This paper, co-authored with Reed T. DeAngelis and published in the journal Population Research and Policy Review, analyzed data from a community sample from Davidson County, Tennessee. The main purpose of this paper was to examine the relationship between parenting and two types of biological functioning: telomere length and allostatic load. Allostatic load represents an index of biomarkers that has been shown to respond to the physiological wear and tear resulting from exposure to stress. Higher levels of stress cause higher levels of allostatic load. Telomeres are considered to be biological indicators of cellular aging that reduce in length over the life course as a natural function of recurring cell division. Exposure to stress and adversity has been shown to accelerate the shortening of telomeres which, in turn, increases the risk of illness and premature death. Gaining a better understanding of these two biological processes has been a growing interest among health researchers because each have been shown to predict future health problems and each can be evaluated to assess who may be at risk for illness prior to the onset of physical health symptoms.

Research on physical burdens of parenting is limited. Most has focused on mental health outcomes or on the caregiving demands of parenting children with special needs. Thus, it is not well known if parenting increases health risks in general populations. There are at least two reasons for this. First, active parenting usually occurs at a stage in the life course that precedes the onset of easily detectable chronic illnesses. Second, until recently population researchers have lacked access to biological data subtle enough to detect the biological processes that precede illness.

We analyzed survey and biomarker data from Vanderbilt University’s Nashville Stress and Health Study to see if parenting was related to telomere length and allostatic load. We compared study participants who were not parents to empty nesters and to parents with children living at home. We statistically controlled for a number of other risk factors including age, race, gender, and socioeconomic status.

The average respondent was 44 years old and had one child living at home. Twenty-four percent of respondents were empty-nest parents and thirty percent were childless. Our analyses showed that physical dysregulation increased with the number of children living at home. In general, we found that each additional child living at home at the time of the interview increased allostatic load and decreased telomere length. Importantly, we were able to identify biological dysregulation of parents in a study population that is generally younger than those who experience the onset of physical symptomatology (i.e., working-age adults).

Our study should not be interpreted as suggesting the solution to the health risks of parenting is to avoid having children altogether. Rather, we believe the current findings signal a need for an increased attentiveness to the health risks of childrearing, particularly for parents with multiple children in the home. We hope the information provided here can inform parents and their healthcare providers of the potential health risks associated with parenting. Still, we hasten to add that more scholarly work is needed to determine (a) the social and biological mechanisms by which childrearing affects parental biological functioning, and (b) whether or to what extent parents can leverage certain resources to buffer the stressors of raising children. Indeed, although we believe the present paper expands our understanding of parenting and health, there remain several important unanswered questions that we could not address in our brief report. For example, we did not assess whether marital status, SES, race, gender, or other psychosocial resources condition the relationship between parenting and biological functioning.

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