Women's Experiences of the Effect of Financial Strain on Parenting and Mental Health.

OBJECTIVE: To develop a conceptual theory to describe how financial strain affects women with young children to inform clinical care and research. DESIGN: Qualitative, grounded theory. SETTING: Participants were recruited from the waiting area of a pediatric clinic and an office of the Special Supplemental Nutrition Program for Women, Infants, and Children embedded within the largest safety-net academic medical center in New England. Participants were interviewed privately at the medical center or in the community. PARTICIPANTS: Twenty-six English-speaking women, mostly single and African American/Black, with at least one child 5 years old or younger, were sampled until thematic saturation was met. METHODS: We used grounded theory methodology to conduct in-depth, semistructured interviews with participants who indicated that they experienced financial strain. We analyzed the interview data using constant comparative analysis, revised the interview guide based on emerging themes, and developed a theoretical model. RESULTS: Five interrelated themes emerged and were developed into a theoretical model: Financial Strain Has Specific Characteristics and Common Triggers, Financial Strain Is Exacerbated by Inadequate Assistance and Results in Tradeoffs, Financial Strain Forces Parenting Modifications, Women Experience Self-Blame, and Women Experience Mental Health Effects. CONCLUSION: For women with young children, financial strain results in forced tradeoffs, compromised parenting practices, and self-blame, which contribute to significant mental health problems. These findings can inform woman-centered clinical practice and advocacy interventions. Women's health care providers should identify families experiencing financial strain, provide referrals to financial services, and join advocacy efforts to advance social policies that address the structural causes of poverty, such as increased minimum wage and paid family leave.

Association of Plasma Amylin Concentration With Alzheimer Disease and Brain Structure in Older Adults.

Importance: Preclinical studies suggest that amylin has a U-shaped dose-response association with risk of Alzheimer disease (AD). The association of plasma amylin with AD in humans is unknown. Objectives: To measure amylin concentration in plasma by using enzyme-linked immunosorbent assay and to study the association between plasma amylin, incidence of AD, and brain structure in humans. Design, Setting, and Participants: This cohort study used data from the Framingham Heart Study offspring cohort from 1998 to 2015. Using a Monte Carlo approach, participants were divided into 3 plasma amylin concentration groups: (1) low (<75 pmol/L), (2) high (75-2800 pmol/L), and (3) extremely high (≥2800 pmol/L). Data analyses were conducted October 5, 2017, to December 18, 2018. Exposures: Baseline plasma amylin concentrations at examination 7. Main Outcomes and Measures: Incidence of dementia or AD and brain volumetric measures from structural magnetic resonance imaging data. Results: From the Framingham Heart Study offspring cohort, 3061 participants (mean [SD] age at baseline, 61.0 [9.5] years; 1653 [54.0%] women) who had plasma amylin measurements, dementia incidence, and brain volume measurements on record were included in this study. The distribution of plasma amylin concentrations was highly skewed (median [interquartile range], 7.5 [4.6-18.9] pmol/L; mean [SD], 302.3 [1941.0] pmol/L; range, 0.03-44 623.7 pmol/L). Compared with the low plasma amylin concentration group, the high plasma amylin concentration group had a lower rate of AD incidence (2.3% vs 5.6%; P = .04), but the extremely high plasma amylin concentration group had a higher rate of AD incidence (14.3%; P < .001). After adjusting for age, sex, education, body mass index, diabetes, cardiovascular disease, high-density lipoprotein level, and APOE4, high plasma amylin was not associated with decreased AD risk (hazard ratio, 0.42 [95% CI, 0.16-1.14]; P = .09) but was positively associated with volume of gray matter in the temporal lobe (ß = 0.17 [SE, 0.05]; P < .001). In contrast, extremely high plasma amylin concentration was associated with a higher AD risk (hazard ratio, 2.51 [95% CI, 1.38-4.57]; P = .003) but not associated with temporal lobe volume (ß = 0.02 [SE, 0.07]; P = .82). Conclusions and Relevance: This study found that plasma amylin concentration was associated with AD incidence and brain structure with a U-shaped pattern. These findings are consistent with preclinical findings that suggest amylin is a neuropeptide that is physiological; however, at extremely high concentrations, it may lead to amylin aggregation and therefore may be a risk factor for AD.