A note before you read

This article discusses body weight, calorie intake, energy balance and weight management in some detail. I know that these topics can be difficult or triggering for some readers, including some members of the LipedemaScience community.

For others, this may be an important and useful discussion, particularly because weight and lipedema are often discussed in ways that are either overly simplistic or scientifically inaccurate.

If conversations about calories, food intake or body weight are difficult for you, I recommend skipping this article. There is no need to engage with content that may negatively affect your relationship with food or your body.

If you choose to continue, the purpose of this article is not to promote weight loss or restrictive eating. It is to examine what current research actually tells us about body weight, energy balance, adipose tissue and lipedema, including where the evidence remains uncertain.

Weight has a complicated place in discussions about lipedema. The disease is frequently mistaken for obesity, and many women have experienced being advised to lose weight without adequate consideration of the characteristic distribution of adipose tissue, pain, tenderness, bruising or heaviness associated with lipedema. This history explains why discussions about weight can be difficult. It does not, however, answer the physiological question of what changes in body weight mean once lipedema is already present.

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My own experience is one reason I have become interested in this distinction. I have remained within the normal BMI range throughout adulthood, but my body weight has varied by approximately 10 kilograms between different periods. I notice those differences most clearly when changes in weight coincide with changes in physical activity.

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I was around 15 when the first dramatic change happened. I had started taking hormonal birth control and gained approximately 12 kilograms in two months. It was not only the number on the scale that frightened me. The shape of my lower body changed too, and it did not feel like ordinary weight gain.

My legs became heavy and swollen. There was a deep, aching pain inside the tissue that I still find difficult to describe. The closest comparison I have is a severe toothache, except that the pain was inside my thighs and lower legs. Some nights, I would lie in bed massaging them because it was the only thing that calmed the pain enough for me to sleep.

At 15, I did not have a framework for understanding any of this. I did not know what lipedema was. I did not know that hormones might be relevant, or that other women had experienced similar changes. I simply knew that my body seemed to respond differently from the bodies around me.

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Food appeared to make a difference too. Sugar became one of my clearest triggers. If I ate a lot of it, my legs could feel more swollen, painful and irritated afterwards. I could not explain why, and I am still careful not to turn my own experience into a universal rule. But the pattern was noticeable enough that I began paying attention to it long before I understood anything about the condition.

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I also noticed something else. When I lost weight, it disappeared from my face and upper body much more readily than from my hips and legs. My proportions remained. This was not a question of refusing to exercise or consistently eating too much, although that is often how disproportionate bodies are judged. I could make my body smaller, but I could not make it respond in the way people expected it to.

Finally, a name

In January 2012, when I was 20, I was assessed at a Norwegian hospital. By then, I had lived with swelling in both legs for several years, and it had become noticeably worse during the previous six months.

My legs felt tight, heavy and tender. Although the discomfort usually increased as the day went on, I sometimes woke up with heavy legs in the morning. During the examination, it was noted that my feet were unaffected, while the tissue from my ankles towards my hips was enlarged and painful to pressure.

Other possible explanations were investigated, including blood clots, venous insufficiency, obstruction and lymphedema. The overall clinical picture was consistent with lipedema.

I was diagnosed at a BMI of 19.

I keep returning to that detail because it challenges one of the most persistent misunderstandings about lipedema. I was lean, and I was also in significant pain. Both things were true. Body size alone could not explain what was happening, nor could it show how much the condition was affecting my life.

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Having a name for it should have provided clarity. In some ways it did, but a diagnosis and an explanation are not the same thing.

I was advised to wear class II knee-high compression garments and to avoid gaining weight. That was essentially the full treatment plan. Most of my symptoms extended well above my knees, so I struggled to understand how knee-high garments were supposed to address them. I did not know what progression might look like, what I could do for the pain or what the diagnosis could mean for my future.

I left the hospital knowing that I had lipedema, but knowing very little about how to live with it.

The loneliness after diagnosis

For several years, lipedema felt like something that existed only inside my own life. I did not know anyone else who had been diagnosed. There were no large online communities where I could recognise myself in other people’s stories, and I could not find a patient-friendly platform that explained the research in language I could actually use.

It took around four years before I heard another Norwegian woman speak publicly about lipedema on television. Four years is a long time to have a diagnosis without hearing another person say its name.

My symptoms remained relatively stable for a while, but in 2018 they became significantly worse during an intensely stressful period of my life. That experience strengthened something I had already begun to suspect: my symptoms did not seem to be governed by body weight alone.

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Hormones appeared to matter. Stress seemed to matter. Sleep, food and movement appeared to influence how my body felt from one period to another. Inflammation and individual biology could also be part of the picture. Some of these relationships are scientifically plausible, but plausibility is not the same as proof, and the research has not yet given us all the answers. What I knew from living in my own body was that my symptoms were not static and that the scale could not explain every change.

When surgery became a real possibility

Around 2020, I learned that the cousin of someone I knew had undergone surgery for lipedema. Until then, surgery had felt distant and almost theoretical. Suddenly, it was something a real person had done.

I began reading everything I could find. I wanted to understand not only the potential benefits, but also the risks, the recovery and the uncertainty. Surgery is sometimes discussed as though it produces one predictable outcome. It does not. It is an invasive treatment, and every person enters it with a different body, symptom history and risk profile.

Between September 2021 and October 2022, I underwent four lipedema surgeries. The first was in September 2021, followed by procedures in November 2021, February 2022 and October 2022. Different areas of my legs and arms were treated across the four operations.

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It was a demanding year. Recovery meant pain, swelling, exhaustion, compression garments and periods when I did not know whether what I was experiencing was normal. Travelling between procedures added another challenge. Flying could cause substantial swelling and fluid retention, and at times I wore two layers of compression to make the journey manageable.

There were complications too. I developed a seroma in my thigh, experienced internal bleeding in my hand and had symptoms consistent with nerve irritation. I mention these things because I do not want to rewrite surgery as a simple success story just because it ultimately helped me. The benefits were real, but so were the risks and the difficult parts of recovery.

Even with those complications, the operations changed my life. The deep pain improved considerably. Movement became easier, and my body felt lighter. I still have areas of fibrosis and sensitivity, and surgery did not remove every symptom. I do not describe myself as cured. Lipedema is still part of my body and part of the way I make decisions about my health.

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The difference is that it no longer controls my daily life in the way it once did.

What living with lipedema looks like now

There is no single thing I do to manage lipedema. It is more like a collection of choices that changes depending on what my body needs.

I use compression when I fly because I know how strongly travelling can affect my legs. I receive manual lymphatic drainage when needed and use pneumatic compression at home. Strength training, running and everyday movement are important to me, as are sleep and stress management. I also pay attention to food, not because I believe there is one magical lipedema diet, but because I have learned that certain choices work better for my symptoms than others. Sea bathing and dry brushing are also part of my personal routine.

I am describing what I do, not prescribing what everyone else should do. People with lipedema can respond very differently to the same intervention. Something that brings relief to one person may do very little for another, or may not be practical or appropriate at all.

My approach has developed through years of observing patterns, getting things wrong, trying again and adjusting when my body changes. It is not a perfect system. It is simply how I have learned to live more comfortably in a body that does not always behave predictably.

The scientist and the patient

My relationship with lipedema has also been shaped by my academic background. I began studying human nutrition in 2014 and later completed a master’s degree in food science. Through my education and professional work, I gained experience in areas including cell biology, inflammation, intestinal cell research, bioactive peptides, microbiology, whole-genome sequencing and scientific writing.

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I have worked in laboratories, managed laboratory operations and contributed to published research. This background taught me how to read scientific papers, but perhaps more importantly, it taught me to notice what a study cannot tell us.

For a long time, these felt like two separate parts of my life. On one side, I was a woman living with lipedema, trying to understand pain, swelling and a changing body. On the other, I was trained to assess evidence, methods and uncertainty. After my surgeries, my surgeon encouraged me to bring those two perspectives together and use my background to help people who were searching for reliable information about nutrition, lifestyle and lipedema.

I initially created a knowledge platform for Norwegian women. Then, in November 2025, I took the next step and launched LipedemaScience for an international audience.

Why I created LipedemaScience

LipedemaScience grew out of the experience I had at 20: receiving a diagnosis, leaving the hospital and realising that I still had almost no idea what it meant.

I wanted to create the resource I had needed then.

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Today, there is far more lipedema content available online, but more information does not automatically mean better information. People with lipedema are exposed to confident claims about diets, supplements, hormones, medications, inflammation, lymphatic treatments and surgery. Some claims are supported by research. Some are based on early biological theories. Others come mainly from personal experience or commercial interests. Those distinctions matter.

A biological mechanism is not proof that a treatment improves lipedema in patients. An association found in a survey cannot establish cause and effect. A presentation at a conference is not the same as a published clinical trial. A registered study may be promising, but it has not produced evidence until the results are available. Personal experiences can help us ask better questions and feel less alone, but one person’s result cannot predict what will happen in everyone else.

This does not mean that we should dismiss everything that has not yet been proven. It means we should be honest about what we know, what we suspect and what remains uncertain.

That is what I want LipedemaScience to do. I want to make research understandable without stripping away the details that determine what the research actually means. People living with lipedema should be able to understand how a study was conducted, what the researchers found, where the limitations are and whether the conclusions being shared online are stronger than the evidence allows.

Scientific information should not be reserved for academics and clinicians. The people living with the condition belong in the conversation too.

More than 14 years have now passed since I received my diagnosis. During that time, I have moved through pain, confusion, isolation, worsening symptoms, four surgeries and a long recovery. I have also developed a much deeper scientific understanding of the condition and a more workable relationship with my own body.

There are still things I do not understand about my lipedema. There are questions that researchers cannot answer yet either. I no longer see that uncertainty as a reason to fill the gaps with easy promises. I see it as a reason to keep reading, questioning and explaining.

For many years, I felt as though I was carrying all those questions alone. I do not anymore. Through LipedemaScience, I hope fewer people with lipedema will have to feel that way.

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New studies have looked at GLP-1 medications, pain processing, lymphatic function, quality of life, inflammation and the relationship between lipedema and obesity. New clinical studies are being registered. At the same time, lipedema has appeared in formal physician education in the United States, Ireland has held its first national lipedema conference, and a major plastic surgery congress in Brazil dedicated an entire course to the condition.

None of this means that we suddenly have all the answers. But taken together, these developments tell us something important. Lipedema is receiving more scientific and medical attention across different parts of the world.

Three things to know

1. There is more research, but there has not been a treatment breakthrough.
Several new studies are important, but most are observational, cross-sectional or reviews. They can identify patterns and generate hypotheses, but they cannot yet tell us that a particular treatment changes the underlying disease.

2. Lipedema is entering more established medical settings.
In the space of two days, lipedema was part of accredited physician education at Texas A&M, the focus of Ireland’s first national conference, and the subject of a dedicated 5.5-hour course at a Brazilian plastic surgery congress.

3. Researchers are looking far beyond fat accumulation.
Recent studies are examining pain processing, lymphatic transport, systemic inflammation, mental health, quality of life, obesity, exercise and potential pharmacological treatment.

Here are some of the most important developments.

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A large study reports better symptoms among GLP-1 users with lipedema

One of the most talked-about new studies is likely to be the first large dataset examining GLP-1 and GLP-1/GIP medications in people with lipedema.

The study, published online on 14 August 2026 in Obesity Pillars, analysed data from 2,719 respondents with lipedema. Around 55% reported currently using a GLP-1 or GLP-1/GIP receptor agonist, most commonly tirzepatide.

Current users reported better physical and mental health and lower levels of pain, swelling and functional limitation than people who had never used these medications. Participants also recalled improvements after starting treatment.

That sounds promising, but there is a very important limitation.

This was a cross-sectional online survey based on self-reported medication use and symptoms. People were not randomly assigned to treatment, and researchers did not follow comparable groups prospectively.

The study therefore does not prove that GLP-1 medications treat lipedema itself.

Weight loss, metabolic changes, differences between people who use and do not use these medications, other treatments, and several forms of selection bias could influence the results.

What the study provides is a strong signal that deserves proper prospective clinical research.

Why this matters for people with lipedema: GLP-1 medications are already being widely discussed within the community. This study gives that discussion more data, but it does not yet give us proof of disease-specific treatment.

Evidence strength: observational and hypothesis-generating.

Source: Srinivasan et al., Obesity Pillars. Published online 14 August 2026. PMID 42656629. DOI 10.1016/j.obpill.2026.100316.

A Swedish study documents a very high burden on quality of life

On 14 August 2026, researchers from Sweden published results from the LISE study in PLOS One.

The study included 104 women with lipedema, 42 healthy controls and an exploratory comparison group of 44 women with advanced cancer.

Women with lipedema reported significantly poorer health-related quality of life than healthy controls across all eight dimensions that were measured. Their quality-of-life scores were comparable to those of women with advanced cancer in several dimensions, and the lipedema group also reported substantial pain, fatigue, anxiety, depression and body-image concerns.

That comparison needs to be handled carefully. The study does not mean that lipedema and advanced cancer are medically equivalent diseases.

What it demonstrates is that the patient-reported burden of living with lipedema can be extremely high, something that can easily be missed when the condition is viewed primarily in terms of body shape or fat distribution.

Why this matters: quality of life is not a secondary issue. These results strengthen the argument that pain, mobility, psychological health and participation in everyday life should be taken seriously when evaluating lipedema.

Evidence strength: controlled cross-sectional study. Important for documenting burden, but it cannot determine cause and effect.

Source: Goodrose-Flores & Björkhem-Bergman, PLOS One. Published 14 August 2026. DOI 10.1371/journal.pone.0355488. PMID 42599946.

New research suggests pain may involve more than painful fat tissue

Another study, published online in Phlebology on 18 August 2026, investigated central sensitization and pain thresholds.

Researchers compared 61 women with lipedema with 20 healthy controls.

Women with lipedema had lower pressure-pain thresholds not only in affected areas of the legs, but also in the forearm, an area not typically considered affected by lower-limb lipedema. They also had higher scores on the Central Sensitization Inventory.

This is interesting because it raises the possibility that pain in lipedema may involve changes in how the nervous system processes painful stimuli, rather than being explained entirely by local pressure or abnormalities within lipedema tissue.

But this distinction is critical: the study found features consistent with central sensitization. It did not establish that central sensitization causes lipedema pain.

Why this matters: understanding why lipedema hurts could eventually influence how pain is assessed and managed. It may also help explain why pain severity does not always correspond neatly with the visible amount of affected tissue or disease stage.

Evidence strength: small cross-sectional study. Mechanistically interesting, but not proof of causation.

Source: Yücel, Candan & Ata, Phlebology. Published online 18 August 2026. DOI 10.1177/02683555261478723. PMID 42613760.

A systematic review looks at what happens in the lymphatic system

Lymphatic dysfunction is one of the major questions in lipedema research.

A systematic review published on 10 August 2026 examined lymphoscintigraphy findings in people with lipedema.

Seven studies were included, covering 470 participants, including 311 with lipedema. Lymphoscintigraphy was reported as normal in 61.4% of patients with lipedema. When abnormalities were present, findings included tortuous lymphatic vessels, collateral vessels and visualization of popliteal lymph nodes.

The authors interpreted the overall pattern as being more consistent with lymphatic overload than clear lymphatic failure.

That is potentially important, but the included studies used different methods and protocols, which made the evidence too heterogeneous for a formal meta-analysis. So this does not settle the debate about lymphatic involvement in lipedema.

Instead, it reinforces a more nuanced picture: the lymphatic system may be involved without lipedema simply being another form of lymphedema.

Evidence strength: systematic review, but based on a small and heterogeneous underlying literature.

Source: Mortada et al., Plastic and Reconstructive Surgery Global Open. Published 10 August 2026. DOI 10.1097/GOX.0000000000008015. PMID 42578114.

Researchers are also challenging simple ideas about lipedema, inflammation and obesity

An August publication examining inflammatory markers compared 78 women with lipedema, 76 women with obesity without lipedema and 75 normal-weight controls.

CRP, erythrocyte sedimentation rate and the CRP-to-albumin ratio were higher in both the lipedema and obesity groups than in normal-weight controls. However, researchers did not find significant differences between the lipedema and obesity groups for these markers, and several other inflammatory indices were similar across all three groups.

This matters because claims that lipedema has a unique systemic inflammatory signature are common. These results are more complicated. They are compatible with low-grade systemic inflammation being present in women with lipedema, but they do not demonstrate that this inflammatory profile is specific to lipedema. Adiposity and obesity may account for at least part of the signal.

That distinction becomes especially important when studies include participants with different body compositions.

A separate narrative review published online on 20 August 2026 also examined the relationship between obesity and lipedema, arguing that the two should be considered distinct conditions that frequently coexist and may biologically and clinically influence one another. Importantly, the authors describe their proposed framework as a tool for clinical reasoning, not a formal guideline.

Why this matters: separating what belongs to lipedema itself from what is associated with obesity, body composition or disease stage remains one of the central challenges in lipedema research.

New clinical studies are being launched

The research pipeline is also growing. A new study from Cairo University was registered in August to compare aquatic exercise, land-based exercise and usual care in women with lipedema.

The randomized trial plans to include 60 women and assess functional capacity, pain, body composition, limb changes and quality of life over a 12-week intervention. The study was first posted on 10 August 2026, with a listed study start of 27 August.

This is worth watching because exercise is routinely recommended to people with lipedema, but we still have limited controlled evidence telling us what types of exercise work best for specific symptoms.

Another study in Turkey is comparing a personalized anti-inflammatory diet plus physical therapy with standard healthy nutrition advice plus the same physical therapy programme. It is designed as a randomized controlled trial with 75 women. The ClinicalTrials.gov record was updated on 29 July 2026, with an expected study start in August.

Again, registration does not mean a treatment works. These studies tell us what researchers are testing. We need to wait for results before drawing conclusions.

A new study is looking for blood-based inflammation markers

Another study became publicly available in the clinical trial registry on 26 August 2026. Researchers in Istanbul have collected data from 192 women, comparing women with lipedema with BMI-matched women with overweight or obesity and normal-weight healthy controls.

The researchers will evaluate several markers derived from routine blood tests, including the systemic immune-inflammation index and CRP-to-albumin ratio, to investigate whether they are associated with lipedema or disease severity.

The BMI-matched comparison group is particularly important because it gives researchers a better opportunity to distinguish inflammation associated with lipedema from inflammation associated with adiposity.

However, no published results are available yet. There is currently no validated blood test for diagnosing lipedema.

Source: ClinicalTrials.gov NCT07787234. First publicly posted 26 August 2026.

Lipedema enters accredited physician education in the United States

The scientific developments are only part of the story. On 28 August 2026, Texas A&M University Naresh K. Vashisht College of Medicine held “Lipedema in Focus: From Symptoms to Standard of Care” in Houston in partnership with the Lipedema Foundation.

The programme was accredited for up to 2.5 AMA PRA Category 1 Credits, meaning physicians could receive formal continuing medical education credit for participating.

The sessions covered adipose tissue dysfunction, recognition and diagnosis, pain and lymphatic transport deficiency.

This is significant because lipedema was not simply included as a small presentation inside an unrelated meeting. It was the subject of dedicated accredited physician education at a medical school.

Why this matters: one of the practical barriers facing people with lipedema is still finding healthcare professionals who understand the condition. Research alone cannot improve care if clinicians never encounter that research.

Evidence strength: this is not new scientific evidence. It is an important development in medical education and professional recognition.

Source: Texas A&M University College of Medicine / Lipedema Foundation. Event held 28 August 2026.

Ireland holds its first National Lipoedema Conference

The following day, 29 August 2026, Ireland held its first National Lipoedema Conference in Cork. The programme brought together healthcare professionals, surgeons, therapists, nutrition specialists, patient advocates and people living with lipedema.

Topics included the LipLeg Study, surgical case discussions, nutrition, metabolic health, GLP-1 treatments and the psychological impact of the condition.

Again, the conference itself is not scientific evidence. But it represents something important for patients: lipedema is becoming a subject around which national professional networks and care discussions are being built.

For a condition that many people still struggle to have recognised by healthcare professionals, that matters.

Source: Lipoedema Support Network Ireland. First National Lipoedema Conference, Cork, 29 August 2026.

Brazil dedicates 5.5 hours of a plastic surgery congress to lipedema

Also on 29 August 2026, the 39th Jornada Norte-Nordeste de Cirurgia Plástica in Natal, Brazil, hosted a dedicated course called “Lipedema 360°.”

The course ran from 08:00 to 13:30 and covered pathophysiology and diagnosis, surgical treatment, compression, manual therapy, postoperative complications, photobiomodulation and thermography.

This is noteworthy because lipedema was given an entire educational track within an established regional plastic surgery congress.

At the same time, the programme illustrates why evidence appraisal remains so important.

The fact that a therapy appears on the programme of a medical congress does not automatically mean that strong clinical evidence supports it. Treatments such as photobiomodulation or the use of thermography in postoperative lipedema care need to be evaluated separately against the published evidence.

Why this matters: medical recognition is growing, but recognition and evidence are not the same thing.

Source: Official programme, 39º Jornada Norte-Nordeste de Cirurgia Plástica, Natal, Brazil, 29 August 2026.

So, are things finally changing?

Possibly.

What stands out is not one single breakthrough. It is the number of different directions moving at the same time.

Researchers are studying the biology of pain. Others are examining lymphatic function, inflammation and obesity. Large patient datasets are beginning to provide clues about medications already being used in the real world. Randomized trials are being designed around exercise, nutrition and conservative treatment.

And outside the laboratory, lipedema is becoming more visible in physician education and professional conferences in different parts of the world.

That is progress. But it also creates a new challenge. As attention grows, so will treatment claims.

A conference presentation is not a clinical trial. A biological mechanism is not proof of benefit in patients. An association in a survey is not proof that a medication treats lipedema. And a promising registered study has not produced evidence until its results are available.

For people living with lipedema, the most encouraging development may therefore be something broader than any individual study:

the scientific conversation around lipedema is getting bigger, more international and more specific.

Now the next step is to make sure the quality of the evidence catches up with the level of attention.

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The evidence is strongest when we look at dietary patterns rather than isolated foods. Mediterranean-style dietary patterns, for example, have been shown in randomised trials to influence inflammatory markers including CRP, TNF-α and several interleukins. These are different substances we can measure in the body that can tell researchers something about inflammatory activity. Tools such as the Dietary Inflammatory Index also attempt to estimate the inflammatory potential of an overall diet based on research linking nutrients and foods with inflammatory biomarkers. But even the DII is a population-level research tool; it is not a test telling us whether broccoli, tomatoes, dairy or almonds are inflammatory for you. The same dietary inflammatory score does not necessarily translate into the same inflammatory state in every individual.

That is why I dislike the idea of an “anti-inflammatory food list” when it is presented as universal truth. Foods commonly placed on those lists tend to contain components that could contribute to a lower-inflammatory dietary pattern - fibre, polyphenols, carotenoids, unsaturated fats, omega-3 fatty acids and so on. That is useful nutritional information. But your body does not read the list.

Two people can eat the same meal and have quite different physiological responses. In PREDICT 1, more than 1,000 adults showed substantial person-to-person variation in glucose, insulin and triglyceride responses after identical meals. Earlier work involving 800 people similarly found large differences in glucose responses to the same foods. That does not mean every different glucose response equals a different inflammatory response, but it demonstrates an important principle: food interacts with a biological system, and our biological systems are not identical.

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There are also much clearer examples where an otherwise nutritious food can produce an undesirable immune response in a particular person. Someone with a genuine food allergy can mount an immune response to a food that would be perfectly healthy for most people. Gluten is another obvious example in someone with coeliac disease. Conversely, feeling bloated after eating a food does not automatically mean that food has caused inflammation. Intolerance, fermentation and gastrointestinal symptoms are frequently confused with inflammation online.

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There is no magical group of foods that enters the body and switches inflammation off.

When scientists describe a food or diet as “anti-inflammatory,” we are usually talking about what has been observed across groups of people: certain dietary patterns are associated with lower concentrations of particular inflammatory biomarkers or a lower risk of inflammation-related disease.

That is very different from saying, “This food is anti-inflammatory for everyone.”

Your response depends on the whole biological context - your health, metabolism, immune system, gut microbiome, allergies, medications, activity, the amount you eat, what you eat it with, how it is prepared and what the rest of your diet looks like.

This is why, as a food scientist, I would much rather teach you how an anti-inflammatory dietary pattern is constructed than hand you a green list and a red list. A blueberry does not become medicine because it appears on an infographic, and a food does not automatically become “inflammatory” because you experience a symptom after eating it.

Nutrition is much more interesting - and much more complex - than that.

There is another part of this that I think is particularly important: personalisation should not turn into nutritional chaos either. Individual variation does not mean that nutrition science has no generalisable findings. We absolutely do have useful evidence about dietary patterns and health. It simply means that we can have strong population-level principles and acknowledge that applying those principles to an individual requires context.

This matters particularly when you have lipedema because “inflammation” has become one of the main explanations used to justify dietary advice in our community, even though the science is much more nuanced.

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There is evidence that inflammatory processes are involved in lipedema biology, and newer studies have found associations between more pro-inflammatory dietary patterns, higher inflammatory markers and, in some studies, greater pain. But this does not yet establish that a particular food causes inflammation in lipedema tissue, or that eliminating foods from an “inflammatory foods” list treats lipedema. A 2025 systematic review found only nine dietary intervention studies in lipedema, involving 269 women, with substantial differences between the studies and mostly moderate-to-high risk of bias. A 2026 review likewise concluded that there is currently no established evidence-based nutritional treatment for lipedema.

This distinction matters because when you live with lipedema, it is very easy to be told:

“Don’t eat dairy.”

“Don’t eat gluten.”

“Don’t eat tomatoes.”

“Don’t eat carbohydrates.”

“Don’t eat seed oils.”

“Don’t eat this because it causes inflammation.”

Eventually, trying to eat “anti-inflammatory” can become an increasingly restrictive way of eating without good evidence that those individual foods are actually worsening your lipedema.

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At the same time, I do not think we should swing too far in the other direction. Dietary pattern probably does matter. A 2026 study of women with lipedema found that a higher Dietary Inflammatory Index was associated with higher TNF-α and IL-6, while greater adherence to a Mediterranean diet was associated with lower concentrations. Importantly, the study was cross-sectional - meaning it looked at relationships at one point in time rather than proving cause and effect - and included only 60 women with stage 2–3 lipedema and BMI 30–40. It therefore cannot demonstrate that particular foods caused their inflammation or that the same relationship applies to every person with lipedema.

That is where the distinction between population evidence and your individual body becomes useful.

Something can be part of a generally health-promoting, lower-inflammatory dietary pattern while still being unsuitable for one particular person because of an allergy, coeliac disease, intolerance or another medical reason. Conversely, feeling pain, swelling or bloating after eating something does not automatically demonstrate that the food has produced systemic inflammation or aggravated your lipedema tissue. Your symptoms are important information, but symptoms are not themselves an inflammatory biomarker.

For those of us living with lipedema, I therefore think the more useful question is not:

“Is this food inflammatory?”

It is:

“What does my overall way of eating look like, what evidence do we have for it, how does my body respond to it, and can I eat this way sustainably while meeting my nutritional needs?”

That changes the whole conversation. Instead of hunting for the perfect anti-inflammatory food list, we can build a dietary pattern around vegetables, fruit, legumes, whole grains where tolerated, nuts and seeds, fish and other appropriate protein sources, unsaturated fats and minimally processed foods - while adjusting it for the individual rather than treating the list as a prescription.

And this is particularly relevant to lipedema because when you live with a chronic condition, you can very quickly accumulate more and more rules in the name of controlling inflammation. The current evidence does not justify making food frightening.

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There is also an interesting scientific tension here. Recent lipedema studies are beginning to show relationships between diet quality and inflammatory biomarkers, but we are still a long way from being able to say, “eat X and your lipedema inflammation will decrease” or “avoid Y because it is inflammatory for lipedema.”

Foods commonly called “anti-inflammatory” that may not work for everyone

Here are some examples that show why a universal list becomes problematic.

• Fatty fish such as salmon, sardines and mackerel
  These are commonly labelled anti-inflammatory because EPA and DHA omega-3 fatty acids can influence inflammatory pathways. But fish is also a major food allergen. In someone with a fish allergy, proteins in that same salmon can activate the immune system and cause a genuine inflammatory allergic response.

• Nuts such as walnuts and almonds
  Nuts provide unsaturated fats, fibre, polyphenols and micronutrients and are commonly included in anti-inflammatory dietary patterns. But tree-nut allergy can produce an immune response, sometimes from very small amounts. The food can therefore be nutritionally beneficial at population level while being completely inappropriate for a particular individual.

• Sesame and seeds
  Seeds are often recommended because of their unsaturated fats, fibre and phytochemicals. However, sesame is a recognised major allergen. For someone allergic to it, sesame is certainly not “anti-inflammatory” in any meaningful practical sense, because the immune system identifies sesame proteins as a threat.

• Whole-grain wheat, barley and rye
  Whole grains are generally associated with beneficial dietary patterns because they provide fibre, minerals and phytochemicals. But for someone with coeliac disease, gluten in wheat, barley and rye triggers an abnormal immune reaction that damages the small intestine. This is one of the clearest examples of why we cannot classify a food solely according to a universal anti-inflammatory list.

• Yoghurt and kefir
  Fermented dairy foods are frequently promoted for their protein, micronutrients and potential effects on the gut microbiome. But someone with a cow’s-milk protein allergy can have an immune reaction to them. Importantly, this is different from lactose intolerance. Lactose intolerance can cause bloating, pain, gas and diarrhoea, but it is not an allergic inflammatory reaction.

• Soy foods such as tofu, edamame and tempeh
  Soy provides protein, unsaturated fat and isoflavones and can fit very well within a Mediterranean-style or plant-rich dietary pattern. At the same time, soy is one of the major food allergens, so an individual with soy allergy can mount an immune response to exactly the same food.

• Legumes such as chickpeas, lentils and beans
  These are rich in fibre, resistant carbohydrate, minerals and phytochemicals and are normally an excellent component of a health-promoting diet. Yet many legumes contain fermentable carbohydrates such as GOS, which can cause substantial bloating, pain and bowel symptoms in some people with IBS. That does not automatically mean the legumes are causing inflammation. Fermentation, movement of water into the bowel and increased sensitivity in the gut can explain symptoms without us needing to label the food “pro-inflammatory.”

• Garlic and onions
  These frequently appear on anti-inflammatory food lists because they contain various organosulfur compounds and phytochemicals. They are also extremely high in fructans, a type of fermentable carbohydrate or FODMAP. For someone with IBS, a meal containing lots of onion or garlic can cause pronounced pain, bloating and distension. Again, the symptoms are real, but they should not automatically be interpreted as evidence that garlic has caused systemic inflammation.

• Fruit such as apples, cherries, mangoes and pears
  Fruit is one of the foundations of many dietary patterns described as anti-inflammatory because it provides fibre, vitamins and thousands of different phytochemicals. But several fruits contain larger amounts of fructose, sorbitol or both, which may produce gastrointestinal symptoms in susceptible people. You can therefore feel significantly worse after a perfectly nutritious fruit without that proving that the fruit is “inflammatory” for your body.

• Cashews and pistachios
  Nuts as a category are usually placed firmly on the anti-inflammatory side of food pyramids. Yet cashews and pistachios are relatively high in GOS and fructans, so they can cause gastrointestinal symptoms in some people with IBS. They can also cause true nut allergy in susceptible individuals. Two completely different mechanisms can therefore make the same supposedly “anti-inflammatory” food unsuitable for two different people.

The important lesson

This is why I would be careful with the sentence “this food becomes pro-inflammatory in my body.” Sometimes that is biologically defensible — for example, gluten in someone with coeliac disease or an allergen in someone with a genuine food allergy.

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But sometimes what you are experiencing is fermentation, intolerance, altered digestion, increased sensitivity in the gut or another physiological response that is not the same thing as systemic inflammation.

So when I hear someone with lipedema say:

“Tomatoes make me inflamed.”

“Dairy causes inflammation in my body.”

“I become inflamed when I eat carbohydrates.”

My next question as a food scientist is:

What exactly do you mean by inflammation?

Pain? Swelling? Bloating? Diarrhoea? Headache? Fatigue? An allergic reaction? A diagnosed autoimmune response? Or has inflammation actually been measured? Those are very different things.

And that is precisely why an anti-inflammatory food list can never tell the whole story. It tells us something about nutritional patterns and average effects across populations. It cannot tell us exactly how your individual body will respond to every food.

So what actually is inflammation?

Inflammation is part of your body’s immune defence and repair system. It is a coordinated biological response that your body activates when it detects something potentially harmful, such as an infection, tissue injury or an immune trigger.

Immune cells release signalling molecules called cytokines and chemokines - essentially chemical messages that allow cells to communicate with one another. Blood vessels change, and additional immune cells are recruited to the affected tissue. This can increase blood flow and fluid movement and produce familiar signs such as heat, redness, swelling and pain. The purpose of this response is to contain the problem, remove damaged material and help the tissue repair itself.

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In acute inflammation, this response is normally temporary and settles once the problem has been dealt with. In chronic inflammation, inflammatory signalling remains active for longer periods and can contribute to tissue dysfunction and disease.

This is also why “feeling inflamed” is not necessarily the same as having inflammation. Bloating, heaviness, pain or fatigue can have many different causes. Inflammation is a specific biological process involving immune cells, signalling molecules, blood vessels and changes within tissues.

For me, this is one of the most important things to understand about nutrition when you live with lipedema. We should absolutely be interested in inflammation, diet quality and how food may influence our health. But we also need to be precise about what the science can and cannot tell us.

Food should be something we learn to understand, not something we learn to fear.

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• There are probably things that help people with lipedema that science has never studied. Lipedema research is still young, and absence of evidence is not evidence that something does nothing.

• That does not make every plausible treatment equally plausible. We need to distinguish direct lipedema evidence from borrowed evidence, biological reasoning, clinical experience and personal experience.

• You do not need to do everything. The goal should be to find the smallest sustainable set of things that gives you meaningful benefit, not to become perfect at managing lipedema.

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Let’s play devil’s advocate when it comes to conservative treatment for lipedema.

The internet is full of tools, routines, protocols, supplements, compression strategies, massage techniques, exercise advice, dietary approaches and “must-do” habits. When you are constantly exposed to all of it, managing lipedema can start to feel like another full-time job.

That can create its own burden. You may start feeling that you are not doing enough, or that you are failing because you do not dry brush, wear compression every day, follow a specific diet, perform lymphatic drainage, use a pneumatic compression device, exercise in exactly the right way, take the right supplements and keep up with everything else someone online says you “should” be doing.

But conservative treatment is supposed to support your life, not take it over. And this is where I think we need more nuance, because there is no single truth here with two lines underneath it.

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There are probably things that work that nobody has studied

I want to start here because otherwise this article could easily become another version of “there is no randomized controlled trial, therefore don’t do it.” That is not what I think, and it would be a particularly poor way of approaching a condition such as lipedema.

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Lipedema remains under-recognized, underfunded and insufficiently studied. The number of clinical trials is small, many studies include few participants, definitions and diagnostic criteria have changed over time, and several commonly recommended treatments have never been properly isolated and tested. In a research field like this, absence of a study often tells us as much about the maturity and funding of the field as it does about the intervention itself.

Behind LipedemaScience is a food scientist and nutritionist with a background in laboratory research and years of experience living with lipedema herself.

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I am a food scientist, nutritionist, and former laboratory researcher who also lives with lipedema. LipedemaScience brings these parts of my life together.

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A new integrative review from a Brazilian physiotherapy group tries to bring this literature together. Published in Jornal Vascular Brasileiro in July 2026, it asks which physiotherapy strategies have been described for assessing and treating lipedema.

The review is helpful, but not quite in the way its evidence labels suggest.

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Three key takeaways

1. Intermittent pneumatic compression has the strongest direct treatment evidence in this review. It is still a small evidence base, but it includes randomized and controlled studies in women with lipedema.

2. Compression and exercise remain reasonable parts of symptom management, but much of their support comes from small studies, indirect physiology and expert consensus. That is not the same as strong proof that they alter the disease itself or prevent progression.

3. Use this review as a map to the primary studies, not as the final authority on them. Its evidence grading is inconsistent, some numbers contradict each other, and one treatment section makes a favorable lipedema recommendation without including any lipedema data.

That does not make the paper useless. It means we must use it for the job it can actually do.

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What the review says

Modena, Baiocchi and Guirro searched five databases between March and August 2025. They identified 745 records and included 28 studies. Instead of organizing the results around outcomes such as pain, function or quality of life, they organized them by assessment method and treatment modality.

The assessment section reads almost like a clinical primer. It covers medical history, including the timing of symptoms around hormonal changes, and physical examination findings commonly associated with lipedema. These include symmetrical disproportion, pain or tenderness, easy bruising, sparing of the feet and usually negative Godet and Stemmer signs. It also presents the familiar three-stage skin classification and Schingale’s five anatomical types.

The authors list several ways clinicians and researchers can follow symptoms and tissue changes over time: circumference and volume measurements, visual analogue scales for pain, the QuASiL symptom questionnaire, WOMAC, SF-36, bioimpedance, standardized photographs and soft-tissue ultrasound. They also discuss differential diagnosis against lymphedema, obesity, chronic venous insufficiency, lipohypertrophy and edema caused by systemic disease.

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This is one of the paper’s more useful sections. It gathers many of the tools used in lipedema practice and research into one place. Still, a checklist is not a validated diagnostic standard. Negative Godet and Stemmer signs can support the clinical picture, but they do not diagnose lipedema on their own or cleanly exclude every overlapping condition.

The treatment section covers eight broad approaches:

• complete decongestive therapy, or CDT

• compression

• exercise and musculoskeletal physiotherapy

• manual treatments, including subcutaneous adipose tissue therapy

• extracorporeal shock wave therapy

• photobiomodulation

• intermittent pneumatic compression

• mechanical vibrotherapy

The review’s general message is that conservative physiotherapy may reduce pain, improve mobility, help manage fluid-related symptoms and support quality of life. It also acknowledges that the literature is limited and that more robust trials are needed.

At that level, the conclusion is fair. The problems begin when the paper tries to tell us how strong the evidence is.

My background combines human nutrition, food science, and laboratory research. My perspective also comes from living with lipedema myself.

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An evidence level is not the same as trustworthy evidence

The authors use a hierarchy that classifies studies mainly according to design. In their own description, Level 1 is a meta-analysis of randomized controlled trials, while Level 2 is an individual randomized controlled trial.

Yet the paper labels both a single vibrotherapy trial and a single intermittent pneumatic compression trial as Level 1. The Brazilian QuASiL validation study is listed as Level 4 in the evidence table, then described as having Level 1 to 2 support in the text.

These are not merely cosmetic errors. Readers may see “Level 1” and reasonably assume that the intervention is supported by the highest-quality evidence. In this paper, the label may tell us little more than that a study was randomized, and sometimes the label does not even follow the paper’s own definition.

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Study design is only the beginning of quality assessment. A randomized trial can still be weakened by poor allocation methods, lack of blinding, attrition, selective reporting, very small groups or inappropriate outcome measures. The review does not formally assess these risks for the included studies. It has no registered protocol, no risk-of-bias tool and no formal appraisal of certainty across outcomes. It reports that two reviewers assessed studies independently, which is a strength, but it does not show an agreement statistic.

This matters because an unblinded trial of thirty participants with subjective outcomes should not be interpreted as if randomization alone settles the question.

There are also basic inconsistencies. The flow diagram reports that 217 records remained after duplicate removal and that 155 were excluded during screening. That should leave 62 records, yet only 44 full texts were assessed. Eighteen records disappear without explanation. The table and discussion give different sample sizes for the Szolnoky intermittent pneumatic compression study and the Ibarra manual therapy pilot. The paper describes three stages, then recommends compression for “stage 4,” even though lipo-lymphedema is not consistently defined as a fourth stage in the classification it has just presented.

Individually, these errors might be minor. Together, they mean that numbers and evidence labels should be checked against the original papers before being repeated.

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When plausibility is promoted into evidence

The photobiomodulation section shows the deeper reasoning problem.

The review cites four studies and grades the evidence as Level 1 to 2. But none of the studies was conducted in people with lipedema. They concern breast cancer-related lymphedema. Evidence can be methodologically strong within one population and still be indirect for another condition. Lymphedema and lipedema can overlap, and lymphatic dysfunction may be relevant in some people with lipedema, but the two diagnoses are not interchangeable.

Two of the cited reviews also reported non-significant effects on volume-related outcomes. Even so, the section ends by calling photobiomodulation a “consistent, safe, and potentially valuable” approach for lipedema.

That conclusion moves too quickly. A plausible mechanism can justify a lipedema trial. It cannot replace one.

I want you to think critically. Learn new things, ask questions, and stay curious. Our understanding of lipedema is still far from complete, but the research is growing. At LipedemaScience, we want to follow that journey as it unfolds.

The same problem appears in softer forms elsewhere. A systematic review does not automatically provide strong evidence simply because it is a review. If its ten included studies are small pilots and quasi-experimental studies, the review inherits those weaknesses. Weak evidence does not become strong when it is wrapped in a higher-ranking study design.

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Co-interventions make interpretation even harder. One shock wave study treated fifteen women with shock wave therapy, kinesio taping, compression and intradermal injections of Lymdiaral, described in the paper as a homeopathic preparation. There was no control group. If pain, circumference and tissue measures improve after four treatments are given together, we cannot identify which component caused the change. The review nevertheless presents the findings within its evidence for shock wave therapy without meaningfully confronting this problem.

There is also a recurring issue with what researchers choose to measure. Several interventions reduced limb volume or circumference over a period ranging from days to weeks. In lymphedema, fluid volume is a central outcome because accumulated fluid is part of the disease. In lipedema, the affected tissue is adipose tissue, even when fluid, microvascular changes and secondary lymphatic dysfunction also contribute to symptoms.

A 5.6 percent reduction in limb volume after five days is therefore much more likely to reflect fluid movement than loss of lipedema fat. That may still be valuable if a person feels less heavy or has less pain. But the biological meaning is different, and the review does not ask whether short-term volume change predicts better function, fewer symptoms or slower progression years later.

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The follow-up periods are generally short in a lifelong condition. No synthesis of durability, harms, costs or access is provided. Adherence is mentioned, especially the discomfort, fit problems and difficulty putting on compression garments, but it is not allowed to influence how strongly compression is recommended. A treatment that works only when used, but is too painful or impractical to use consistently, has a real-world limitation that belongs in the evidence assessment.

What the individual treatment sections can really tell us

Complete decongestive therapy and compression are widely recommended, but much of that recommendation comes from clinical experience and consensus rather than large, high-quality lipedema trials. The randomized CDT study cited in the review included 33 women divided across three groups, leaving roughly eleven participants per arm. That can generate an important signal, but it cannot settle which component works best, for whom, or for how long.

The review also cites a five-person pilot using sodium MRI as evidence that multimodal physiotherapy reduced tissue inflammation. This deserves more caution. Tissue sodium is an interesting imaging signal, but a change in sodium after a combined program of CDT, exercise, compression and education does not directly demonstrate that inflammation was reduced. It certainly does not tell us which part of the program produced the change.

LipedemaScience is not about pretending that we already have all the answers. It is about examining what we know, questioning what we think we know, and staying open to what new research may reveal. Knowledge about lipedema is still developing, and I want us to follow that development with curiosity, honesty, and critical thinking.

Exercise is supported by modest lipedema-specific research, together with strong general knowledge about muscle strength, mobility, cardiovascular health and the muscle pump. It is reasonable to include movement in long-term care, especially when adapted to pain, joint stability and current capacity. The safest conclusion is that exercise can support function and general health and may improve symptoms. Claims that it prevents lipedema progression or meaningfully changes the diseased adipose tissue require stronger evidence.

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Manual therapy may help some people with pain, tissue mobility or the feeling of tightness. But the SAT therapy evidence presented here comes mainly from two uncontrolled pilots with seven participants each. These studies are useful for generating hypotheses, not confirming effectiveness.

Shock wave therapy and vibrotherapy remain preliminary. The vibrotherapy section rests on one trial of thirty women, while the shock wave studies are small and complicated by combined treatments. Photobiomodulation has no direct lipedema evidence in this review and should not be presented as an established treatment for the condition.

Intermittent pneumatic compression is the modality that survives the review most clearly. It has several small studies pointing in the same direction, including a randomized study of 46 women with stage 2 lipedema. Participants using an advanced pneumatic compression device at home for thirty days were compared with a group continuing compression garments alone. The study reported improvements in several fluid, ultrasound and patient-reported measures.

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Even here, caution is needed. The paper highlights a statistically significant reduction in the left leg volume. In a bilateral condition, a significant result on only one side raises questions about multiple testing, variability and why the other leg did not show the same result. The trial was also short. Still, among the interventions assembled by this review, intermittent pneumatic compression has the clearest direct trial support.

What this review leaves unresolved

The review gives no effect sizes or confidence intervals, does not pool comparable outcomes and does not systematically examine adverse events. Without effect sizes, it is difficult to know whether a statistically significant change was large enough to matter in daily life. Without confidence intervals, we cannot see how uncertain the estimate is.

The prevalence section is another warning sign. It gives a prevalence range of 0.06 to 11 percent, then mentions an estimate of 39 percent in Germany without explaining why it lies far outside that range. It also places an estimate of 8.8 million Brazilian women with symptoms suggestive of lipedema close to statements about diagnosed disease. Screening estimates and clinical diagnoses are not the same.

The paper notes that lipedema has no accepted biomarker or universal diagnostic standard. That should make us more cautious about prevalence estimates, not less. When estimates span several orders of magnitude, part of what we are seeing is likely variation in definitions, sampling and ascertainment.

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The paper also states that a positive family history in up to 60 percent of cases supports autosomal dominant inheritance. Familial clustering can support a genetic contribution, but it does not by itself establish a specific inheritance pattern. Shared environments, referral patterns and the way family history is collected also matter.

I am a food scientist and nutritionist with a background in laboratory research, and I have lived with lipedema since long before I knew its name.

Finally, the same researchers recur across consensus documents and primary studies in this small field. Herbst is an author on the US consensus guideline, a SAT therapy pilot and the pneumatic compression trial included in the review. This is not evidence of misconduct. It is what a young and relatively small research field often looks like. But it means that guidelines and studies should not always be counted as independent layers of confirmation when they partly arise from the same research network.

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How I would use this paper

I would keep it. The table is a useful index of conservative treatment studies, and the assessment section can help clinicians and readers see which symptoms, differential diagnoses and measurement tools are commonly discussed. If I wanted to learn more about compression, SAT therapy, shock wave therapy or intermittent pneumatic compression, this review would help me find the relevant primary papers.

I would not use it as proof that every listed treatment works. I would not quote its evidence levels without checking how they were assigned. I would not cite it for prevalence or for the effectiveness of photobiomodulation in lipedema. And I would verify every sample size and numerical result against the original study before publishing it.

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For someone living with lipedema, the practical message is narrower than the review’s treatment list:

• Compression may help pain, heaviness and fluid-related symptoms, but it should be individually fitted and tolerable enough to use.

• Movement and strength work are sensible for function, circulation and general health, even though lipedema-specific trials remain limited.

• Intermittent pneumatic compression currently has the best direct trial evidence among the modalities reviewed and may be a useful addition for some people.

• Manual therapy, shock wave therapy and vibrotherapy remain experimental or supported mainly by small pilots.

• Photobiomodulation is biologically interesting, but this review does not provide direct clinical evidence that it works for lipedema.

Most importantly, symptom relief is not the same as removing lipedema tissue, and a short-term change in circumference is not proof that a treatment changes long-term disease progression. Those distinctions matter when people are deciding where to spend their money, effort and hope.

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My verdict is simple: this is a useful inventory and a weak evidence synthesis. It tells us where the studies are. It is less reliable when it tells us how much confidence to place in them.

Use it as a bibliography, then read the primary research.

This article discusses research and is not individual medical advice. Treatment decisions should be adapted to symptoms, health status, contraindications and personal tolerance together with qualified healthcare professionals.

1. The role of physical therapy in the treatment of lipedema: an integrative review of therapeutic strategies and the current clinical landscape (DOI: 10.1590/1677-5449.202501962)

• 4.12 billion are women and girls

• 4.18 billion are men and boys

The 2026 Lipedema World Alliance consensus states that prevalence among adult women remains unknown, with published estimates ranging from less than 1% to 12%.

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If those percentages were applied very approximately to the world’s female population, they would suggest:

• 1%: approximately 41 million

• 5%: approximately 206 million

• 10%: approximately 412 million

• 12%: approximately 494 million

Lipedema has also been documented in men, but published cases remain rare and no reliable global prevalence estimate exists. Although a figure of 0.2% has appeared in parts of the literature, the evidence is not strong enough to conclude that approximately 8.4 million men have lipedema.

These calculations are illustrations of scale, not reliable estimates of how many people have lipedema. The prevalence range relates to adult women, while the global female population also includes children, and diagnostic recognition varies considerably between countries. We therefore cannot conclude that more than 400 million women have lipedema. What we can say is that… lipedema may affect tens or even hundreds of millions of people worldwide, while the true number remains unknown. Men can also develop lipedema, but no credible global prevalence estimate currently exists.

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One Global Community, Many Different Lives

At LipedemaScience, we bring people from all over the world together under one umbrella. Your gender, age, location, stage of lipedema and personal management choices do not determine whether you belong here. What matters is that we meet one another with kindness, share what we know, support each other and cheer one another on.

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The LipedemaScience community now reaches 63 countries. The people represented by these numbers live in different climates, cultures and healthcare systems, but geography is only one part of the picture. We also differ in how lipedema presents, how advanced it is, which symptoms affect us most and whether we live with other conditions alongside it. Age, hormonal life stages, work, family responsibilities, financial resources and access to qualified healthcare can all influence which forms of management are realistic, appropriate or sustainable.

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Personal goals and preferences matter too. One person may be trying to reduce pain enough to remain at work, while another is preparing for surgery, rebuilding strength after treatment or trying to manage symptoms without access to specialist care. Some people can obtain compression garments, physiotherapy and medical follow-up. Others must navigate lipedema largely on their own.

This is why one universal lipedema management protocol cannot meet everyone’s needs. Shared principles and evidence-based guidance are valuable, but they must leave room for individual symptoms, health conditions, circumstances and choices. We are each navigating our own journey, but we can learn from one another and support each other along the way.

Top 10:
🇺🇸 United States (45.10%)
🇳🇴 Norway (11.67%)
🇦🇺 Australia (8.36%)
🇬🇧 United Kingdom (7.93%)
🇨🇦 Canada (4.83%)
🇹🇷 Türkiye (3.75%)
🇸🇪 Sweden (1.44%)
🇩🇪 Germany (1.30%)
🇪🇸 Spain (1.15%)
🇳🇿 New Zealand (1.08%)

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The full LipedemaScience map:
🇮🇹 Italy (1.01%)
🇳🇱 Netherlands (1.01%)
🇫🇷 France (0.86%)
🇮🇪 Ireland (0.65%)
🇮🇳 India (0.58%)
🇿🇦 South Africa (0.58%)
🇧🇪 Belgium (0.58%)
🇵🇹 Portugal (0.50%)
🇧🇷 Brazil (0.50%)
🇮🇱 Israel (0.43%)
🇨🇭 Switzerland (0.43%)
🇭🇷 Croatia (0.36%)
🇵🇱 Poland (0.36%)
🇩🇰 Denmark (0.29%)
🇲🇽 Mexico (0.29%)
🇷🇴 Romania (0.29%)
🇦🇪 United Arab Emirates (0.29%)
🇦🇹 Austria (0.22%)
🇭🇺 Hungary (0.22%)
🇫🇮 Finland (0.22%)
🇮🇸 Iceland (0.22%)
🇧🇬 Bulgaria (0.22%)
🇰🇼 Kuwait (0.22%)
🇸🇦 Saudi Arabia (0.14%)
🇦🇷 Argentina (0.14%)
🇨🇿 Czechia (0.14%)
🇬🇪 Georgia (0.14%)
🇬🇷 Greece (0.14%)
🇰🇪 Kenya (0.14%)
🇱🇺 Luxembourg (0.14%)
🇱🇻 Latvia (0.14%)
🇲🇰 North Macedonia (0.14%)
🇲🇹 Malta (0.14%)
🇵🇰 Pakistan (0.14%)
🇵🇷 Puerto Rico (0.14%)
🇸🇮 Slovenia (0.14%)
🇮🇩 Indonesia (0.07%)
🇪🇬 Egypt (0.07%)
🇺🇦 Ukraine (0.07%)
🇪🇪 Estonia (0.07%)
🇧🇲 Bermuda (0.07%)
🇩🇿 Algeria (0.07%)
🇶🇦 Qatar (0.07%)
🇩🇴 Dominican Republic (0.07%)
🇷🇺 Russia (0.07%)
🇦🇩 Andorra (0.07%)
🇨🇴 Colombia (0.07%)
🇸🇬 Singapore (0.07%)
🇦🇱 Albania (0.07%)
🇧🇸 The Bahamas (0.07%)
🇲🇺 Mauritius (0.07%)
🇳🇬 Nigeria (0.07%)
🇱🇧 Lebanon (0.07%)

I learned that I had lipedema back in 2012, after years of severe pain. The best way I can describe it is like having a toothache inside the fat tissue. Sometimes the pain was so intense that I couldn’t sleep. I would lie in bed massaging my thighs and legs because the pressure from my hands gave me some relief.

But this was 2012.

There wasn’t much information about lipedema available to me. I didn’t find communities like the ones we have today. I didn’t know anyone else with the disease. I was completely alone with this diagnosis.

It actually took four years before I heard about another woman with lipedema. She appeared on a television programme in Norway, and I remember what a relief that was. For the first time, there was something I could send to my family and friends and say: this is what I have. There was finally another person I could relate to.

And then several more years passed.

It wasn’t until around 2020 that I started hearing about more women with lipedema. A cousin of a friend had lipedema and had undergone surgery. That became an important turning point for me. I started researching surgery myself, and before New Year’s 2021, I made a promise to myself that I would finally start that journey.

My first lipedema surgery was in September 2021. My last was in October 2022. During that period, I had four surgeries.

Interestingly, it was my surgeon who encouraged me to start sharing my knowledge about lipedema, particularly when it came to food, nutrition, lifestyle and food science. She met so many women who had received a diagnosis or undergone surgery but were still trying to figure out how to live with lipedema afterwards.

That eventually became the beginning of what I am doing today.

At first, I shared mainly with a Norwegian audience. Then, in November 2025, I decided to take LipedemaScience international.

One of the reasons was that I kept seeing how much interesting work was happening in different parts of the world. Lipedema doesn’t belong to one country, one healthcare system or one community. A study from Turkey can be relevant to a woman in Canada. Research from Germany, Poland, the US, Australia or France can teach all of us something.

I also think we can learn a lot from each other beyond research.

Women with lipedema live in completely different cultures, climates and food environments. We have different traditions, different resources, different healthcare systems and very different access to food.

I travel a lot myself, and my diet changes depending on where I am. If I am somewhere where beetroot is everywhere and tastes amazing, I eat more beetroot. If I am somewhere with beautiful avocados, I eat more avocado. I adapt to the food culture around me, and I actually see that flexibility as a strength.

I love food. I want variety. I want to experience different cuisines and learn from the way people eat around the world.

That doesn’t mean everyone with lipedema should eat the same way I do.

Some people have very clear food triggers. Some have allergies, intolerances or other diseases that need to be considered. For some people, a more restrictive diet may genuinely make sense. And I think learning to understand your own body is incredibly important.

But your solution is not automatically everyone else’s solution.

That is something I want LipedemaScience to communicate much more clearly.

When we are talking about millions of women across the world, we cannot build one extremely narrow definition of the “correct” lipedema lifestyle. Even recommendations that sound simple can look very different depending on where you live. I personally like eating organic food when I can, for example. In countries such as Germany, organic food can be relatively easy to find. Somewhere else, the same products may be difficult to access or far too expensive.

I never want this platform to become a place where women are made to feel that they are managing their lipedema incorrectly because they cannot afford a certain food, follow a particular diet, buy a supplement or live in a particular way.

We can share knowledge. We can discuss evidence. We can share experiences. We can ask difficult questions.

But we should also remain curious about each other.

That is probably the best description of what I want LipedemaScience to be.

I want to be curious. I want to stay open-minded. I want to be active. I want to see the world. I want to understand the science better. I want to learn from women with lipedema living completely different lives from mine.

And yes, I also want to eat everything the world has to offer.

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This is interesting..

91.7 % of an international lipedema panel agreed that active self-management can help control symptoms and improve quality of life. When the same panel rated the strength of the evidence behind that statement, 36.1 % called it high or very high quality. A statement that progression of lipedema-associated symptoms is not universal received 95.1 % agreement and 47.5 % for evidence strength. A recommendation that lipedema surgery should be performed by providers with extensive knowledge of lipedema management received 98.3 % agreement and 53.3 % for evidence strength.

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Before going further, it is worth asking who this international panel actually was. The 71 participants in the final Delphi round were founding members of the Lipedema World Alliance, representing 19 countries across 5 continents and a wide range of professional and patient perspectives. The group included 17 surgeons, the largest professional group, 12 patient representatives, 7 medical researchers, and professionals from lymphology, angiology, phlebology, physical and lymphedema therapy, dermatology and other areas of healthcare. 16 of the 71 participants were from Germany. This does not make the consensus less valuable, but it matters when interpreting percentages such as 91.7 % or 98.3 %. Consensus becomes much more informative when we know who reached it.

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When we talk about lipedema, most of the attention is usually placed on fat tissue, pain, swelling, bruising, and the lymphatic system. But our legs are not made up of separate parts that work independently. Fat tissue, connective tissue, muscles, tendons, fascia, blood vessels, lymphatic vessels, nerves, and joints all have to work together every time we stand, walk, climb stairs, or exercise.

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A new study titled Ultrasonographic Evaluations of Tendons/Fascia in Lower Limb Lymphedema and Lipedema looked at something that is discussed much less often: whether chronic swelling in the legs may also be linked to physical changes in tendons and fascia.

The researchers studied 53 people with chronic swelling in the lower legs and compared them with 55 people of similar age and sex who did not have chronic edema. They used ultrasound to examine several important structures in the legs and feet, including the Achilles tendon, the tibialis posterior tendon, the peroneal tendons, the patellar tendon, and the plantar fascia.

To understand why this matters, it helps to first understand what these structures actually do. Tendons are strong bands of connective tissue that connect muscles to bones. When a muscle contracts, the tendon transfers that force to the bone and helps create movement. The Achilles tendon, for example, connects the calf muscles to the heel. It is heavily involved every time you walk, run, climb stairs, or rise onto your toes.

The plantar fascia is slightly different. It is a strong band of connective tissue that runs along the bottom of the foot from the heel toward the toes. It helps support the arch of the foot and absorbs some of the forces created when we walk. When this tissue becomes irritated or changes structurally, it can contribute to plantar fasciitis, which often causes pain around the heel or underneath the foot.

The researchers wanted to know whether these tissues looked different in people who had chronic leg swelling. They did.

Most of the tendons they examined were thicker in the group with chronic edema than in the control group. The Achilles tendon, tibialis posterior tendon, peroneal tendons, and plantar fascia were all thicker. The patellar tendon, which is located around the knee, was the main exception.

At first, this might sound like a very small anatomical detail. But tendon thickness can tell us something about what is happening inside the tissue. A thicker tendon is not necessarily a stronger tendon. Tendons can become thicker when they are exposed to repeated mechanical stress, tissue remodeling, inflammation, degeneration, or other long-term changes.

The Achilles tendon and plantar fascia were particularly interesting because the differences remained even after the researchers adjusted for body mass index, or BMI.

This matters because body weight itself can affect the feet and lower legs. A person with a higher body weight may naturally place more mechanical load on structures such as the Achilles tendon and plantar fascia. If the people with chronic edema also had higher BMI, it would therefore be reasonable to ask whether body size alone explained the thicker tissues.

The researchers tried to account for this statistically. Even after adjusting for BMI, the Achilles tendon and plantar fascia were still significantly thicker in the edema group. That suggests that the difference may not simply be explained by body weight.

The researchers also found another important relationship: people with greater edema volume tended to have thicker Achilles tendons and thicker plantar fascia. In simple terms, the more swelling the participants had, the greater the changes in these particular tissues tended to be.

This is called a correlation. It tells us that two things appear to be related, but it does not tell us that one directly causes the other. The study cannot prove that swelling itself makes the Achilles tendon or plantar fascia thicker. There may be several explanations.

For example, chronic swelling could change the physical environment around these tissues. It could influence how forces are distributed through the foot and ankle. People with painful or heavy legs may also change the way they walk without even realizing it. Small changes in walking pattern, foot position, stride length, or weight distribution may not seem important during a single step, but over thousands of steps every day they may alter the load placed on tendons and fascia.

It is also possible that the same biological processes that contribute to swelling may affect connective tissue elsewhere in the leg. The study does not tell us which explanation is correct. What it does show is that chronic edema and changes in these musculoskeletal tissues appear to occur together.

The researchers also looked at actual tendon and foot problems, not only tissue thickness. They found that plantar fasciitis was present in 50.9% of the patients in the chronic edema group. In other words, about half of the patients had plantar fascia problems. Achilles tendinopathy was found in 22.6%, which is roughly one in five.

Both conditions were more common in the edema group than in the control group. That is an important finding because plantar fasciitis and Achilles tendinopathy can have a major effect on everyday movement.

Plantar fasciitis often causes pain underneath the heel or along the bottom of the foot. Some people notice it most strongly when taking their first steps in the morning or after sitting for a long time.

Achilles tendinopathy can cause pain, tenderness, stiffness, or discomfort at the back of the ankle. It may become noticeable when walking uphill, climbing stairs, running, standing on the toes, or increasing physical activity.

The researchers also asked the participants about pain, leg function, and quality of life. The people with chronic edema reported more pain, poorer lower-limb function, and worse quality of life than the control group. This is where the study becomes especially interesting for people living with lipedema.

Lipedema is often described mainly as a disorder of abnormal fat tissue. That is an important part of the condition, but it may not tell the whole story of why the legs can feel painful, heavy, weak, stiff, or difficult to use. The human body is a mechanical system as well as a biological one.

If the legs become heavier, swollen, tender, or painful, a person may gradually start moving differently. They may shorten their stride, shift more weight onto one side, avoid pushing strongly through the foot, rotate the leg differently, or reduce certain movements because they hurt. These changes can happen subconsciously.

Over time, altered movement can change which tissues carry the greatest load. The Achilles tendon and plantar fascia are especially important because they repeatedly absorb and transfer force during walking.

This could potentially help explain why some people with lipedema describe symptoms that do not seem to come directly from the fat tissue itself. Heel pain, pain beneath the foot, tightness around the calf, Achilles pain, ankle stiffness, difficulty standing for long periods, or pain during walking may sometimes have a musculoskeletal component.

That does not mean every person with lipedema has tendon disease. It also does not mean that lipedema directly causes plantar fasciitis or Achilles tendinopathy. The study cannot prove that.

There is also an important limitation that needs to be understood before applying these findings specifically to lipedema.

Although the title of the paper refers to both lymphedema and lipedema, the abstract describes the study group more broadly as patients with chronic lower-extremity edema. From the abstract alone, we cannot see exactly how many participants had lipedema, how many had lymphedema, whether some had both conditions, or whether the researchers analyzed the lipedema patients separately.

That means we should not take the figure of 50.9% and say that half of all people with lipedema have plantar fasciitis. The study does not establish that.

The correct interpretation is that plantar fasciitis and Achilles tendinopathy were more common among the patients with chronic lower-limb edema included in this study.

This distinction is important because good science is not only about finding interesting results. It is also about being careful not to claim more than the data actually show.

The study was also observational. The researchers compared people who already had chronic edema with people who did not. They did not follow healthy people for many years to see whether swelling developed first and tendon changes appeared afterwards. Because of that, they cannot prove cause and effect.

We therefore cannot say, based on this study, that chronic edema damages the Achilles tendon. What we can say is that people with chronic leg edema had measurable differences in several tendons and in the plantar fascia, and that greater edema volume was associated with greater thickness of the Achilles tendon and plantar fascia. That is still an interesting finding.

For people with lipedema, the study encourages a broader way of thinking about the condition. Pain and reduced function may not always come from one tissue or one biological process. Fat tissue, fluid balance, connective tissue, movement patterns, muscles, tendons, fascia, joints, and the nervous system may all contribute to how the legs feel and function. This may also have practical importance.

If someone with lipedema has persistent heel pain, Achilles pain, foot pain, or difficulty walking, it may be worth considering the musculoskeletal system rather than assuming every symptom is simply “the lipedema.” A clinician may need to look at tendon health, foot mechanics, strength, mobility, gait, and the way the person loads their legs during movement.

Ultrasound may also become useful in some cases because it allows clinicians to look directly at tendon and fascial structure without surgery or radiation.

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The larger message from this study is therefore not that lipedema automatically damages tendons. It is that chronic swelling in the legs may be connected to changes in tissues that are essential for movement, especially the Achilles tendon and plantar fascia.

For people living with lipedema, that adds another piece to a much more complex picture. Lipedema may be visible in the fat tissue, but its effects on how a person feels and moves can involve the entire leg.

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1. Ultrasonographic Evaluations of Tendons/Fascia in Lower Limb Lymphedema and Lipedema (DOI: 10.1097/PHM.0000000000003118.)

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When I eat carbohydrates, I often think about what else is on my plate or what I combine them with. Is there enough protein? Healthy fats? Fibre? How will this meal affect satiety, blood glucose, and the overall nutritional quality of the meal rather than just one ingredient?

I think about food quality. Not only calories or macronutrients, but the quality of the raw ingredients, how the food has been processed, the soil they have grown in or the environment around them, and whether the food provides vitamins, minerals, fibre, and bioactive compounds alongside energy. And energy is often the one thing I think the least about, because I get enough protein, healthy fats, and carbohydrates anyway.

I also think about nutrient interactions. Like, I take fat-soluble supplements such as vitamin D and omega-3 with meals that contain fat because absorption depends on it. I try to eat vitamin C-rich foods such as kiwi, oranges, or bell peppers separately from coffee when possible, since coffee can reduce iron absorption. When I think about my bone health, I don’t think about calcium alone. I also think about vitamin D, vitamin K, physical activity like lifting weights, and the many factors that work together.

I think a lot about my gut microbiome. I don’t avoid antibiotics when I genuinely need them, but I don’t want to use them unnecessarily either. I enjoy eating fermented foods, fibre-rich vegetables, legumes, and other foods that nourish beneficial bacteria.

I think about phytochemicals. I find it fascinating that cooking tomatoes actually increases the bioavailability of lycopene, or that different colours of fruits and vegetables contain different families of protective plant compounds.

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I generally try to minimise highly refined foods, large amounts of added sugar, refined flour, alcohol, and products with long ingredient lists when there are simpler alternatives. Not because I believe every ingredient is harmful, but because my overall dietary pattern matters more than individual foods.

I also find intermittent fasting interesting. I usually eat two or sometimes three meals per day because it suits my lifestyle, and I appreciate the emerging research on fasting, including its potential effects on metabolic health and autophagy. At the same time, I recognise that fasting is not appropriate for everyone.

Perhaps most importantly, I think about balance. I live by an 80/20 rule, where those 20 percent make me able to eat everything I want.

I genuinely love food. I love cooking. I love restaurants. I love discovering local markets when I travel. I went to a very nice one in France today, in a very nice small town called Senlis. And my partner wanted us to have a full French experience since we have had scrambled eggs for lunch and chicken with salad every day now, so we bought a lot at the market. The food was amazing, but to be honest, I felt full very fast and hungry not long after, so my daily routines are often the best.

But I never want nutrition to become a source of fear or unnecessary restriction. Some of my favourite memories have been created around meals in places like Italy, Portugal, France, and Spain. I have no interest in giving that up, ever. My goal has never been to eat a perfect diet.

My goal is to eat a nutrient-dense diet most of the time, while leaving plenty of room for joy, curiosity, culture, and flexibility.

Living with lipedema has taught me that every body is different, and my body is what I need to focus on. Not everybody else’s. Some people have clear food triggers. Others do not. Some thrive on one dietary pattern, while others feel better with another. I don’t think there is one universal way to eat with lipedema.

What I hope to demonstrate through LipedemaScience is that it is possible to care deeply about nutrition without becoming trapped by food rules. We can appreciate scientific evidence, remain curious about new research, pay attention to our own bodies, and still enjoy eating.

For me, that is what a healthy relationship with food looks like.

Some of them may never speak to each other. Their paths may never cross. But perhaps they can cross here, in the comments. I also want to give space to the stories that are not my own.

I do not have endometriosis, but some of you do.

This is something I often notice in lipedema communities. People are trying to understand their bodies by asking questions like “Does anyone else experience this too?”

In a large community, you will often find someone who recognises your experience. But that does not automatically mean there is a biological connection. Sometimes two conditions simply exist in the same body. Sometimes they may share a mechanism. And sometimes we do not yet know.

Lipedema research is still young. We do not have strong consensus on how lipedema may be connected to many other conditions. We do know that lipedema often appears or changes during hormonal stages of life, including puberty, pregnancy and menopause. This is one of the reasons researchers suspect that hormones are involved in some way. But we do not yet know exactly how.

Some possible connections are still more interesting than others. One of them is the relationship between lipedema and other conditions that mainly affect women, such as endometriosis and PCOS.

These are not conditions I live with myself, so this article is not really written for “me”. But it may be written for you.

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There is a new study that looks at endometriosis and lipedema side by side and asks whether some of the pain in both conditions may be driven by similar communication between hormones, immune cells and the nervous system. Become a LipedemaScience member to access every article in the library.

It is called From Endometriosis to Lipedema: Toward a Neuroimmune Framework for Pain Amplification in Hormone-Sensitive Disorders. It was published in July 2026.

The authors are not saying that lipedema and endometriosis are the same disease, since they affect different tissues and have different symptoms. What they are asking and exploring is whether both may create a local environment where inflammation and pain signals start reinforcing each other, which could make symptoms worse in both conditions.

The interesting part here is that there is much stronger evidence for this in endometriosis than in lipedema. Researchers have found increased sensory nerves, mast cells close to nerve fibres, changes in pain receptors such as TRPV1, and CGRP-related signalling in endometriosis tissue. These findings may help explain why pain can sometimes be severe even when the visible extent of the disease is limited, and why pain can continue after surgery in some women. Personally, I have noticed that hormones, refined white sugar and periods of intense stress seem to trigger more pain and inflammation in my lipedema tissue. For you, the triggers might be something else.

In lipedema, the picture is much less complete, and this is something I really want you to be aware of, since social media can often give you the impression that the science is already bulletproof. It is not. We are not there at all. But we are on our way. We are still learning and still discovering, and this is why asking questions is so important. We do know that lipedema tissue can contain mast cells, higher histamine levels, macrophages, vascular changes, fibrosis and altered local estrogen metabolism. These findings are interesting because they are some of the same upstream conditions that could irritate or sensitise nerves. But the nerves themselves have not been studied well enough in lipedema. TRPV1, CGRP and nerve growth factor have not yet been properly mapped in the tissue, so this part of the model is still a hypothesis.

I think one of the most relevant parts for women living with either condition is the discussion about pain flares. The authors suggest that sleep loss, stress, hormonal changes, infection or gastrointestinal symptoms may sometimes add pressure to an already sensitive pain system. That may sound familiar to many people. Still, the proposed flare types have not been tested, and the study does not prove that histamine, food, the gut or hormones are causing an individual woman’s symptoms.

The study is therefore useful for some of us, including those of us who do not have endometriosis but may have other conditions also related to inflammation. But it is not useful because it gives us a new treatment. It gives researchers better questions. Are mast cells located close to nerves in lipedema tissue? Are the same pain receptors involved? Do women with both lipedema and endometriosis show more pain amplification? Those studies have not been done yet. For now, this paper gives us a possible explanation for why the pain can feel much bigger than what is visible from the outside. It is an interesting model, but it is still a model.

If you like what I do for the lipedema community, I would really appreciate it if you shared this article, recommended LipedemaScience to a friend with lipedema, or simply helped the community grow.

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I love spending time building this, and I want it to become something unique that is not already out there. A place where you can ask questions and find more nuance in all the social media noise that is sometimes presented as hard science, but may also be more connected to a lipedema trend that gets more views and followers.

Maybe you simply prefer to learn and read lipedema news. I will never give you a black-and-white answer, because that would be too simple. I am not built that way, and my brain is very critical when it comes to strong claims. Some studies are given more weight than they deserve because of poor study design, serious weaknesses, too short a timeframe, too few participants, or because they are funded by companies selling the product being studied, as we have seen with some studies on lipedema and vibration plates.

Vibration plates are trending heavily on social media. They might work, but some of the effect could also be placebo. If it is something you feel motivated to try and it gives you energy, I say go for it. But if it adds more stress to your life, more guilt or a feeling of failure, then skip it and focus on the things that actually motivate you.

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1. From Endometriosis to Lipedema: Toward a Neuroimmune Framework for Pain Amplification in Hormone-Sensitive Disorders (DOI: 10.3390/biomedicines14071510)

What you see here is translated directly from my medical record, from Norwegian into English. I thought it might be interesting to share. I was only 20 years old and already struggling with pain, heaviness and swelling in my legs.

Imagine receiving this information from a doctor at the age of 20, and then being sent home with almost nothing else.

There was no social media community like the one we have today. Very little information was available, and I was not given any real guidance on how to understand the condition, manage my symptoms or possibly reduce the risk of progression.

As you can see, I received only one practical recommendation which was to wear Class II compression stockings up to my knees. But I was 20 years old. I did not wear them. My lipedema did not noticeably progress for several years. Then, in 2018, during a period of intense stress, everything changed.

Members can continue reading the full article below and access the rest of the LipedemaScience library. You can also read about what happened to me in 2018. That article is open to everyone, including free subscribers.

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It took 4 years before I met another person with lipedema. There was nothing like the community we have today. I didn’t have you. I didn’t have anyone.

My Medical Record from 2012

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That energy is needed for movement, repair, communication and the ordinary work of staying alive. Every tissue depends on it, although different cells depend on mitochondria in different ways.

I think that is part of why I find them so interesting. Mitochondria are not separate from the rest of the body. They sit quietly inside cells and influence how those cells manage energy, stress and change.

Over time, I have also started wondering what this might mean in relation to lipedema. I want to be careful with that question. Some of what follows is established biology. Some of it comes from early research. Some of it is my own reflection on what may be worth paying attention to. I do not want to make those things sound more certain than they are.

What mitochondria do

Mitochondria are found in almost every cell in the body. Some cells contain only a few, while cells with a high energy demand may contain thousands. Their best known role is to produce ATP, which is the form of energy cells can use directly. They do this through a series of chemical reactions involving nutrients and oxygen.

This process is not only about producing energy. Mitochondria also take part in cellular signalling, stress responses, inflammation and decisions about whether damaged cells should repair themselves or be removed.

They are therefore not just small power plants. They are part of the systems that help cells respond to what is happening around them. This is also true in fat tissue.

Fat cells are not passive storage containers. They constantly respond to hormones, nutrients, immune signals and changes in energy demand. Mitochondria help regulate whether energy is stored, released or used. They also influence how fat tissue communicates with the rest of the body. Healthy fat tissue depends on cells that can adapt. Mitochondria are part of that adaptability.

Thank you so much for being here and reading LipedemaScience. I live with lipedema myself and have a background in Human Nutrition, Food Science, and laboratory research. Many articles are available to everyone, while members receive access to the full library. Your support means more than you know.

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What we know about lipedema

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So I want to be honest before I write anything else. Salt is not one of my triggers. When I eat too much of it my legs do not light up with the deep, tender, pressing pain I know from sugar, or from certain hormonal weeks when my body seems to work against itself. I can still swell and feel heavy. That happens to me for many reasons. But the sharp inflammatory reaction, the kind that leaves the tissue sore to the touch, does not come from salt for me.

I could have left it there. My body was not asking me to think about salt. But lipedema has taught me that the quiet things are often the ones worth understanding, and salt turned out to be one of the most interesting quiet things in this disease. What it is built upon reaches straight into the part of lipedema that I have come to believe matters most, which is the tissue around the fat rather than the fat itself.

Where this started for me

The first time salt and lipedema came together in my mind was in a webinar with Dr. Karen Herbst. I watched it years ago now. It must have been not long after my own surgery period ended in late 2022, because I remember watching it in that strange recovery stretch when I was reading and listening to everything about this disease that I could get my hands on.

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Herbst said something that reorganised how I thought about my own legs. Lipedema, she explained, is not only a disorder of fat. It is a disorder of the loose connective tissue, the living scaffolding that sits between and around our cells. And that scaffolding, she said, has a particular relationship with salt.

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One idea about GAGs

To follow why, you need one idea, and it is not a hard one.

The connective tissue in our bodies is filled with long molecules called glycosaminoglycans. The name is a mouthful, so most people shorten it to GAGs. You can picture them as long sugar chains woven all through the tissue. Two of them matter for this story, hyaluronan and chondroitin sulfate, and the important thing about them is that they carry a strong negative electrical charge along their whole length.

Salt, once it is inside the body, splits into charged pieces. Sodium is the positively charged one. Opposite charges pull toward each other, so sodium is drawn to the negatively charged GAGs and collects around them. And where sodium collects, water tends to be pulled in as well. Connective tissue that is rich in these molecules therefore holds on to more sodium and more water than tissue that is not.

Now bring lipedema into it. The tissue in lipedema is not built like ordinary tissue. Studies describe a remodelled matrix with more of these GAG molecules, more fibrosis, which is a kind of internal scarring, and more fluid held in the spaces between the cells. Put plainly, the lipedema matrix is by its very construction better at holding sodium and water. That was the sentence Herbst planted in my head, and it has stayed there ever since.

The part that surprised me

There is a second piece that makes this stranger and more interesting than I first expected. For a long time medicine taught that salt lives in the blood, and the kidneys deal with whatever is left over. In the last fifteen years or so that picture has changed. We now know that sodium can also be stored inside the connective tissue itself, in the skin and the fascia, held against those same charged GAGs. Some of this stored sodium simply sits there quietly, without dragging along the amount of water we used to assume. Immune cells and the lymphatic system, the drainage network of the body, help manage these stores.

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This is why lipedema is such a natural place to ask the question. The three parts of the body most involved in storing and clearing tissue sodium, the connective tissue, the immune cells, and the lymphatic system, are all altered in lipedema. It would be strange if sodium handling turned out to be completely normal in a disease that touches all three at once.

If you’d like full access to the entire LipedemaScience library, consider becoming a member. LipedemaScience is where you’ll find the articles you didn’t even know you were looking for, written by food scientist CarinaW, who was diagnosed with lipedema at a Norwegian hospital in 2012. With a background in human nutrition, food science, and research on human cells, bacterial DNA, and peptides, she translates complex science into practical knowledge for women living with lipedema.

This is not only theory

The part I find most convincing is that we can now look, not just reason. Dr. Rachelle Crescenzi and her colleagues built a way to see sodium in living tissue using a special form of MRI. When they scanned women with lipedema, they found more sodium in the tissue of the legs than in women of a similar body size who did not have lipedema. The arms did not show the same difference, which fits the way lipedema settles in the lower body. The extra sodium was present even when there was no loose, visible fluid to point to.

Then they went one step further. In a small study, women with early lipedema were given hands on physical therapy, the manual work and compression that helps move fluid out of a limb. Afterward, the sodium in the tissue had dropped, and the size of that drop tracked with less pain and better quality of life. It was a small, early study, and the authors were careful to say so. But it showed something that matters. The sodium in lipedema tissue is not locked in place forever. It can be moved, and when it moves, people can feel better.

Two different clocks

Here is where I want to slow down, because this is where a lot of confusion lives.

When people talk about salt and swelling, two separate things get folded into one, and they run on very different clocks.

The fast one is the heavy, tight feeling many of us know after a salty restaurant meal or a long flight. It can arrive within hours. That quick swelling is mostly ordinary fluid shifting into the tissue, the same kind of thing that comes with heat, with sitting still too long, and with the premenstrual phase. It is real. It is also not the deep matrix storage.

The slow one is the sodium held against the GAGs over days and weeks. That is the storage system, the one Herbst and Crescenzi are describing, and it does not swing up and down because of a single dinner.

This distinction matters because so many of us quietly blame ourselves for a body that seemed to change overnight. If your legs feel enormous the morning after salty food, that is almost certainly the fast fluid response, not proof that you have permanently packed your tissue full of salt. The two are related, but they are not the same thing, and it helps to stop treating them as one.

What we actually know, and what we do not

I will not tell you something is proven when it is not, so let me be exact.

The biology is real. GAGs bind sodium. The lipedema matrix is remodelled. Imaging shows more sodium in lipedema legs, and shows that it can be reduced. That much stands on solid ground.

What has never been done is the obvious next study. Nobody has taken a group of women with lipedema, carefully changed how much salt they eat, and measured what happens to their tissue and their symptoms. In heart disease and in kidney disease, that kind of controlled salt study has been done many times over. In lipedema it has not been done even once. So there is no evidence that eating less salt changes lipedema. There is a believable mechanism and an open question, and those are not the same as proof.

That is why I do not tell anyone to cut salt. I do not know that it helps, and I am not willing to build a rule for your body on a mechanism that has never been tested in ours.

The one small thing I did

What I did was smaller and more personal than a rule. When I was still living in Norway and this idea was new to me, I made one quiet change. I started reaching for a salt where part of the sodium is replaced, a salt made to carry less sodium for the same taste on the tongue. I did not stop salting my food. I love it far too much for that, and salt was never my trigger in the first place. I only changed the kind of salt in my hand, because understanding how the GAGs work made it an easy and low cost thing to try.

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I cannot tell you it did anything measurable for me. It was not an experiment and I ran no numbers on it. It was a small choice I felt comfortable making with what I understood at the time, and I am sharing it as my choice, not as a plan for yours.

Why I wanted to write this anyway

The reason I wanted to write about salt, even though salt does not hurt me, is that the salt question is really a doorway. Walk through it and you end up standing in front of the tissue around the fat, the connective tissue, the matrix, the fluid, the drainage. That is the part of lipedema I think we have underestimated for far too long. For years the entire conversation was about fat cells. The more I read, the more convinced I am that the scaffolding around them is doing at least as much of the work in how our legs feel, how they swell, and how much they hurt.

Salt is one small window into that larger idea. I still love it. I still use it. But I understand my own tissue a little better because I stopped to ask what salt was actually doing inside it, and understanding, for me, has always been its own quiet kind of relief.

Comment

1. Tissue Sodium Content is Elevated in the Skin and Subcutaneous Adipose Tissue in Women with Lipedema (DOI: 10.1002/oby.22090)

2. Upper and Lower Extremity Measurement of Tissue Sodium and Fat Content in Patients with Lipedema (DOI: 10.1002/oby.22778)

3. Physical Therapy in Women with Early Stage Lipedema (DOI: 10.1089/lrb.2021.0039)

4. Sodium magnetic resonance imaging of tissue sodium (DOI: 10.1161/HYPERTENSIONAHA.111.183517)

ReCARB. Not rehab. ReCARB.

That strange feeling when you come home from holiday and suddenly crave vegetables, water, your running shoes, and a normal bedtime more than another pizza.

I am writing this on the flight from Milan to Lisbon, already looking forward to getting back into my usual routine. Not because I feel guilty. Not because I think I have “ruined” anything. Simply because my body is asking for something different now. And I have learned that it is worth listening.

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Holidays are part of a healthy life too

This has honestly been one of the best weeks I have had in a long time.

We travelled through Lake Como, Milan, Rapallo, Camogli, Portofino, and Santa Margherita. We laughed until late at night, had conversations that only happen when nobody is checking the clock, ate incredible food, and created memories that will probably become stories we tell for years.

That is not a distraction from health. That is health.

Sometimes we forget that when we live with a chronic condition. We become so focused on managing symptoms that the management itself quietly becomes the centre of our lives. I never want that to happen.

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Lipedema deserves attention. It does not deserve to become my entire identity.

Italy is not just pizza

Of course we enjoyed pizza. And yes, I may have eaten the best carbonara I have ever tasted.

But something interesting happens when people imagine an Italian holiday. They picture endless pasta and wine. The reality is much more varied. We also walked for hours every day.

Lunch was often seafood, salads or avocado toast. Fresh vegetables appeared almost automatically. Olive oil replaced butter. Portions were surprisingly moderate. We spent much more time moving than sitting.

Without really trying, we ended up eating remarkably close to a Mediterranean dietary pattern.

As someone who studied both nutrition and food science, I cannot help noticing these things.

What actually happens to lipedema after a holiday?

This is probably the question I receive most often. The short answer is reassuring.

A couple of weeks with more pasta, pizza and wine does not rebuild lipedema tissue.

Lipedema tissue changes slowly. It is famously resistant to dieting in both directions. It does not suddenly appear because you enjoyed your holiday.

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What usually changes much faster is something else.

Fluid. Inflammation. The way your legs feel.

If your legs become heavier after a holiday, alcohol is actually one of the most plausible explanations. Alcohol causes blood vessels to dilate, influences fluid balance, and may temporarily affect lymphatic drainage. Many women notice increased heaviness or tenderness the following day.

Restaurant food also tends to contain considerably more sodium than home cooking, which may increase fluid retention, particularly if you already have some degree of lymphatic involvement.

Carbohydrates themselves are probably less interesting than many people think.

Yes, ketogenic diets have been studied in lipedema, and a few small studies have reported reductions in pain. But those studies are short, involve relatively few participants, and they certainly do not demonstrate that eating carbohydrates damages lipedema tissue. Those are two very different conclusions.

Sometimes research quietly supports what you are already doing

One thing I found funny afterwards was realising that this holiday looked remarkably healthy from a research perspective. We ate plenty of seafood. That matters.Fatty fish provide EPA and DHA, the marine omega-3 fatty acids that become part of our cell membranes. From these, the body produces specialised signalling molecules called resolvins and protectins, compounds involved in actively helping inflammation resolve rather than simply suppressing it.

Shellfish such as mussels provide iron, selenium, zinc, iodine and vitamin B12 in amounts that are surprisingly difficult to match elsewhere.

Extra virgin olive oil contributes polyphenols and oleocanthal, compounds that have been associated with lower inflammatory markers in Mediterranean diet studies.

There is an important scientific caveat here.

We have reasonably good evidence that Mediterranean dietary patterns can reduce inflammatory markers such as CRP and IL-6 in the general population.We do not yet have studies demonstrating that these foods specifically improve lipedema tissue itself. That distinction matters.

One of the biggest challenges in lipedema research is resisting the temptation to make stronger conclusions than the evidence allows.

My body still gives me feedback

Even though I know the science, I still pay attention to my own body.

During this trip my legs became noticeably swollen after several hours on the train. The next thing I did was head straight into the Mediterranean Sea. Cold water has always made my legs feel better.

Was it changing my lipedema? Probably not. Did it help the swelling and heaviness I was experiencing in that moment? Absolutely.

Sometimes listening to your body is just as important as reading another research paper.

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If your body tells you it needs rest, give it rest. If it needs movement, move. If it needs vegetables after several days of pasta, that is probably a perfectly reasonable request.

The mindset that changed my own life

There is another lesson this trip reminded me of. Life becomes surprisingly heavy when every decision feels like a health decision.

Should I eat this?

Should I skip that?

Should I have another glass of wine?

Should I stay home because my legs are swollen?

At some point, the pursuit of perfect health quietly steals your happiness.

I would rather live differently.

I want to smile more.

Talk to strangers.

Stay curious.

Have long dinners with friends.

Walk through beautiful towns without counting every calorie burned.

Laugh so much that I forget to think about my legs for a while.

The interesting thing is that when I stop trying to control everything, I often make better choices anyway. Not because somebody told me to. Because my body naturally wants balance.

Why I write about lipedema

People sometimes ask why someone with my background spends so much time writing about lipedema. The answer is actually quite simple.

I have a bachelor’s degree in Human Nutrition and a master’s degree in Food Science. Those are different disciplines that complement each other remarkably well. One focuses on what food does inside the body. The other focuses on what food actually is, its chemistry, microbiology, composition and processing.

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I also spent time working in laboratory research, studying inflammation, intestinal cells, bioactive food compounds and the gut.

But the most valuable thing my education gave me was not facts. It taught me method. How to read a scientific paper. How to separate an interesting hypothesis from convincing evidence. How to recognise when conclusions extend beyond the data.

That skill has become surprisingly valuable in lipedema, where research is still limited and ideas often spread through patient communities much faster than the science itself. And perhaps most importantly, I also live with lipedema.

I know what it feels like to desperately want answers. That is why I care so much about getting the science right.

Balance, balance, balance

If there is one thing this week reminded me of, it is this.

Your lipedema management should support your life.

Your life should not revolve around your lipedema management.

Eat the carbonara.

Enjoy the seafood.

Walk along the Mediterranean.

Drink enough water.

Go back to your routine when you get home.

Listen to your body.

Read the science.

Question exaggerated claims.

And never postpone making beautiful memories because you are waiting for the day when your legs finally become perfect.

Life is happening now. And none of us will ever be younger than we are today.

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But redox reactions are not a minor detail hidden inside a textbook. They are happening in us every second. They allow our cells to turn food into energy, help immune cells respond to infections and influence how blood vessels, nerves and tissues communicate.

Years later, as I started reading more about lipedema, I found myself returning to redox biology. Not because oxidative stress has been proven to cause lipedema. It has not. But because redox reactions sit at the centre of several processes that may be relevant to our symptoms: mitochondrial activity, vascular permeability, inflammation, bruising, pain and tissue remodelling.

What is a redox reaction?

The word redox comes from reduction and oxidation. It describes a reaction in which electrons move from one molecule to another. The molecule losing electrons is oxidised. The molecule receiving them is reduced. The two processes always happen together.

This movement of electrons is what makes energy production possible. When we metabolise carbohydrates, fats and proteins, electrons are transferred to carriers such as NADH and FADH₂. These molecules transport them into the mitochondria, where they pass through the electron transport chain.

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Oxygen receives the electrons at the end of the chain, and the energy released during the process is used to produce ATP, the form of energy our cells can use. In other words, our metabolism depends on controlled oxidation.

When oxygen becomes reactive

The transfer of electrons inside the mitochondria is not perfectly contained. Some electrons can escape and react with oxygen before reaching the end of the chain. This creates reactive oxygen species, commonly called ROS.

You may have heard ROS described as harmful waste products, but that is only part of the story. At normal levels, they act as signals. They help regulate immunity, blood-vessel function, tissue repair and the adaptations we gain from exercise.

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The problem begins when ROS production becomes greater than the body’s ability to control it. This is what we call oxidative stress. When that happens, reactive molecules can begin to modify fats, proteins and DNA. The fats in cell membranes are particularly vulnerable, as oxidation can start a chain reaction known as lipid peroxidation.

The body has several systems designed to prevent this. Glutathione, superoxide dismutase, catalase, glutathione peroxidase and peroxiredoxins all help control reactive compounds. Vitamins C and E also participate, but they are only smaller parts of a much larger internal defence network. The aim is not to remove all ROS. It is to keep the system in balance.

What affects redox balance?

Redox balance changes according to what the body is dealing with. Our mitochondria produce more energy when demand rises, such as during physical activity. Immune cells deliberately produce ROS when they need to destroy microorganisms. Sleep loss, smoking, air pollution, persistent high blood sugar, illness and some forms of chronic stress can also increase oxidative pressure.

Nutrition matters, but not because one “superfood” can neutralise oxidative stress. The body needs protein and micronutrients to build its own defence systems. Glutathione contains amino acids, while several antioxidant enzymes depend on nutrients such as selenium, zinc, copper and manganese.

This does not mean that taking large doses of these nutrients will automatically improve the system. Too little can be a problem, but too much can also disturb normal biology.

Physical activity is a good example of why the conversation is more complicated than “oxidation is bad”. Exercise produces a temporary increase in ROS. These molecules then help signal the body to strengthen its mitochondria and increase its own antioxidant capacity. A small, controlled challenge can make the system more resilient.

Why might this matter in lipedema?

Much of what we know about oxidative stress in fat tissue comes from obesity research. In metabolically unhealthy obesity, enlarged fat cells, impaired blood flow, inflammation and mitochondrial stress may reinforce one another. It is tempting to place lipedema inside the same model. But lipedema is not simply obesity located in the legs.

Lipedema has its own pattern. The tissue is often painful and tender. Bruising can happen easily. Fluid handling and the small blood vessels appear to be affected. At the same time, many women with lipedema have relatively good glucose regulation and other signs of preserved metabolic health.

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A few small studies have found higher levels of markers connected with lipid oxidation in the blood of women with lipedema. They have also found increased activity of antioxidant enzymes such as superoxide dismutase and catalase.

That could mean the body is experiencing greater oxidative pressure. It could also mean the defence system is responding appropriately. Blood tests cannot tell us exactly where the signal came from, and they do not prove that oxidative stress causes lipedema.

More recent tissue studies have complicated the story further. Some have found increased expression of pathways involved in mitochondrial respiration and energy production, together with less classical immune activation than researchers might expect.

So the honest answer is that we do not yet know whether mitochondria in lipedema are struggling, compensating or behaving differently for another reason.

The blood vessels may be especially important

One area I find particularly interesting is the relationship between fat tissue and the smallest blood vessels. Research suggests that signals from lipedema tissue can make endothelial cells, which form the inner lining of blood vessels, more permeable. A weaker vascular barrier could allow more fluid and proteins to move into the surrounding tissue.

Redox reactions are known to influence endothelial cell junctions, nitric oxide signalling and blood-vessel function in other conditions. It is therefore plausible that local redox signals could be involved in the vascular changes seen in lipedema.

But plausible is not the same as proven. Researchers have found altered permeability. They have not yet shown that ROS are the cause. Still, this could be one place where the pieces meet: altered tissue signals, more vascular leakage, increased tissue pressure and greater stress on nerves and connective tissue.

Could bruising create local oxidative stress?

The tendency to bruise easily also raises an interesting question. When red blood cells escape from a damaged vessel, haemoglobin and iron must be cleared from the tissue. Iron is essential, but when it is poorly controlled it can take part in reactions that produce highly reactive radicals.

Macrophages help clean up haemoglobin and damaged cells. Lipedema tissue appears to contain many CD163-positive macrophages, a type involved in tissue repair and the handling of blood products.

Could repeated microscopic bleeding create local episodes of iron-related oxidative stress? Could that contribute to tenderness or tissue remodelling?

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At the moment, this is a research hypothesis rather than an established explanation. But it connects a very recognisable symptom - easy bruising - with a biological process that could be measured in future studies.

Redox and pain

Redox biology may also be relevant to pain. Products formed when fats are oxidised can influence sensory nerves. In other pain conditions, reactive molecules can make nerve endings more sensitive and lower the threshold at which they begin to signal pain.

In lipedema, this could interact with swelling, pressure, fibrotic tissue and mechanical stress. Redox products may not create the problem alone, but they could amplify pain in tissue that is already vulnerable. Again, this has not been demonstrated directly in lipedema. We need studies that measure oxidised lipids and redox-sensitive pain pathways inside affected tissue.

Where hormones may fit

Lipedema frequently appears or changes around puberty, pregnancy and menopause, which makes hormonal biology difficult to ignore.

Oestrogen can influence fat-cell development, blood vessels, mitochondrial activity and the body’s antioxidant systems. Early lipedema studies have found changes in genes involved in local oestrogen metabolism.

This creates a possible connection between hormonal transitions and redox regulation. A change in local oestrogen signalling could alter how cells use energy, respond to stress or maintain the vascular barrier.

But the full chain has not been established. We cannot yet say that oestrogen causes oxidative stress in lipedema, or that redox imbalance explains the hormonal pattern of the disease.

What can we do with this information?

The practical message is not that everyone with lipedema should start taking antioxidant supplements. There is currently no evidence that high-dose antioxidants treat lipedema. More is not necessarily better, and very large doses may interfere with useful redox signals, including some of the signals involved in exercise adaptation.

A better approach is to support the systems the body already uses:

• Eat enough protein and a varied diet containing vegetables, fruit, nuts, seeds, fish, eggs and other nutrient-dense foods that suit you.

• Stay physically active in ways your body tolerates. Walking, strength training, swimming and other regular movement can support mitochondrial and vascular health.

• Prioritise sleep and recovery, especially during periods when symptoms are worse.

• Avoid smoking and limit unnecessary exposure to pollutants where possible.

• Manage blood sugar and body weight without assuming that lipedema can be dieted away.

• Correct confirmed nutrient deficiencies with appropriate guidance rather than taking large doses “just in case”.

None of these removes lipedema. But they may improve the general environment in which our cells, blood vessels and tissues have to function. For me, that is a more useful way to think about redox health than searching for the strongest antioxidant supplement.

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Redox reactions are not the enemy. They are the chemistry that keeps us alive. There are early signs that oxidative balance may be altered in lipedema, but the evidence is still limited and sometimes contradictory. The most likely explanation may not be a dramatic, whole-body state of oxidative stress.

Instead, redox biology may matter locally around small blood vessels, macrophages clearing damaged cells, sensitive nerve endings and mitochondria adapting to changes in the tissue.

It may not be the mechanism that starts lipedema. But it could influence how the tissue responds, how much it leaks, how easily it bruises and how painful it becomes. That is still only part of the picture. But it is a part worth studying.

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She wanted to know why it is that lipedema ladies have hEDS or EDS. She thinks she may have vascular EDS. She has mitral valve prolapse, and another valve less affected. And she wrote something that stayed with me, that for years she has been saying she can feel her bones moving out of joint.

I read it, and my first instinct was to answer quickly. I know this comes up constantly. Every lipedema group I have ever been in has a version of this conversation running somewhere in the comments. Someone posts a photo of their thumb folded back to their wrist. Someone else says she always knew she was double jointed. And underneath it all sits the assumption that these two things belong together, that lipedema and Ehlers-Danlos are somehow the same story told twice.

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Then I sat down to actually look, and I could not answer quickly at all.

First, a confession about my own body. I do not have hypermobility.

My lipedema has never pointed that way. No unstable joints, no dislocations, no bendy thumbs, none of it. My picture is the classic one, swollen legs, pain in the tissue, hormonal timing, bruising, the whole familiar shape of it.

I am telling you this because it matters for how you read what follows. If I only wrote about what I recognise from the inside of my own body, LipedemaScience would be very small and very boring. Connie's question is not my question. And that is exactly why I wanted to take it seriously, because a lot of you are living something I am not, and you deserve better than a shrug.

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So I went to the literature. Here is what is actually there.

Before any of the studies make sense, we have to separate four things that get blended together in almost every conversation I see.

Joint hypermobility just means that a joint moves further than average. That is all it means. It can be entirely painless and entirely harmless. Plenty of people are bendy and perfectly fine.

HSD, hypermobility spectrum disorder, was introduced in the 2017 classification for people whose hypermobility actually causes problems, pain, instability, injury, but who do not meet the criteria for hEDS or any other named condition. It is not a mild version of hEDS. That is a misunderstanding I want to kill on sight. The symptom burden can be every bit as heavy. The line between them is a formal boundary, not a severity scale.

hEDS, hypermobile Ehlers-Danlos syndrome, is a clinical diagnosis with three requirements that all have to be met. Generalised hypermobility measured on the Beighton score, adjusted for age. Then at least two of three feature groups, which include a list of twelve systemic connective tissue signs, family history, and musculoskeletal complications. And then exclusion of other diagnoses. A high Beighton score alone does not give you hEDS. Neither does being bendy plus tired plus in pain, however real all of that is.

vEDS, vascular Ehlers-Danlos syndrome, is not on this spectrum at all. It is a rare, genetically defined disease, caused by a pathogenic variant in the COL3A1 gene, which codes for type III collagen. It accounts for roughly 5 percent of all EDS cases. The defining problem is fragility of arteries, intestines and the uterus. Arterial dissection or rupture, bowel perforation, organ rupture. It shortens life expectancy. It is diagnosed by finding the variant, not by recognising yourself in a symptom list.

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Hold on to that last distinction. I will come back to it, because it is the part of Connie's question that I most want to answer properly.

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This article highlights the work of Dr. Julie Caroline Sæther, Postdoctoral Researcher at the Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences at NTNU, located at St. Olavs Hospital in Trondheim, Norway. With a background in Human Movement Science, Exercise Physiology and Medicine and Health Sciences, her research brings together clinical exercise science, cardiovascular health and biomarker analysis in the study of lipedema.

Special thanks also go to photographer Jan Inge Haga, whose photographs from the LipidEx research project help document the people, the training environment and the important work taking place in Trondheim.

Most importantly, this article is dedicated to the women who participated in the studies. By showing up, completing demanding training programmes, undergoing tests and sharing their experiences, they have made a vital contribution to a field in which knowledge is still far too limited. Their participation is helping researchers build a stronger evidence base for women living with lipedema.

This is why exercise research designed specifically for women with lipedema is so important. General knowledge about the benefits of physical activity cannot automatically answer the questions that matter most to this patient group.

• Does exercise reduce lipedema-related pain?

• Can it improve daily function and quality of life even when the characteristic adipose tissue remains?

• Does the tissue itself change in response to training?

• Are some forms of exercise more effective or more tolerable than others?

• And what biological processes take place in the blood and adipose tissue when women with lipedema improve their cardiovascular fitness?

Researchers at the Norwegian University of Science and Technology, NTNU, and St. Olavs Hospital in Trondheim are now investigating these questions through the LipidEx research programme. The work is being conducted by a multidisciplinary team that includes researchers in exercise physiology, clinical medicine, body composition, adipose tissue biology, analytical chemistry and statistics. Postdoctoral researcher Dr. Julie Caroline Sæther has played a central role in the project alongside Professor Anja Bye and the wider research team.

The significance of their work lies partly in the fact that they are not treating exercise as a generic lifestyle recommendation. They are studying it as a possible therapeutic intervention for a chronic and painful adipose tissue disorder. Their aim is not simply to demonstrate that exercise is beneficial for general health. Instead, they are trying to determine whether a defined training programme can produce measurable changes in pain, quality of life, physical fitness, body composition and biological processes among women diagnosed with lipedema.

The first LipidEx study: high-intensity interval training

The first study in the programme, often referred to as LipidEx HIIT, examines the effects of twelve weeks of high-intensity interval training. Approximately 60 women between the ages of 18 and 65 with a diagnosis of lipedema were recruited. The participants completed three endurance-training sessions each week. Two sessions were supervised at St. Olavs Hospital, while one was completed independently.

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The training included high-intensity intervals based on the Norwegian 4 × 4 model. This involves four periods of four minutes at a high exercise intensity, with active recovery between the intervals. Although the programme was adapted to each participant’s physical capacity, it was intended to be demanding. This was not a study of occasional light movement or general advice to become more active. It was a structured intervention designed to improve cardiovascular fitness and to test how women with lipedema respond to repeated high-intensity exercise over time.

The study uses a randomized controlled design with sequential intervention and control periods. Pain is the primary outcome, while secondary outcomes include quality of life and adipose tissue mass. The research team is also examining physical fitness, body composition, blood pressure and biomarkers in blood and adipose tissue. This allows the researchers to study both the participants’ experiences and the physiological changes that may accompany training.

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This combination is particularly valuable in lipedema research. Pain and quality of life cannot be fully understood through laboratory measurements alone, because they are experienced in daily life. At the same time, changes in blood markers, tissue characteristics or body composition cannot be reliably evaluated through personal experience alone. By combining questionnaires, clinical tests, fitness measurements and biological samples, the LipidEx team may be able to connect subjective improvements or difficulties with measurable changes in the body.

The study protocol was made publicly available before the final results were reported. This means that the research questions, outcomes and planned analyses were described in advance. The currently available paper explains what the researchers intend to investigate, but it does not yet provide the final answer as to whether high-intensity interval training reduces lipedema pain or changes the affected tissue.

That distinction is important. The public coverage of the project includes encouraging observations, but these should not be confused with final study results. A participant becoming fitter, progressing from walking to running or feeling a stronger sense of mastery is meaningful, but it does not by itself prove that the intervention has reduced lipedema pain or altered the biology of lipedema tissue. Those conclusions require analysis of the complete dataset and publication of the findings.

What the team has observed during the training period

Even before the final results are available, the project has provided a rare view of how women with lipedema respond to a supervised and demanding exercise intervention. Julie and the research team have described women improving their fitness during the twelve-week period. Some participants initially walked on the treadmill but gradually developed the capacity to run. The researchers also observed a strong social element, with participants encouraging one another, exchanging experiences and creating a sense of community around the training sessions.

This matters because many women with lipedema have a difficult relationship with exercise. Some have been repeatedly told that they simply need to move more or lose weight. Others have learned to distrust their bodies because physical activity has caused pain, heaviness or exhaustion. Entering a supervised research environment where symptoms are taken seriously and exercise is individually adapted may therefore have effects beyond cardiovascular fitness. It can offer a safer setting in which participants can explore their physical capacity without having their symptoms dismissed.

Several participants have described both positive and difficult aspects of the intervention. One woman reported considerable cramping and fatigue during the training period, while also recognising that her physical fitness had improved and that the exercise felt beneficial overall. Another described being in good physical condition and feeling better after extensive training, despite having lived with painful and heavy legs since puberty.

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These experiences illustrate why research in this area must avoid overly simple conclusions. Exercise can be demanding and beneficial at the same time. A participant may improve her fitness while still experiencing cramping. She may feel stronger without seeing a major change in the appearance of her legs. She may gain confidence in her body even if her lipedema symptoms do not disappear. Treatment effects in a chronic condition are often multidimensional, and progress cannot always be reduced to a single number.

The team has also been clear that lipedema tissue does not appear to respond to exercise in the same way as ordinary adipose tissue. This is an essential point. The purpose of the study is not to prove that women can exercise away the characteristic fat distribution. Rather, it is to investigate whether exercise can improve symptoms, health and function, and whether it influences the tissue or related biological processes in ways that are not necessarily visible from the outside.

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For women with lipedema, this represents a more meaningful understanding of exercise. A training intervention should not be judged solely by whether the legs become smaller. It may still be valuable if it improves cardiovascular capacity, muscle function, mobility, confidence, mental health or the ability to participate in everyday life. The relevant question is not only whether exercise removes affected tissue, but whether it helps the person living with that tissue to function and feel better.

Compression was generally not used during the exercise sessions

Compression garments are frequently discussed as part of conservative lipedema management, but their role during different forms of exercise remains insufficiently studied. I therefore asked Julie whether the LipidEx participants used compression while training.

She explained that the women mainly did not wear compression garments during the exercise sessions. Many, and in her impression most of them, used compression at other times in their daily lives.

This practical detail helps us understand the conditions under which the intervention was carried out. The women were not required to complete the supervised high-intensity sessions while wearing compression. However, because many continued using compression outside the training sessions, the study should not be interpreted as a direct comparison between exercising with and without compression.

A study designed to answer that question would need to assign participants to clearly defined groups and standardize compression use. LipidEx HIIT was designed to investigate the effect of the exercise intervention compared with a control period, not to determine whether compression improves exercise outcomes.

Nevertheless, the information may be reassuring for some women. It shows that participants with diagnosed lipedema were able to complete a supervised high-intensity programme without routinely wearing compression during the sessions. This does not mean that the same approach will suit everyone. Symptoms, disease stage, joint health, mobility, lymphatic complications and personal preference will continue to influence what is tolerable for the individual.

The next step: moderate-intensity endurance training

The Norwegian researchers are not stopping with high-intensity intervals. The next study, LipidEx MICT, examines moderate-intensity continuous training. This is an important development because the question is not simply whether exercise can help, but which form of exercise provides the most useful balance between effect, symptom tolerance and long-term sustainability.

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The moderate-intensity study is expected to include approximately 38 women with lipedema. Participants will train three times a week for twelve weeks, with two supervised sessions at St. Olavs Hospital and one independent session. They will be randomized to either a training group or a control group. The researchers will investigate pain, quality of life, body composition, physical fitness and biomarkers in blood.

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Moderate-intensity continuous training differs from high-intensity interval training because the participant exercises at a steadier and less intense level rather than alternating between very demanding intervals and recovery periods. For some women, this may be easier to tolerate. It may produce fewer episodes of cramping or excessive fatigue and may be more realistic to maintain without close supervision. On the other hand, high-intensity training may produce larger or faster improvements in cardiovascular fitness. These possibilities need to be tested rather than assumed.

By studying both high- and moderate-intensity approaches, the researchers are beginning to address a much more clinically relevant question than whether exercise is broadly “good” for lipedema. They are asking how exercise should be prescribed. This could eventually help healthcare professionals move away from generic advice and towards recommendations based on intensity, frequency, symptoms and individual capacity.

It is also possible that there will not be one universally superior form of exercise. Some women may benefit from high-intensity intervals and enjoy the sense of achievement they provide. Others may respond better to moderate continuous training. Disease severity, pain sensitivity, previous fitness, body weight, joint problems, age and other health conditions may all influence the response. The long-term goal should therefore not necessarily be to identify one perfect programme, but to develop a better basis for individualized exercise guidance.

Why this research is important for women with lipedema

Women with lipedema have often been left to manage exercise through personal experimentation. We learn from our own bodies, from other patients and from practitioners with varying levels of knowledge. Some discover that swimming or walking in water reduces heaviness. Others prefer strength training, cycling, slow jogging or short intervals. Many adapt the intensity according to pain, hormonal changes, heat, stress and recovery. This practical knowledge is valuable, but it cannot replace systematic research.

The LipidEx programme may help clarify whether exercise affects more than general fitness. If the studies find reductions in pain or changes in quality of life, they may support the development of structured exercise as part of conservative treatment. If the researchers identify changes in biomarkers or adipose tissue, this could also contribute to a better understanding of the biological mechanisms involved in lipedema.

Negative or limited findings would also be important. If high-intensity exercise improves fitness but does not reduce pain, women should know that. If moderate training is easier to tolerate but produces similar benefits, that would be clinically useful. If some participants improve substantially while others do not, researchers may be able to investigate which characteristics predict the response.

This is what serious treatment research should do. It should not begin with the assumption that exercise must work because it is healthy in the general population. Nor should it dismiss exercise because lipedema fat is considered resistant to weight loss. It should test specific interventions, measure outcomes that matter to patients and report both benefits and limitations.

Julie’s background also brings useful expertise to this work. She has previously worked with biomarkers, including microRNAs and lipoprotein subfractions, and now conducts women’s health research through the LipidEx and CorFemina projects at NTNU. This combination of exercise research and biomarker experience may help the team explore how clinical changes relate to processes in blood and tissue.

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The research environment is also internationally connected. The LipidEx protocol includes German collaborators Tobias Bertsch and Gabriele Erbacher, and the moderate-intensity study lists the Földi Clinic in Germany among its partners. These relationships matter because lipedema research is still a comparatively small field. Stronger international collaboration may make it easier to compare methods, develop common outcome measures and build larger studies in the future.

A more useful way of thinking about exercise

Exercise is sometimes discussed in lipedema communities in absolute terms. It is either presented as essential treatment or dismissed because it cannot remove the abnormal fat. Both positions are too narrow.

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Exercise does not need to cure lipedema in order to improve life with the condition. Better cardiovascular fitness may make walking, travelling and working easier. Stronger muscles may support joints and improve mobility. Greater physical capacity may provide more freedom and reduce the secondary consequences of inactivity. Exercise may also improve sleep, mood and confidence, although these outcomes must still be examined specifically in women with lipedema.

At the same time, women should not be blamed if exercise does not change the size or shape of their limbs. Nor should severe pain or fatigue be interpreted as a lack of discipline. A scientifically responsible approach must recognise that the tissue may respond differently, that symptoms vary considerably and that the optimal intensity is still uncertain.

This is what makes the Norwegian work so valuable. Julie and the LipidEx team are creating a research framework in which women with lipedema are not reduced to their body weight or told to exercise without further guidance. Their pain, quality of life and lived experiences are being studied alongside fitness, body composition, blood markers and adipose tissue.

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The final results from the high-intensity study will be needed before we can say whether HIIT is an effective treatment for lipedema-related pain. The moderate-intensity study will add another part of the picture. Further research will then be needed to reproduce the findings, examine long-term effects and identify which women benefit most from different approaches.

Even so, the work already represents progress. It acknowledges that exercise in lipedema is a legitimate and complex research question. It recognises that improving life with a chronic disease may involve more than changing the amount of affected tissue. Most importantly, it begins to replace assumptions with evidence.

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For a patient community that has spent years navigating contradictory advice, that is an important step forward.

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It made me think about my own life, because I realized that I have had one hobby for almost half of it.

Food..

Not dieting. Not restriction. Not calorie counting. Not turning every meal into a rule. Food itself.

Those of you who have followed me for a while probably already know this about me. I genuinely love food. I love walking through markets, looking at ingredients, tasting local specialties, learning why foods taste the way they do, and understanding what happens inside the body after we eat them. I do not think I have ever been able to separate food from curiosity. For me, they have always belonged together.

Looking back, I think this hobby really began when I was around sixteen. It eventually became six years of university studies, first in Human Nutrition and later in Food Science. It led me into research, where I worked with food compounds, bioactive peptides, intestinal cells, absorption, bioactivity, and inflammatory signaling. It also brought me into the food industry, where I worked with quality, laboratories, food safety, production, and product understanding.

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Long before that, I was the young girl working in cafés and smoothie bars because I simply loved being around food, flavors, routines, ingredients, and people.

It has never really stopped..

Today, I spent the day in Setúbal, a Portuguese fishing town just outside Lisbon. We walked through the local market, surrounded by fish, shellfish, vegetables, fruit, herbs, and people who seemed to know exactly what they came for. We started the afternoon with oysters that actually came from Setúbal. Over the past few days, we have eaten a lot of seafood, and much of it has been prepared in the simple way that only works when the ingredients are already good.

There is something deeply satisfying about food that does not need much fixing. Fresh fish, olive oil, vegetables, fruit, good bread, and seafood that was in the ocean not long ago.

As someone who lives with lipedema, I cannot help noticing how my body responds to the life I am living right now. At the moment, I have no signs of lipedema pain. My body feels calm. My legs feel light. I feel well.

Can I prove that Portugal is the reason? Of course not.

Travel changes many things at once. I walk more. I spend more time outside. I sleep differently. My stress level is lower. I eat slowly. I share meals. I am in a different rhythm. The slower pace probably matters just as much as the food.

But I also do not think it is random that my body feels good while I am eating high-quality, minimally processed meals built around fresh ingredients every day.

My life at the moment is quite fragmented. I do not live in one fixed rhythm all year. I live more in chapters, or maybe in eras. Right now, I travel a lot, stay in different places, and work remotely. That kind of life is not for everyone, and I do not think it has to be. But for me, in this season of life, it works. I love the life I am living now. More importantly, my lipedema body seems to love it too.

That has made me think differently about hobbies and health.

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Caring for the body does not always have to look like a treatment plan. It does not always have to happen in a clinic, through a protocol, or inside a strict routine. Sometimes it can happen through the way we build our days. Through the places we walk. Through the food we choose. Through the people we eat with. Through the things we stay curious about.

For me, food markets are a hobby. Cooking is a hobby. Learning nutrition is a hobby. Reading research is a hobby. Writing LipedemaScience is a hobby. They all connect, and they all support my health in different ways.

But I also know that food is not everyone’s thing.

Some people may find this same feeling through walking in nature, swimming, strength training, gardening, dancing, yoga, or slow morning routines. Others may find it through reading, learning, writing, photography, music, sewing, painting, volunteering, book clubs, faith, friendship, or spending time with family. Some people need hobbies that move the body. Some need hobbies that quiet the nervous system. Some need hobbies that make them feel creative again. Some need hobbies that remind them they still belong somewhere.

I think that is the point!

A hobby does not have to be impressive. It does not have to become a business, a performance, or a self-improvement project. It can simply be something that helps you feel more alive inside your own life.

Living with lipedema can make life feel very body-focused. We can spend years searching for treatments, reading about symptoms, trying therapies, buying compression garments, changing our diets, and wondering what our tissue is doing. Some of that is necessary. I have done a lot of it myself. But I also think we need to build lives that are not only centered around managing disease.

We need things that make us want to wake up in the morning.

Not because they cure lipedema, but because they remind us that we are still whole people.

For me, that has always been food. It has shaped my education, my work, my research interests, my travels, and now LipedemaScience. Looking back, I do not think I was only building knowledge. I was slowly building a life around something that made me feel alive.

And right now, sitting here in Portugal with a calm body, good food, and no lipedema pain, I feel very grateful for that.

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The last couple of weeks..