Relation between place of residence and postpartum depression

Background:

The relation between place of residence and risk of postpartum depression is uncertain. We evaluated the relation between place of residence and risk of postpartum depression in a population-based sample of Canadian women.

Methods:

Female postpartum respondents to the 2006 Canadian Maternity Experiences Survey (n = 6126) were classified as living in rural (< 1000 inhabitants or population density < 400/km²), semirural (nonrural but < 30 000 inhabitants), semiurban (30 000–499 999 inhabitants) or urban (≥ 500 000 inhabitants) areas. We further subdivided women living in rural areas based on the social and occupational connectivity of their community to larger urban centres. We compared the prevalence of postpartum depression (score of ≥ 13 on the Edinburgh Postnatal Depression Scale) across these groups and adjusted for the effect of known risk factors for postpartum depression.

Results:

The prevalence of postpartum depression was higher among women living in urban areas than among those living in rural, semirural or semiurban areas. The difference between semiurban and urban areas could not be fully explained by other measured risk factors for postpartum depression (adjusted odds ratio 0.60, 95% confidence interval 0.42–0.84). In rural areas, there was a nonsignificant gradient of risk: women with less connection to larger urban centres were at greater risk of postpartum depression than women in areas with greater connection.

Interpretation:

There are systematic differences in the distribution of risk factors for postpartum depression across geographic areas, resulting in an increased risk of depression among women living in large urban areas. Prevention programs directed at modifiable risk factors (e.g., social support) could specifically target women living in these areas to reduce the rates of postpartum depression.Postpartum depression is an internationally recognized health concern for women and their families. Depression during the perinatal period is associated with serious negative consequences for both mother and baby, particularly if the depression is untreated.¹ Outcomes among women include impaired functioning, poor quality of life and death.² Outcomes for infants include developmental delay, poor growth, malnutrition and illness.^3–5 Numerous risk factors for postpartum depression have been identified; low levels of social support and history of depression are among the variables most consistently associated with postpartum depression.^6–8 However, previous reports are inconsistent as to whether geographical size or location is associated with the risk of postpartum depression.⁹ In Canada, about 30% of the population lives in rural or remote areas, a large proportion live in several large urban areas, and the remainder live in smaller urban settings.¹⁰ To design appropriate supports and services for the prevention and treatment of postpartum depression among Canadian women, it is important to identify and target geographical variation in the risk of postpartum depression.Our primary objective was to compare the risk of postpartum depression among Canadian women living in rural and urban areas. Our secondary objective was to identify factors that could explain any associations between place of residence and risk of postpartum depression. We used multiple definitions of rural and urban locations to more accurately reflect differences between communities and to account for the level of social and occupational connectivity of smaller areas to more urban areas.     

Association of postpartum depression with weight retention 1 year after childbirth

Objective: To examine the extent to which early postpartum depression is associated with weight retention 1 year after childbirth. Methods and Procedures: In a prospective cohort study of 850 women enrolled in Project Viva, mothers reported depressive symptoms on the Edinburgh Postnatal Depression Scale (EPDS) at midpregnancy and 6 months postpartum. A score >12 indicated probable depression. We assessed associations of antenatal and postpartum depression with risk of substantial weight retention (at least 5 kg) 1 year after childbirth. Results: Seven‐hundred thirty‐six women (87%) were not depressed during or after pregnancy, 55 (6%) experienced antenatal depression only, 22 (3%) experienced both antenatal and postpartum depression, and 37 (4%) experienced postpartum depression only. At 1 year, participants retained a mean of 0.6 kg (range ?16.4 to 25.5), and 12% retained at least 5 kg. In multivariate logistic regression analyses, after adjustment for weight‐related covariates, maternal sociodemographics, and parity, new‐onset postpartum depression was associated with more than a doubling of risk of retaining at least 5 kg (odds ratio (OR): 2.54, 95% confidence interval (CI): 1.06, 6.09). Antenatal depression, either alone or in combination with postpartum depression, was not associated with substantial weight retention. Discussion: New‐onset postpartum depression was associated with substantial weight retention in the first postpartum year. Interventions to manage depressive symptoms may help reduce excess weight retained postpartum and aid in the prevention of obesity among women.     

Association between endometritis and endometrial cytokine expression in postpartum Holstein cows

The endometrium regulates the inflammatory response after infection by production and release of cytokines and chemokines. The objective was to compare gene expression of important pro-inflammatory (TNFα, IL-1β, IL-6) and anti-inflammatory (IL-10) cytokines, and the main neutrophil chemokine (IL-8), from calving to Week 7 after calving, in cows that developed endometritis and healthy control cows. Uterine biopsies were obtained at calving and at Weeks 1, 3, 5 and 7. Endometritis was evaluated at Week 5 by uterine lavage and cytology; cows with ≥ 10% neutrophils were considered to have endometritis. Real-time RT-PCR threshold values (Ct) were used to calculate the fold difference in gene expression, using the 2^−ddCt method, normalized to GAPDH and calibrated to the average dCt for all cows at calving. Serum IL-8 concentrations were measured with ELISA. The analysis included 28 cows (11 had endometritis) for the PCR data and 44 cows (20 had endometritis) for ELISA. Expression of the TNFα gene in uterine tissue was decreased in cows with endometritis compared to control cows at calving (P = 0.09) and at Week 1 (P = 0.05). Iterleukin-1β gene expression tended to be decreased (P = 0.08) in cows with endometritis compared to control cows at Week 1, but tended to be increased (P ≤ 0.10) at Weeks 5 and 7. Cows with endometritis had increased (P < 0.05) IL-6 gene expression at calving and at Week 7 compared to control cows. Interleukin-8 gene expression was increased (P = 0.03) in endometritic cows compared to control cows at Week 7. Uterine disease was not significantly associated with IL-10 gene expression. A lower local level of expression of pro-inflammatory cytokines in the endometrium soon after calving might impair activation of inflammation and clearance of bacteria, and lead to development of endometritis.     

Association between depression and hospital outcomes among older men

Background:

Studies that have investigated the relation between depression and the type, nature, extent and outcome of general hospital admissions have been limited by their retrospective designs and focus on specific clinical populations. We explored this relation prospectively in a large, community-based sample of older men.

Methods:

A cohort of 5411 men aged 69 years and older enrolled in the Health in Men Study was assessed at baseline for depressive symptoms, defined as a score of 7 or higher on the 15-item Geriatric Depression Scale. Participants were followed for 2 years for occurrence and number of hospital admissions, type of hospital admission, length of hospital stay and inpatient death as recorded in the Western Australian Data Linkage System.

Results:

Of 339 men with depressive symptoms, 152 (44.8%) had at least 1 emergency hospital admission, compared with 1164 of 5072 (22.9%) nondepressed men (p < 0.001). In multivariate analyses, the presence of depressive symptoms was a significant independent predictor of hospital admission (hazard ratio 1.67, 95% confidence interval [CI] 1.38–2.01), number of hospital admissions (incidence rate ratio [IRR] 1.22, 95% CI 1.07–1.39) and total length of hospital stay (IRR 1.65, 95% CI 1.36–2.01).

Interpretation:

Participants with depressive symptoms were at higher risk of hospital admission for nonpsychiatric conditions and were more likely to have longer hospital stays and worse hospital outcomes, compared with nondepressed participants. These results highlight the potential to target this high-risk group to reduce the burden of health care costs in an aging population.Older people are the most frequent users of health services, and the progressive aging of the world’s population may lead to a saturation of available services. Therefore, we must find ways to reduce preventable admissions to hospital and uncover the factors associated with potentially preventable use of health services. An association between depression and hospital admission for nonpsychiatric conditions has been postulated, although the data have been limited to specific clinical populations and the interpretation of the results hampered by the retrospective study design and the use of self-reported outcomes.^1–8 Consequently, these findings cannot be easily generalized or used to develop data-driven interventions.We addressed this gap in the literature by using a community-based population survey with prospective data linkage to measure important health-related outcomes. Our main objective was to investigate whether community-dwelling older men with depressive symptoms were more likely than nondepressed men to be admitted to general hospitals. Our other aims were to determine whether the long-term clinical outcomes of these 2 groups differed in relation to the number of future hospital admissions, length of hospital stay and inpatient deaths.     

Association of tryptophan hydroxylase gene polymorphism with depression, anxiety and comorbid depression and anxiety in a population-based sample of postpartum Taiwanese women

Depression and anxiety disorders often coexist clinically and both are known to have a genetic basis, but the mode of inheritance is too complicated to be determined so far. Serotonin is the biogenic amine neurotransmitter most commonly associated with depression and anxiety. Since tryptophan hydroxylase (TPH1) is the rate-limiting enzyme in serotonin biosynthesis, its role in the pathophysiology of these psychiatric diseases has been intensively studied. In this study, we examined whether polymorphism of the TPH1 gene is related to the etiology of major depression, anxiety and comorbid depression and anxiety. Five single nucleoside polymorphisms of the TPH1 gene were studied in a population-based sample of postpartum Taiwanese women consisting of 120 subjects with depression or/and anxiety and 86 matched normal controls. A significant difference (P = 0.0107) in genotype frequency for the T27224C polymorphism was found between the comorbid and normal groups, and risk analysis showed that the C allele conferred a strong protective effect (odds ratio = 0.27; 95% confident interval = 0.11-0.7). Three-allele haplotypes involving T27224C polymorphism were constructed and haplotype associations between particular haplotype combinations and various diseases identified. However, the associations were weak and the overall haplotype frequency profiles in all groups were similar. The results suggest that depression, anxiety, and comorbid depression and anxiety disorders may have related etiologies. In addition, this study suggests that the TPH1 gene might play a role in the pathogenesis of these closely related disorders.     

Association between coronary endothelial dysfunction and local inflammation of atherosclerotic coronary arteries

We have examined a possibility whether or not severity and extent of coronary atherosclerosis may associate with degree of local inflammation in relation to endothelial dysfunction as is indicated by reduced NO formation. Blood samples were obtained from aortic root (Ao) and coronary sinus (CS) of 39 patients who underwent coronary angiography. Plasma NOx levels (nitrite + nitrate, stable NO end-products) were evaluated by HPLC-Griess system, and markers of inflammation, C-reactive protein (CRP) and serum amyloid A protein (SAA), were measured by Latex Turbidimetric Immunoassay. To evaluate the changes of these substances through coronary circulation, the percentage changes of respective markers [(CS – Ao) × 100/Ao] were calculated. The extent and severity of atherosclerosis of left coronary arteries were evaluated with Gensini Score (GS). The GS correlated with the percentage changes of NOx (r = –0.35, p < 0.05) and that of SAA (r = 0.43, p < 0.05) across coronary circulation, but not with changes in CRP. Moreover, the percentage changes of NOx correlated with that of SAA (r = –0.36, p < 0.05). These results indicated that severity and extent of coronary atherosclerosis related to degree of local inflammation which has a possible association with coronary endothelial dysfunction.     

Association between plasma metal elements and platelet dysfunction in trauma-induced coagulopathy rat model

BackgroundDisorders of metal elements and platelet dysfunction are common in patients with trauma-induced coagulopathy (TIC).AimThe aim of this study was to explore the potential role of plasma metal elements in platelet dysfunction in TIC.MethodsThirty Sprague-Dawley rats were divided into control, hemorrhage shock (HS) and multiple injury (MI) groups. At timepoints of 0.5 and 3 h after trauma and being documented as _{HS 0.5 h}, HS_3 h, _{MI 0.5 h} or MI_3 h, blood samples were harvested for inductively coupled plasma mass spectrometer, conventional coagulation function and thromboelastograph.ResultsThe plasma zinc (Zn), vanadium (V) and cadmium (Ca) decreased initially in HS _0.5 h and recovered slightly in HS_3 h, whereas their plasma concentrations continued to decrease from beginning till MI_3 h (p < 0.05). In HS, plasma Ca, V and nickel were negatively correlated to the time taken to reach the initial formation (R), whereas R was positively correlated to plasms Zn, V, Ca and selenium in MI (p < 0.05). In MI, plasma Ca was positively correlated to maximum amplitude, and plasma V was positively correlated to platelet count (p < 0.05).ConclusionThe plasma concentrations of Zn, V and Ca appeared to contribute to platelet dysfunction in _{HS 0.5 h}, HS_3 h, _{MI 0.5 h} and MI_3 h, which were trauma type sensitive.     

Association between airway hyperreactivity and bronchial macrophage dysfunction in individuals with mild asthma

Little is known about the functional capabilities of bronchial macrophages (BMs) and their relationship to airway disease such as asthma. We hypothesize that BMs from asthmatics may be modulated in their function compared with similar cells from healthy individuals. BMs obtained by induced sputum from mild asthmatics (n = 20) and healthy individuals (n = 20) were analyzed using flow cytometry for CD16, CD64, CD11b, CD14, and human leukocyte antigen-DR expression, phagocytosis of IgG opsonized yeast, and oxidant production. Asthma status was assessed by lung function [percent predicted forced vital capacity and forced expiratory volume in 1 s (FEV(1))], percent sputum eosinophils, and nonspecific airway responsiveness [provocative concentration that produces a 20% fall in FEV(1) (PC(20,FEV1))]. Asthmatics with >5% airway eosinophils (AEo+) had decreased BM CD64 expression and phagocytosis compared with asthmatics with <5% eosinophils (AEo-). Among asthmatics, a significant correlation was found between CD64 expression and BM phagocytosis (R = 0.7, P < 0.009). Phagocytosis was also correlated with PC(20,FEV1) (R = 0.6, P < 0.007), lung function (%predicted FEV(1), R = 0.7, P < 0.002) and percent eosinophils (R = -0.6, P < 0.01). In conclusion, BM from asthmatics are functionally modulated, possibly by Th2 cytokines involved in asthma pathology.     

Pigmentation and dysfunction of Gunn rat thyroid

The thyroid gland of homozygous Gunn rats is moderately enlarged and displays a brownish-black discoloration. Light microscopic examination discloses that the follicular cells are filled with brown granules, which are shown, under the electron microscope, to be modified colloid droplets. Most of them possess a strong acid phosphatase and a mild peroxidase activity and contain a melanin-like pigment, according to histochemical analysis. In comparison with normal Wistar rats, Gunn rats possess significantly higher plasma thyroxine and lower triiodothyronine as well as an increased plasma TSH level. The soluble protein content of the thyroid is reduced in the Gunn rat, as is the total intrathyroid iodine content. The hyperthyroxinaemia of homozygous Gunn rats is due to a hereditary deficiency in hepatic glucuronyl transferase activity. The excess circulating thyroxine is of little functional importance because it is firmly bound to plasma proteins. But Gunn rats have a slight hypothyroid goitre for reasons not yet elucidated. The functional as well as morphological data at present available suggest a modified thyroid iodine metabolism and an altered composition of the thyroglobulin which may induce abnormalities in colloid proteolysis. The observed pigment may result from peroxidation of tyrosine. These alterations are probably independent of the sole enzymatic deficiency so far encountered in these animals and may probably be ascribed to a primary enzymatic defect in the thyroid gland itself.