Pregnancy and liver health: delivering new collaborations to advance the MASLD and MASH field

We read with great interest the article by Allen et al. (Envisioning how to advance the MASH field. Nat. Rev. Gastroenterol. Hepatol. 21, 726–738 (2024))¹, and particularly welcomed the acknowledgement of the intrauterine environment’s contribution to metabolic dysfunction-associated steatotic liver disease (MASLD; formerly known as nonalcoholic fatty liver disease) development in the offspring. The concept of the Developmental Origins of Health and Disease, pioneered by David Barker in 1986 (ref. ²), highlights pregnancy as a valuable period to influence public health by addressing the intergenerational effect of non-communicable diseases, and it is highly fitting that MASLD is now recognized in this paradigm. But perhaps it is time to shine a brighter spotlight on pregnancy as a tool to advance the MASLD public health agenda.

In addition to offering insights into future offspring disease, pregnancy events can be used to predict long-term maternal outcomes. The International Federation of Gynecology and Obstetrics has emphasized the value of using pregnancy as a screening tool for a range of conditions³, highlighting the immediate postpartum period as an important window for early preventive interventions⁴. The antenatal period, often the first regular point of contact with healthcare professionals, also offers a unique triad of opportunity composed of engagement, motivation and receptivity to healthcare advice. Although this concept has mostly been applied to subsequent cardiovascular disease and type 2 diabetes⁵, evidence suggests that it is equally relevant to the field of MASLD. For instance, literature demonstrates that women affected by gestational diabetes are 50% more likely to develop MASLD within 16 months to 25 years of pregnancy than those without⁶. Although a causal relationship has not been confirmed, it is important to consider whether the metabolic challenges of pregnancy and associated dyslipidaemia, exacerbated by certain gestational disorders, could trigger or accelerate the pathway towards MASLD and metabolic dysfunction-associated steatohepatitis (MASH; formerly known as nonalcoholic steatohepatitis).