My research program consists of three parallel, synergistic aims to maximize replicability, streamline theory progression and refinement, and ultimately maximize clinical impact (described in more detail in my article in Brain, Behavior, and Immunity-Health's special issue on "Emerging PNI research: Future Leaders in Focus").
First, I aspire to inspire methodological reform in biological psychiatry. A solid methodological foundation is key to building a robust and efficient field of study. Namely, I believe this efficiency applies to both the research-to-practice pipeline as well as fiscal efficiency. More methodologically rigorous studies result in fewer false positive/false negatives, reducing the investment required for impactful research. Further, more reliable methods can increase power, resulting in less expensive research projects. To this aim, I have published on "physiometric" (the measurement properties of biological variables) papers spanning from empirical studies to didactic resources. Additionally, I have prioritized statistical approaches that isolate conceptually-important variance (e.g., within-person variance) to increase etiological/treatment implications. Finally, I have also published a tutorial paper highlighting common analytic concerns in immunopsychiatry, complete with template code for researchers to easily implement into their next project.
Second, my work also investigates the inflammatory phenotyping of psychopathology. Specifically, interrogating at what level (e.g., broadly vs. specific symptoms) inflammation is associated with mental health and vice-versa. Most recently, I have challenged theories that inflammation is only associated with depression generally OR specific symptoms, considering that these are not mutually exclusive concepts in what I describe as "hierarchical phenotypes". Extending beyond DSM-categories and embracing curiosity about how biology is related to psychopathology, in my view, is a necessary step to embracing the complexity of psychiatry in pursuit of refining theory, enhancing replicability, and advancing precision medicine.
Finally, my work seeks to integrate immunological processes into extant, robust, clinically-established psychosocial models of risk. Effect sizes between immunological variables and mental health are often small and variable. Thus, it is important to identify for whom and how inflammation might play a role in mental health risk/resilience/recovery. While I believe phenotyping work to play a large role in this pursuit, considering psychosocial moderators is also key. Specifically, there is robust evidence that cognitive vulnerabilities that amplify or extend physiological arousal influence baseline physiology. As such, I am working on an immunocognitive model of psychopathology in which cognitive vulnerabilities amplify arousal, resulting in changes to inflammatory physiology, in ways that confer risk for mental health. By moving away from studies strictly testing the relationship between inflammation and symptoms, I believe we can contextualize inflammatory mechanisms in maximally comprehensive models, allowing clinicians to provide flexible and exhaustive treatment plans.
First, I aspire to inspire methodological reform in biological psychiatry. A solid methodological foundation is key to building a robust and efficient field of study. Namely, I believe this efficiency applies to both the research-to-practice pipeline as well as fiscal efficiency. More methodologically rigorous studies result in fewer false positive/false negatives, reducing the investment required for impactful research. Further, more reliable methods can increase power, resulting in less expensive research projects. To this aim, I have published on "physiometric" (the measurement properties of biological variables) papers spanning from empirical studies to didactic resources. Additionally, I have prioritized statistical approaches that isolate conceptually-important variance (e.g., within-person variance) to increase etiological/treatment implications. Finally, I have also published a tutorial paper highlighting common analytic concerns in immunopsychiatry, complete with template code for researchers to easily implement into their next project.
Second, my work also investigates the inflammatory phenotyping of psychopathology. Specifically, interrogating at what level (e.g., broadly vs. specific symptoms) inflammation is associated with mental health and vice-versa. Most recently, I have challenged theories that inflammation is only associated with depression generally OR specific symptoms, considering that these are not mutually exclusive concepts in what I describe as "hierarchical phenotypes". Extending beyond DSM-categories and embracing curiosity about how biology is related to psychopathology, in my view, is a necessary step to embracing the complexity of psychiatry in pursuit of refining theory, enhancing replicability, and advancing precision medicine.
Finally, my work seeks to integrate immunological processes into extant, robust, clinically-established psychosocial models of risk. Effect sizes between immunological variables and mental health are often small and variable. Thus, it is important to identify for whom and how inflammation might play a role in mental health risk/resilience/recovery. While I believe phenotyping work to play a large role in this pursuit, considering psychosocial moderators is also key. Specifically, there is robust evidence that cognitive vulnerabilities that amplify or extend physiological arousal influence baseline physiology. As such, I am working on an immunocognitive model of psychopathology in which cognitive vulnerabilities amplify arousal, resulting in changes to inflammatory physiology, in ways that confer risk for mental health. By moving away from studies strictly testing the relationship between inflammation and symptoms, I believe we can contextualize inflammatory mechanisms in maximally comprehensive models, allowing clinicians to provide flexible and exhaustive treatment plans.