Inequities in access to directly-funded home care in Canada: a privilege only afforded to some.

BACKGROUND: Directly-funded home care (DF) provides government funds to people who need assistance with the activities of daily living, allowing them to arrange their own services. As programs expand globally, many allow DF clients to hire home care agencies to organize their services rather than finding their own workers. In Canada, half of the DF home care programs allow users to purchase agency services. The goal of this research is to describe the role of agency providers in DF home care in Canada and consider potential equity implications for service access from the perspectives of clients and families. METHODS: Framed with intersectionality, the study included online focus groups with families and clients (n = 56) in the two Canadian provinces of Alberta and Manitoba between June 2021-April 2022. All transcripts underwent qualitative thematic analysis using open and axial coding techniques. Each transcript was analyzed by two of three possible independent coders using Dedoose qualitative analysis software. RESULTS: The article presents five thematic findings. First, the focus groups document high rates of satisfaction with the care regardless of whether the client uses agency providers. Second, agency providers mediate some of the administrative barriers and emotional strain of using DF home care, and this is especially important for family caregivers who are working or have additional care responsibilities. Third, there are out-of-pocket expenses reported by most participants, with agency clients describing administrative fees despite lower pay for the frontline care workers. Fourth, agencies are not generally effective for linguistic and/or cultural matching between workers and families. Finally, we find that DF care programs cannot compensate for a limited informal support network. CONCLUSIONS: Clients and families often intentionally choose DF home care after negative experiences with other public service options, yet the results suggest that in some Canadian contexts, DF home care is a privilege only afforded to some. Given the growing inequalities that exist in Canadian society, all public home care options must be open to all who need it, irrespective of ability to pay, degree of social support, or competence in the English language.

Intersectionality, health equity, and EDI: What's the difference for health researchers?

Many countries adopted comprehensive national initiatives to promote equity in higher education with the goal of transforming the culture of research. Major health research funders are supporting this work through calls for projects that focus on equity, resulting in a proliferation of theoretical frameworks including "intersectionality," "health equity," and variations of equity, diversity and inclusion, or EDI. This commentary is geared at individual principal investigators and health research teams who are developing research proposals and want to consider equity issues in their research, perhaps for the first time. We present histories and definitions of three commonly used frameworks: intersectionality, health equity, and EDI. In the context of health research, intersectionality is a methodology (a combination of epistemology and techniques) that can identify the relationships among individual identities and systems of oppression; however, it should also be used internally by research teams to reflect on the production of knowledge. Health equity is a societal goal that operationalizes the social determinants of health to document and address health disparities at the population level. EDI initiatives measure and track progress within organizations or teams and are best suited to inform the infrastructure and human resourcing "behind the scenes" of a project. We encourage researchers to consider these definitions and strive to tangibly move health research towards equity both in the topics we study and in the ways we do research.

Suppression of estrogen receptor beta classical genomic activity enhances systemic and adipose-specific response to chronic beta-3 adrenergic receptor (ß3AR) stimulation.

White adipose tissue (WAT) dysfunction independently predicts cardiometabolic disease, yet there is a lack of effective adipocyte-targeting therapeutics. B3AR agonists enhance adipocyte mitochondrial function and hold potential in this regard. Based on enhanced sensitivity to B3AR-mediated browning in estrogen receptor (ER)alpha-null mice, we hypothesized that ERß may enhance the WAT response to the B3AR ligand, CL316,243 (CL). Methods: Male and female wild-type (WT) and ERß DNA binding domain knock-out (ERßDBDKO) mice fed high-fat diet (HFD) to induce obesity were administered CL (1 mg/kg) daily for 2 weeks. Systemic physiological assessments of body composition (EchoMRI), bioenergetics (metabolic chambers), adipocyte mitochondrial respiration (oroboros) and glucose tolerance were performed, alongside perigonadal (PGAT), subcutaneous (SQAT) and brown adipose tissue (BAT) protein expression assessment (Western blot). Mechanisms were tested in vitro using primary adipocytes isolated from WT mice, and from Esr2-floxed mice in which ERß was knocked down. Statistical analyses were performed using 2 × 2 analysis of variance (ANOVA) for main effects of genotype (G) and treatment (T), as well as GxT interactions; t-tests were used to determine differences between in vitro treatment conditions (SPSS V24). Results: There were no genotype differences in HFD-induced obesity or systemic rescue effects of CL, yet ERßDBDKO females were more sensitive to CL-induced increases in energy expenditure and WAT UCP1 induction (GxT, p < 0.05), which coincided with greater WAT B3AR protein content among the KO (G, p < 0.05). Among males, who were more insulin resistant to begin with (no genotype differences before treatment), tended to be more sensitive to CL-mediated reduction in insulin resistance. With sexes combined, basal WAT mitochondrial respiration trended toward being lower in the ERßDBDKO mice, but this was completely rescued by CL (p < 0.05). Confirming prior work, CL increased adipose tissue ERß protein (T, p < 0.05, all), an effect that was enhanced in WAT and BAT the female KO (GxT, p < 0.01). In vitro experiments indicated that an inhibitor of ERß genomic function (PHTPP) synergized with CL to further increase UCP1 mRNA (p = 0.043), whereas full ERß protein was required for UCP1 expression (p = 0.042). Conclusion: Full ERß activity appears requisite and stimulatory for UCP1 expression via a mechanism involving non-classical ERß signaling. This novel discovery about the role of ERß in adipocyte metabolism may have important clinical applications.

White Adipose Tissue Depots Respond to Chronic Beta-3 Adrenergic Receptor Activation in a Sexually Dimorphic and Depot Divergent Manner.

Beta-3 adrenergic receptor activation via exercise or CL316,243 (CL) induces white adipose tissue (WAT) browning, improves glucose tolerance, and reduces visceral adiposity. Our aim was to determine if sex or adipose tissue depot differences exist in response to CL. Daily CL injections were administered to diet-induced obese male and female mice for two weeks, creating four groups: male control, male CL, female control, and female CL. These groups were compared to determine the main and interaction effects of sex (S), CL treatment (T), and WAT depot (D). Glucose tolerance, body composition, and energy intake and expenditure were assessed, along with perigonadal (PGAT) and subcutaneous (SQAT) WAT gene and protein expression. CL consistently improved glucose tolerance and body composition. Female PGAT had greater protein expression of the mitochondrial uncoupling protein 1 (UCP1), while SQAT (S, p < 0.001) was more responsive to CL in increasing UCP1 (S×T, p = 0.011) and the mitochondrial biogenesis induction protein, PPARγ coactivator 1α (PGC1α) (S×T, p = 0.026). Females also displayed greater mitochondrial OXPHOS (S, p < 0.05) and adiponectin protein content (S, p < 0.05). On the other hand, male SQAT was more responsive to CL in increasing protein levels of PGC1α (S×T, p = 0.046) and adiponectin (S, p < 0.05). In both depots and in both sexes, CL significantly increased estrogen receptor beta (ERß) and glucose-related protein 75 (GRP75) protein content (T, p < 0.05). Thus, CL improves systemic and adipose tissue-specific metabolism in both sexes; however, sex differences exist in the WAT-specific effects of CL. Furthermore, across sexes and depots, CL affects estrogen signaling by upregulating ERß.