Kimberly Brown, MD, is division chief of gastroenterology and hepatology and the Associate Medical Director of the Henry Ford Hospital Transplant Institute at Henry Ford Hospital. She is also a Professor of Medicine at Wayne State University

Kimberly A. Brown, MD

Are We Screening Women for MASLD Often Enough?

metabolic dysfunction-associated steatotic liver disease (MASLD)

 continues to rise, clinicians are increasingly questioning whether current screening approaches fully capture risk in women. While existing guidelines identify key metabolic risk factors, concerns exist regarding their ability to adequately account for the physiologic changes women experience across the lifespan, particularly during transitions like menopause and pregnancy that significantly influence disease progression.

Current MASLD screening guidelines effectively identify at-risk populations but may not fully account for sex-specific risk across a woman’s lifespan.

The interval of monitoring is important, especially during high-risk transitions such as menopause, when fibrosis progression may accelerate.

Women with metabolic risk factors and early fibrosis may benefit from more frequent noninvasive assessments rather than standard multi-year follow-up.

PCOS screening and recognition should be part of risk assessment in younger women, given its link to insulin resistance and MASLD.

Greater engagement of OB/GYN providers is needed, as they often serve as primary care providers and are well-positioned to identify at-risk patients.

Patient empowerment is essential, including encouraging women to understand their risk, calculate FIB-4 scores, and advocate for further evaluation when steatosis is identified.

Liver Lineup: Updates and Unfiltered Insights

, Meena Bansal, MD, joins Nancy Reau, MD, and Kimberly Brown, MD, to examine a critical but often overlooked question in hepatology: should screening strategies for MASLD differ for women?

The discussion begins with Brown raising the possibility that while current guidelines effectively identify at-risk populations like individuals with diabetes, insulin resistance, or metabolic syndrome, they may not fully account for key transitions in a woman’s life. Bansal agrees that existing frameworks are generally sound but emphasizes that timing and frequency of screening are where clinicians may need to adapt their approach.

Rather than redefining who should be screened, Bansal highlights the importance of adjusting monitoring intervals during periods of increased risk, particularly around menopause. As hormonal changes accelerate metabolic dysfunction and fibrosis progression, she suggests that women in this transition, especially those with additional risk factors like diabetes or early fibrosis, may benefit from more frequent noninvasive assessments. Tools such as vibration-controlled transient elastography or serum-based biomarkers can help identify disease progression earlier, creating an opportunity for timely intervention.

Reau reinforces this point with clinical experience, noting that some patients previously considered low risk can return years later with advanced disease, often after significant metabolic changes and menopause, underscoring the need for greater vigilance during these inflection points.

Beyond hepatology, the conversation further expands to the role of multidisciplinary care. Bansal stresses the importance of engaging obstetricians and gynecologists, who often serve as primary care providers for many women. While awareness is growing, she notes that more education is needed to ensure these clinicians incorporate liver disease screening into routine care for at-risk patients. This includes using simple tools like the FIB-4 index as an initial step, followed by additional testing when indicated.

The group also highlights the importance of patient empowerment. Women are frequently told that “fatty liver” is benign, which may delay further evaluation. Encouraging patients to understand their risk factors, calculate their own FIB-4 scores, and advocate for follow-up care can play a meaningful role in earlier detection.

Editors’ note: Relevant disclosures for 

 include AbbVie, Gilead, Salix, Arbutus, and VIR. Relevant disclosures for 

 include Mallinckrodt Pharmaceuticals, Gilead, Salix, Intercept, Ipsen, and Madrigal. Relevant disclosures for 

 include Boeheringer-Ingelheim, Boston Pharma, Fibronostics, GSK, Madrigal, Merck, NOVO Nordisk, and The Kinetix Group.

DiStefano JK. NAFLD and NASH in Postmenopausal Women: Implications for Diagnosis and Treatment. Endocrinology. 2020;161(10):bqaa134. doi:10.1210/endocr/bqaa134

Sarkar M, Kushner T. Metabolic dysfunction-associated steatotic liver disease and pregnancy. J Clin Invest. 2025;135(10):e186426. Published 2025 May 15. doi:10.1172/JCI186426

Mass General Brigham. Patients Who Discontinued GLP-1s Had More Weight Gain, Complications During Pregnancy. November 24, 2025. Accessed April 20, 2026. 

https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/pregnancy-effects-from-discontinued-glp-1-use

Videos

Experts call for greater awareness, improved collaboration with OB/GYNs, and more proactive MASLD screening strategies for women.

Screening Smarter: Identifying MASLD Risk in Women

PCOS, Pregnancy, and MASLD Risk: What Clinicians Need to Know

 continues to grow, increasing attention is being paid to how reproductive and metabolic conditions uniquely shape risk in women. Among these, 

 and pregnancy represent critical but often underrecognized periods where hormonal and metabolic factors intersect to influence liver health.

In this segment from a recent episode of 

, Meena Bansal, MD, joins hosts Nancy Reau, MD, and Kimberly Brown, MD, to examine the complex relationship between PCOS, pregnancy, and MASLD.

Bansal emphasizes that PCOS is a well-established risk factor for MASLD and its more advanced form, MASH, largely driven by underlying insulin resistance. While the condition is widely recognized in endocrinology, its implications for liver health are often underappreciated. She notes that patients with PCOS should be evaluated for liver fibrosis using noninvasive tools, and those with evidence of stage 2 or 3 fibrosis may be appropriate candidates for currently approved therapies.

The discussion then shifts to pregnancy as a critical period of risk. Women entering pregnancy with metabolic comorbidities such as obesity or diabetes may already be predisposed to MASLD, and the physiologic changes of pregnancy, including weight gain, can further exacerbate disease progression. According to Bansal, emerging data suggest that MASLD during pregnancy is associated with increased risks of adverse maternal outcomes, including gestational diabetes and preeclampsia, as well as complications for the fetus, such as preterm birth and abnormal growth patterns.

The conversation also touches on the potential for long-term, intergenerational effects. Bansal highlights research suggesting that maternal metabolic health may influence fetal outcomes through epigenetic mechanisms, potentially increasing a child’s lifetime risk of metabolic disease and liver dysfunction. While she says these findings require further validation, they underscore the broader implications of MASLD beyond the individual patient.

Reau and Brown further explore how current therapies fit into this landscape, particularly for younger, premenopausal women. Although GLP-1 receptor agonists have shown benefits in weight loss and metabolic regulation and may even improve menstrual regularity in some patients with PCOS, their use is contraindicated during pregnancy. Bansal points out the challenges this creates in preconception care, including uncertainty around weight regain after discontinuation and its potential impact during pregnancy.

As Bansal notes, more research is needed to better understand how to tailor care for women with MASLD, especially during periods of hormonal and metabolic transition.

Mass General Brigham. Patients Who Discontinued GLP-1s Had More Weight Gain, Complications During Pregnancy. November 24, 2025. Accessed April 17, 2026. 

Experts discuss how metabolic and hormonal factors in women influence MASLD risk, progression, and potential long-term outcomes.

MASLD and Women’s Health: The Roles of PCOS and Pregnancy

Liver Lineup: Updates & Unfiltered Insights

Liver Lineup: Closing the Gap in Women’s Liver Health

, hosts Nancy Reau, MD, and Kimberly Brown, MD, are joined by Meena Bansal, MD, to examine how liver disease uniquely affects women across the lifespan. While conditions like 

 are often discussed in broad terms, the trio highlights how risk, progression, and outcomes can differ significantly based on sex and hormonal status.

From reproductive years through menopause and beyond, physiologic changes play a central role in shaping liver health, but these distinctions have historically been underrecognized in both research and clinical care.

0:00:00 – Welcome & women’s liver health framework

0:03:17 – Menopause, estrogen loss, and fibrosis risk

0:10:57 – PCOS, young women, and high‑risk metabolic phenotypes

0:13:54 – Pregnancy, MASH, and maternal-fetal outcomes

0:18:45 – Screening strategy, menopause as a pivot, and intervals

0:28:03 – Practical toolkit: FIB‑4, second‑line tests, and who to test

0:31:27 – Management, GLP‑1s, resmetirom, and key takeaways

Bansal frames MASLD through the lens of a woman’s life course, emphasizing that risk is not static but evolves from reproductive years through menopause and beyond. While premenopausal women may have some degree of protection against liver disease, this advantage diminishes with the loss of estrogen.

As Bansal explains, the postmenopausal transition is associated with increased visceral adiposity and heightened fibrogenic activity, contributing to a rise in MASLD prevalence and severity that begins to parallel, and in some cases exceed, that seen in men. These physiologic shifts mirror patterns observed in cardiovascular disease and underscore the need for more tailored approaches to screening and monitoring in women.

The discussion also underscores critical gaps in the evidence base, with much of the existing literature historically extrapolating findings from predominantly male populations or failing to account for hormonal status among women. As Brown notes, even when women are included in studies, they are rarely stratified by life stage, limiting the ability to draw meaningful conclusions about disease behavior in specific subgroups such as those with polycystic ovary syndrome (PCOS), during pregnancy, or after menopause.

Pregnancy represents another key inflection point. Women with MASLD face increased risks of adverse maternal outcomes, including gestational diabetes and preeclampsia, as well as potential downstream effects on fetal health. Emerging data suggesting epigenetic influences further reinforce the importance of early identification and management. However, therapeutic decision-making in this population remains challenging, particularly given contraindications for commonly used agents such as GLP-1 receptor agonists during pregnancy and the lack of robust safety data for newer therapies.

Across the discussion, Bansal and the hosts repeatedly emphasize the importance of proactive screening and patient advocacy. Tools such as the FIB-4 index offer accessible, scalable approaches to risk stratification, but clinicians must remain attentive to timing and frequency, particularly during periods of hormonal transition. The group also calls for greater collaboration with obstetrics and gynecology providers, who often serve as primary care touchpoints for women, to improve early detection and intervention.

Ultimately, this episode highlights a critical shift in hepatology: moving beyond a one-size-fits-all model toward a more nuanced understanding of how sex and gender influence liver disease. As Bansal notes, empowering women with knowledge about their risk and encouraging clinicians to recognize these distinctions will be essential to improving outcomes in MASLD and beyond.

Mass General Brigham. Patients Who Discontinued GLP-1s Had More Weight Gain, Complications During Pregnancy. November 24, 2025. Accessed April 16, 2026. 

Podcasts

Hosts are joined by Meena Bansal, MD, to discuss long-standing research gaps and what clinicians need to understand about sex-specific drivers of liver disease today.

Genetic Testing in Liver Disease: Interpreting Results and Clinical Impact

As genetic testing becomes more integrated into hepatology, clinicians are increasingly faced with challenges regarding how to interpret results and incorporate them into a broader diagnostic framework. In this segment of 

, guests Robert Gish, MD, and Saul Karpen, MD, PhD, explore the complexities of genetic interpretation, the evolving role of multidisciplinary evaluation, and how traditional tools like biopsy remain essential in the era of genomics.

Genetic panels often require clinical correlation, especially when results return as variants of uncertain significance

“Synergistic heterozygosity” may explain disease when multiple variants are present rather than a single mutation

Genetic testing can uncover rare, actionable diagnoses such as lysosomal acid lipase deficiency

Liver biopsy remains critical when genetic results are inconclusive or do not fully explain the clinical picture

Referral to genetics is most useful for targeted cases, including rare diseases and reproductive counseling

Whole-exome sequencing may be needed when standard panels are unrevealing but suspicion for genetic disease remains

Gish highlighted the limitations of relying solely on genetics, noting that referrals to major academic centers for additional interpretation often yield limited new insights unless more expansive approaches, such as whole-exome or whole-genome sequencing, are pursued. Instead, he has shifted toward a more selective and clinically driven use of genetic consultation, reserving referrals for targeted scenarios such as rare diagnoses, complex counseling questions, or reproductive planning.

At the same time, genetic testing can uncover unexpected and actionable findings. Gish described a patient with atypical cholestatic liver disease who was ultimately diagnosed with lysosomal acid lipase deficiency, a rare condition that would have been difficult to identify without genetic evaluation. In another case, identification of dual heterozygous variants helped explain overlapping pulmonary and hepatic disease, reinforcing the concept that multiple genetic factors can interact to shape clinical presentation.

This concept, referred to as “synergistic heterozygosity,” is gaining increasing recognition in hepatology. Rather than a single causative mutation, patients may harbor multiple variants that collectively contribute to disease. This paradigm challenges traditional binary thinking and underscores the importance of interpreting genetic results in clinical context.

A major continued barrier to adoption, however, is the interpretation of variants of uncertain significance (VUS). Gish argued that this terminology can be misleading and counterproductive, preferring instead a more pragmatic approach that emphasizes clinical correlation. For hepatologists, this means integrating genetic findings with other core elements of liver disease evaluation, including laboratory testing, imaging, and histology.

Indeed, both Gish and Karpen emphasized that genetic testing should complement established diagnostic tools rather than replace them. Liver biopsy, in particular, continues to play a critical role, especially when genetic findings are inconclusive. Histologic evidence of cholangiopathy or other structural abnormalities can help validate the clinical relevance of a genetic variant and, in some cases, contribute to its reclassification as pathogenic.

Karpen also highlighted the dynamic nature of genetic interpretation. A result considered inconclusive today may be better understood in the future as additional data emerge. In some cases, reanalysis of prior genetic testing has led to new diagnoses, reflecting the rapidly evolving knowledge base in genomics.

Editors’ note: Relevant disclosures for Reau include AbbVie, Gilead, Salix, Arbutus, and VIR. Relevant disclosures for Brown include Mallinckrodt Pharmaceuticals, Gilead, Salix, Intercept, Ipsen, and Madrigal. Relevant disclosures for Karpen include Mirum and Ipsen. Relevant disclosures for Gish include Abbott, AbbVie, Aligos, Altimmune, Arrowhead, AstraZeneca, Corcept, Genentech, Gilead Sciences, GSK, Intercept, Janssen, Merck, Perspectum, Pfizer, and others.

Experts discuss interpreting genetic testing in liver disease, the role of biopsy, and how to integrate variants into clinical decision-making.

Kimberly A. Brown, MD

Articles