Hallvard Heiberg

• Jonassen, Rune; Øverli, Øyvind; Hilland, Eva; Nilsen, Hilde; Esbensen, Qin Ying & Lirussi, Lisa [Vis alle 13 forfattere av denne artikkelen] (2026). Serotonin transporter polymorphism (5-HTTLPR) is associated with post-awakening cortisol measures in previous depression. Comprehensive Psychoneuroendocrinology. 27, s. 1–7. doi: 10.1016/j.cpnec.2026.100363. Fulltekst i vitenarkiv Vis sammendrag

  Elevated cortisol levels have been linked to major depressive disorder (MDD), but cortisol dynamics vary substantially across individuals and clinical states. Genetic variation in the serotonin transporter polymorphism (5-HTTLPR) has been proposed as one contributor to differences in hypothalamic-pituitary-adrenal axis functioning. The present study examined associations between cortisol awakening measures and 5-HTTLPR genotype groups in individuals with a history of depression compared with healthy controls, and explored whether current depressive symptom severity was related to cortisol indices. A total of 108 individuals with a history of depression were genotyped and compared with 59 healthy controls. Participants completed structured diagnostic interviews and self-reported depressive symptoms. Salivary cortisol was sampled in the evening and at five consecutive timepoints after awakening (15-min intervals). Cortisol was analyzed using a linear mixed-effects model of repeated measures and by cortisol awakening response (CAR) summary indices: area under the curve with respect to ground (AUCg) and area under the curve with respect to increase (AUCi). Cortisol changed significantly over time, but there was no evidence that genotype groups differed in the overall cortisol timecourse. In CAR summary analyses, group differences were observed for AUCg, whereas AUCi did not show corresponding group differences. Regression analyses indicated that BDI-II was not associated with AUCg or AUCi after adjustment for covariates. These findings suggest that 5-HTTLPR-related differences, when present, may be more detectable in overall post-awakening cortisol output than in baseline-relative increase.

• Bø, Ragnhild; Jonassen, Rune; Harmer, Catherine; Øverli, Øyvind; Nilsen, Hilde & Esbensen, Qin Ying [Vis alle 13 forfattere av denne artikkelen] (2025). 5-HTTLPR does not moderate the effect of attention bias modification for depression: a randomized sham-controlled trial. Translational Psychiatry. 15, s. 1–6. doi: 10.1038/s41398-025-03581-3. Fulltekst i vitenarkiv Vis sammendrag

  Abstract The 5-HTTLPR polymorphism in the serotonin transporter gene SLC6A4 has previously been dubbed a plasticity marker. Within the 5-HTTLPR polymorphism, a SNP (rs25531) in the L-allele in the promoter region, affects the transcription efficacy of the SCL6A4 , leading to functionally important differences related to serotonin transporter availability in the synapses. 5-HTTLPR has been implicated in magnitude of negative attentional bias, a causal risk factor for depression, and the modifiability of attentional biases both in positive and negative directions. Hence, this genotype may moderate the outcomes of attention bias modification (ABM) targeted at reducing depressive symptoms. We conducted a registered randomized sham-controlled trial of ABM in a sample of 301 participants with a history of Major Depressive Disorder (MDD) who had residual symptoms. They were randomized and underwent 14 days of two daily session of either ABM or sham at home. Of these, 264 provided genetic samples for determining the functionally important variant of the gene SLC6A4 . We investigated if the SNP ( rs25531 ) moderated the effect of ABM on symptoms of depression (HDRS, BDI-II) and anxiety (BAI), and attention bias post-intervention. None of the outcomes were moderated by the allelic variation in the promoter region of 5-HTTLPR . Limitations include low level of depressive symptoms, lack of data on ethnicity, current and prenatal level of stress, and early traumatic experiences. The 5-HTTLPR polymorphism did not moderate the effect of ABM on the symptom scales, nor attentional bias. Combination or interactions with other genes may be required for prescribing personalized interventions.

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• Sætra, Marte Julie & Heiberg, Hallvard (2018). Kommunikasjon mellom hjerneceller. Fulltekst i vitenarkiv
• Sætra, Marte Julie & Heiberg, Hallvard (2018). Kommunikasjon mellom hjerneceller. Fulltekst i vitenarkiv

Se alle arbeider i NVA