This work would not have been possible without my amazing co-authors: Kristen Kelly, @lukas-schaffer.bsky.social, Jeremy Lawrence, Heather Lee, Elizabeth Karlson, and @andrewgrotzinger.bsky.social! 🦡

Finally, some psychiatric – immune disease relationships are mediated by multiple markers, likely tapping into similar biological processes. We clarify this overlap by modeling these markers together in a multiple mediation framework.

Immune markers exhibited a wide range of mediating effects. For example, IL-6 mediated 60% of the genetic link between internalizing disorders and Crohn’s disease, while a TNF-α/CCL3 factor mediated 100% of the link between substance use and autoimmune disorders.

Furthermore, the study shows that specific markers mediate psychiatric – immune disease relationships, rather than more general wide-spread inflammation, as indicated by a pattern of null results alongside specific sets of mediating markers.

A major finding challenges a widely held view: The psychiatric relevance of C-reactive protein (CRP) is better explained by its precursor, IL-6. When modeled together, the effect of CRP on psychiatric and immune diseases becomes non-significant.

As a continuation of our previous work genetically linking immune-mediated diseases with psychiatric disorders, we now explore some of the intermediate mechanisms further by investigating the role of immune and inflammatory markers in those relationships.

Immune markers exhibited a wide range of mediating effects. For example, IL-6 mediated 60% of the genetic link between internalizing disorders and Crohn’s disease, while a TNF-α/CCL3 factor mediated 100% of the link between substance use and autoimmune disorders.

Furthermore, the study shows that specific markers mediate psychiatric – immune disease relationships, rather than more general wide-spread inflammation, as indicated by a pattern of null results alongside specific sets of mediating markers.

A major finding challenges a widely held view: The psychiatric relevance of C-reactive protein (CRP) is better explained by its precursor, IL-6. When modeled together, the effect of CRP on psychiatric and immune diseases becomes non-significant.

As a continuation of our previous work, genetically linking immune-mediated diseases with psychiatric disorders, we now explore some of the intermediate mechanisms further by investigating the role of immune and inflammatory markers in those relationships.

Congrats Fiona! So well deserved! 🥳

Congrats, Leo!! So proud of you! 🎉