Associations between child marriage and food insecurity in Zimbabwe: a participatory mixed methods study.

BACKGROUND: Child marriage is a global crisis underpinned by gender inequality and discrimination against girls. A small evidence base suggests that food insecurity crises can be both a driver and a consequence of child marriage. However, these linkages are still ambiguous. This paper aims to understand how food insecurity influences child marriage practices in Chiredzi, Zimbabwe. METHODS: Mixed methods, including participant-led storytelling via SenseMaker® and key informant interviews, were employed to examine the relationship between food insecurity and child marriage within a broader context of gender and socio-economic inequality. We explored the extent to which food insecurity elevates adolescent girls' risk of child marriage; and how food insecurity influences child marriage decision-making among caregivers and adolescents. Key patterns that were generated by SenseMaker participants' interpretations of their own stories were visually identified in the meta-data, and then further analyzed. Semi-structured guides were used to facilitate key informant interviews. Interviews were audio-recorded, and transcribed and translated to English, then imported into NVivo for coding and thematic analysis. RESULTS: A total of 1,668 community members participated in SenseMaker data collection, while 22 staff participated in interviews. Overall, we found that food insecurity was a primary concern among community members. Food insecurity was found to be among the contextual factors of deprivation that influenced parents' and adolescent girls' decision making around child marriage. Parents often forced their daughters into marriage to relieve the household economic burden. At the same time, adolescents are initiating their own marriages due to limited alternative survival opportunities and within the restraints imposed by food insecurity, poverty, abuse in the home, and parental migration. COVID-19 and climate hazards exacerbated food insecurity and child marriage, while education may act as a modifier that reduces girls' risk of marriage. CONCLUSIONS: Our exploration of the associations between food insecurity and child marriage suggest that child marriage programming in humanitarian settings should be community-led and gender transformative to address the gender inequality that underpins child marriage and address the needs and priorities of adolescent girls. Further, programming must be responsive to the diverse risks and realities that adolescents face to address the intersecting levels of deprivation and elevate the capacities of adolescent girls, their families, and communities to prevent child marriage in food insecure settings.

Tolerogenic signaling by pulmonary CD1c+ dendritic cells induces regulatory T cells in patients with chronic obstructive pulmonary disease by IL-27/IL-10/inducible costimulator ligand.

BACKGROUND: Increased mortality rates in patients with chronic obstructive pulmonary disease (COPD) are largely due to severe infectious exacerbations. Impaired respiratory immunity is linked to the enhanced susceptibility to infections. Dendritic cells (DCs) direct host immune responses toward immunity or tolerance. Pulmonary CD1c(+) DCs elicit robust antiviral immune responses in healthy subjects. Nevertheless, their functional specialization in patients with COPD remains unexplored. OBJECTIVE: We sought to better understand the mechanisms that suppress respiratory immunity in patients with COPD by examining the immunostimulatory and tolerogenic properties of pulmonary CD1c(+) DCs. METHODS: We analyzed the expression of costimulatory and tolerogenic molecules by pulmonary CD1c(+) DCs from patients with COPD (CD1c(+)DCCOPD) and former smokers without COPD. We isolated lung CD1c(+) DCs and determined their ability to stimulate allogeneic T-cell responses. The suppressive effects of lung CD1c(+) DCs and CD1c(+) DC-primed T cells on mixed leukocyte reactions were examined. An experimental human model of COPD exacerbation was used to investigate the levels of critical immunosuppressive molecules in vivo. RESULTS: CD1c(+) DCs from patients with COPD hinder T-cell effector functions and favor the generation of suppressive IL-10-secreting CD4(+) T cells that function through IL-10 and TGF-ß. IL-27, IL-10, and inducible T-cell costimulator ligand signaling are essential for CD1c(+)DCCOPD-mediated differentiation of IL-10-producing suppressive T cells. Exposure of lung CD1c(+) DCs from nonobstructed subjects to lungs of patients with COPD confers tolerogenic properties. IL-27 and IL-10 levels are increased in the lung microenvironment on rhinovirus-induced COPD exacerbation in vivo. CONCLUSION: We identify a novel tolerogenic circuit encompassing suppressive CD1c(+) DCs and regulatory T cells in patients with COPD that might be implicated in impaired respiratory immunity and further highlight IL-10 and IL-27 as potent therapeutic targets.

Smoking cessation increases serum adiponectin levels in an apparently healthy Greek population.

BACKGROUND: Smoking has been associated with low serum levels of adiponectin, an adipocytokine with insulin-sensitizing, anti-inflammatory and anti-atherogenic properties. The objective of this study was to assess the early effect on adiponectin levels of smoking cessation supported by bupropion. METHODS: Apparently healthy smokers of both sexes with no additional cardiovascular risk factors were administered 150mg sustained-release bupropion twice daily for 9 weeks. Quitters constituted the active group and non-quitters the control group. Sandwich enzyme-linked immunosorbent assays were employed for the measurement of serum adiponectin and cotinine, the latter used for validation of self-reported abstinence. RESULTS: Among the 106 participants (mean age 44.5+/-11.3 years, 57 females, Brinkman index 512.2+/-98.4, basal adiponectin 7.2+/-1.5mg/L), 45 (42.5%) had quitted smoking at week 9. Quitters' post-cessation adiponectin levels were significantly increased (mean difference with baseline 1.9+/-0.8mg/L, 95% CI 1.2, 2.3; p<0.001), while non-quitters' adiponectin remained unaltered. A multiple regression model including female gender (standardized beta coefficient=0.480, p=0.002), age (0.355, p=0.003), body mass index (BMI) (-0.308, p=0.005), waist circumference (-0.276, p=0.008), smoking status (-0.255, p=0.010), and cotinine levels (-0.233, p=0.021) explained about two thirds of the variation in adiponectin levels (adjusted R(2)=0.656). CONCLUSIONS: Serum adiponectin levels appear to increase considerably within 2 months after smoking cessation. This finding may provide further insight into the mechanisms related to the detrimental effects of smoking and the benefits of quitting.

Low circulating adiponectin and resistin, but not leptin, levels are associated with multiple myeloma risk: a case-control study.

Accumulating evidence supports a role for obesity in the etiology of multiple myeloma (MM). The distinct possibility exists that obesity may be linked to MM through altered adipokine secretion and circulating levels, one of which, adiponectin, has a protective role in several malignancies, including leukemia. In this case-control study, we investigated the role of serum adiponectin, resistin, and leptin levels in the etiopathogenesis of MM and we explored their association with several established prognostic factors. Seventy three patients with incident, histologically confirmed MM and 73 controls matched on gender and age were studied between 2001 and 2007, and blood samples were collected. Serum adiponectin, leptin, resistin, as well as MM prognostic parameters were determined. Statistical analysis of the data was performed using univariate and multivariate analyses. Lower serum adiponectin and resistin levels were associated with higher risk of MM by bivariate analysis and after adjusting for age, gender, BMI, and serum levels of leptin (p < 0.0001). Adiponectin may have a protective role in MM, whereas leptin was not associated with risk for MM at a comparable level of significance and resistin levels may be decreased via a compensatory mechanism. Further studies are needed to confirm these associations and to explore the mechanisms underlying adiponectin's role in MM and plasma cell dyscrasias.