Introduction
Lipoedema is increasingly being investigated as more than a disorder of abnormal fat distribution. Research now implicates adipose tissue, loose connective tissue, fascia, microvasculature and extracellular matrix remodelling, while clinical studies continue to identify a striking number of women with lipoedema who also report joint hypermobility and other symptoms associated with connective-tissue laxity.
Lipoedema and hypermobile Ehlers-Danlos syndrome (hEDS) are frequently discussed together. However, they are not the same condition, and being hypermobile does not automatically mean that someone automatically has Ehlers-Danlos syndrome.
In an earlier Lymph Fusion article, I looked more broadly at Lipoedema and Ehlers-Danlos Syndrome, including the possible relationship between connective tissue, hypermobility spectrum disorder (HSD) and hEDS.
This article looks at what newer research may mean in practice: What can help symptomatic hypermobility? What substantial weight loss with medications such as tirzepatide (Mounjaro) and semaglutide (Wegovy) may mean for skin and muscle, and whether hypermobility or Ehlers-Danlos syndrome should change the way surgery and recovery are approached.
Hypermobility, HSD and hEDS Are Not the Same Thing
Joint hypermobility simply means that one or more joints move beyond the range expected for most people.
Some people are naturally flexible and experience no problems at all. Hypermobility becomes clinically important when it is accompanied by problems such as recurrent sprains, instability, subluxations, pain, fatigue or other connective-tissue symptoms.
Hypermobility Spectrum Disorder, or HSD, describes symptomatic joint hypermobility that cannot be better explained by another condition and does not meet the diagnostic criteria for hEDS or another genetic connective-tissue disorder.
Hypermobile Ehlers-Danlos syndrome is a genetic connective-tissue disorder characterised by generalised joint hypermobility together with a broader pattern of musculoskeletal and systemic features.
These diagnoses overlap considerably, but they are not interchangeable.
What Is the Evidence in Lipoedema?
Hypermobility has been reported in lipoedema populations for some time, but recent research has brought the relationship into sharper focus.
A 2025 cross-sectional observational study by Fiengo & Sbarbati specifically examining lipoedema and Hypermobility Spectrum Disorders found that 44% of participants with lipoedema reported joint hypermobility and 60% recalled being hypermobile in childhood.
The women also reported a broader collection of symptoms including joint pain, low muscle tone, exercise-related fatigue and gastrointestinal symptoms.
These findings are significant, but they need to be interpreted carefully. The study used questionnaire data and does not establish that 44% of all women with lipoedema have HSD, nor does it demonstrate that one condition causes the other.
The 2026 Lipedema World Alliance consensus also reflects how much remains uncertain in lipoedema research. The emerging picture is that a subgroup of women with lipoedema appears to have a broader phenotype involving connective-tissue laxity and hypermobility.
Looking Beyond Flexible Joints
Hypermobility is often trivialised as simply being unusually bendy. For people with symptomatic hypermobility, hEDS or HSD, the consequences can be much wider.
Joint instability can lead to recurrent sprains, subluxations, dislocations and persistent musculoskeletal pain. Muscles may have to work harder to provide active stability around joints that have less passive support from connective tissues.
Proprioception- the body’s awareness of where a joint is positioned; may also be relevant to movement control and rehabilitation.
Someone who was extremely flexible as a child may no longer appear particularly hypermobile later in life. Injury, pain, surgery and ageing can all alter mobility, which is why childhood history can be useful when assessing adults.
Pelvic Floor Dysfunction and Prolapse
One of the less obvious areas associated with hEDS and HSD is pelvic-floor dysfunction.
A published review by Hoffman & Yeh identified a broad range of urogenital and pelvic problems in people with EDS and HSD, including urinary incontinence, pelvic-floor dysfunction and different forms of pelvic-organ prolapse.
While Pregnancy, childbirth, age, menopause, obesity and many other factors affect pelvic-floor function, recurrent or unusually early prolapse in a woman who is also hypermobile, has recurrent joint problems or has other signs of connective-tissue laxity may be relevant to the wider clinical picture.
Gastrointestinal and Autonomic Symptoms
hEDS and HSD can also be associated with symptoms beyond the musculoskeletal system.
Gastrointestinal symptoms and disorders are frequently reported, including constipation and disorders of gut-brain interaction. Autonomic symptoms, including orthostatic intolerance, are also recognised within the wider hEDS/HSD clinical picture.
Gastrointestinal and autonomic symptoms are common and can have many different causes, so they should not automatically be attributed to hypermobility. However, where they occur alongside other features of HSD or hEDS, they should be considered in the assessment criteria.
Can Hypermobility Be Treated?
At present, there is no medication that corrects the underlying connective-tissue abnormality in hEDS or HSD.
Treatment therefore concentrates on improving function and managing individual symptoms.
For musculoskeletal hypermobility, appropriately designed physiotherapy and exercise remain central
Treatment usually focuses on:
- progressive muscle strengthening
- core and limb stability
- proprioception
- movement control
- posture and biomechanics
- gradual physical conditioning
- protection of repeatedly unstable joints.
Braces, splints and other supports can sometimes be useful, particularly for unstable or repeatedly injured joints.
Pain treatment needs to be personalised. Gastrointestinal, autonomic and other associated symptoms may require their own management.
What About Tirzepatide (Mounjaro) and Semaglutide (Wegovy)?
This is becoming increasingly relevant for women with lipoedema.
Tirzepatide, Mounjaro in the UK, and semaglutide, Wegovy in the UK, can produce substantial weight loss in people who meet the appropriate indications.
I have discussed the emerging research around Mounjaro and lipoedema separately. Neither tirzepatide nor semaglutide is a treatment for hEDS or HSD.
However, major weight loss creates a separate issue for somebody who already has unusually lax connective tissue.
Rapid or substantial loss of adipose tissue reduces the volume supporting the overlying skin. Published medical literature now describes facial volume loss, skin laxity and body-contour changes following substantial weight loss associated with medications such as semaglutide.
The changes are not confined to the face. Skin laxity following major weight loss can affect areas including the neck, arms, abdomen and thighs, and excess folds can sometimes cause functional as well as aesthetic problems.
There is not currently good evidence demonstrating that people with hEDS or HSD develop more loose skin following tirzepatide- or semaglutide-associated weight loss than otherwise comparable people without these conditions.
Nevertheless, pre-existing connective-tissue laxity is an important consideration when discussing expectations following major weight loss.
Age, genetics, the amount and speed of weight loss, previous pregnancies, smoking, sun exposure, muscle mass and starting skin quality can all influence the final result.
Muscle Loss During Major Weight Loss
Another consideration is muscle loss.
A 2025 study followed 269 adults receiving either semaglutide or tirzepatide and measured changes in weight, fat mass, visceral fat and skeletal muscle mass over 12 months.
Both drugs produced substantial reductions in body weight and fat mass. The study also recorded changes in skeletal muscle mass, while reporting that lifestyle measures including strength training and adequate protein intake supported muscle preservation.
This is potentially particularly relevant for someone with symptomatic hypermobility because muscle provides active stability around lax joints, as there is no evidence that tirzepatide or semaglutide makes hEDS or HSD worse.
However, preserving muscular strength during substantial weight loss is a sensible consideration in somebody who already depends heavily upon muscular control for joint stability.
Excess Skin After Major Weight Loss
Increasingly effective obesity treatments mean that more people may subsequently consider body-contouring surgery.
Large folds of redundant skin are not necessarily only an aesthetic concern. They can cause rubbing, irritation, difficulty exercising, problems with clothing and physical discomfort.
Procedures including abdominoplasty, brachioplasty, thigh lift, breast uplift and other forms of body contouring may therefore be considered after substantial weight loss.
For someone with lipoedema, there may be another issue. Loss of non-lipoedema adipose tissue can change body proportions considerably without necessarily removing the characteristic distribution of lipoedema tissue.
A patient may therefore reach a much lower body weight while still having disproportionate lipoedema tissue and, at the same time, redundant skin following major weight loss.
For somebody who is also hypermobile or has hEDS, the quality and laxity of that connective tissue deserves consideration when planning what happens next.
Does Ehlers-Danlos Syndrome Affect Surgery?
Potentiallybut the answer is more nuanced than simply saying that people with EDS heal badly.
The Ehlers-Danlos syndromes are a group of different connective-tissue disorders with different surgical risk profiles.
An International Consortium Skin Working Group reviewed skin fragility and wound management across the Ehlers-Danlos syndromes, emphasising that tissue fragility and wound-healing problems vary between EDS types.
Vascular EDS in particular should never be confused with hEDS when discussing surgical risk.
Does EDS Mean You Cannot Have Plastic Surgery?
No. A diagnosis of EDS should not automatically exclude somebody from elective plastic surgery.
A 2025 matched cohort study compared 100 people with EDS undergoing elective plastic surgery with 100 matched controls. Hypermobile EDS was the most common subtype, representing 41% of the EDS group.
Complications occurred in 25% of the EDS group and 35% of controls. There was no statistically significant difference in either major or minor complication rates between the groups.
The authors concluded that elective plastic surgery can be performed safely in patients with EDS, particularly those with hEDS, but that patients with EDS should receive individual surgical assessment to assess any additional risks.
Preparing for Surgery When Hypermobility or hEDS Is Present
For somebody with significant hypermobility, HSD or hEDS considering lipoedema liposuction, skin-removal surgery or another substantial procedure, the surgical team should know about the diagnosis or suspected diagnosis beforehand.
Relevant considerations may include:
Tissue and wound quality
The surgeon may need to take account of tissue fragility, laxity, bruising or previous problems with wound healing.
Previous wound healing
A personal history of wound breakdown, unusually wide scars, prolonged healing or troublesome bleeding may provide useful information when planning future surgery.
Joint positioning
A hypermobile patient may have joints that are vulnerable to excessive positioning or prolonged loading during a long operation.
Known unstable shoulders, hips, knees, neck or other vulnerable joints should therefore be considered during positioning.
Autonomic symptoms
If somebody has significant orthostatic intolerance or another diagnosed autonomic disorder, this should be discussed with the surgical and anaesthetic team before surgery.
Rehabilitation
Rehabilitation should not simply focus on restoring maximum range of movement.
For a hypermobile patient, the priority may instead be controlled movement, muscular stability and return to function without repeatedly moving unstable joints into excessive end ranges.
Compression
After lipoedema surgery or body-contouring procedures, compression may be needed for surgical or lymphatic reasons.
In a hypermobile patient, garments may also need to be considered in relation to joint positioning, skin tolerance and the person’s ability to put them on and remove them safely.
Lipoedema Surgery Does Not Treat hEDS
This is an important expectation to establish before surgery.
Liposuction can remove lipoedema adipose tissue and may improve symptoms in appropriately selected patients but it cannot change an underlying connective-tissue disorder.
Someone with lipoedema and hEDS may therefore experience improvement in lipoedema-related symptoms while continuing to experience joint instability, pelvic-floor dysfunction, autonomic symptoms or other manifestations of hEDS.
What Should Clinicians Ask to Determine hEDS?
When assessing someone with lipoedema, it may be useful to ask about more than limb shape.
A wider connective-tissue history can include:
- marked childhood flexibility
- recurrent ankle sprains
- joints that repeatedly give way
- subluxations or dislocations
- chronic musculoskeletal pain
- unusually soft or stretchy skin
- easy bruising
- hernias
- unexplained or early pelvic-organ prolapse
- urinary or pelvic-floor problems
- gastrointestinal symptoms
- orthostatic symptoms
- previous problems with wound healing or unusual scars
- family members with similar joint or connective-tissue problems.
The Beighton score can contribute to assessment, but it should not replace the wider clinical history.
Where Does the Research Stand Now?
The evidence has moved forward, but there is still a great deal we do not know.
There is increasing interest in the role of connective tissue and extracellular-matrix biology in lipoedema and repeated evidence of hypermobility within lipoedema populations.
What has not been established is how many women with lipoedema have an Ehlers-Danlos syndrome.
Similarly, there is now evidence that substantial medication-associated weight loss can be accompanied by skin laxity and loss of underlying tissue volume.
But we do not yet know is whether people with hEDS or HSD develop more severe excess skin following tirzepatide or semaglutide treatment than people without a connective-tissue disorder.
Conclusion
Lipoedema, Hypermobility Spectrum Disorder and hypermobile Ehlers-Danlos syndrome remain separate diagnoses but the overlap between them is becoming increasingly difficult to dismiss.
New research has strengthened the evidence that hypermobility and wider connective-tissue symptoms occur within lipoedema populations.
There is currently no drug that treats the underlying hypermobility of HSD or hEDS. Management remains centred on muscular strength, proprioception, joint stability, symptom management and appropriate multidisciplinary care.
For people considering substantial weight loss with tirzepatide (Mounjaro), semaglutide or related medications, skin and muscle deserve consideration alongside the number on the scales. Major weight loss can leave significant skin laxity and redundant tissue, and maintaining muscle may be particularly relevant to somebody who relies upon muscular stability around hypermobile joints.
For those subsequently considering lipoedema surgery or body-contouring surgery, an EDS diagnosis should not automatically exclude them from treatment.
As our understanding of lipoedema moves beyond fat alone, recognising the connective tissue in which that fat exists may prove increasingly important.
References
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Kruppa P, Crescenzi R, Faerber G, et al. Lipedema World Alliance Delphi Consensus-Based Position Paper on the Definition and Management of Lipedema: Results from the 2023 Lipedema World Congress in Potsdam. Nature Communications. 2026;17:427. doi:10.1038/s41467-025-68232-z. PMID: 41519859. PMCID: PMC12796449.
Gilliam E, Hoffman JD, Yeh G. Urogenital and pelvic complications in the Ehlers-Danlos syndromes and associated hypermobility spectrum disorders: A scoping review. Clinical Genetics. 2020;97(1):168–178. PMCID: PMC6917879.
Thwaites PA, Gibson PR, Burgell RE. Hypermobile Ehlers-Danlos syndrome and disorders of the gastrointestinal tract: What the gastroenterologist needs to know. Journal of Gastroenterology and Hepatology. 2022;37(9):1693–1709. PMCID: PMC9544979.
Angwin C, Doolan BJ, Hausser I, et al. Skin fragility and wound management in Ehlers-Danlos syndromes: a report by the International Consortium on Ehlers-Danlos Syndromes and Hypermobility Spectrum Disorders Skin Working Group. Clinical and Experimental Dermatology. 2024;49(12):1496–1503. doi:10.1093/ced/llae201. PMID: 38767179.
Fodor R, Marlar R, Ku Y, et al. Revisiting Ehlers-Danlos Syndrome as a Relative Contraindication to Elective Plastic Surgery: A Retrospective Matched Cohort Study. Plastic and Reconstructive Surgery. 2025;156(5):695e–702e. doi:10.1097/PRS.0000000000012205. PMID: 40366279.
Haykal D, Hersant B, Cartier H, Meningaud JP. The Role of GLP-1 Agonists in Esthetic Medicine: Exploring the Impact of Semaglutide on Body Contouring and Skin Health. Journal of Cosmetic Dermatology. 2025;24(2):e16716. doi:10.1111/jocd.16716. PMID: 39645647. PMCID: PMC11845967.
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