Hormonal
Premenopausal women are protected from developing NAFLD due to estrogen-mediated partitioning of fatty acids toward ketone body production and sex-specific browning of white adipose tissue, whereas postmenopausal estrogen deficiency facilitates massive hepatic steatosis and fibrotic progression.
For women, reproductive status is a critical factor in liver health. Before menopause, estrogen helps protect the liver by directing fat away from storage in the liver and towards energy use (ketones). After menopause, this protection vanishes, significantly increasing the risk of fatty liver and scarring, even if weight doesn't change drastically. Maintaining metabolic health becomes even more crucial post-menopause to counteract this hormonal shift.
female sex is protected from dysmetabolic traits thanks to young individuals’ ability to partition fatty acids towards ketone body production rather than very low density lipoprotein (VLDL)-triacylglycerol, and to sex-specific browning of white adipose tissue which contributes in protecting female mice from experimental NAFLD... ovarian senescence, via hypoestrogenemia, facilitates both the development of massive hepatic steatosis and the fibrotic progression of liver disease
Why this rating
The paper is a narrative review citing multiple longitudinal human studies, animal models (zebrafish, mice), and mechanistic studies, though it acknowledges conflicting epidemiological data in specific subgroups.
Source
NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk
Stefano Ballestri et al. · Advances in Therapy · 2017
DOI 10.1007/s12325-017-0556-1
More from this paper
- Postmenopausal women have a higher prevalence of NAFLD than premenopausal women, and this risk is independently associated with menopause status even after adjusting for metabolic factors in some studies.Good
- Early menarche is associated with an increased risk of NAFLD in adulthood, primarily driven by excess adiposity rather than estrogen activation itself.Moderate
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