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The Estrogen-Lipedema Connection: New Insights into the Impact of Hormones

By November 7, 2024 November 8th, 2024 No Comments
Lipedema Simplified - Estrogen and Lipedema

The Estrogen-Lipedema Connection:
New Insights into the Impact of Hormones

Hello everyone! It’s Leslyn Keith here, Director of Research and President of the Board for the Lipedema Project. We are thrilled to share a groundbreaking paper on the relationship between estrogen and lipedema. This paper, titled Estrogen as a Contributing Factor to the Development of Lipedema,” sheds new light on the hormonal aspects of our condition.  It was published online and will be a chapter in an open-access peer-reviewed book.  The working title of the book is Hot Topics in Endocrinology and Metabolism.

The hypotheses put forward in this paper could have an impact on how we understand and treat lipedema, potentially improving the lives of many in our community.

Estrogen’s Role in Fat Metabolism

Estrogen is more than just a reproductive hormone – it’s a key player in how our bodies handle fat. It regulates appetite, energy use, and where fat is stored in our bodies. When estrogen levels drop or estrogen receptors aren’t working properly, we see an increase in subcutaneous fat – exactly what happens in lipedema [1]Szél et al. (2014) Pathophysiological dilemmas of lipedema. Med Hypotheses, 83(5), 599-606.. This connection supports the idea that lipedema might be a hormonal disease at its core.

I’d like to point out that estrogen also controls leptin, the hormone that manages hunger and body weight [2]Yi et al. (2008) Role of estrogen receptor-alpha and -beta in regulating leptin expression in 3T3-L1 adipocytes. Obesity (Silver Spring), 16(11), 2393-2399.. If estrogen or its receptors are lacking in lipedema, it could explain why traditional weight loss methods often fall short for people with lipedema. This hormonal imbalance might be why our bodies stubbornly hold onto fat, especially in the lower body.

Estrogen and Inflammation in Lipedema

Inflammation is a hot topic in lipedema research, and estrogen plays a significant role here too. When estrogen levels decrease, we see an increase in proinflammatory substances in the body. This happens during menopause or after ovary removal. On the flip side, during pregnancy or when taking estrogen supplements, inflammation tends to decrease [3]Monteiro et al. (2014). Estrogen signaling in metabolic inflammation. Mediators Inflamm.

What’s really interesting is how this relates to lipedema. As estrogen levels change throughout our lives, it might explain why some may experience flare-ups or worsening symptoms of lipedema at certain times. Post-menopausal women with high inflammation markers saw a decrease in these markers after estrogen treatment [4]Monteiro et al. (2014). Estrogen signaling in metabolic inflammation. Mediators Inflamm. This suggests that managing estrogen levels could potentially help manage lipedema symptoms.

Potential Hormonal Treatments for Lipedema

Now, let’s talk about what this all means for treatment. Some exciting studies have shown that estrogen therapy might be beneficial for lipedema patients. In one study, applying topical estrogen to the lower body decreased the activity of an enzyme that promotes fat storage [5]Price et al. (1998) Estrogen regulation of adipose tissue lipoprotein lipase–possible mechanism of body fat distribution. Am J Obstet Gynecol, 178, 101-107.. Other research found that estrogen treatment reduced the expression of genes related to fat formation [6]Jeong & Yoon (2011). 17β-Estradiol inhibition of PPARγ-induced adipogenesis and adipocyte-specific gene expression. Acta Pharmacologica Sinica, 32(2), 230-238..

It’s worth noting that estrogen seems to help transform white fat (the stubborn, storage kind) into brown fat, which is more metabolically active and easier to burn [7]Ponnusamy et al. (2017). Pharmacologic activation of estrogen receptor β increases mitochondrial function, energy expenditure, and brown adipose tissue. FASEB journal: official publication of the … Continue reading. This could be a significant breakthrough for those of people struggling with stubborn lipedema fat.

As we wrap up, I want to emphasize how crucial these findings are. They suggest that lipedema might indeed be a hormonal disease, which opens up new avenues for treatment. While more research is needed, this gives us hope for more effective management strategies in the future.

What can you do with this information? 

First, stay informed. Keep up with the latest research by subscribing to our daily Flash Briefings. You can find these on Apple, Spotify, Amazon Alexa, or at lipedema-simplified.org/flash. Second, discuss these findings with your healthcare provider. They might help inform your treatment plan or lead to new approaches tailored to your unique situation.

Remember, understanding lipedema better is the first step to managing it more effectively. Keep learning, stay hopeful, and know that research is constantly moving forward to improve our lives with lipedema.

~Leslyn Keith, OTD, CLT-LANA
Board President, Director of Research | The Lipedema Project


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Citations

Citations
1 Szél et al. (2014) Pathophysiological dilemmas of lipedema. Med Hypotheses, 83(5), 599-606.
2 Yi et al. (2008) Role of estrogen receptor-alpha and -beta in regulating leptin expression in 3T3-L1 adipocytes. Obesity (Silver Spring), 16(11), 2393-2399.
3, 4 Monteiro et al. (2014). Estrogen signaling in metabolic inflammation. Mediators Inflamm
5 Price et al. (1998) Estrogen regulation of adipose tissue lipoprotein lipase–possible mechanism of body fat distribution. Am J Obstet Gynecol, 178, 101-107.
6 Jeong & Yoon (2011). 17β-Estradiol inhibition of PPARγ-induced adipogenesis and adipocyte-specific gene expression. Acta Pharmacologica Sinica, 32(2), 230-238.
7 Ponnusamy et al. (2017). Pharmacologic activation of estrogen receptor β increases mitochondrial function, energy expenditure, and brown adipose tissue. FASEB journal: official publication of the Federation of American Societies for Experimental Biology, 31(1), 266-281.