Many studies have found an association between mood-disorder-related traits and endometriosis and adenomyosis. However, the cause–effect relationship remains unclear.

We conducted Mendelian randomisation analyses to evaluate any causal relationship between mood disorders and endometriosis as well as different sites of endometriosis.

Summary-level statistics for mood-disorder-related traits and endometriosis (8288 cases, 68 969 controls) in European populations were derived from large-scale data-sets of genome-wide association studies. A two-sample Mendelian randomisation was performed using the inverse-variance weighted and weight median methods. Further sensitivity analyses, including heterogeneity, pleiotropy and leave-one-out analyses, were conducted to test the consistency of the results.

Genetically determined mood swings (odds ratio = 2.557, 95% CI: 1.192–5.483, P = 0.016) and major depression (odds ratio = 1.233, 95% CI: 1.019–1.493, P = 0.031) were causally associated with an increased risk of endometriosis. Mood swings (odds ratio = 4.238, 95% CI: 1.194–15.048, P = 0.025) and major depression (odds ratio = 1.512, 95% CI: 1.052–2.173, P = 0.025) were also causally associated with the risk of adenomyosis. Sensitivity analyses confirmed the reliability of the results.

Our results suggest that mood-disorder-related traits increase the risk of endometriosis and adenomyosis. This study provides new insights into the potential pathogenesis of endometriosis and adenomyosis, and highlights the importance of preventing endometriosis and adenomyosis in patients with mood-disorder-related traits.

Sleep and mood are known to be linked and this is particularly evident in people with a diagnosis of bipolar disorder (BD). It has been proposed that psychological interventions improving sleep can be a pathway for improving mood. In order for a psychological sleep intervention to be appropriate, the common cognitive processes maintaining the range of sleep disturbances need to be investigated.

This study aimed to explore and identify expert consensus on positive and negative sleep appraisals in the context of low and high mood states, using the Integrative Cognitive Model as a theoretical guide.

A Delphi approach was utilized to allow clinical and research professionals, with experience in the field of BD, to be anonymously consulted about their views on sleep appraisals. These experts were invited to participate in up to three rounds of producing and rating statements that represented positive and negative sleep appraisals.

A total of 38 statements were developed and rated, resulting in a final list of 19 statements that were rated as ‘essential’ or ‘important’ by >80% of the participants. These statements represent the full range of extreme sleep appraisals this study had set out to explore, confirming the importance of better understanding and identifying positive and negative sleep cognitions in the context of high and low mood.

The statements reviewed in this study will be used to inform the development of a sleep cognition measure that may be useful in cognitive therapy addressing sleep disturbances experienced along the bipolar spectrum.

In bipolar-II (BP-II) disorder impulsivity (defined as excessive risky activities by DSM-IV-TR) is one of the symptoms of hypomania. It is unclear if impulsivity is also a trait in BP-II.

The aim was to test if impulsivity was also a trait in BP-II.

Consecutive 136 remitted BP-II outpatients (assessed when presenting for depression by a mood disorder specialist psychiatrist using the Structured Clinical interview for DSM-IV), self-assessed trait impulsivity during follow-ups, using the Personality Questionnaire of the Structured Clinical interview for DSM-IV Axis II Disorders, in a private practice. Trait mood swings were also self-assessed, using the TEMPS-A. A trait nature of impulsivity in BP-II could be supported by finding (1) a relatively high frequency, (2) association between trait impulsivity and symptoms of past hypomania, especially impulsivity, (3) dose–response relationship between number of past hypomania symptoms and trait impulsivity, and (4) association between trait impulsivity and trait mood swings (a trait feature of BP-II).

Trait impulsivity was present in 41.1% of BP-II. BP-II with, versus BP-II without, trait impulsivity had significantly more males, trait mood swings, past hypomania symptoms (irritable mood, talkativeness, increased goal-directed activity), and excessive risky activities (i.e. state impulsivity), corresponding to an irritable risky overactivity. Past state impulsivity and trait impulsivity were significantly associated. Number of past hypomania symptoms and trait impulsivity were significantly correlated. A dose–response relationship was found between number of past hypomania symptoms and trait impulsivity.

Findings suggest that trait impulsivity may be a feature of BP-II. Limitation of self-assessment of personality traits should be taken into account. Findings may have treatment impacts, as the combination of trait impulsivity and mood swings may facilitate relapses and mixed states, which mood stabilising agents could prevent/delay.