Death of a child and parents' later dementia risk

Does the Death of a Child Prior to Midlife Increase Later Dementia Risk for Parents? is This Disadvantage Greater for Black Parents Than for White Parents?

Debra Umberson, Rachel Donnelly, Minle Xu, Mateo Farina, and Michael A. Garcia

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Introduction

Dementia is a growing public health concern in the United States. Like other health outcomes in the U.S., the burdens of dementia are borne more heavily by black Americans than by white Americans. Indeed, the prevalence of dementia is two times higher for black than for white Americans, and dementia emerges at substantially younger ages among black Americans.

Growing evidence points to stress as a contributor to dementia risk, and one of the most stressful events one can experience is the death of a child. Compared to white Americans, black Americans have higher rates of premature death at every age. This means that black parents are much more likely to experience the death of a child, and to experience this loss at an earlier age compared with white parents.

The death of a child could trigger biological, psychological, social, and behavioral mechanisms that are associated with increased risk for dementia, but this possibility has not been previously explored. For example, bereavement is associated with increased risk for depression, sleep disorders, substance abuse, and cardiovascular risk—all factors known to influence dementia risk. Moreover, if the death of a child occurs prior to midlife (by age 40), there may be many years after which these mechanisms of risk are activated, thereby increasing the risk of dementia in later life.

This brief reports on a study that uses Health and Retirement Study (HRS) data to explore the impact of the death of a child prior to midlife on later dementia risk for parents, to ask whether biosocial processes might explain increased dementia risk, and to consider how the loss of a child might add to disadvantage in dementia risk for non-Hispanic black parents compared to non-Hispanic white parents.

Key Findings

• The death of a child prior to midlife is a traumatic life course stressor with consequences that appear to increase dementia risk for both black and white parents. See Figure, next page.
• This increased dementia risk is explained by biosocial processes—such as health damaging behaviors (smoking, drinking), depression, and poor physical health—likely activated by bereavement.
• Black parents are disadvantaged in that they are more likely than white parents to experience the death of a child and because such losses add to the already substantial racial disadvantage in dementia risk.

Parents who lose a child by age 40 are more likely to develop dementia than parents who do not lose a child by that age

This figure [1] shows that parents who lose a child prior to midlife are more likely to develop dementia compared to parents who do not lose a child. Moreover, black parents are almost three times more likely than white parents to develop dementia over the study period. That is, black parents who are bereaved by age 40 have a 3.6% probability of developing dementia, whereas white parents who are bereaved by age 40 have a 1.3% probability of developing dementia.

Policy Implications

Dementia is associated with increased demands for medical and personal care as well as premature death. These burdens are borne more heavily by black than white families. Moreover, given that the death of a child occurring prior to midlife contributes to later life dementia, policymakers are urged to shift their thinking about dementia as a public health problem of old age to a public health problem that has its origins earlier in the life course. Policymakers should also consider racial disadvantage wherein black parents are more likely to experience the death of a child and such losses add to the already substantial racial disadvantage in dementia risk.

It is therefore important to target parents who have lost a child for early intervention strategies to reduce long-term health risk, perhaps by focusing on the specific biosocial factors most strongly triggered by loss and known to increase dementia risk, such as depression, heart disease, stroke, diabetes, and hypertension.

Attention to specific life course turning points associated with later life dementia may provide the impetus to dedicate resources to specific and modifiable risk and protective factors for dementia earlier in the life course. This approach should recognize that effective interventions must also address the greater barriers to screening and treatment that black Americans face. Finally, although more challenging to address, premature mortality of Americans, especially black Americans, is at the heart of the matter and is in dire need of immediate remedies.

Reference

[1] Umberson, D., Donnelly, R., Xu, M., Farina, M & Garcia, M.A. (2019). Death of a child prior to midlife, dementia risk, and racial disparities. Journal of Gerontology: Social Sciences. Published online ahead of print.

Suggested Citation

Umberson, D., Donnelly, R., Xu, M., Farina, M & Garcia, M.A. (2019). Does the death of a child prior to midlife increase later dementia risk? Is this disadvantage greater for black parents than for white parents? PRC Research Brief 4(11). DOI: 10.26153/tsw/5800.

About the Authors

Debra Umberson (umberson@prc.utexas.edu) is a professor of sociology; Christine and Stanley E. Adams, Jr. Centennial Professorship in Liberal Arts; and director of the Population Research Center, The University of Texas at Austin; Rachel Donnelly is an assistant professor of sociology at Vanderbilt University and former graduate student trainee in the PRC; Minle Xu was a postdoctoral fellow at the PRC at the time the reference paper was written; and Mateo Farina and Michael A. Garcia are PhD students in sociology and graduate student trainees in the PRC. 

Acknowledgements

This work was supported by the National Institutes of Health (R01AG054624 and R01 AG054624- 01A1S); and Eunice Kennedy Shriver National Institute of Child Health and Human Development (P2C HD042849 and T32 HD00708). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.