Recall bias and major depression lifetime prevalence

BACKGROUND: Epidemiological studies have reported lifetime prevalence rates for major depression that have typically ranged between 10 % and 20 %, and have typically been fairly stable across age groups. This contradicts the intuitive expectation that lifetime prevalence should accumulate with age. Some authors have hypothesized that a cohort effect may account for this puzzling pattern, but another possible explanation is recall bias. In principle, differential mortality could also account for a failure of age-specific lifetime prevalence to increase with age. The objective of this study was to describe the relationship between recall failure (failure to recall previous depressive episodes) and bias in the evaluation of age-specific lifetime major depression prevalence. METHOD: A framework recently described by Hill et al. was used in this analysis. Hill's model relates the slope of an age-specific prevalence curve for an irreversible disease to incidence and mortality. The model is applicable in the current context since lifetime major depression is, by definition, an irreversible condition (albeit one typically characterized by recurring episodes). In the current investigation, an extra term for recall failure was added to the model. In order to incorporate mortality, a structured literature review was conducted and the impact of plausible levels of differential mortality was explored. RESULTS: Relatively low rates of recall failure (e. g. 2-4 % per year) can account for a flat or declining age-specific lifetime prevalence curve in most age groups, with higher rates of recall failure being necessary in the adolescent age range. Among the elderly, where mortality rates are higher, differential mortality may also contribute to the pattern. CONCLUSIONS: Available data about the incidence of major depression, and the mortality associated with this condition, suggest that plausible rates of recall failure can explain a flat or declining lifetime major depression prevalence across age groups. A corollary of this result is that many existing estimates of major depression lifetime prevalence may be too low. A cohort effect can be inferred from cross-sectional lifetime prevalence data only when the diagnostic instruments employed make recall failure very unlikely.     

Waist-to-hip ratio and breast cancer mortality

High insulin levels have been associated with increased risk of breast cancer and poorer survival after a breast cancer diagnosis. Waist-to-hip ratio (WHR) is a marker for insulin resistance and hyperinsulinemia. In this study, the authors tested the hypothesis that elevated WHR is directly related to breast cancer mortality. For identification of modifiable factors affecting survival, data were collected on 603 patients with incident breast cancer who visited the Vancouver Cancer Centre of the British Columbia Cancer Agency (Vancouver, British Columbia, Canada) in 1991-1992, including body measurements and information on demographic, medical, reproductive, and dietary factors. These patients were followed for up to 10 years. Cox proportional hazards regression models were used to relate the variables to breast cancer mortality (n = 112). After adjustment for age, body mass index, family history, estrogen receptor (ER) status, tumor stage at diagnosis, and systemic treatment (chemotherapy or tamoxifen), WHR was directly related to breast cancer mortality in postmenopausal women (for highest quartile vs. lowest, relative risk = 3.3, 95% confidence interval: 1.1, 10.4) but not in premenopausal women (relative risk = 1.2, 95% confidence interval: 0.4, 3.4). Stratification according to ER status showed that the increased mortality was restricted to ER-positive postmenopausal women. Elevated WHR was confirmed as a predictor of breast cancer mortality, with menopausal status and ER status at diagnosis found to be important modifiers of that relation.     

Head CT in new geriatric psychiatry patients: a prospective study

Computed tomography of the head (HCT) was studied prospectively in 42 new geriatric psychiatry patients. Scans were obtained in 88% of the sample. Subjects underwent a complete evaluation by a geriatric psychiatrist who was blind to the HCT results. The HCT was abnormal in 32 (86%) of the 37 patients who had a scan. The most frequent finding was atrophic changes, which were discovered in ten (27%) of the 37 patients. Subcortical vascular disease was found in 14 patients (38%). Mixed pictures with both vascular disease and atrophic changes were found in nine (24%). The only statistically significant predictor of an abnormal HCT was an abnormal neurobehavioral examination. While the information gained from the HCT did not add appreciably to the clinical evaluation in determining whether there was an organic or idiopathic psychiatric syndrome, it was crucial in determining the location and nature of the central nervous system lesions.     

Proficiency testing for creatine kinase isoenzyme CK-2 (CK-MB) in Ontario

Three surveys of the measurement and interpretation of creatine kinase (CK; EC 2.7.3.2) isoenzyme 2 (CK-MB) were conducted in Ontario, Canada, in 1989. Of the clinical laboratories participating, 66% used immunological methods and 24% used electrophoretic methods. Although reference ranges and interpretative routines varied widely, 95% of the laboratories reported correct interpretations for 10 of the 15 vials tested. The only major problems occurred with samples with very low total CK activity. Within-survey duplicate results compared well, and 89% of the laboratories had consistent between-survey results, even for specimens with low total CK activity. Errors were proportional to the frequency of use of the different analytical methods. The lyophilized testing material gave higher results with methods for measuring the mass of CK-2, suggesting that the material contained inactive but immunologically intact CK-2. The surveys indicate that laboratories should review their protocols for measuring CK-2 when only a single sample from the patient is available.     

Propranolol and depression: evidence from the antihypertensive trials

The relationship between propranolol and depression is a subject of controversy. Numerous case reports suggest that propranolol can cause depression, but two small prospective trials have failed to confirm this. The contemporary psychiatric literature is divided as to whether propranolol can cause depression. This study addresses this issue by re-analyzing side effect data from clinical trials of propranolol as an antihypertensive agent. A literature review was carried out and the data were analyzed using meta-analytic statistical techniques. Propranolol was found to cause depression as a side effect with a statistically greater frequency than the control medications used in these trials. As other side effects of propranolol include fatigue, diminished energy, decreased libido, anorexia and poor concentration, it is suggested that propranolol is a cause of organic mood disorder, depressed type.     

Radionuclide imaging of epithelial ovarian tumours with 123I-labelled monoclonal antibody (H317) specific for placental-type alkaline phosphatase

A murine monoclonal antibody, H317, specific for placental-type alkaline phosphatase was labelled with 123I and assessed as an imaging agent using a gamma camera computer system in 18 patients suspected of possible recurrent or metastatic ovarian cancer 1-4 years after removal of the primary tumour. Four patterns of distribution were visible: (1) normal uptake; (2) focal accumulation; (3) diffuse uptake; and (4) 'cold' areas. Six patients, five of whom were clinically negative for ovarian cancer, had normal scans; 11 patients, eight of whom were clinically positive, had increased uptake. One patient had visibly 'cold' areas. Findings were confirmed, where possible, at surgery.