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PACEs in Pediatrics

ACEs, biomarkers and the cost of adversity

 

How useful and necessary are biomarkers in telling the story of how toxic stress from adverse childhood experiences and resilience can impact a child’s long-term health? In the introduction to an article in the journal BioEssays, Dr. Kathryn Ridout, a Kaiser Permanente San Jose psychiatrist, and her co-authors examine what is known about two biomarkers and quote data on child maltreatment and its economic burden over time that says it all.  

 “When totaling the costs of health care, child welfare services, criminal justice involvement and productivity losses over the lifespan, the lifetime economic burden of childhood adversity exceeds $124 billion annually,” according to the article “Adverse Childhood Experiences Run Deep: Toxic Early Life Stress, Telomeres and Mitochondrial DNA Copy Number, the Biological Markers of Cumulative Stress,” published in August.

Every year in the United States, about 700,000 children are determined by state agencies to be victims of maltreatment, the article notes. But that’s just the tip of the iceberg. Based on the 2016 National Survey of Children’s Health, note Ridout and her colleagues, an estimated 15 million children have experienced 2 or more ACEs in their lifetime. And they note that children with higher ACE scores typically seek more medical care as adults, have higher unemployment, lower earning capacity and less schooling than their peers with no ACEs. Left without supports, some might pass their own ACEs on to their children.

These data are the backdrop for looking at what the scientific literature demonstrates about how well two different biomarkers measure toxic stress in children. The article also looks at the next steps needed to use biomarkers to pinpoint the impact of toxic stress on young children.

Telomeres are DNA molecules at the end of chromosomes that shorten in length with aging. Toxic stress that constantly triggers the brain and body to go into a “flight and flight” response, can also lead to abnormal shortening of telomeres. For this reason, according to Ridout and her co-authors, it’s one biomarker that can measure how toxic stress impacts a child. (Telomere length is determined by analyzing blood drawn from a blood test).

What’s lacking in most existing studies is a point of comparison between a baseline telomere test and one done later on in time, according to Ridout, the director of research and quality, and co-director of behavioral medicine for Kaiser San Jose’s Family Medicine Residency Program.

KRidout headshot2
Dr. Kathryn Ridout

“This is my view: There are European countries that take telomere length at birth of all of their population, because they think that’s important, because it’s a marker of overall stress or illness in their population,” she says, which may help them identify who needs interventions. “So, the true way to tell if your telomeres are shorter, is you have a baseline from birth, and then another one at another point in time.” That, says Ridout, would be a next step.

But it’s certainly not the only step. There haven’t been studies that rule out other factors that can shorten telomeres, says Ridout. For example, certain habits, like smoking or drinking alcohol or lack of exercise can all contribute to decreased telomere length.

“So, the question is: How? What’s the mechanism that causes telomere shortening? If someone is physically inactive, is it because they’re depressed? Is it the depression that causes it or that they’re inactive that contributes to telomere shortening?” asks Ridout. “We know these are associations, but we don’t know cause and effect yet.”

And to the question of childhood maltreatment and telomere length, Ridout and her coauthors said that since the first reported study that showed a link between childhood maltreatment and shorter telomere length in adulthood appeared in the journal Biological Psychiatry in 2010, subsequent studies have continued to support that finding.

Telomere length may provide clues to cumulative stress over the life span, according to Ridout and her colleagues. Mitochondria, the energy powerhouse of the cell, can also be a marker of wear and tear on the body, including how early life stress from ACEs contributes to aging. The more stress on the cell, she explains, the more demand you place on your mitochondria, which is reflected in mitochondrial DNA copy number.  The copy number goes up with more stress and an increased level of stress hormones in the body.  

“I think the takeaway is that these biomarkers are sensitive to stressful exposures, especially ones in childhood and really should be viewed as potential markers of risk and resilience for negative health outcomes imparted by ACEs exposures,” says Ridout. “Because right now we have this really well-defined relationship between ACEs and early life and disease risk. And we know that the relationship is beyond risky health behaviors. It’s not just because  you start smoking, or have less access to healthy foods. We think there’s something actually about adverse exposures in childhood that get under the skin and change your risk for heart disease, diabetes, depression, anxiety.”

 

 

 

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