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- Järvelä-Reijonen, E., et al.
(författare)
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The effects of acceptance and commitment therapy on eating behavior and diet delivered through face-to-face contact and a mobile app : A randomized controlled trial
- 2018
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Ingår i: International Journal of Behavioral Nutrition and Physical Activity. - : BioMed Central Ltd.. - 1479-5868. ; 15:22, s. -14
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Tidskriftsartikel (refereegranskat)abstract
- Background: Internal motivation and good psychological capabilities are important factors in successful eating-related behavior change. Thus, we investigated whether general acceptance and commitment therapy (ACT) affects reported eating behavior and diet quality and whether baseline perceived stress moderates the intervention effects. Methods: Secondary analysis of unblinded randomized controlled trial in three Finnish cities. Working-aged adults with psychological distress and overweight or obesity in three parallel groups: (1) ACT-based Face-to-face (n = 70; six group sessions led by a psychologist), (2) ACT-based Mobile (n = 78; one group session and mobile app), and (3) Control (n = 71; only the measurements). At baseline, the participants' (n = 219, 85% females) mean body mass index was 31.3 kg/m2 (SD = 2.9), and mean age was 49.5 years (SD = 7.4). The measurements conducted before the 8-week intervention period (baseline), 10 weeks after the baseline (post-intervention), and 36 weeks after the baseline (follow-up) included clinical measurements, questionnaires of eating behavior (IES-1, TFEQ-R18, HTAS, ecSI 2.0, REBS), diet quality (IDQ), alcohol consumption (AUDIT-C), perceived stress (PSS), and 48-h dietary recall. Hierarchical linear modeling (Wald test) was used to analyze the differences in changes between groups. Results: Group x time interactions showed that the subcomponent of intuitive eating (IES-1), i.e., Eating for physical rather than emotional reasons, increased in both ACT-based groups (p = .019); the subcomponent of TFEQ-R18, i.e., Uncontrolled eating, decreased in the Face-to-face group (p = .020); the subcomponent of health and taste attitudes (HTAS), i.e., Using food as a reward, decreased in the Mobile group (p = .048); and both subcomponent of eating competence (ecSI 2.0), i.e., Food acceptance (p = .048), and two subcomponents of regulation of eating behavior (REBS), i.e., Integrated and Identified regulation (p = .003, p = .023, respectively), increased in the Face-to-face group. Baseline perceived stress did not moderate effects on these particular features of eating behavior from baseline to follow-up. No statistically significant effects were found for dietary measures. Conclusions: ACT-based interventions, delivered in group sessions or by mobile app, showed beneficial effects on reported eating behavior. Beneficial effects on eating behavior were, however, not accompanied by parallel changes in diet, which suggests that ACT-based interventions should include nutritional counseling if changes in diet are targeted.
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- Tiihonen, J, et al.
(författare)
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Correction: Neurobiological roots of psychopathy
- 2020
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Ingår i: Molecular psychiatry. - : Springer Science and Business Media LLC. - 1476-5578 .- 1359-4184. ; 25:12, s. 3455-3456
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- A correction to this paper has been published and can be accessed via a link at the top of the paper.
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- Tiihonen, J, et al.
(författare)
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Neurobiological roots of psychopathy
- 2020
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Ingår i: Molecular psychiatry. - : Springer Science and Business Media LLC. - 1476-5578 .- 1359-4184. ; 25:12, s. 3432-3441
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Tidskriftsartikel (refereegranskat)abstract
- Psychopathy is an extreme form of antisocial behavior, with about 1% prevalence in the general population, and 10–30% among incarcerated criminal offenders. Although the heritability of severe antisocial behavior is up to 50%, the genetic background is unclear. The underlying molecular mechanisms have remained unknown but several previous studies suggest that abnormal glucose metabolism and opioidergic neurotransmission contribute to violent offending and psychopathy. Here we show using iPSC-derived cortical neurons and astrocytes from six incarcerated extremely antisocial and violent offenders, three nonpsychopathic individuals with substance abuse, and six healthy controls that there are robust alterations in the expression of several genes and immune response-related molecular pathways which were specific for psychopathy. In neurons, psychopathy was associated with marked upregulation of RPL10P9 and ZNF132, and downregulation of CDH5 and OPRD1. In astrocytes, RPL10P9 and MT-RNR2 were upregulated. Expression of aforementioned genes explained 30–92% of the variance of psychopathic symptoms. The gene expression findings were confirmed with qPCR. These genes may be relevant to the lack of empathy and emotional callousness seen in psychopathy, since several studies have linked these genes to autism and social interaction.
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- Tiihonen, J, et al.
(författare)
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Neurobiological Roots of Schizophrenia
- 2018
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Ingår i: NEUROPSYCHOPHARMACOLOGY. - 0893-133X. ; 43, s. S481-S482
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 8. |
- Tiihonen, J, et al.
(författare)
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Sex-specific transcriptional and proteomic signatures in schizophrenia
- 2019
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1, s. 3933-
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Tidskriftsartikel (refereegranskat)abstract
- It has remained unclear why schizophrenia typically manifests after adolescence and which neurobiological mechanisms are underlying the cascade leading to the actual onset of the illness. Here we show that the use of induced pluripotent stem cell-derived neurons of monozygotic twins from pairs discordant for schizophrenia enhances disease-specific signal by minimizing genetic heterogeneity. In proteomic and pathway analyses, clinical illness is associated especially with altered glycosaminoglycan, GABAergic synapse, sialylation, and purine metabolism pathways. Although only 12% of all 19,462 genes are expressed differentially between healthy males and females, up to 61% of the illness-related genes are sex specific. These results on sex-specific genes are replicated in another dataset. This implies that the pathophysiology differs between males and females, and may explain why symptoms appear after adolescence when the expression of many sex-specific genes change, and suggests the need for sex-specific treatments.
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