There is some evidence suggesting that childhood poverty may contribute to insulin resistance and advanced cell aging. Several studies have shown that children growing up in low-income households are at higher risk for developing insulin resistance, a condition in which the body’s cells become less responsive to insulin and blood sugar levels rise. Insulin resistance is a hallmark of type 2 diabetes, a chronic disease that is more prevalent among people living in poverty.
A study found that childhood poverty and adolescent beliefs about their future prospects were associated with accelerated immune cell aging and higher levels of insulin resistance in young adulthood. Researchers discovered that black adolescents who lived in poverty and were less optimistic about the future had accelerated aging in their immune cells and were more likely to have elevated insulin resistance at the age of 25-29.
The study’s first author, Allen W. Barton, a professor of human development and family studies at the University of Illinois Urbana-Champaign, followed the health of 342 African Americans from adolescence to their mid- to late-twenties for 20 years. The researchers’ goal was to explore links between the individuals’ childhood social environment and insulin resistance, a precursor to diabetes where cells don’t respond well to insulin or use blood glucose for energy.
The participants lived in rural Georgia, a region with one of the highest poverty rates and shortest life expectancies in the U.S.
Once we found some compelling evidence that childhood poverty was related to participants’ insulin resistance in their late 20s, we looked at immune cell aging as a possible mediator, something that transmits the effect.
Allen W. Barton
“Once we found some compelling evidence that childhood poverty was related to participants’ insulin resistance in their late 20s, we looked at immune cell aging as a possible mediator, something that transmits the effect,” Barton explained. “And we were able to find support for it. Immune cell aging was one mechanism by which poverty was linked to insulin resistance.”
The findings, published in the journal Child Development, support the hypothesis that chronic diseases such as diabetes and metabolic syndrome, which affect Black adults and low-income populations at significantly higher rates, may have their origins much earlier in life – even during childhood – and that such disadvantages can influence individuals’ cognition and physiology.
“Understanding these health disparities associated with race and socioeconomic status really requires a developmental perspective, but prospective research with these populations is scarce,” Barton said.
“In addition to focusing on contemporaneous stressors – such as their socioeconomic status in adulthood, where they currently live, and their access to health care – prospective studies like this that follow participants into adulthood are important to explore developmental pathways originating in childhood to see associations between individuals’ early social environment and their subsequent health outcomes as adults,” he said.
Recent research cited in the current study also indicates that Type 2 diabetes and other diseases are affecting certain populations – especially Blacks – at much younger ages. Data used in the new study were drawn from the Strong African American Families Healthy Adult Project, also called SHAPE, that enrolled 667 Black fifth-grade students and their caregivers. SHAPE began collecting data in 2001.
Young adults in the sample provided at least one blood sample at age 20 and again between the ages of 25-29. From these samples, researchers assessed participants’ biological age using DNA methylation and compared this age with their chronological age. Participants’ blood samples also were used to quantify their levels of insulin resistance at ages 25, 27, and 29.
Caregivers completed questionnaires about their family’s need-to-income ratios at six-time points, beginning when the children were 11 and continuing until the children were 18, which were used to calculate their poverty status and the number of years they lived below the federal poverty line.
The youths completed the Perceived Life Chances Scale three times between the ages of 16 and 18, a 10-item inventory that asked them whether they thought they would go to college or get a good-paying job, and how likely they thought that was.
In their initial analyses, the researchers found that living in poverty between ages 11-18 was associated with insulin resistance at ages 25-29. The longer participants lived in poverty during adolescence, the higher their risk of insulin resistance and diabetes in adulthood, the researchers found. This risk was calculated using a Homeostatic Model of Insulin Resistance, or HOMA, score. Each additional year of poverty was associated with a greater than one-point higher HOMA score.
When the children reached age 19-20, the researchers examined DNA methylation in a subset of participants. DNA methylation is a normal aging process that can affect gene function.
When the researchers took into account whether the teens believed they would be able to achieve their goals as adults, they discovered that more years spent in poverty were associated with fewer perceived life chances. According to Barton, the team discovered links between youths’ perceived life chances and premature immune cell aging at 20 years old, which was then linked to insulin resistance.
“We don’t know what happened to them prior to the age of 11, so maybe there were things put in place that we just can’t assess yet,” Barton said of the study’s limitations.
According to him, the researchers will continue to follow the sample individuals and investigate the role of resilience in participants’ health outcomes as they age. “It’s a huge data set that can start answering some important public health questions, shed light on some of these racial disparities, and help find ways to mitigate them,” Barton said.
