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Pressbild John Axelsson. Foto: Sara Appelgren

John Axelsson

Professor

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Arbetar vid Stressforskningsinstitutet
E-post john.axelsson@su.se
Besöksadress Frescati Hagväg 16 A
Rum A 128
Postadress Stressforskningsinstitutet 106 91 Stockholm

Om mig

Varför vi sover är en av biologins största gåtor. Vi vet dock att sömn är ett livsviktigt biologiskt fenomen som är både komplext och dynamiskt. Jag är fascinerad av hur dagens moderna 24-timmars samhälle påverkar hur vi sover och vilka konsekvenserna är.

Forskning

Vårt forskarteam på Stressforskningsinstitutet vill öka kunskapen och medvetenheten om hur sömn och sjukdom i det moderna samhället påverkar vår biologi, kognition och hälsa. Några av de frågor vi arbetar med att besvara är:

- Hur hjärnan påverkas av sömnbrist och varför är vissa mer sårbara än andra? 

- Hur snabbt vaknar hjärnan upp från sömn?

- Hur dåligt sover småbarnsföräldrar och vad kan man göra åt det? 

- Kan mer sömn stödja återhämtning när vi är sjuka? 

 

Publikationer

I urval från Stockholms universitets publikationsdatabas
  • 2019. Julie Lasselin (et al.). Brain, behavior, and immunity 79, 236-243

    There is strong experimental support that infections increase the drive for sleep in animals, and it is widely believed that more sleep is part of an adaptive immune response. While respiratory infections (RI) are very prevalent in humans, there is a striking lack of systematic knowledge on how it affects sleep. We recruited 100 people, among whom 28 became sick with an RI during the study period (fulfilling criteria for influenza-like illness, ILI, or acute respiratory infection, ARI). We measured sick participants' sleep at home, both objectively (actigraphy) and subjectively (diary ratings), for one week as well as four weeks later when healthy. During the week with RI, people spent objectively longer time in bed and had a longer total sleep time compared to the healthy week. During the infection, participants also had more awakenings, but no significant differences in sleep latency or sleep efficiency. While sick, people also reported increased difficulties falling asleep, worse sleep quality, more restless sleep and more shallow sleep, while they did not report sleep to be less sufficient. Most problems occurred at the beginning of the sickness week, when symptoms were strong, and showed signs of recovery thereafter (as indicated by interactions between condition and day/night of data collection for all the 10 sleep outcomes). The degree of symptoms of RI was related to a worse sleep quality and more restless sleep, but not to any of the objective sleep outcomes or the other subjective sleep variables. Having a higher body temperature was not significantly related to any of the sleep variables. This study suggests that having a respiratory infection is associated with spending more time in bed and sleeping longer, but also with more disturbed sleep, both objectively and subjectively. This novel study should be seen as being of pilot character. There is a need for larger studies which classify pathogen type and include baseline predictors, or that manipulate sleep, in order to understand whether the sleep alterations seen during infections are adaptive and whether sleep interventions could be used to improve recovery from respiratory infections.

  • 2018. John Axelsson (et al.). Proceedings of the Royal Society of London. Biological Sciences 285 (1870)

    Detection and avoidance of sick individuals have been proposed as essential components in a behavioural defence against disease, limiting the risk of contamination. However, almost no knowledge exists on whether humans can detect sick individuals, and if so by what cues. Here, we demonstrate that untrained people can identify sick individuals above chance level by looking at facial photos taken 2 h after injection with a bacterial stimulus inducing an immune response (2.0 ng kg-1 lipopolysaccharide) or placebo, the global sensitivity index being d' = 0.405. Signal detection analysis (receiver operating characteristic curve area) showed an area of 0.62 (95% confidence intervals 0.60-0.63). Acutely sick people were rated by naive observers as having paler lips and skin, a more swollen face, droopier corners of the mouth, more hanging eyelids, redder eyes, and less glossy and patchy skin, as well as appearing more tired. Our findings suggest that facial cues associated with the skin, mouth and eyes can aid in the detection of acutely sick and potentially contagious people.

  • 2017. Christina Regenbogen (et al.). Proceedings of the National Academy of Sciences of the United States of America 114 (24), 6400-6405

    Throughout human evolution, infectious diseases have been a primary cause of death. Detection of subtle cues indicating sickness and avoidance of sick conspecifics would therefore be an adaptive way of coping with an environment fraught with pathogens. This study determines how humans perceive and integrate early cues of sickness in conspecifics sampled just hours after the induction of immune system activation, and the underlying neural mechanisms for this detection. In a double-blind placebo-controlled crossover design, the immune system in 22 sample donors was transiently activated with an endotoxin injection [lipopolysaccharide (LPS)]. Facial photographs and body odor samples were taken from the same donors when sick (LPS-injected) and when healthy (saline-injected) and subsequently were presented to a separate group of participants (n = 30) who rated their liking of the presented person during fMRI scanning. Faces were less socially desirable when sick, and sick body odors tended to lower liking of the faces. Sickness status presented by odor and facial photograph resulted in increased neural activation of odor-and faceperception networks, respectively. A superadditive effect of olfactory-visual integration of sickness cues was found in the intraparietal sulcus, which was functionally connected to core areas of multisensory integration in the superior temporal sulcus and orbitofrontal cortex. Taken together, the results outline a disease-avoidance model in which neural mechanisms involved in the detection of disease cues and multisensory integration are vital parts.

  • 2017. Ellen R. Stothard (et al.). Current Biology 27 (4), 508-513

    Reduced exposure to daytime sunlight and increased exposure to electrical lighting at night leads to late circadian and sleep timing [1-3]. We have previously shown that exposure to a natural summer 14 hr 40 min:9 hr 20 min light-dark cycle entrains the human circadian clock to solar time, such that the internal biological night begins near sunset and ends near sunrise [1]. Here we show that the beginning of the biological night and sleep occur earlier after a week's exposure to a natural winter 9 hr 20 min:14 hr 40 min light-dark cycle as compared to the modern electrical lighting environment. Further, we find that the human circadian clock is sensitive to seasonal changes in the natural light-dark cycle, showing an expansion of the biological night in winter compared to summer, akin to that seen in non-humans [4-8]. We also show that circadian and sleep timing occur earlier after spending a weekend camping in a summer 14 hr 39 min:9 hr 21 min natural light-dark cycle compared to a typical weekend in the modern environment. Weekend exposure to natural light was sufficient to achieve similar to 69% of the shift in circadian timing we previously reported after a week's exposure to natural light [1]. These findings provide evidence that the human circadian clock adapts to seasonal changes in the natural light-dark cycle and is timed later in the modern environment in both winter and summer. Further, we demonstrate that earlier circadian timing can be rapidly achieved through natural light exposure during a weekend spent camping.

  • 2017. Benjamin C. Holding (et al.). Sleep 40 (11)

    Objectives: Insufficient sleep has been associated with impaired recognition of facial emotions. However, previous studies have found inconsistent results, potentially stemming from the type of static picture task used. We therefore examined whether insufficient sleep was associated with decreased emotion recognition ability in two separate studies using a dynamic multimodal task.

    Methods: Study 1 used a cross-sectional design consisting of 291 participants with questionnaire measures assessing sleep duration and self-reported sleep quality for the previous night. Study 2 used an experimental design involving 181 participants where individuals were quasi-randomized into either a sleep-deprivation (N = 90) or a sleep-control (N = 91) condition. All participants from both studies were tested on the same forced-choice multimodal test of emotion recognition to assess the accuracy of emotion categorization.

    Results: Sleep duration, self-reported sleep quality (study 1), and sleep deprivation (study 2) did not predict overall emotion recognition accuracy or speed. Similarly, the responses to each of the twelve emotions tested showed no evidence of impaired recognition ability, apart from one positive association suggesting that greater self-reported sleep quality could predict more accurate recognition of disgust (study 1).

    Conclusions: The studies presented here involve considerably larger samples than previous studies and the results support the null hypotheses. Therefore, we suggest that the ability to accurately categorize the emotions of others is not associated with short-term sleep duration or sleep quality and is resilient to acute periods of insufficient sleep.

  • 2016. Göran Kecklund, John Axelsson. BMJ. British Medical Journal 355

    This review summarises the literature on shift work and its relation to insufficient sleep, chronic diseases, and accidents. It is based on 38 meta-analyses and 24 systematic reviews, with additional narrative reviews and articles used for outlining possible mechanisms by which shift work may cause accidents and adverse health. Evidence shows that the effect of shift work on sleep mainly concerns acute sleep loss in connection with night shifts and early morning shifts. A link also exists between shift work and accidents, type 2 diabetes (relative risk range 1.09-1.40), weight gain, coronary heart disease (relative risk 1.23), stroke (relative risk 1.05), and cancer (relative risk range 1.01-1.32), although the original studies showed mixed results. The relations of shift work to cardiometabolic diseases and accidents mimic those with insufficient sleep. Laboratory studies indicate that cardiometabolic stress and cognitive impairments are increased by shift work, as well as by sleep loss. Given that the health and safety consequences of shift work and insufficient sleep are very similar, they are likely to share common mechanisms. However, additional research is needed to determine whether insufficient sleep is a causal pathway for the adverse health effects associated with shift work.

  • 2016. Göran Kecklund, Mikael Sallinen, John Axelsson. Principles and Practice of Sleep Medicine, 742-749
  • 2016. John Axelsson, Göran Kecklund. FYSS 2017: fysisk aktivitet i sjukdomsprevention och sjukdomsbehandling, 171-183
Visa alla publikationer av John Axelsson vid Stockholms universitet

Senast uppdaterad: 12 december 2019

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