Elle Lipedema Fit

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Elle Lipedema Fit

Lipedema Coach BHSc | Complex Bodies
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31/08/2026

The lipedema genetics conversation is changing 👀🧬

Not just “what genes did you inherit?” but “what’s happening inside the affected tissue?”
That’s the idea behind somatic mosaicism - when a genetic change happens after fertilization, so only SOME cells carry it. Blood can look normal while affected tissue tells a different story.
This isn’t proven in lipedema - it’s an emerging hypothesis researchers are starting to explore. Lipedema is currently understood as polygenic/complex, not caused by one single gene.
I used the case of Mandy Sellars (PIK3CA-related overgrowth spectrum / PROS is not lipedema) in the slides to show how mosaicism can work in overgrowth conditions. Same lesson: sometimes you have to look in the tissue, not just the blood.
Fascinating shift, right?

References:
Michelini S, et al. Unraveling lipedema: comprehensive insights and the path to future discoveries. npj Metabolic Health and Disease. 2024.
2. Child AH, et al. Lipedema: An Inherited Condition. Familial clustering suggests genetic etiology but mode is challenging; supports polygenic model with multiple susceptibility genes.
3. Keppler-Noreuil KM, et al. PIK3CA-related overgrowth spectrum (PROS): Diagnostic and testing criteria. PROS disorders can be caused by mosaic PIK3CA mutations. Example of somatic mosaicism in overgrowth.
4. Luks VL, et al. Case reports: Whole-exome sequencing on resected tissue revealed PIK3CA c.3140A>G with 11% mosaicism leading to PROS diagnosis (CLOVES). Illustrates tissue-specific mosaicism detection.

24/08/2026

Yes your estrogen can be LOW on a blood test… and that still doesn’t tell you everything about what’s happening in your tissues.

This is where the conversation around lipedema and hormones gets much more interesting as gynoid adipose tissue isn’t simply passive storage. It is metabolically active tissue that can participate in steroid hormone production, conversion and metabolism.

And your estrogen status is influenced by more than the number printed on one serum blood test, we also have to consider:

→ local aromatase activity
→ steroid-converting enzymes
→ genetic variation
→ liver conjugation
→ gut microbiome activity
→ enterohepatic recycling
→ bowel regularity
→ HRT, if applicable
→ and the individual hormonal environment of the tissue

This does NOT mean that low serum estrogen = “estrogen dominance.” And it certainly doesn’t mean every woman with lipedema needs to “detox estrogen.”

It means we need to stop treating one blood marker as the complete picture because it isn’t. Especially when we’re talking about a condition that has such a strong sex-hormone-associated, gynoid distribution.

So the real goal isn’t to chase estrogen lower, it is to understand the system because lipedema is complex and your biology deserves more than a single number on a lab report.

Educational content only. Not medical advice.

DM CLEARANCE if you are interested in my coaching waitlist or see Lindsay Huelse | Weight Loss for Moms for in-depth lab analysis like DUTCH

22/08/2026

Why are scientists suddenly so interested in one gene - AKR1C1 - for lipedema? 🧬

Well, for decades lipedema was dismissed as “just fat” or a lifestyle issue.
Then in 2020 they found the first mutated gene linked to non-syndromic lipedema in one family - 3 women with autosomal dominant lipedema all shared an AKR1C1 variant. AKR1C1 is the off-switch that turns active progesterone into its inactive form inside the fat tissue.
Their variant only worked at ∼50%. So active progesterone hung around longer in the subcutaneous fat and kept the fat-storage machinery switched ON.
This is why researchers are excited and why that line in thos reel states “pointing to new therapeutic targets BEYOND diet and exercise”:
1. Because it explains the pattern - 11% of women, female predominance, onset at puberty / pregnancy / menopause - it was always hormonal. This shows it’s about how fat tissue metabolizes hormones locally, not just blood levels.
2. It’s not just one family anymore either, in late 2023 they found AKR1C2 (the second gene) overexpressed in 24% of patients.

The BIG 2026 reviews now call the whole AKR1C pathway a central biological pathway for lipedema. Plus 3 common polymorphisms linked to higher risk.

3. It basically explains why diet and exercise don’t fix it, because it’s a pre-receptor metabolism + genetics + environment.
4. For us, this opens more doors.. if it’s hormone metabolism, then we can finally look at biomarkers, targeted therapies, personalized approaches, and why mental health is now considered a CORE part of lipedema, not just a consequence of living with it - because these same enzymes make neurosteroids 👀

That’s why 19 countries just agreed in the first international consensus: it’s never just an abnormal fat condition.
This doesn’t mean low progesterone or that HRT will fix or worsen lipedema - that wasn’t tested. It means hormone metabolism matters, and that’s why research beyond compression and liposuction is finally happening.

Educational only. Save this for your clinician appointment.

20/08/2026

I have one spot left Sept for coaching. Not only do I coach - I teach. You will learn to understand how your body works, build muscle and learn how to fuel yourself correctly. This is no quick fix, this is a journey that needs to be fully committed to for atleast 6 months. So you go away understanding and learning how to manage Lipedema for life.

20/08/2026

Your daily reminder that compression care IS self-care.

We wash them every wear, we air dry them... and then we absolutely cheat with the hair dryer when we need them NOW 🤣

Pro tip: low heat, keep it moving, and never high heat directly on flat knit 👀

18/08/2026

SPEND THE MORNING WITH ME: sclerotherapy for beginner varicose veins lipedema edition.

I get asked a lot - “Elle, should I treat small varicose veins if I have lipedema?”
Yes - early.
With lipedema our fascia / connective tissue is lax and our venous return is already working harder. Small superficial varicose + reticular veins can progress to pain, heaviness, itching, and worse swelling if we leave them.
Sclerotherapy is a common treatment for small varicose tributaries and reticular / spider veins. A sclerosant solution is injected into the targeted vein to irritate the lining, causing it to collapse and be reabsorbed over weeks.

What to know:
• Duplex ultrasound should come first to rule out deep system reflux
• Best for beginner / small veins - often needs 2-3 sessions
• You walk immediately after
• Compression + daily walking + no heat / heavy leg workout for a few weeks after is standard

This is not medical advice - venous treatment is individualized. Talk to a vein specialist / phlebologist about what’s appropriate for you.

Comment VEINS and I’ll DM you:
• My self-check checklist
• Daily habits that support venous return
• When to see your GP / vascular specialist and what to ask for

*Not medical Advice.

15/08/2026

Can men get lipedema? Yes. But the reason they almost never do explains the whole disease.

Every documented male case had low testosterone, high estrogen, Klinefelter XXY or hypogonadism.

When the male hormone brake comes off, the lipedema pattern can appear. That tells us this is hormone-sensitive tissue. It’s estrogen = store, testosterone = protect, plus a receptor imbalance (low ER-alpha, high ER-beta, low GPER)
that drives leaky vessels and poor lymphatic drainage.

That’s also why it flares at puberty, pregnancy, menopause for women.

Do you have more questions about this? And want the actual research papers behind this carousel?

I break down all the studies + answer your hormone questions inside my subscriber community. That’s where I share the research, not just the slides.

Tap Subscribe to support me on my profile to get access 🧬

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