University of Cincinnati psychiatrist, Dr. Jeffery Strawn talks about flame retardants and anxiety disorders in children and teens.
Interview conducted by Ivanhoe Broadcast News in 2023.
Can you describe for me what you and your colleagues were looking at and why?
Strawn: I’m fortunate to work with a really talented group of individuals who have been evaluating the impact of exposures to different chemicals that exist in the environment from very early ages. This is a study that’s called the homes study that began here in Cincinnati back in the early 2000s. What’s really interesting about this study as opposed to a lot of other studies where kids or adults are followed over time, is that the follow up actually started while the moms were pregnant with these kids. It started roughly during the second trimester and then these children had been followed over time and they’re now at a point that they’re in their early teens.
What exposure were you measuring for?
Strawn: The team has looked at a number of exposures. They’ve looked at things like air pollution. They’ve looked at things like flame retardants, which is what our study focused on, but also at things like lead and other chemicals that exists pretty ubiquitously in the environment. Our study focused, as I mentioned on the flame retardants, which is a group of compounds that are often referred to as PBDEs. Those chemicals really have now been banned in many places. But the issue is that they were added to a number of products. Chairs, foam, cushions, carpets, car seats, even as flame retardants. These compounds actually tend not to be tightly bound to the surface that they’re aimed to protect against catching on fire. Because of that, they tend to be released into the environment and that facilitates them being a fairly prominent exposure for a lot of folks. The other issue is that these chemicals tend to persist in the environment for a long period of time. Then when we think about the fact that car seats and other furniture tend to get held onto for a number of years or even resold in a secondhand store, that further extends the lifespan of these chemicals.
What did you find?
Strawn: What we found was that exposure to these chemicals during a fairly critical time period during the pregnancy, when there’s a lot happening in terms of brain maturation and specific brain cells moving to different areas of the brain, and also a time when these connections between nerve cells in the brain are really being formed. Exposure during that period was associated with a small but a significant increase in anxiety. I think one of the things that’s probably important to emphasize here is that we’re looking at a large group of kids. This is not necessarily individuals that are coming to see me as a child and adolescent psychiatrists for anxiety or worries. This is across the general population, and so even looking at a small but significant increase in anxiety across a whole population has a lot of public health implications.
What are the implications? We certainly have talked about with the pandemic, with mental health being such an issue for both adults and for kids, but especially for kids and adolescents who’ve really felt the brunt of being close to it away.
Strawn: Certainly. We’ve seen a surge really in mental health problems potentially as a result of the pandemic. It may also be because of other factors that are related to the pandemic in terms of isolation, in terms of disruption of school, processes and normal friend relationships, as well as just normal family activities. With that being said, in terms of recognizing this small but significant impact, when it’s multiplied across this large number of individuals can have some pretty significant impacts. For example, if we have somebody that has mild anxiety, but this increase raises the anxiety level to the point that it now starts interfering with things, where we cross that line into this becoming anxiety disorder. That’s something that’s really important in terms of now that individual needs treatment, or it’s affecting school function and family life.
How are you and your colleagues able to determine that it was the toxins and exclude other factors? How did you control for other factors?
Strawn: I’m fortunate that the team includes some very talented epidemiologists and statisticians who really have tremendous expertise in terms of creating these fairly complicated models where they’re able to control for many of the other things that we know increase the risk of anxiety. Things like the birth weight of the child and family history. In other words, having a family member with an anxiety disorder or the mothers or parent’s anxiety symptoms themselves. In these fairly sophisticated models, they’re able to control for the influence of all of those other factors and environmental exposures.
What if someone was pregnant around that time? Do you have any guidance? What do people do if they have kids that are in that age range in the early 2000s?
Strawn: This is probably a point where I’d step away from the study, and in looking at that situation, I would probably look at this like I might look at any other individual or perhaps even patient coming in to see me as a child and adolescent psychiatrist. I’d be thinking about that anxiety in terms of how does it impact that particular child. The thing that we tend to go back to is in determining whether anxiety is a problem or whether anxiety is normal, is a couple of aspects of it. First look to see if the the anxiety is expected. We know that there are certain times where it’s appropriate to have anxiety. The second is determining if the anxiety is proportional? In other words, if there is some anxiety producing event that’s upcoming, is the amount of anxiety that that child is experiencing or the amount of distress that they’re having proportional to what other kids might have with that same event. The third piece is really looking at how it impacts other things. Deterining what it interferes with and if there is interference either in family or friend relationships or in terms of other things. That’s somewhat removed from the actual study, but I think that’s still a fair approach to evaluating things.
Again, you and the team looked at exposure to the mom, in utero and not children wearing pajamas with the flame retardants still in it or being in those car seats. Was this more the impact of the toxins on mom while she was pregnant?
Strawn: During the pregnancy. It’s an important point because as of right now, we have pretty limited data in terms of what exposures at other points during development may have had on the risk of anxiety or depression or quite frankly, many other conditions.
Would the implications of having the information that exposure during that point in time be making a difference?
Strawn: I think the one important consideration is how is that actually happening. That has some pretty significant implications for further research. It’s one thing to know that an environmental exposure increases the risk of anxiety, but really understanding how that happens is ra critical piece. Right now there are some studies that are ongoing looking at actual brain imaging, trying to identify if this produces differences in terms of how regions are connected to one another or the activity in specific regions.
PBDE, what does that stand for? Can you give me a list of some other places that you might find that?
Strawn: Certainly carpets. Maybe it was predominantly used in furniture, and a number of just household products for many years.
What does PBDE stand for?
Strawn: Polybrominated Diphenyl Ether.
Is there anything else I didn’t ask you about this particular study that you want to make sure that people know?
Strawn: The only other thing to mention would just be the effect in terms of right now what we’re seeing with screening for anxiety disorders with the U.S. prevention screening task force recommendation and others that we should be screening for now and individuals between eight and 17. That’s not only because of functional impact, but also due to the fact that they increase the risk of developing other anxiety disorders. If you have an anxiety disorder, you increase your risk of developing another type of anxiety disorde and you also doubling your risk of developing depression. If you have anxiety and depression, both of those conditions are now more difficult to treat than if you just had anxiety or just had a depressive disorder.
That U.S. Preventative Prevention Task Force, is that just a recommendation at this point? Has anyone implemented it?
Strawn: It’s like any other screening test. It’s a recommendation for this one in particular for primary care settings working with kids.
Are most states doing that or most doctors doing that?
Strawn: It’s local. I think one of the issues with the Screening Task Force is that it provided a recommendation, but it provided very limited evidence or guidance in terms of how to screen. That’s something that our team addressed in accompanying editorial in JAMA looking at when and in particular how to screen for anxiety disorders in kids.
I know you and your colleagues are doing some work on this, in terms of individualized and personalized medicine, in what way can that be a benefit when it comes to mental health medications?
Strawn: Certainly. I think when we’re looking at genetic testing, and specifically pharmacogenetic testing, the bulk of the evidence in the pediatric setting is probably more for the antidepressant medications. I think it’s also important when people are thinking about genetic testing and how that guides treatment. It doesn’t necessarily replace the clinician or pick the medication. It allows clinicians to believe that medication or antidepressant medication would be helpful. This testing can help individualize treatment because we know that some patients breakdown the medicine much more quickly than other patients. Those patients that break down the medication more quickly, potentially have a slower improvement over time. Optimizing the dosing based on how the patient metabolizes the medicine allows us to create a blood level that might be about the same across all different types of patients based on their ability to metabolize the medicine. The other piece to that is that we know that there are some people that break down the medicine much more slowly. Those are individuals who are actually at higher risk for side effects. In those patients, we might decrease the dose of the medicine below even what is the recommended starting dose of the medicine in that age range.
Is this something that you and your colleagues are testing now, is it a clinical trial? Can you tell me a little bit about your research?
Strawn: This is something that with colleagues at Cincinnati Children’s and at the University of Cincinnati we’ve been very interested in for a number of years and like anything else in science, oftentimes, before we start the clinical trial, the groundwork is really laid by a number of preliminary studies. What we’ve looked at, is how these differences in metabolism produce differences in weight gain with some medications or other specific side effects. We’ve also looked at how it influences how quickly someone improves. Now, we’re in the process of doing a large trial that’ll actually look at normal dosing of these medications versus the genetically guided dosing of these medications and that trials are sponsored by the National Institutes of Health.
Are there certain medications in particular?
Strawn: When we’re looking at antidepressants in the pediatric population, there are several that have FDA approval. Now, certainly, we often use many of them, what we call off label. In the absence of having these specific indication, although I think what’s important is recognizing that off label doesn’t mean without evidence. In terms of the specific medications that we often use, these would be things like fluoxetine, prozac, escitalopram, lexapro, sertraline, or zoloft. Now, among those that I’ve mentioned, not all of them are heavily influenced by these differences in metabolism. Some of the ones that we’re looking at in particular are actually escitalopram, which is strongly influenced by one particular enzyme in the liver in terms of how it’s metabolized. We know that there’s a tremendous amount of variation in the population in terms of how much activity for that particular enzyme an individual has and consequently, how much variation we would see in blood levels with that medicine.
Why is it so important to get the dosage right when it comes to anxiety medication?
Strawn: We know when we’re thinking about the treatments for anxiety disorders, we have two main treatments. We have psychotherapy and we have medication. Unfortunately, we know that either with psychotherapy or with medication, only about two to three in five patients fully get better. In other words, they get to a point where they no longer had any functional impairment or residual symptoms. Getting the treatment right allows us potentially to optimize that. Maybe that means getting to the point that we can get four or aspirationally maybe even five of those five patients better. The other thing that I think is important is the speed of improvement. When we’re thinking about these disorders, we often allow ourselves to go a bit slower. As a physician that specializes in treating anxiety disorders, this is a kin to bringing a patient with pneumonia in the hospital and watching while the patient continues to suffer and has tremendous morbidity, I just don’t think that’s ethically acceptable.
END OF INTERVIEW
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