Background and Objectives Marital dissolution has become more common in midlife with the doubling of the divorce rate among middle-aged adults. Guided by the stress model that stipulates losing economic, social, and psychological resources lowers well-being, we posited that midlife adults who experienced divorce or widowhood were at greater risk of cognitive impairment than the continuously married. Subsequent repartnering was expected to negate the increased risk. Research Design and Methods We used data from the 1998-2016 Health and Retirement Study to estimate discrete-time event history models using logistic regression to predict cognitive impairment onset for men and women. Results Roughly 27% of men who experienced spousal death in midlife went on to experience mild cognitive impairment by age 65. For women, experiencing divorce or widowhood was associated with higher odds of cognitive impairment onset although these differentials were accounted for by economic, social, and psychological resources. Men and women who repartnered after marital dissolution did not appreciably differ from their continuously married counterparts in terms of their likelihoods of cognitive impairment onset. Discussion and Implications A stressful life event, midlife marital dissolution can be detrimental to cognitive well-being, placing individuals at increased risk of developing dementia in later life. The growing diversity of partnership experiences during the second half of life points to the continued importance of examining how union dissolution and formation shape health and well-being.
Objective Divorce is now widespread in later life, yet little is known about how older adults and their adult children respond in the aftermath of gray divorce. Guided by the life course perspective, this study examines the consequences of gray divorce and subsequent repartnering for parent-adult child relationships from the parent’s perspective. Method Using longitudinal data from the 1998-2014 Health and Retirement Study in the United States, we estimated growth curve models to compare fathers’ and mothers’ frequent contact with and financial support to their adult children prior to, during, and following gray divorce. Results Gray divorce and repartnering had disparate effects on father- versus mother-adult child relationships. Following divorce, fathers’ frequent contact with their adult children decreased but financial support to their adult children increased. Fathers’ repartnering had an enduring negative effect on frequent contact with their children. Gray divorce did not alter mothers’ financial support to adult children and it actually increased interaction between mothers and adult children as the odds of frequent contact doubled upon divorce. Repartnering had no appreciable effects on mothers’ relationships with their adult children. Discussion The results of our study are consistent with prior research showing that divorce creates a matrifocal tilt in our kinship system. The shifting dynamics of parent-adult child relationships in response to gray divorce and repartnering raise questions about whether gray divorced parents will be able to rely on their adult children for care as they age.
The gray divorce rate, which describes divorce among individuals aged 50 and older, has doubled since 1990. Extending prior research that showed the transition to parenthood has a “braking effect” on divorce, we examined whether the transition to grandparenthood, an emotionally meaningful midlife event that typically renews midlife marriages, exerts an analogous “braking effect” on gray divorce. Using panel data from the 1998–2014 Health and Retirement Study, we found that becoming biological grandparents has a large deterrent effect on gray divorce that persists even after accounting for a host of other factors known to be associated with divorce. However, the transition to step grandparenthood has no protective effect on gray divorce. Our study demonstrates the importance of the larger family system and in particular the life webs connecting the generations for promoting marital stability among midlife couples.
Objectives We introduced a unique form of kinlessness: sole family survivorship, which describes the lack of family of origin (i.e., biological parents and siblings) kin. This form of kinlessness may be particularly consequential for older adults who experience other forms of kinlessness (e.g., no spouse/partner or no children) as they are especially likely to have relied on their family of origin for support. Methods Data from the 1998-2014 Health and Retirement Study (N = 148,346 person-waves) were used to estimate the prevalence of sole family survivorship among adults aged 55 and older and men and women aged 55-74 and 75+. Variation in prevalence levels of sole family survivorship across sociodemographic characteristics, health indicators, and family factors were also estimated. Finally, we tracked cohort trends in sole family survivorship. Results More than 1 in 10 adults aged 55+ were sole family survivors and this figure rose to more than 1 in 4 among those aged 75+. Adults with no spouse/partner and no children were especially likely to be sole family survivors, meaning they face a double burden of kinlessness. Discussion Sole family survivorship represents the culmination of loss of multiple, lifelong kin ties. It is more common among those lacking other close kin, signaling the presence of a uniquely vulnerable group of older adults who experience multiple forms of kinlessness. Future research should address how older adults and society at large adapt to kinlessness to ensure successful aging.
IntroductionCerebral malaria is one of the most severe manifestations of malaria and is a leading cause of acquired neurodisability in African children. Recent studies suggest acute kidney injury (AKI) is a risk factor for brain injury in cerebral malaria. The present study evaluates potential mechanisms of brain injury in cerebral malaria by evaluating changes in cerebrospinal fluid measures of brain injury with respect to severe malaria complications. Specifically, we attempt to delineate mechanisms of injury focusing on blood-brain-barrier integrity and acute metabolic changes that may underlie kidney-brain crosstalk in severe malaria.MethodsWe evaluated 30 cerebrospinal fluid (CSF) markers of inflammation, oxidative stress, and brain injury in 168 Ugandan children aged 18 months to 12 years hospitalized with cerebral malaria. Eligible children were infected with Plasmodium falciparum and had unexplained coma. Acute kidney injury (AKI) on admission was defined using the Kidney Disease: Improving Global Outcomes criteria. We further evaluated blood-brain-barrier integrity and malaria retinopathy, and electrolyte and metabolic complications in serum.ResultsThe mean age of children was 3.8 years (SD, 1.9) and 40.5% were female. The prevalence of AKI was 46.3% and multi-organ dysfunction was common with 76.2% of children having at least one organ system affected in addition to coma. AKI and elevated blood urea nitrogen, but not other measures of disease severity (severe coma, seizures, jaundice, acidosis), were associated with increases in CSF markers of impaired blood-brain-barrier function, neuronal injury (neuron-specific enolase, tau), excitatory neurotransmission (kynurenine), as well as altered nitric oxide bioavailability and oxidative stress (p < 0.05 after adjustment for multiple testing). Further evaluation of potential mechanisms suggested that AKI may mediate or be associated with CSF changes through blood-brain-barrier disruption (p = 0.0014), ischemic injury seen by indirect ophthalmoscopy (p < 0.05), altered osmolality (p = 0.0006) and through alterations in the amino acids transported into the brain.ConclusionIn children with cerebral malaria, there is evidence of kidney-brain injury with multiple potential pathways identified. These changes were specific to the kidney and not observed in the context of other clinical complications.
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