Profiles

Mats Lekander

Mats Lekander

Enhetschef

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Arbetar vid Stressforskningsinstitutet
Telefon 08-553 789 33
E-post mats.lekander@su.se
Besöksadress Frescati Hagväg 16 A
Rum 339
Postadress Stressforskningsinstitutet 106 91 Stockholm

Om mig

Mats arbetar i skärningspunkten mellan psykologi och biomedicin. Framförallt studerar han samverkan mellan hjärnan och immunsystemet och beteendets roll i detta samspel. Detta kan exempelvis gälla effekter av stress eller otillräcklig sömn på immunsystemets och hjärnans funktion. Flera relevanta studier är inriktade på allergi. Ett särskilt intresse ligger i hur immunsystemet påverkar hjärnans aktivitet och därigenom den subjektiva hälsoupplevelsen. Inom detta område studerar han hur både akut och kronisk inflammation påverkar smärtkänslighet, trötthet och så kallad självskattad hälsa. Mats intresse för mekanismer bakom generella hälsoaspekter och stress har de senaste åren också tillämpats inom behandlingsforskning, där flera studier pågår. Ett exempel är akupunktur och den roll placebo och interaktionen mellan behandlare och patient har för behandlingens effektivitet. Andra studier gäller bland annat behandling av insomni eller hälsoångest (hypokondri) med hjälp av kognitiv beteendeterapi, eller hur ACT (Acceptance and Commitment Therapy) kan användas vid kroniska smärttillstånd. I nästan alla studier kompletterar biologiska och psykologiska observationsnivåer varandra för att ge ökad förståelse. Mats är föreståndare för Stockholm Stress Center.

Utbildning

Psykologexamen 1990,
Doktor i medicinsk vetenskap 1996

Publikationer

I urval från Stockholms universitets publikationsdatabas
  • Helena Schiller (et al.).

    Purpose: Sleep disturbance is common in the working population, often associated with work stress, health complaints and impaired work performance. This study evaluated a group intervention at work, based on Cognitive Behavioral Therapy (CBT) for insomnia, and the moderating effects of burnout scores at baseline.

    Methods: This is a randomized controlled intervention with a waiting-list control group. Participants were employees working at least 75% of full time, reporting self-perceived regular sleep problems. Data were collected at baseline, post-intervention and at a three-month follow-up through diaries, wrist-actigraphy and questionnaires including the Insomnia Severity Index (ISI) and the Shirom-Melamed Burnout Questionnaire (SMBQ). Fifty-one participants (63% women) completed data collections.

    Results: A multilevel mixed model showed no significant differences between groups for sleep over time, while there was a significant effect on insomnia symptoms when excluding participants working shifts (N=11) from the analysis (p=0.044). Moreover, a moderating effect of baseline-levels of burnout scores was observed on insomnia symptoms (p=0.009). A post-hoc analysis showed that individuals in the intervention group with low burnout scores at baseline (SMBQ<3.75) displayed significantly reduced ISI scores at follow-up, compared to individuals with high burnout scores at baseline (p=0.005).

    Conclusions: Group CBT for insomnia given at the workplace did not reduce sleep problems looking at the group as a whole, while it was indicated that the intervention reduced insomnia in employees with regular daytime work. The results also suggest that workplace-based group CBT may improve sleep in employees with primary insomnia if not concomitant with high burnout scores. 

  • Tina Sundelin, Mats Lekander, John Axelsson.
  • Helena Schiller (et al.).

    Objectives: A 25% reduction of weekly work hours for full-time employees has been shown to improve sleep and alertness and reduce stress during both workdays and days off. The aim of the present study was to investigate how employees use their time during such an intervention: does total workload (paid and non-paid work) decrease, and recovery time increase, when work hours are reduced?

    Methods: Full-time employees within the public sector (N=636; 75% women) were randomized into intervention group and control group. The intervention group (N=370) reduced worktime to 75% with preserved salary during 18 months. Data were collected at baseline, after 9 months and 18 months. Time-use was reported every half hour daily between 06 and 01 a.m. during one week at each data collection. Data were analyzed with multilevel mixed modeling.

    Results: Compared to the control group, the intervention group increased the time spent on domestic work and relaxing hobby activities during workdays when worktime was reduced (p≤0.001). On days off, more time was spent in free-time activities (p=0.003). Total workload decreased (-65 minutes) and time spent in recovery activities increased on workdays (+53 minutes). The pattern of findings was similar in subgroups defined by gender, family status and job situation.

    Conclusions: A worktime reduction of 25% for full-time workers resulted in decreased total workload and an increase of time spent in recovery activities, which is in line with the suggestion that worktime reduction may be beneficial for long-term health and stress.

  • 2019. Daniel S. Albrecht (et al.). Brain, behavior, and immunity 75, 72-83

    Fibromyalgia (FM) is a poorly understood chronic condition characterized by widespread musculoskeletal pain, fatigue, and cognitive difficulties. While mounting evidence suggests a role for neuroinflammation, no study has directly provided evidence of brain glial activation in FM. In this study, we conducted a Positron Emission Tomography (PET) study using [C-11]PBR28, which binds to the translocator protein (TSPO), a protein upregulated in activated microglia and astrocytes. To enhance statistical power and generalizability, we combined datasets collected independently at two separate institutions (Massachusetts General Hospital [MGH] and Karolinska Institutet [KI]). In an attempt to disentangle the contributions of different glial cell types to FM, a smaller sample was scanned at KI with [C-11]-L-deprenyl-D2 PET, thought to primarily reflect astrocytic (but not microglial) signal. Thirty-one FM patients and 27 healthy controls (HC) were examined using [C-11]PBR28 PET. 11 FM patients and 11 HC were scanned using [C-11]-L-deprenyl-D2 PET. Standardized uptake values normalized by occipital cortex signal (SUVR) and distribution volume (V-T) were computed from the [C-11]PBR28 data. [C-11]-L-deprenyl-D2 was quantified using lambda k(3). PET imaging metrics were compared across groups, and when differing across groups, against clinical variables. Compared to HC, FM patients demonstrated widespread cortical elevations, and no decreases, in [C-11]PBR28 ITT and SUVR, most pronounced in the medial and lateral walls of the frontal and parietal lobes. No regions showed significant group differences in [C-11]-L-deprenyl-Ds signal, including those demonstrating elevated [C-11] PBR28 signal in patients (p's >= 0.53, uncorrected). The elevations in [C-11]PBR28 V-T and SUVR were correlated both spatially (i.e., were observed in overlapping regions) and, in several areas, also in terms of magnitude. In exploratory, uncorrected analyses, higher subjective ratings of fatigue in FM patients were associated with higher [C-11] PBR28 SUVR in the anterior and posterior middle cingulate cortices (p's < 0.03). SUVR was not significantly associated with any other clinical variable. Our work provides the first in vivo evidence supporting a role for glial activation in FM pathophysiology. Given that the elevations in [C-11]PBR28 signal were not also accompanied by increased [C-11]-deprenyl-D2 signal, our data suggests that microglia, but not astrocytes, may be driving the TSPO elevation in these regions. Although [C-11]-L-deprenyl-D2 signal was not found to be increased in FM patients, larger studies are needed to further assess the role of possible astrocytic contributions in FM. Overall, our data support glial modulation as a potential therapeutic strategy for FM.

  • 2018. Anna Andreasson (et al.). Journal of Health Psychology 23 (11), 1452-1463

    Symptoms after inflammatory activation, so-called sickness behaviour, overlap with trans-diagnostic complaints. As no self-report questionnaire to assess sickness behaviour exists, we aimed to develop such an instrument, the Sickness Questionnaire. Items responsive to experimentally induced inflammatory activation (randomized double-blind study endotoxin (0.6 ng/kg) versus placebo, n = 52) were selected and the statistical properties were examined in 172 primary care patients. A principal component analysis indicated a one-factor solution (Cronbach's alpha = .86). This 10-item scale correlated with depression ( β = .41, p < .001), anxiety ( β = .36, p < .001), self-rated health ( β = .28, p < .001) and a single item of feeling sick ( β = .55, p < .001). The results support the adequacy of Sickness Questionnaire as a brief assessment instrument of perceived sickness behaviour.

Visa alla publikationer av Mats Lekander vid Stockholms universitet

Senast uppdaterad: 15 mars 2019

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