A national profile of kinlessness at the end of life among older adults: Findings from the Health and Retirement Study.

BACKGROUND/OBJECTIVES: The majority of end-of-life (EOL) caregiving is provided by unpaid family members. An increasing number of older adults are kinless (without close family/partnerships) and may have insufficient caregiver support to remain at home at the EOL. We therefore determined what proportion of older adults are kinless at the EOL and assessed the association of kinlessness with EOL care. DESIGN: Retrospective analysis of Health and Retirement Study decedents, 2002-2015. SETTING: US population-based sample. PARTICIPANTS: Decedents age 51+ who died within 1 year of interview (n = 3844) and subset who are community-dwelling at last interview. MEASUREMENTS: Kinlessness was defined as lacking a spouse/partner and children. Primary outcome measure was location of death. Secondary outcome measures included contextual EOL measures such as symptom burden and caregiver support. RESULTS: A total of 7.4% of decedents were kinless at the EOL. Kinless decedents were more likely to be female, nonwhite, enrolled in Medicaid, living alone, or living in a nursing home prior to death. Although community-dwelling kinless decedents received fewer hours of caregiving per week at the EOL (34.7 vs. 56.2, p < 0.05) and were more likely to die in nursing homes (18.1% vs. 10.3%, p < 0.05) than those with kin, they did not have higher EOL symptom burden or treatment intensity (e.g., intensive care unit use). In multinomial logistic analysis controlling for demographic and illness characteristics, kinless decedents living in the community before death had a twofold increased risk of dying in the nursing home (odds ratio [OR] = 2.02 [95% confidence interval (CI) = 1.09-3.72]) and a trend toward increased risk of hospital death (OR = 1.60 [95% CI = 0.96-2.69]) versus home setting. CONCLUSIONS: Kinless individuals are more likely to die in nursing homes, even if they are living in the community in their last year of life. Expanded long-term care services and policies are needed to enable all older adults regardless of their family support systems to receive high-quality EOL care.

Impact of Coffee and Cacao Purine Metabolites on Neuroplasticity and Neurodegenerative Disease.

Increasing evidence suggests that regular consumption of coffee, tea and dark chocolate (cacao) can promote brain health and may reduce the risk of age-related neurodegenerative disorders. However, the complex array of phytochemicals in coffee and cacao beans and tea leaves has hindered a clear understanding of the component(s) that affect neuronal plasticity and resilience. One class of phytochemicals present in relatively high amounts in coffee, tea and cacao are methylxanthines. Among such methylxanthines, caffeine has been the most widely studied and has clear effects on neuronal network activity, promotes sustained cognitive performance and can protect neurons against dysfunction and death in animal models of stroke, Alzheimer's disease and Parkinson's disease. Caffeine's mechanism of action relies on antagonism of various subclasses of adenosine receptors. Downstream xanthine metabolites, such as theobromine and theophylline, may also contribute to the beneficial effects of coffee, tea and cacao on brain health.

Dioxin Exposure Alters Molecular and Morphological Responses to Thyroid Hormone in Xenopus laevis Cultured Cells and Prometamorphic Tadpoles.

Amphibian metamorphosis is driven by thyroid hormone (TH). We used prometamorphic tadpoles and a cell line of the African clawed frog (Xenopus laevis) to examine immediate effects of dioxin exposure on TH. Gene expression patterns suggest cross-talk between the thyroid hormone receptor (TR) and aryl hydrocarbon receptor (AHR) signaling pathways. In XLK-WG cells, expression of Cytochrome P450 1A6 (cyp1A6), an AHR target, was induced 1000-fold by 100 nM TCDD (2, 3, 7, 8 tetrachlorodibenzo-p-dioxin). Krüppel-Like Factor 9 (klf9), the first gene induced in a cascade of TH responses tied to metamorphosis, was upregulated over 5-fold by 50 nM triiodothyronine (T3) and 2-fold by dioxin. Co-exposure to T3 and TCDD boosted both responses, further inducing cyp1A6 by 75% and klf9 about 60%. Additional canonical targets of each receptor, including trßa and trßb (TR) and udpgt1a (AHR) responded similarly. Induction of TH targets by TCDD in XLK-WG cells predicts that exposure could speed metamorphosis. We tested this hypothesis in two remodeling events: tail resorption and hind limb growth. Resorption of ex vivo cultured tails was accelerated by 10 nM T3, while a modest increase in resorption by 100 nM TCDD lacked statistical significance. Hind limbs doubled in length over four days following 1 nM T3 treatment, but limb length was unaffected by 100 nM TCDD. TCDD co-exposure reduced the T3 effect by nearly 40%, despite TCDD induction of klf9 in whole tadpoles, alone or with T3. These results suggest that tissue-specific TCDD effects limit or reverse the increased metamorphosis rate predicted by klf9 induction.