Trying to think of potential biological bridges between stress or high-emotionality disorders like anxiety and increased risk for depression. We have a fairly good understanding of how these things are tied together psychologically and have psychotherapy techniques to improve emotion regulation, but identifying biological mechanisms can guide us toward supplemental medications or lifestyle changes. This might inform treatments and give us insight into how psychological processes increase the risk for physiological diseases.

Broadly speaking, difficulties regulating emotion—either in ways that allow emotions to get very high and/or thinking styles that extend the duration of negative emotions—seem to increase the inflammatory impact of stressors. In my view, there is strong enough experimental and longitudinal evidence that it is plausible this association is causal.

I don’t think that immune panels make sense as diagnostic biomarkers for these types of disorders; they are more expensive and less scalable than existing diagnostic measures and lack sensitivity/specificity. That said, for disorders that inflammation seems to be a risk factor for (rather than a consequence of), I think that inflammatory screening, in combination with careful case conceptualization, might be useful in determining if inflammation could be something worth targeting in treatment as part of a holistic plan.

This depends on what you want the information for but, I think that trait measures of emotion regulation like the Difficulties in Emotion Regulation Scale, The Emotion Regulation Questionnaire, the Cognitive Emotion Regulation Questionnaire, and the Behavioral Emotion Regulation Questionnaire capture many aspects of emotion regulation that people care about. Regarding inflammation, blood samples to assay for proteins like C-reactive protein, interleukin-6, interleukin-10, and tumor necrosis factor-α are the most common to see in both research and standard clinical labs.

In our recent systematic review on the topic, we found that characteristics such as how susceptible people are to large spikes in negative emotions, their tendency to suppress negative emotions rather than address them, and their proneness to focus on negative emotions repeatedly (also referred to as rumination and worry) were most consistently associated with elevated inflammation. Conversely, the ability to cope with negative emotions in positive ways (including seeking social support) and the ability to disengage with negative emotions were associated with lower levels of inflammation.

One of the exciting things about this field is that there are so many ways to target inflammation, ranging from anti-inflammatory medications (though, it is important to note that these are still being studied to determine when they are safe and helpful for mental health disorders), to psychotherapy (which has consistent evidence as good for immune health), to diet and exercise. Lots of flexibility which means lots of room to tailor treatment recommendations to individual patients.

There is evidence that antidepressants, mindfulness, and lifestyle interventions like exercise decrease inflammation in some individuals (particularly those with elevated inflammation to begin with) and that this might contribute to the treatment effects we see in these individuals.

Most of the research I see in this area focuses on depression, and it doesn’t seem like anti-inflammatory medications will be helpful for everyone. However, current research is helping to identify a subgroup of individuals who might benefit. For example, those with elevated inflammation who show specific symptoms like appetite changes and fatigue (associated with immune functioning) might find anti-inflammatory medications helpful as adjunctive treatments.

Something that’s important to emphasize is that inflammation is a natural, necessary part of our immune system—it is not inherently bad. We really want there to be acute inflammatory reactions when our body needs to fend off illness or help us recover. However, more negative emotion regulation styles seem to amplify and extend these acute reactions in ways that increase the risk for our inflammatory baseline to shift upward in what is referred to as a “chronic inflammatory phenotype”. This can increase the risk of negative health outcomes associated with immune dysregulation.

Broadly speaking, I’m very excited about projects and ideas that attempt to flesh out the nuances that will facilitate informed treatment planning—especially for medications which are often more-or-less trial-and-error in many clinics. A lot of my work focuses on looking at specific symptoms rather than broad diagnostic constructs to help improve screening measures—and there are a lot of open questions on how precise we need to think about mental health (for example, disorders vs disorder subtypes vs subsets of symptoms vs individual symptoms) for our research to be maximally useful in the clinic. I find these types of projects both conceptually fascinating but also incredibly necessary to synergize how we as a field do research with the nuances that patients and clinicians work with every day.