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Recorded onsite in Washington DC, Scott Friedman, Jörn Schattenberg, Rachel Zayas and Roger Green discuss takeaways from the first three days at the 73rd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD). The group encapsulates the dynamic, vibrant energy of returning to this momentous event which welcomed back over 7,000 in-person attendees.

In this conversation, Rachel injects fascinating new considerations to the podcast through her lens from the microbiome. She begins by highlighting a poster presented by Curtis Gabriel. The study, titled Diabetic Persons with HIV and Hepatic Steatosis Have Reduced Intestinal Microbial Diversity, links intestinal dysbiosis and hepatic steatosis in patients with HIV. Rachel notes the topic to be compelling yet underexplored. Her curiosity questions, what does the normal microbiome look like initially and how does this change over time? Scott suggests society-wide changes in our food and use of antibiotics are important indices to investigate. Discussion digresses to other related phenomena as antibiotics are not the only agent society has introduced to ecosystems.

Scott distills what he determined to be an eye-opening theme of the meeting in saying, “the Devil is in the details.” He describes himself as always looking to reduce complex topics to main, big picture themes. Contrarily, this meeting made clear to him how complex NAFL-D really is. He regards the complexities and differences in cell backgrounds, microbiota and treatment patterns as components of a longer-term challenge. Despite this challenge, he is confident the disease will yield to therapies incrementally and effectively.

NAFLD is noted to be a complex disease with a set of interrelated issues. Scott provides several examples of this, including Stephen Harrison’s presentation on a fatty acid synthase inhibitor (discussed in a later conversation). Jörn points out that a drug does not have to affect every key target to have an impact on the disease. This leads Rachel to ask in addition to what is driving disease, what are the protective mechanisms? Do they lie in epigenetics? Scott concurs and provides an example based on hyperlipidemia and the PCSK9 class. As this session winds down, Roger comments that we might not need to know exactly why an agent or therapeutic approach works to know that it does work. Instead, we can expect to solve the why as reverse engineers.