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The aetiology of nausea and vomiting during pregnancy (NVP) is multifactorial, but the relative contribution of biological and psychological determinants is insufficiently understood. We examined the association of human chorionic gonadotropin (hCG), thyroid hormones (thyroid-stimulating hormone and thyroxin) and psychological factors with NVP.
Blood chemistry and psychological measures were obtained in 1682 pregnant women participating in the Holistic Approach to Pregnancy and the first Postpartum Year (HAPPY) study between 12 and 14 weeks of gestation. The presence of NVP was measured using the Pregnancy-Unique Quantification of Emesis scale. Depressive symptoms were assessed using the Edinburgh Depression Scale. Multivariable logistic regression analyses were used to investigate the independent role of hCG, thyroid hormones and depression as related to NVP, adjusting for age, body mass index, education, parity, smoking status, unplanned pregnancy and history of depression.
Elevated levels of NVP were observed in 318 (18.9%) participants. High hCG levels [odds ratio (OR) = 1.47, 95% confidence interval (CI) = 1.11–1.95], elevated depressive symptoms in the first trimester (OR = 1.67, 95% CI = 1.15–2.43) and a history of depression (OR = 1.53, 95% CI = 1.11–2.11) were independently related to high NVP. Multiparity (OR = 1.47, 95% CI = 1.12–1.92) and younger age (OR = 0.91, 95% CI = 0.87–0.94) were also associated with high NVP, whereas (sub)clinical hyperthyroidism was not related to high NVP.
The current study is the first to demonstrate that a combination of hCG hormone and psychological factors are independently related to nausea and vomiting during early pregnancy.
The prevalence and severity of neurocognitive dysfunctioning of patients with somatic symptom and related disorders (SSRD) is unknown. Furthermore, the influence of comorbid depression and anxiety has not been evaluated. This study examines neurocognitive dysfunctioning of patients with SSRD and explores if comorbid depression and anxiety is associated with specific neurocognitive dysfunctioning.
Cross-sectional study with consecutive patients suffering from SSRD visiting an outpatient specialty mental health care Centre of Excellence for SSRD. Extensive neuropsychological assessment and assessment of depression and anxiety symptom levels using the Patient-Health-Questionnaire-9 and General Anxiety Disorder questionnaire-7 were performed at intake. Multivariate analysis was performed.
The study sample consisted of 201 SSRD patients, with a mean age of 43 years (Standard deviation = 13) years; 37.8% were male. Neurocognitive dysfunction in the domains information processing speed, sustained and divided attention, working memory, verbal and visual memory were reported, compared with normative data. Comorbid depression and anxiety occurred frequently within the sample (75.1% and 65.7%, respectively). Neurocognitive dysfunctioning was worse in patients suffering from comorbid depression [multivariate F (7,161) = 2.839, p = 0.008] but not in patients with comorbid anxiety.
Poor neurocognitive performance of patients with SSRD is common and worsens in case of comorbid depression. This may explain treatment dropout of patients with SSRD from neurocognitive behavioral therapy. Research on novel interventions is needed targeting neurocognitive functioning of patients with SSRD, particularly those with comorbid depression.
Systematic research on behavioural patterns related to increased risk of coronary artery disease (CAD) and its clinical manifestation as myocardial infarction was initiated by Friedman and Rosenman in the 1950s. The Type A Behaviour Pattern (TABP) was documented to be predictive of future myocardial infarction. TABP is defined as: ‘an action-emotion complex that can be observed in any person who is aggressively involved in a chronic, incessant struggle to achieve more and more in less and less time, and if required to do so, against the opposing efforts of other things or persons …’ (Friedman & Rosenman, 1959). Later research (reviewed below) has documented that hostility may be the ‘toxic’ component of TABP. Type A behaviour is characterized by an excessive competitive drive, impatience, hostility and vigorous speech characteristics. The complement of TABP was called Type B behaviour and was described as the relative absence of Type A characteristics.
The early reports by Friedman, Rosenman and co-workers have resulted in numerous epidemiological and experimental investigations on the relationship between TABP and manifestations of coronary artery disease. In the 1960s and 1970s, most epidemiological studies supported the association between TABP and risk of future coronary artery disease (CAD) in men and women. The magnitude of these associations was comparable to that of traditional risk factors for CAD and also independent of these factors, such as hypertension and elevated lipid levels.
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