<b><i>Background:</i></b> The innovative treatment model Improving Access to Psychological Therapies (IAPT) and its Norwegian adaptation, Prompt Mental Health Care (PMHC), have been evaluated by cohort studies only. Albeit yielding promising results, the extent to which these are attributable to the treatment thus remains unsettled. <b><i>Objective:</i></b> To investigate the effectiveness of the PMHC treatment compared to treatment as usual (TAU) at 6-month follow-up. <b><i>Methods:</i></b> A randomized controlled trial with parallel assignment was performed in two PMHC sites (Sandnes and Kristiansand) and enrolled clients between November 9, 2015 and August 31, 2017. Participants were 681 adults (aged ≥18 years) considered for admission to PMHC due to anxiety and/or mild to moderate depression (Patient Health Questionnaire [PHQ-9]/Generalized Anxiety Disorder scale [GAD-7] scores above cutoff). These were randomly assigned (70:30 ratio; <i>n</i> = 463 to PMHC, <i>n</i> = 218 to TAU) with simple randomization within each site with no further constraints. The main outcomes were recovery rates and changes in symptoms of depression (PHQ-9) and anxiety (GAD-7) between baseline and follow-up. Primary outcome data were available for 73/67% in PMHC/TAU. Sensitivity analyses based on observed patterns of missingness were also conducted. Secondary outcomes were work participation, functional status, health-related quality of life, and mental well-being. <b><i>Results:</i></b> A reliable recovery rate of 58.5% was observed in the PMHC group and of 31.9% in the TAU group, equaling a between-group effect size of 0.61 (95% CI 0.37 to 0.85, <i>p</i> &#x3c; 0.001). The differences in degree of improvement between PMHC and TAU yielded an effect size of –0.88 (95% CI –1.23 to –0.43, <i>p</i> &#x3c; 0.001) for PHQ-9 and –0.60 (95% CI –0.90 to –0.30, <i>p</i> &#x3c; 0.001) for GAD-7 in favor of PMHC. All sensitivity analyses pointed in the same direction, with small variations in point estimates. Findings were slightly more robust for depressive than anxiety symptoms. PMHC was also more effective than TAU in improving all secondary outcomes, except for work participation (<i>z</i> = 0.415, <i>p</i> = 0.69). <b><i>Conclusions:</i></b> The PMHC treatment was substantially more effective than TAU in alleviating the burden of anxiety and depression. This adaptation of IAPT is considered a viable supplement to existing health services to increase access to effective treatment for adults who suffer from anxiety and mild to moderate depression. A potential effect on work participation needs further examination.

An understanding of the origin of cancer is critical for cancer prevention and treatment. Complex biological mechanisms promote carcinogenesis, and there is increasing evidence that pregnancy‐related exposures influence foetal growth cell division and organ functioning and may have a long‐lasting impact on health and disease susceptibility in the mothers and offspring. Nulliparity is an established risk factor for breast, ovarian, endometrial and possibly pancreatic cancer, whilst the risk of kidney cancer is elevated in parous compared with nulliparous women. For breast, endometrial and ovarian cancer, each pregnancy provides an additional risk reduction. The associations of parity with thyroid and colorectal cancers are uncertain. The timing of reproductive events is also recognized to be important. Older age at first birth is associated with an increased risk of breast cancer, and older age at last birth is associated with a reduced risk of endometrial cancer. The risks of breast and endometrial cancers increase with younger age at menarche and older age at menopause. The mechanisms, and hormone profiles, that underlie alterations in maternal cancer risk are not fully understood and may differ by malignancy. Linking health registries and pooling of data in the Nordic countries have provided opportunities to conduct epidemiologic research of pregnancy exposures and subsequent cancer. We review the maternal risk of several malignancies, including those with a well‐known hormonal aetiology and those with less established relationships. The tendency for women to have fewer pregnancies and at later ages, together with the age‐dependent increase in the incidence of most malignancies, is expected to affect the incidence of pregnancy‐associated cancer.

ObjectiveHigh-level alcohol consumption is common in, and central to, the student community. Among adults, high-level alcohol consumption, and sometimes also low, has been associated with poorer social integration and mental health. We aimed to investigate how alcohol consumption relates to life satisfaction and mental health among students in higher education.MethodsData from the Norwegian study of students' health and well-being (SHoT, 2014, n = 9632) were used. Associations between alcohol consumption (AUDIT; abstainers, low risk, risky and hazardous consumption) and life satisfaction and mental health complaints, as well as number of close friends, and social and emotional loneliness were investigated using linear regression models. Crude models and models adjusted for age, gender and relationship status were conducted.ResultsStudents reporting hazardous consumption reported lower life satisfaction, more mental health complaints, and more emotional and social loneliness than students with low risk consumption. Students reporting risky consumption reported slightly reduced life satisfaction and more mental health complaints, but more close friends and less social loneliness. Abstainers did not report reduced life satisfaction or more mental health complaints, despite reporting fewer close friends and more social loneliness.ConclusionHigh-level alcohol consumption among students might indicate increased risk of several problems in the future – but also currently. Our findings further imply that the quality of friendships might be more important for life satisfaction and mental health than the number of friends, but also that social integration in student communities might be more difficult for students who do not drink.

ObjectiveTo examine associations between birth defects and cancer from birth into adulthood.DesignPopulation based nested case-control study.SettingNationwide health registries in Denmark, Finland, Norway, and Sweden.Participants62 295 cancer cases (0-46 years) and 724 542 frequency matched controls (matched on country and birth year), born between 1967 and 2014.Main outcome measuresRelative risk of cancer in relation to major birth defects, estimated as odds ratios with 99% confidence intervals from logistic regression models.ResultsAltogether, 3.5% (2160/62 295) of cases and 2.2% (15 826/724 542) of controls were born with major birth defects. The odds ratio of cancer for people with major birth defects compared with those without was 1.74 (99% confidence interval 1.63 to 1.84). For individuals with non-chromosomal birth defects, the odds ratio of cancer was 1.54 (1.44 to 1.64); for those with chromosomal anomalies, the odds ratio was 5.53 (4.67 to 6.54). Many structural birth defects were associated with later cancer in the same organ system or anatomical location, such as defects of the eye, nervous system, and urinary organs. The odds ratio of cancer increased with number of defects and decreased with age, for both non-chromosomal and chromosomal anomalies. The odds ratio of cancer in people with any non-chromosomal birth defect was lower in adults (≥20 years: 1.21, 1.09 to 1.33) than in adolescents (15-19 years: 1.58, 1.31 to 1.90) and children (0-14 years: 2.03, 1.85 to 2.23). The relative overall cancer risk among adults with chromosomal anomalies was markedly reduced from 11.3 (9.35 to 13.8) in children to 1.50 (1.01 to 2.24). Among adults, skeletal dysplasia (odds ratio 3.54, 1.54 to 8.15), nervous system defects (1.76, 1.16 to 2.65), chromosomal anomalies (1.50, 1.01 to 2.24), genital organs defects (1.43, 1.14 to 1.78), and congenital heart defects (1.28, 1.02 to 1.59) were associated with overall cancer risk.ConclusionsThe increased risk of cancer in individuals with birth defects persisted into adulthood, both for non-chromosomal and chromosomal anomalies. Further studies on the molecular mechanisms involved are warranted.