A recent study published in BMC Medicine has revealed that a Western diet (WD) significantly accelerates the growth of endometriotic lesions and alters gut microbiota in mice. This research highlights the potential of dietary modifications as a strategy for managing endometriosis, a condition that affects approximately 10% of women of reproductive age and is characterized by the growth of tissue similar to the uterine lining outside the uterus.
The study found that the Western diet not only promotes the development of endometriotic lesions but also activates macrophage markers associated with inflammation, potentially exacerbating the condition. Despite being classified as benign, endometriosis can lead to considerable morbidity, and previous research has suggested that anti-inflammatory diets may alleviate pain associated with the disease by influencing gut bacteria and metabolism.
The gut microbiome plays a crucial role in regulating immune responses and inflammation. Specific bacterial components can modulate macrophage activity, enhancing their inflammatory response through a mechanism known as trained immunity.
In this study, researchers surgically implanted endometriotic tissue into female mice and monitored lesion development over several weeks. The mice were divided into two groups: one consuming a control diet and the other a Western diet, which is typically high in fat and low in fiber. Importantly, the study avoided high-fat diets that could lead to obesity-related changes.
After seven weeks, the results showed that mice on the Western diet had a mean lesion volume of 148.3 mm³, compared to 69.7 mm³ in the control group, indicating a doubling of lesion size in the WD group. While inflammatory markers remained unchanged, the lesions in WD mice exhibited increased fibrotic characteristics and greater macrophage activity, suggesting a link between diet and trained immunity.
The study also noted that serum glucose levels were lower in mice with endometriosis compared to their original, endometriosis-free state, possibly due to increased glucose consumption. Both the Western diet and endometriosis independently altered gut microbiota composition, revealing distinct differences from the control group, even in the absence of overt dysbiosis.
Mice on the Western diet with endometriosis produced higher levels of lactate during anaerobic glucose metabolism, indicating a potential metabolic shift associated with dietary influences. The research suggested that leptin pathway activation may play a role in endometriotic lesion development.
Many women with endometriosis also experience functional bowel disorders, such as irritable bowel syndrome, which could be alleviated through dietary changes. Previous studies have indicated that probiotics may reduce the size of endometriotic lesions, although the specific metabolic changes involved remain unclear.
Significant changes in gut microbiota were observed in relation to dietary patterns. Notably, mice on the Western diet with larger endometriotic lesions showed a depletion of Akkermansia muciniphila, a beneficial gut bacterium associated with reduced inflammation and improved intestinal barrier function. Despite normal levels of this bacterium in the WD group, its depletion after endometriosis induction suggests a protective role in gut health.
While the current study did not find evidence of intestinal dysbiosis, other research has indicated that gut microbiota alterations are common in individuals with endometriosis.
Conclusion
The findings of this study suggest that a Western diet significantly accelerates the growth of endometriotic lesions in a mouse model, indicating that dietary choices may play a critical role in the progression of endometriosis. This underscores the potential for dietary interventions to alleviate symptoms and improve the quality of life for women affected by this condition. Further research is needed to explore the mechanisms behind these observations and to evaluate dietary strategies in human populations.
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