ecological interactions in the environment out side of host has been developed before. Yet it is essential to develop this kind of theoretical model so that the development and dynamics of opportunistic diseases could be predicted and prevented. In this work, an opportunistic disease model was developed that considers both the opportunistic reproduction and the influence of a superior competitor as compared to pathogenic strain on pathogen growth in the environment outside of host. Differential equations in the model represent the density changes in time in the populations of susceptible and infected host, pathogen and rival strain outside host that is not pathogenic. Evolution of virulence of the new opportunistic pathogen meaning the ability to grow from low density in presence of superior competing strain was modeled in differing circumstances. Opportunistic disease dynamics was modeled in differing circumstances, when non-pathogenic competing strain was either present or absent. Equilibrium equations were solvable to a system, where non-pathogenic competing strain was absent, but to a system where non-pathogenic competing strain was present. Analyses of the model were performed with Math Works MATLAB – program. Reproducing inside host gives an opportunity for new opportunistic pathogen to increase in density under circumstances where competition is moderate enough so that the reproduction in the environment outside host may compensate opportunistic pathogen's weaker ability to compete. Reproduction and competition in the environment outside host produce disease dynamics that differ from more traditional SI-models. Density dependence of the reproduction in the environment outside host stabilizes host-parasite system in the absence of competition in the environment outside host. Instead, in the presence of competition the competitive advantage of the non-pathogen strain destabilizes disease dynamics and prevents extinction of the susceptible host. Reproduction in the environment outside host also enables opportunistic pathogen to remain in the environment in the absence of susceptible hosts and functions thus as a potential mechanism for disease out breaks when circumstances change. However, increasing competition in the environment outside host at the expense of opportunistic pathogen may potentially prevent epidemics. Among other things, the model could be applied to biological control with the intension of removing an opportunistic pathogen naturally by weakening its survival in the environment out side of host in a competiotion situation. This kind of biological control could for example be possible in the case of saprotrophic Flavobacterium columnare –fish pathogen that is found in fish farms.Monet taudinaiheuttajat kykenevät selviytymään ja lisääntymään isännän ulkopuolisessa ympäristössä esimerkiksi saprotrofismin avulla. Tällaisia taudinaiheuttajia kutsutaan opportunistiksi erotuksena obligatorisista taudinaiheuttajista, jotka eivät vuorovaikuta tai lisäänny isännän ulkopuolisessa ympäristössä. Opportunistiset taudinaiheuttajat altistuvat isännän ulkopuolisessa ympäristössä voimakkaille valintapaineille, esimerkiksi kilpaillessaan samoista resursseista muiden mikrobien kanssa. Ekologiset vuorovaikutukset isännän ulkopuolella voivat siten vaikuttaa opportunististen taudinaiheuttajien tautidynamiikkaan ja virulenssin evoluutioon. Kattavaa teoreettista mallia, joka huomioisi sekä opportunistisen lisääntymisen että isännän ulkopuoliset ekologiset vuorovaikutukset ei ole aiemmin kehitetty. Kuitenkin tällaisen mallin kehittäminen on oleellista, jotta opportunististen tautien syntyä voidaan ehkäistä ja dynamiikkaa ennakoida. Tässä työssä kehitettiin opportunistinen tautimalli, joka huomioi sekä taudinaiheuttajan isännän ulkopuolisen kasvun että taudinaiheuttajaa voimakkaamman kilpailevan kannan vaikutuksen isännän ulkopuoliseen kasvuun. Mallin differentiaaliyhtälöt kuvaavat alttiiden ja tartunnan saaneiden isäntien, taudinaiheuttajan ja sen kanssa isännän ulkopuolella kilpailevan tautia aiheuttamattoman kannan tiheysmuutoksia ajassa. Uuden opportunistisen taudinaiheuttajan virulenssin evoluutiota eli taudinaiheuttajan kykyä runsastua alhaisesta tiheydestä tautia aiheuttamattoman kilpailijan läsnä ollessa mallinnettiin erilaisissa olosuhteissa. Opportunistista tautidynamiikkaa sen sijaan mallinnettiin olosuhteissa, jossa tautia aiheuttamattoman kannan läsnäoloa manipuloitiin. Mallin vakautta tutkittiin analyyttisesti ratkaisemalla tasapainotilat systeemille, jossa tautia aiheuttamaton kanta ei ollut läsnä, sekä numeerisin analyysein tilanteessa jossa tautia aiheuttamaton kanta oli läsnä. Lisääntyminen isännissä mahdollistaa uuden opportunistisen taudinaiheuttajan runsastumisen olosuhteissa, joissa kilpailu on riittävän heikkoa, siten että isännästä riippumaton kasvu voi kompensoida opportunistisen taudinaiheuttajan heikomman kilpailukyvyn. Isännän ulkopuolinen lisääntyminen ja kilpailu tuottavat perinteisistä obligatorisen taudinaiheuttajan SI-malleista eroavan tautidynamiikan. Isäntien ulkopuolisen kasvun tiheysriippuvaisuus voi vakauttaa isäntä-loissysteemin isännän ulkopuolisen kilpailun puuttuessa. Lajien välisen kilpailun läsnä ollessa tautia aiheuttamattoman kannan kilpailuetu sen sijaan lisää tautidynamiikan epävakautta ja ehkäisee alttiiden isäntien sukupuuttoa. Isäntien ulkopuolinen kasvu mahdollistaa myös opportunistisen taudinaiheuttajan säilymisen ympäristössä alttiiden isäntien puuttuessa ja toimii siten mahdollisena mekanismina tautien puhkeamiselle olosuhteiden muuttuessa. Kilpailun lisääminen isännän ulkopuolella taudinaiheuttajan kustannuksella voi kuitenkin toimia epidemioita potentiaalisesti ehkäisevänä keinona. Mallia voidaan soveltaa mm. biologisessa kontrollissa, jossa opportunistinen taudinaiheuttaja pyritään poistamaan luontaisesti heikentämällä sen selviytymistä isännän ulkopuolisessa ympäristössä kilpailu-olosuhteessa. Tällainen biologinen kontrolli voisi olla mahdollista esimerkiksi kalankasvatuslaitoksissa esiintyvän saprotrofisen Flavobacterium columnare –kalapatogeenin kohdalla

Disease dynamics, invasion and biological control of environmentally growing pathogens

Many existing and emerging microbial infectious diseases are caused by environmentally growing opportunist pathogens. These pathogens are, contrary to obligatory pathogens, able to survive and replicate in the outside-host environment as free-living microbes that use within-host growth as an alternative replication strategy. This disease class has eco-evolutionary implications in natural populations and causes a serious health and economical threat to humans, our food production and to wildlife. Because of the ability of environmentally growing opportunists to survive and replicate independently of hosts, these diseases are hard to eradicate with conventional methods. The conditions that favor or disfavor environmental opportunism are still poorly understood. Better understanding of the dynamics of these diseases is needed in order to develop proper control methods against them. In this thesis I have developed novel epidemiological models to describe the disease dynamics of environmentally growing pathogens. These models modify the traditional Susceptible-Infected host (SI-model) framework by combining it to the outside-host community of an environmentally growing pathogen. I have considered how the environmental growth of the pathogens and the antagonistic ecological interactions these pathogens face in the outside-host environment, such as competition, predation and parasitism, affect the disease dynamics, invasion of novel pathogens and biological control of environmentally growing infectious diseases. The analyses show that the disease dynamics of environmentally growing pathogens differ from obligatory pathogens. Importantly, ability to grow in the outside-host environment promotes disease outbreaks and can lead to the extinction of the host, which is untypical in the case of obligatory pathogens. Antagonistic interactions the pathogen faces in the outside-host environment can on the other hand limit disease outbreaks and prevent extinction of the hosts that would otherwise occur due to the disease. I conclude that the eradication can be accomplished 1) by increasing the outside-host competition, 2) through predation of pathogens, or 3) through viral infections in pathogens.Monet tartuntataudit ovat ympäristössä kasvavien opportunististen taudinaiheuttajien tuottamia. Nämä taudinaiheuttajat eroavat pelkästään isännässä kasvavista obligatorisista taudinaiheuttajista kykenemällä kasvamaan vapaina mikrobeina ympäristössä isännästä riippumattomasti. Ne siis tartuttavat alttiita isäntiä ainoastaan vaihtoehtoisena kasvustrategiana. Tämä tautiluokka esittää kuitenkin merkittävän terveydellisen että taloudellisen uhan sekä ihmisille, ruoantuotannolle sekä luonnon populaatioille. Ympäristössä kasvavia opportunistisia tartuntatauteja on vaikeaa kontrolloida perinteisin hoitomenetelmin, kuten antibiootein, johtuen niiden kyvystä selviytyä isännästä riippumattomasti isännän ulkoisessa ympäristössä. Parempaa ymmärrystä näiden taudinaiheuttajien tautidynamiikasta ja olosuhteista jotka suosivat tai heikentävät opportunistista kasvustrategiaa tarvitaan, jotta tehokkaita kontrollimenetelmiä voitaisiin kehittää ympäristössä kasvavia opportunistisia tartuntatauteja vastaan. Väitöskirjassani esitän uusia epidemiologia tautimalleja kuvaamaan ympäristössä kasvavia opportunistisia tartuntatauteja. Mallini yhdistävät perinteisen alttiiden ja tartunnan saaneiden isäntien tautiteorian (SI-mallit) ympäristössä kasvan taudinaiheuttajan ekologiaan. Olen tutkinut miten taudinaiheuttajan ympäristökasvu ja antagonistiset ekologiset vuorovaikutukset taudinaiheuttajan isännän ulkoisessa ympäristössä, kuten kilpailu mikrobien kesken, saalistus ja bakteerien virustartunnat, vaikuttavat tautidynamiikkaan, uusien taudinaiheuttajien invaasioon ja ympäristössä kasvavien opportunististen tautien biologiseen kontrolloimiseen. Tutkimukseni osoittaa ympäristössä kasvavien opportunististen tautien dynamiikan eroavan obligatorisista taudeista: kyky kasvaa isännästä riippumattomasti ympäristössä suosii tautiepidemioita ja voi myös johtaa isäntäpopulaation sukupuuttoon vaarantamatta kuitenkaan taudinaiheuttajan selviytymistä. Taudinaiheuttajan kohtaamat antagonistiset vuorovaikutukset isännän ulkoisessa ympäristössä puolestaan voivat heikentää tautiepidemioiden esiintymistä sekä estää taudista johtuvan isäntäpopulaatioiden sukupuuton. Ympäristössä kasvavia opportunistisia tauteja voitaisiin siis tehokkaasti kontrolloida ja mahdollisesti hävittää paikallisesti heikentämällä ympäristökasvua esimerkiksi lisäämällä isännän ulkoista kilpailua taudinaiheuttajan ja muiden mikrobien välillä, kasvattamalla taudinaiheuttajaan kohdistuvaa saalistusta sekä edistämällä taudinaiheuttajien virusinfektioita

Outside-host phage therapy as a biological control against environmental infectious diseases

Background: Environmentally growing pathogens present an increasing threat for human health, wildlife and food production. Treating the hosts with antibiotics or parasitic bacteriophages fail to eliminate diseases that grow also in the outside-host environment. However, bacteriophages could be utilized to suppress the pathogen population sizes in the outside-host environment in order to prevent disease outbreaks. Here, we introduce a novel epidemiological model to assess how the phage infections of the bacterial pathogens affect epidemiological dynamics of the environmentally growing pathogens. We assess whether the phage therapy in the outside-host environment could be utilized as a biological control method against these diseases. We also consider how phage-resistant competitors affect the outcome, a common problem in phage therapy. The models give predictions for the scenarios where the outside-host phage therapy will work and where it will fail to control the disease. Parameterization of the model is based on the fish columnaris disease that causes significant economic losses to aquaculture worldwide. However, the model is also suitable for other environmentally growing bacterial diseases. Results: Transmission rates of the phage determine the success of infectious disease control, with high-transmission phage enabling the recovery of the host population that would in the absence of the phage go asymptotically extinct due to the disease. In the presence of outside-host bacterial competition between the pathogen and phage-resistant strain, the trade-off between the pathogen infectivity and the phage resistance determines phage therapy outcome from stable coexistence to local host extinction. Conclusions: We propose that the success of phage therapy strongly depends on the underlying biology, such as the strength of trade-off between the pathogen infectivity and the phage-resistance, as well as on the rate that the phages infect the bacteria. Our results indicate that phage therapy can fail if there are phage-resistant bacteria and the trade-off between pathogen infectivity and phage resistance does not completely inhibit the pathogen infectivity. Also, the rate that the phages infect the bacteria should be sufficiently high for phage-therapy to succeed.Peer reviewe

Late-Night Digital Media Use in Relation to Chronotype, Sleep and Tiredness on School Days in Adolescence

Funding Information: This study was conducted at the University of Helsinki and was funded by the Faculty of Educational Sciences, University of Helsinki, The Alfred Kordelin Foundation (grant 210196, Kortesoja) and by The Academy of Finland (project 322312, Merikanto). The funders played no role in the study design, data collection/ interpretation, or the decision to submit the work for publication. Open Access funding provided by University of Helsinki including Helsinki University Central Hospital. Publisher Copyright: © 2022, The Author(s).Previous studies on late-night digital media use and adolescent sleep have not considered how chronotype, a natural tendency to be awake or asleep at certain time, is associated with this relationship. Therefore, the nature of the relationship between late-night digital media use and sleep in different chronotypes remains still unknown. The sample consisted of 15–20-year-old Finnish adolescents (n = 1084, mean age = 16.9 years, SD = 0.93, 45.7% female). This study examined whether chronotype, measured as diurnal type and midpoint of sleep, was associated with the time of evening/night when digital media was used. Associations between the use of different forms of digital media and sleep quality, sleep duration and tiredness on school days were also investigated. Finally, the mediation effect of late-night digital media use to the relationship between chronotype and sleep was examined. Generalized linear models showed that evening chronotype, weekend midpoint of sleep, and the time of evening or night at which digital media was used were associated with more insufficient sleep and tiredness, lower sleep quality and shorter sleep duration on school days. The total use of all media forms, i.e., late-night digital media for music, movies/series, social media, and studying, were associated with shorter sleep duration and more insufficient sleep and daytime tiredness. Late-night social media use also mediated the association between diurnal type and sleep quality. Watching movies or listening to music late at night was the strongest mediator of the association between diurnal type and sleep and tiredness. The most prominent finding shows that of the all different media forms, watching movies or listening to music late at night were associated with increased daytime tiredness, whereas late social media use was associated with poor sleep quality. These interactions were pronounced especially for evening-types. The findings of the current study suggest that the negative effects of late-night media use are reflected especially in sleep quality and daytime tiredness among evening-types during adolescence.Peer reviewe

Outside-host growth of pathogens attenuates epidemiological outbreaks

Opportunist saprotrophic pathogens differ from obligatory pathogens due to their capability in host-independent growth in environmental reservoirs. Thus, the outside-host environment potentially influences host-pathogen dynamics. Despite the socio-economical importance of these pathogens, theory on their dynamics is practically missing. We analyzed a novel epidemiological model that couples outside-host density-dependent growth to host-pathogen dynamics. Parameterization was based on columnaris disease, a major hazard in fresh water fish farms caused by saprotrophic Flavobacterium columnare. Stability analysis and numerical simulations revealed that the outside-host growth maintains high proportion of infected individuals, and under some conditions can drive host extinct. The model can show stable or cyclic dynamics, and the outside-host growth regulates the frequency and intensity of outbreaks. This result emerges because the density-dependence stabilizes dynamics. Our analysis demonstrates that coupling of outside-host growth and traditional host-pathogen dynamics has profound influence on disease prevalence and dynamics. This also has implications on the control of these diseases.Peer reviewe

Eveningness intensifies the association between musculoskeletal pain and health-related quality of life : a Northern Finland Birth Cohort Study 1966

People with an evening (E)-type preference (ie, chronotype) experience musculoskeletal (MSK) pain and reduced health-related quality of life (HRQoL) more often than morning (M) types. Musculoskeletal pain is a well-established contributor to reduced HRQoL. This study aimed to evaluate whether eveningness amplifies the association between MSK pain and HRQoL in contrast to morningness. Questionnaire data on MSK pain dimensions (intensity, disability at work, number of pain sites [NPSs], and frequency), chronotype, covariates (sex, sufficiency of sleep duration, mental distress, and presence of coexisting diseases), and HRQoL (measured by 15D) were collected among 46-year-old individuals belonging to the Northern Finland Birth Cohort 1966 (N = 4257). Individuals without any MSK pain were excluded. General linear models were conducted to estimate the associations between chronotypes, MSK pain dimensions, and HRQoL. The interaction terms (chronotype x pain dimension) were tested in the models. There were 13% E-types and 43% M-types in the study sample. Each pain dimension and chronotype were related to HRQoL. In the sex-adjusted chronotype-specific models, the reduction in HRQoL in relation to pain appeared to be stronger among E-types than among M-types in respect to all pain dimensions. After adjustments, this was particularly seen in terms of NPS and pain frequency. Our findings suggest that eveningness intensifies the association between MSK pain and HRQoL, and, thus, they are indicative of E-types being more sensitive than M-types to the consequences of MSK pain. As such, MSK pain treatment and rehabilitation actions to improve HRQoL should be especially targeted at E-types.Peer reviewe

Evoluution säilyttämä uni

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Eveningness associates with lower physical activity from pre- to late adolescence

Objective: Adolescence is often associated with decline in physical activity (PA) and a circadian shift towards eveningness, but it is not known whether these transitions are intertwined. We explored longitudinally and in cross-section how chronotype and genetic liability for morningness associate with PA as self-reported and measured by actigraphy in early and late adolescence. Methods: Our sample comes from a longitudinal Finnish community-cohort born in 1998 with information on actigraph-based PA and objectively measured sleep-wake rhythm based on midpoint of sleep at ages 12 (N = 353, girls = 187) and 17 (N = 171, girls = 98). Information on self-reported circadian preference and subjective PA was available at age 17. The summarized genetic effects of multiple single nucleotide polymorphism for morningness was assessed by calculating polygenic score (PGS) based on the results on a recent genome-wide association study (GWAS). Results: PA declined by 40% (p = 0.36). However, those with circadian preference more towards eveningness at age 17 had more sedentary behavior (p <0.01) and a lower level of general (p = 0.01), light (p <0.01) and moderate to vigorous PA (p <0.05). They also had poorer subjective assessment of their fitness level (p <0.01) and they exercised less (all p = 0.13). Conclusions: Findings of this study highlighted the influence of circadian preference on physical activity behavior in adolescence. Self-assessed circadian preference towards eveningness associated with lower PA and greater decline of it during adolescence. Furthermore, PA declined significantly especially among boys from early to late adolescence. Interventions encouraging physical activity should target specifically evening-oriented adolescents. (C) 2020 Elsevier B.V. All rights reserved.Peer reviewe