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..

Here on LipedemaScience, I often write about food, inflammation, blood sugar, insulin, swelling, pain, hormones, and the complicated relationship many of us with lipedema have with our bodies and our diets. Not because I believe there is one perfect “lipedema diet” that works for everyone, but because I believe food knowledge can give us more freedom, not less.

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So I wanted to make this little guide for you. If you are curious about nutrition and lipedema, but feel overwhelmed by all the strong opinions online, this is a good place to start. Below, I have gathered some of my articles and reflections on food, anti-inflammatory eating, insulin, sugar, weight, symptoms, and what I have learned from both science and my own body over many years of living with lipedema.

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By then, I already knew that I had lipedema. I had been diagnosed in 2012, after years of confusing symptoms that did not fit the body I was living in. My symptoms had started much earlier, around the age of fifteen, when my body changed dramatically after I started hormonal birth control. Within two months, the change was visible. Something had shifted in my lower body, and none of it made sense to me at the time.

In 2011 and 2012, I was often at my general practitioner’s office because of unexplained pain in my fat tissue. It was not normal soreness. It was not muscle pain. It felt deeper than that, almost like toothache inside the fat itself. Later, that pain finally got a name: lipedema.

But this story is not about 2012. It is about 2018.

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That year, my body was living in constant stress. I had just moved from Oslo to Ås to study food science. I had finished my bachelor’s degree in human nutrition, and I wanted to continue into a master’s degree in food science. Five of us from human nutrition started together. On paper, the transition might sound natural because both fields involve food, but in reality, human nutrition and food science are very different disciplines. Nutrition is about the human body. Food science is chemistry, microbiology, processing, technology, quality systems, and the material behavior of food itself.

We were not simply accepted straight into the master’s programme. We had to prove that we could qualify. That meant taking an entire year filled with some of the most demanding subjects from the food science bachelor’s degree, and performing well enough to show that we belonged there. It was exciting, but it was also intense. I was ambitious, under pressure, and trying to rebuild myself academically in a new environment.

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My lipedema body reacted. And I mean really, really badly. My calves did not just feel swollen. They felt balloon-level swollen, as if they could have lifted me straight to the moon.

I have always had several different lipedema symptoms. I have had the deep, toothache-like pain in the fat tissue, symmetrically on both sides. I have had swelling, always a little worse on my right side. I have had fibrotic nodules, the small hard fat lumps that make the tissue feel structurally different from normal fat. But in 2018, the swelling became something else. It felt as if my calves were turning into two balloons.

When I look back at photos from that year, I still feel shocked by them. My BMI was still low to normal. From a healthy physiological perspective, there was no obvious reason why my lower legs should look and feel like that. I was not living in a body that could be explained by the usual “eat less and move more” story. My upper body did not match my lower body. My feet did not swell in the same way. The swelling stopped around the ankles in that characteristic lipedema pattern, as if the disease had drawn its own anatomical border.

That is one of the reasons BMI is such a poor language for lipedema. BMI says something about total body mass relative to height. It says nothing about regional disease in the subcutaneous fat. A person can have a normal BMI and still have pathological tissue expansion, fibrosis, pain, fluid dysregulation, and vascular changes in the legs. Lipedema is not simply “more fat.” It is a different kind of fat tissue behaving differently in specific areas of the body.

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In 2018, my legs often felt as if they were under pressure from the inside. The pain was not only aching. It was tight, heavy, and urgent. It felt like there was no room left for the swelling. I remember the sensation very clearly: as if the skin and tissue could not stretch any further, as if the legs were about to burst.

This type of pain is different from the toothache-like pain I had known for years. The toothache pain feels like it comes from inside the fat itself, deep and gnawing. The swelling pain feels more mechanical. It feels like too much volume inside tissue that cannot expand freely.

I did not have the vocabulary for this distinction back then, but I do now. Lipedema pain is not one single sensation. For me, there have been at least two patterns. One is the deep, internal, almost hormonal-feeling ache inside the fat tissue. The other is the bursting pressure pain that seems to arrive when fluid, inflammation, heat, stress, or stillness pushes the tissue past its limit.

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What exactly happens inside lipedema tissue during these episodes is still not fully understood. That uncertainty matters. I do not want to pretend that science has answered everything. It has not. But research does point toward several mechanisms that make sense of what many of us experience.

Lipedema tissue is often described as hypertrophic, fibrotic, inflamed, and structurally altered. The fat cells may be enlarged. The extracellular matrix, the structural environment around the cells, can become stiffer and more fibrotic. There may be immune cell involvement, microvascular dysfunction, and changes in how fluid moves through the tissue. This is not just passive storage. It is active, biologically disturbed tissue.

LipedemaScience is not only my learning journey. It is becoming a community of people who want to understand this disease more deeply, together.

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When small blood vessels become fragile or more permeable, fluid can leak more easily into the space between cells. The lymphatic system then has to clear that extra fluid. Even if the main lymphatic vessels are not completely damaged, the system can still become relatively overloaded if the tissue produces more fluid burden than it can drain efficiently. Add fibrosis to that picture, and the tissue becomes less compliant. It cannot simply stretch and adapt. Pressure builds.

That is what I imagine when I think back to my 2018 legs. I imagine a tissue environment where fluid handling, vascular fragility, connective tissue stiffness, inflammation, and stress physiology were all interacting. Not in a simple line. Not one cause and one effect. More like a network, where several small disturbances could add up to a much larger physical sensation.

Stress is the part I keep coming back to.

I am not saying that stress “causes” lipedema. I am not interested in making women responsible for a disease they did not choose. But I do believe that stress can affect how lipedema feels in the body. Stress changes sleep, hormones, inflammation, fluid retention, blood flow, pain sensitivity, eating patterns, recovery capacity, and the nervous system. In a healthy body, that may be uncomfortable. In a lipedema body, it can feel like the tissue reacts with much more force.

In 2018, my body was not only studying food science. My body was surviving the pressure of change. New town, new studies, difficult subjects, high expectations, and the constant feeling that I had to prove myself. I was intellectually stimulated, but physiologically overwhelmed. My legs told the story before I was ready to hear it.

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I have experienced similar swelling episodes in other stressful periods before surgery. The same tightness. The same heavy calves. The same feeling of tissue under pressure. But what is interesting to me is that this specific bursting sensation has not happened in the same way after my lipedema surgeries.

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That does not mean surgery removed the disease. It did not. Liposuction removed diseased tissue and changed my mechanical baseline, but I still live in a lipedema-affected body. I still think about hormones, inflammation, lymphatic support, food quality, recovery, and stress. I still have to manage my body. But the extreme swelling pressure I had before surgery has not returned in the same way.

I find that fascinating.

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Maybe reducing the amount of diseased, fibrotic tissue reduced the pressure dynamics. Maybe the lymphatic load changed. Maybe there is less tissue available to trap fluid. Maybe the mechanical environment of my legs became more forgiving. I do not know the full answer yet. But I know what I experienced, and I know that the before-and-after difference is real in my body.

This is why I keep reading. This is why I keep writing. Something is happening inside lipedema fat tissue that we still do not fully understand, and my mantra is to find out what. I want to understand it for myself, but also for my future children and for every other person living with this disease.

Because when your legs feel like they are about to burst, and your BMI is normal, and your blood tests look fine, and people still try to explain your body through ordinary weight logic, you need better language. You need biology. You need a framework that does not turn your symptoms into a character flaw.

You can read all LipedemaScience articles by becoming a member at LipedemaScience.com. This is where I share the full archive of personal science essays, research reflections, and deeper explanations about lipedema, hormones, inflammation, pain, nutrition, surgery, and the biology behind this disease.

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For me, 2018 was one of the clearest examples of lipedema not being static. My body changed with stress. My symptoms intensified with pressure. My tissue behaved as if it had its own internal weather system, and I was living inside it without a map.

Today, stress management has become one of the most important tools in my lipedema management toolbox, together with nutrition, movement, surgery history, recovery, and listening carefully to my body. I do not see stress management as a soft lifestyle idea. I see it as tissue management. Nervous system management. Pain management. Fluid management. It is not always easy, and it does not solve everything, but ignoring stress is no longer an option for me.

I have learned to take my body seriously earlier. If I feel overloaded, I try to respond before my body has to shout. If my legs feel heavy, I ask what else is going on. Am I sleeping enough? Am I carrying too much mentally? Am I eating in a way that supports me? Am I recovering, or am I just pushing?

Looking back at 2018, I feel compassion for that version of myself. She was working so hard. She was trying to build a future. She was studying food science, trying to qualify, trying to keep up, and trying to live in a body that felt unpredictable. She did not yet know that one day she would write about lipedema not only from the inside of the pain, but also from the inside of the science.

Eight years later, I can see that year differently.
It was not just a hard year. It was data.

It showed me that my lipedema body is responsive. It showed me that swelling and pain are not random. It showed me that a low or normal BMI does not protect you from diseased fat tissue. It showed me that stress can amplify symptoms in ways that deserve serious biological attention. And it showed me that my body had been communicating long before I had the words to understand it.

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I still do not have all the answers. But I know this: lipedema is not simply a body shape. It is not simply fat. It is not laziness, weakness, or poor discipline. It is a disease of tissue behavior, and we need to understand that tissue much better.

Do you recognize this bursting pressure feeling in your own legs? Or is your pain more like the deep toothache-like ache inside the fat itself? For me, learning to separate those two sensations changed how I understood my body. Both are real. Both are biological. And both deserve to be taken seriously.

I am building this space because I believe we deserve better knowledge about what is happening inside our bodies, not simplified explanations that make us blame ourselves. If there is a topic you want me to explore, a symptom you want explained, or a question you keep coming back to, please share it in the comments.

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I have seen how a food-derived compound can appear biologically interesting in a controlled cell model, and I have also seen how far that is from saying that a specific food will have the same effect in a living human body. That experience shaped the way I think about “anti-inflammatory food.” It made me both fascinated and cautious. Fascinated, because food really can communicate with biology. Cautious, because the path from a molecule in a lab to symptom relief in a person with lipedema is long, complex, and often misunderstood.

If you have lipedema, you have probably seen the lists.

“Ten anti-inflammatory foods you should eat”

“Avoid these foods to reduce inflammation”

Turmeric, berries, green tea, ginger, olive oil, salmon, walnuts.. They appear everywhere, and they make nutrition sound beautifully simple. Eat from the good list, avoid the bad list, and the body will become calmer.

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I understand why that is tempting. When you live with a condition like lipedema, you want something concrete to do. Food is one of the few things we interact with every single day, and it can feel empowering to believe that the right foods might help reduce pain, swelling, heaviness, or that strange tissue pressure many of us know so well.

But this is where I think we need to slow down.

“Anti-inflammatory food” is not a fixed category of foods that works the same way for every person. It is one of the biggest misunderstandings I see in the lipedema community. And when we look at the actual lipedema research, the picture becomes even more interesting.

The popular story often goes something like this: lipedema is an inflammatory disease, therefore you need an anti-inflammatory diet. But the science is not that clean. Lipedema tissue may involve local tissue remodeling, fibrosis, immune cell activity, vascular changes, lymphatic stress and pain. But whether lipedema is primarily a systemic inflammatory condition is still much more unclear than many online discussions suggest.

That does not mean nutrition is irrelevant. It means we need a better question.

Not: which foods are anti-inflammatory for everyone?

But: how does this dietary pattern, in this person, with this biology, affect markers, symptoms, pain, swelling, quality of life and long-term health?

That is a very different conversation.

What inflammation actually is

Inflammation is not automatically bad. It is part of the body’s normal defense and repair system. If you cut your finger and the area becomes red, warm, swollen and tender, that is inflammation doing its job. Immune cells arrive, signals are released, damaged tissue is cleaned up and repair begins.

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The problem is not inflammation itself. The problem is when inflammatory signaling becomes long-lasting, low-grade and harder to resolve. This is the type of inflammation people usually mean when they talk about diet and inflammation. It is not the dramatic inflammation of an infected wound. It is a quieter biological background noise that can interact with metabolism, blood sugar regulation, fat tissue, vascular function, gut health, stress, sleep and immune activity.

But even here, we need to be precise. Inflammation is not one thing. It is a whole language of immune cells, cytokines, hormones, enzymes, tissue signals and repair mechanisms. Two people can both be described as having “inflammation”, but the reasons may be completely different. One person may have inflammation driven by insulin resistance. Another by autoimmune disease. Another by gut barrier dysfunction. Another by stress, poor sleep, infection, obesity, endometriosis or chronic tissue injury.

Already, the idea of one universal anti-inflammatory food list starts to fall apart.

A food does not enter an empty laboratory system. It enters a living body with a history.

Lipedema inflammation is more complicated than the online version

This is where the lipedema-specific research matters.

For years, many of us have heard that lipedema is an inflammatory disease. In one sense, that is understandable. Lipedema tissue hurts. It can feel swollen, heavy, bruised, tender and reactive. Several studies describe changes in the affected subcutaneous fat tissue, including fibrosis, adipocyte enlargement, immune cell involvement and tissue remodeling. In later stages, the tissue often becomes more fibrotic and clinically harder. Something is clearly happening in the tissue.

But the immune picture is not the same as in ordinary obesity-related adipose tissue inflammation.

Several recent reviews and tissue studies point toward something surprising: lipedema fat often shows a predominance of M2-like macrophages. Macrophages are immune cells that can take on different roles depending on the tissue environment. Very simplified, M1-like macrophages are often associated with more classic pro-inflammatory immune activation, while M2-like macrophages are often associated with repair, remodeling and more anti-inflammatory signaling.

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That does not mean lipedema tissue is “healthy” in the way a person with lipedema experiences it. It hurts. It can be disabling. It can become fibrotic. It can profoundly affect quality of life. But biologically, it may not follow the same inflammatory pattern we see in typical obesity-associated metabolic disease.

Some researchers have even suggested that lipedema may represent a kind of metabolically protected subcutaneous fat expansion, at least in some patients and stages. A population-based study using a lipedema-like body phenotype found lower insulin resistance and a lower neutrophil-to-lymphocyte ratio compared with controls. That does not prove that all clinically diagnosed lipedema is metabolically protective, and it does not erase the lived symptoms of the disease. But it does challenge the simplistic claim that lipedema automatically equals systemic inflammation.

This matters because the popular nutrition logic depends on a very simple chain:

• lipedema equals inflammation

• inflammation is bad

• anti-inflammatory foods reduce inflammation

• therefore everyone with lipedema should eat the same anti-inflammatory foods

The research does not support such a straight line.

A more accurate statement would be this: lipedema involves abnormal adipose tissue biology, local tissue changes, immune activity and fibrosis, and some dietary patterns may influence systemic inflammatory markers. But the exact role of inflammation in lipedema is still unresolved, and reducing a blood marker is not the same as reducing pain, swelling or disease burden. That distinction is important.

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Where the idea of “anti-inflammatory foods” comes from

When someone says a food is anti-inflammatory, it sounds like a settled fact. But when you look more closely at where much of this knowledge comes from, the picture becomes more complicated.

A lot of anti-inflammatory food research begins in cells, animals or supplement studies. Scientists may take immune cells in a dish, expose them to a purified compound from a plant and measure whether certain inflammatory signals go up or down. Or they may feed a high dose of an extracted compound to animals. Or they may study an isolated substance from a food, not the food as you would actually eat it.

This is not bad science. This is often how science has to begin. If we want to understand whether a plant compound can influence inflammatory signaling, we need controlled experiments. A cell dish or animal model can help us understand mechanisms that would be impossible to study directly in humans at first.

But the problem starts when this early-stage research is translated too quickly into human advice.

There is a very big difference between saying “this compound reduced an inflammatory marker in immune cells in a dish” and saying “this food will reduce inflammation in your lipedema tissue.” Many things can disappear along the way. The dose may be unrealistic. The compound may not be absorbed well. The food matrix may change its effect. The person’s gut bacteria may transform it into something different. The inflammatory pathway studied in the lab may not be the pathway driving symptoms in a real human body.

This is why I become cautious when I see very confident claims about single foods.

Turmeric is a good example. Curcumin, the active compound often discussed in turmeric, has been studied intensely for its anti-inflammatory potential. It is biologically interesting. It may have effects in certain contexts. But curcumin is also poorly absorbed in the human body, and studies in humans are much more complex than the online claims suggest. Eating turmeric in food is not the same as taking a concentrated curcumin supplement, and neither of those is the same as exposing cells directly to curcumin in a laboratory.

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The same applies to many other “superfoods.” Berries, green tea, olive oil, ginger, cocoa, grapes, herbs and spices may all contain compounds with interesting biological properties. But that does not make them universal medicine. A food can be nutritious and still not be a proven treatment. A compound can be promising and still not have strong evidence for your specific condition.

This distinction matters, especially for people with lipedema, because we are often vulnerable to oversimplified answers. Many of us have spent years not being believed, not being diagnosed, or being told that our painful tissue is just a weight problem. When someone finally gives us a clear list of what to eat, it can feel like relief. But clarity is not the same as truth.

The lipedema diet studies exist, but they do not give us a simple answer

There is now a small but growing cluster of studies looking at diet, inflammation and lipedema. That is important, and it is more than we had a few years ago. But these studies do not prove that there is one anti-inflammatory diet for everyone with lipedema.

They mostly point toward dietary patterns, not single foods.

Several studies have explored ketogenic diets, low-carbohydrate high-fat diets, Mediterranean-style diets and modified Mediterranean-ketogenic approaches. Some show improvements in body composition, pain, inflammatory markers or quality of life. That is promising. But the studies are still limited, often small, and sometimes come from the same research environments. They are useful, but they are not the same as a large, diverse, long-term evidence base.

One study is especially useful for understanding the difference between biomarkers and symptoms. In women with lipedema, a more pro-inflammatory diet score was associated with higher TNF-alpha and IL-6, two inflammatory markers measured in the blood. A higher Mediterranean Diet Score was associated with lower levels of those markers. On paper, that looks like a clean anti-inflammatory diet story.

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But then comes the important part: in that study, the diet score was not significantly associated with pain scores or physical quality of life.

In other words, the blood markers moved with the diet pattern, but the things patients actually feel, such as pain and quality of life, did not clearly move with them in that study.

That does not make the study unimportant. It makes it more important. It shows us that “anti-inflammatory” cannot automatically be translated into “you will feel better.” Blood markers are useful, but they are not the whole disease. Lipedema pain may involve tissue pressure, fibrosis, nerves, vascular fragility, lymphatic load, central sensitization, hormones and mechanical factors. A cytokine in the blood may not capture all of that.

Other newer studies do report associations between more pro-inflammatory dietary patterns, ultra-processed food intake, pain, inflammatory markers and quality of life. So the symptom story is not absent. It is simply not settled. The evidence is early, cross-sectional in several cases, and unable to prove cause and effect. This is exactly why we need nuance.

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A Mediterranean-style diet may be helpful for many people. A lower-carbohydrate or ketogenic approach may be helpful for some people. Reducing ultra-processed food may be a very sensible starting point. But none of this proves that all people with lipedema need the same diet, or that one food list can predict what will happen in your body.

The stronger evidence is about patterns, not magic foods

If there is one place where nutrition research is more useful, it is not in single foods. It is in dietary patterns.

A dietary pattern means the overall way you eat over time. Not one cup of green tea. Not one serving of berries. Not one spoon of olive oil. But the broader rhythm of your diet: how much fiber you eat, how much ultra-processed food you consume, how often you eat fish, whether most meals contain protein, how much refined sugar you eat, whether your carbohydrates are mostly whole or refined, whether you get enough micronutrients, and whether your meals keep your blood sugar relatively stable.

Anti-inflammatory dietary patterns often look similar to Mediterranean-style eating. They usually include vegetables, fruit, berries, legumes, whole grains if tolerated, fish, seafood, nuts, seeds, olive oil, herbs and other minimally processed foods. They are typically rich in fiber, unsaturated fats, polyphenols, minerals and other compounds that support metabolic and immune function.

On the other side, more pro-inflammatory dietary patterns are often characterized by high intake of ultra-processed foods, refined carbohydrates, sugar-sweetened drinks, low fiber intake, excess alcohol, frequent fried foods and large amounts of processed meats.

But even this needs nuance.

This does not mean that one dessert causes inflammation. It does not mean that white rice is poison. It does not mean that bread is always bad, or that everyone with lipedema must avoid dairy, gluten, fruit, potatoes or carbohydrates. The body does not judge foods morally. It responds biologically. And biology depends on context.

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A slice of bread alone is not the same as a slice of bread with eggs, olive oil, vegetables and protein. Fruit alone is not the same as fruit eaten with Greek yogurt, chia seeds or nuts. Rice alone is not the same as rice eaten with fish, vegetables and fat. A dessert after a balanced meal is not the same as sugar on an empty stomach after a night of poor sleep.

The body responds to the whole meal, the amount, the timing, the person eating it and the biological state that person is in.

This is why the same food can feel fine one day and not fine another day. You may tolerate carbohydrates better after exercise than after several days of poor sleep. You may tolerate salty food differently in hot weather. You may react more strongly to alcohol before your period. You may find that certain foods trigger heaviness only when you are already stressed, inflamed, swollen or sleep deprived.

For people with lipedema, this is often very familiar. The tissue can feel more reactive in certain phases of life, certain phases of the cycle, or certain combinations of heat, hormones, stress and food. That does not mean you are imagining it. It means your body is not a simple machine.

Why the same food affects people differently

Even if a food truly has a mild anti-inflammatory effect in some people, the next question is still: why do some people notice a difference while others notice nothing?

One reason is the gut microbiome. Many plant compounds do not act in the body exactly as they exist in the food. They are transformed by bacteria in the gut. These bacteria help convert fibers and polyphenols into metabolites that may influence the immune system, gut barrier, vascular function and metabolism. But gut microbiomes vary enormously from person to person. Two people can eat the same food and produce different metabolites from it.

In a very real sense, the food does not become the same thing inside every body.

Genes also matter. Small genetic differences can influence how we absorb, transport, metabolize and respond to compounds in food. So can age, sex hormones, medication use, body composition, insulin sensitivity, physical activity and health status.

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Dose matters too. Many lab studies use concentrations that are far beyond what we would ever reach through a normal meal. The effect of a purified compound at a high dose in a cell dish tells us very little about the effect of a cup of tea, a handful of blueberries or a spice used in cooking.

Then there is the rest of life. Sleep, stress, grief, trauma, economic pressure, social support, movement, pain and hormones are not separate from nutrition. They shape how the body responds to food. Food does not work in a vacuum. It works inside a life.

This is why I think we need to stop treating “anti-inflammatory” as a property that simply lives inside a food. It is more accurate to say that an anti-inflammatory effect may emerge in the meeting between a food, a gut microbiome, a metabolism, an immune system and a life context. That is a much less marketable sentence. But it is much closer to biology.

Supplements and “anti-inflammatory” treatments deserve the same skepticism

The same logic applies to supplements and treatments marketed toward inflammation or fibrosis.

Many compounds sound convincing because they have a plausible mechanism. They may influence inflammatory pathways in cells. They may affect fibrosis-related signaling. They may have antioxidant properties. They may make sense on paper. But plausible is not the same as proven.

Serrapeptase is one example. It has been promoted as an anti-inflammatory or antifibrotic enzyme, including after lipedema surgery. But a controlled study looking at serrapeptase after liposuction for lipedema did not find evidence strong enough to support routine use for fibrosis, pain or stiffness.

GLP-1 receptor agonists are another example. They are very interesting drugs, especially for metabolic disease, obesity and insulin resistance. They may have anti-inflammatory and antifibrotic effects in some biological contexts. But when it comes to lipedema itself, the direct evidence is still extremely limited. A small case series is not enough to conclude that these medications modify lipedema tissue.

Resveratrol is similar. It has interesting mechanisms related to inflammation, metabolism, estrogen signaling and oxidative stress. But for lipedema, much of the discussion remains mechanistic and speculative. It is not the same as evidence that taking resveratrol improves lipedema symptoms in real patients.

This does not mean these things are useless. It means we should place them in the right evidence category.

Interesting? Yes.

Worth studying? Yes.

A proven lipedema treatment? Not yet.

For a disease community that has been neglected for so long, this distinction is not pessimistic. It is protective.

The problem with universal food lists

The biggest problem with universal anti-inflammatory food lists is not that the foods are bad. Many of the foods on those lists are genuinely nutritious. I have nothing against berries, olive oil, fish, ginger, vegetables or green tea.

The problem is the certainty.

When foods are divided too neatly into “good” and “bad,” people often stop listening to their own bodies. A person may keep forcing themselves to eat something that gives them digestive distress because it is supposed to be anti-inflammatory. Another person may remove entire food groups they tolerate perfectly well because someone online said those foods are inflammatory. Someone else may feel guilty for eating rice, bread, dairy, fruit, potatoes or an occasional dessert, even though those foods may not be a problem for them at all.

This can become especially harmful in chronic illness communities, where people are already desperate for control.

Food fear is not anti-inflammatory. Chronic guilt is not anti-inflammatory. A diet that makes your life smaller, more anxious and more socially isolated is not necessarily healing, even if every ingredient on the plate looks perfect.

A more useful approach is to think in patterns and personal responses.

What happens when your meals contain enough protein? What happens when you reduce refined sugar? What happens when you eat more fiber? What happens when you drink alcohol several days in a row? What happens when you eat carbohydrates alone compared with carbohydrates in a balanced meal? What happens in the week before your period? What happens after poor sleep? What happens during travel, heat, grief, stress or hormonal treatment?

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These questions are more useful than asking whether one food is officially anti-inflammatory.

What this means in practice

I do not want to replace one rigid list with another. That would defeat the point.

But I do think there are some gentle principles that make sense for many people with lipedema.

A good starting point is to build most meals from minimally processed foods. Make sure you get enough protein. Include vegetables, berries, fruit, legumes, grains or starches according to your own tolerance. Use fat sources such as olive oil, fatty fish, nuts, seeds, avocado or other foods that work for you. Pay attention to fiber, because fiber influences gut bacteria, blood sugar response, bowel function and the production of metabolites that may affect immune signaling.

Then look at the things that most often create problems for many people, even though not always for everyone: large amounts of refined sugar, sugar-sweetened drinks, frequent ultra-processed foods, heavy alcohol intake, very low fiber intake and meals that create large blood sugar swings.

For some people with lipedema, lowering carbohydrate intake may be useful. For others, it may be enough to change carbohydrate quality and meal composition. Some may feel best with a ketogenic approach. Others may feel better with a Mediterranean-style diet that includes legumes, fruit, oats, potatoes or whole grains. Some tolerate dairy. Some do not. Some tolerate gluten. Some do not. Some react strongly to sugar. Others react more to alcohol, heat, lack of sleep or hormonal changes.

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The point is not to find the strictest diet. The point is to find the most supportive pattern.

A symptom diary can be helpful, but only if it is used calmly. The goal is not to obsess over every bite. The goal is to notice patterns over weeks and months. What did you eat? How did you sleep? Where are you in your cycle? How stressed were you? How did your legs feel that evening and the next day? Did you feel swelling, heaviness, pain, pressure, cravings, fatigue or digestive symptoms?

Over time, patterns often become clearer.

Maybe gluten is not the issue, but large amounts of white bread without protein are. Maybe dairy is not the issue, but ice cream with sugar is. Maybe carbohydrates are not the issue, but fast carbohydrates alone are. Maybe you tolerate wine occasionally, but not in heat, not before your period and not after poor sleep. Maybe fruit is fine, but candy is not. Maybe your body handles rice well after strength training, but poorly after a sedentary day.

This is not about perfection. It is about learning.

Anti-inflammatory eating should not make your life smaller

I think one of the most important things we can say in the lipedema community is this: food should support the body, not become another source of punishment.

Many people with lipedema have already been blamed for their bodies. They have been told to lose weight, exercise more, try harder, eat less, be more disciplined. They have lived with pain that others could not see, tissue changes that were dismissed, and symptoms that were reduced to lifestyle.

So when we talk about food, we need to be careful.

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Yes, nutrition matters. Yes, food can influence inflammation markers, blood sugar, fluid balance, gut function and symptoms. Yes, many people with lipedema do notice clear food triggers. I believe those experiences should be taken seriously.

But we should not turn nutrition into another moral test.

An anti-inflammatory way of eating is not just about what is missing from your plate. It is also about whether the pattern is sustainable, nourishing, flexible, socially possible and emotionally safe. A diet you can live with for years will usually be more useful than a perfect protocol you can follow for three weeks while feeling miserable.

For people with lipedema, the goal is not to eat like a machine. The goal is to reduce pain, support tissue health, protect metabolic health and still have a life.

“Anti-inflammatory food” is not one recipe.
And it is certainly not one universal recipe for lipedema.

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There are anti-inflammatory dietary patterns. There are foods that contain compounds with interesting biological properties. There are nutrients that support immune regulation, vascular function, gut health and metabolic stability. There are also food patterns that may worsen blood sugar swings, gut symptoms, fluid retention or systemic inflammatory burden in some people.

The lipedema research makes the story more complicated, not less

Lipedema tissue is not simply ordinary inflamed fat. Its immune profile may differ from obesity. M2-like macrophages, fibrosis, tissue remodeling, pain and possible metabolic protection can all exist in the same conversation. A diet can be associated with lower inflammatory markers in blood without clearly improving pain or quality of life in every study. And a promising mechanism is not the same as a proven treatment.

So no, there is no single anti-inflammatory food list that works the same way for every person with lipedema. The same food can help one person, do nothing for another and trigger symptoms in a third. That does not mean anyone is doing it wrong. It means biology is personal.

For lipedema, this is not a disappointing conclusion. It is a freeing one. You do not have to chase every online list. You do not have to fear every food someone calls inflammatory. You do not have to copy another person’s diet to prove that you are taking your condition seriously.

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You can begin with the science, stay honest about what we do not yet know, and then carefully observe your own body. Because the most useful anti-inflammatory diet is not the one that looks best on paper. It is the one that helps your body feel calmer, without making your life smaller.

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Welcome to LipedemaScience.com!

can cytokines be detected in a blood test?

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The two lab photos are from my research days, when I was studying cytokine responses in human intestinal cells. I added bioactive pea peptides to the cell growth medium together with a pro-inflammatory signaling molecule called interleukin-8, or IL-8.

In the control sample, the cells were exposed only to IL-8. In the sample where I also added the pea peptides, I observed a reduction in the inflammatory marker I was measuring. This was part of my work exploring how bioactive food compounds may influence inflammatory responses at the cellular level.

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This is why a new 2026 study on lipedema metabolism caught my attention. The study does not give us a final answer, and it does not prove that lipedema has a diagnostic blood signature. But it asks an important question. Do women with lipedema have a different fasting metabolic profile from women without lipedema who have a similar BMI?

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That question matters because many lipedema studies are difficult to interpret when the comparison groups are very different in body size. If women with lipedema are compared with much leaner controls, it becomes hard to know whether a finding is related to lipedema itself or simply to differences in weight, fat mass or obesity related metabolism. In this study, the researchers compared 24 premenopausal women with clinically confirmed lipedema with 21 BMI matched controls. That does not make the study perfect, but it makes the question much more useful.

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The researchers used NMR metabolomics, a method that can measure many small molecules in the blood. Instead of looking only at standard clinical markers, they examined a broader biochemical picture of fasting metabolism, including amino acids, glycolysis related metabolites, ketone bodies and lipoprotein markers. This is the kind of approach that may become important in lipedema research, because lipedema is unlikely to be explained by one isolated blood value. It appears to involve adipose tissue, connective tissue, blood vessels, lymphatic function, pain, hormones and metabolism at the same time.

The first important finding was about body shape. Even though the lipedema group and the control group had similar BMI, the women with lipedema had lower waist circumference, lower waist to hip ratio and lower waist to height ratio. In other words, their fat distribution was more peripheral. This supports something many patients already know from lived experience. BMI can make two bodies look similar on paper while hiding major biological differences.

This matters because BMI does not tell us where fat is stored. It does not tell us whether tissue is painful, fibrotic, pressure sensitive or prone to bruising. It does not tell us whether fat is stored around the abdomen or disproportionately in the limbs. For lipedema, those distinctions are not minor details. They are central to the disease.

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That sentence can be hard to hear when you live with a disease that is not caused by your weight. But after 14 years of living as lipedema diagnosed, I understand why it matters.

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Those of us with lipedema often have to live much healthier than people without this disease. And sometimes, that feels incredibly unfair. I watch my friends enjoy waffles, chocolate and crisps without it seeming to leave any trace in their bodies. But in my body, these things often do leave a trace. Because my lipedema tissue is fibrotic and chronically inflamed, I often imagine that every indulgence makes a deeper mark in the tissue. Maybe not visibly overnight, but biologically. It feels as if the tissue remembers.

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That is why I always think carefully before and after I eat something that I know may affect my lipedema negatively. Is it worth it..? Was it worth it..?

I am very analytical about my 20 percent. If I truly enjoy what I eat, I can say to myself, yes, that was worth it. But if it was not actually that good, I can also say, no, that was not worth it. Remember that next time.

I have a bachelor’s degree in nutrition, which is a field where lifestyle change and lifestyle related disease are central topics. Because of that, I have now created a new category of articles called Weight Control. In my Lifestyle category, I also share more about how I live my eighty twenty rule, where I still enjoy life and take breaks from perfectly composed meals.

If you are someone who struggles with weight, I would encourage you to keep a food diary for a period of time. Weigh your meals for a while, or use AI to estimate the calories for you. Many people have real aha moments when they do this. Is there really that much energy in butter. Does this chocolate bar contain almost a full day’s worth of calories. Are the adjustments needed to stay within my energy needs actually much smaller than I thought.

Many people with lipedema find it difficult to talk about calories, lifestyle and excess weight because they have been told that these things have nothing to do with lipedema. And in one important sense, that is true. Lipedema is not caused by calories, lifestyle or body weight.

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But here is the nuance that matters. The biological cause of lipedema is not the same as the biological environment that lipedema tissue has to live in every day. A body with lipedema is already under a lot of pressure. It is already dealing with pain, swelling, inflammation, tissue changes, heaviness, bruising and often impaired mobility. That body needs the best possible conditions you can give it.

I sometimes think of it like having a cold. When you are sick, you may become more focused on supporting your immune system. You rest more. You try not to stress. You eat a little better because you know your body is already dealing with something. I think about lipedema in a similar way. My body is already dealing with a lot.

My partner can eat sweets every day. He trains hard. He pushes his body hard. He can do many things that I cannot do, because my underlying biology is already pushing my body hard. So I have to think differently. I have to say no to more things.

This is a perspective I deeply want more women with lipedema to understand. It has taken me fourteen years of living with this disease to fully understand it in my own body. There have been periods where I have been careless, where I stopped paying attention, where I simply did not care as much. And for me, that has left lasting marks in my lipedema. My tissue is very fibrotic. Maybe yours is not. Maybe you do not need to be as strict as I do.

But my body feels best when I manage to balance my eighty twenty rule well. When I manage stress. When I move regularly. When I use my eighty percent to truly nourish the cells in my body with antioxidants, polyphenols, bioactive compounds, prebiotics, probiotics, protein, healthy fats, fiber, vitamins, minerals and all the small things that help create a better internal environment.

This is not about perfection. It is not about blame. And it is definitely not about saying that lipedema can be dieted away.

It is about understanding that when you live in a body that is already carrying a chronic disease, your daily choices can either add more pressure or give that body a little more support.

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At 23, I looked healthy and normal from the outside. Inside, my legs were already painful, heavy, swollen, and reacting to a disease most people could not see.

And I know what many people might think when they see this photo.
She looks normal. And that is exactly the point.

Looking back at this photo feels strange, because I know how much I was already carrying in my body, even though I did not yet understand the full picture. I had a diagnosis, but I still had so many unanswered questions. I was still trying to understand why my legs could feel painful, heavy, swollen, and different from the rest of me.

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Lipedema is not always obvious from the outside, especially in the earlier years, or in people who are otherwise lean, active, or young. You can look healthy in photos and still live with deep aching pain, tenderness, swelling, heaviness, bruising, and tissue that feels different from the rest of your body.

At that time, I still had so many unanswered questions. I had a diagnosis, but I did not yet understand the biology of what was happening in my tissue. I did not understand why sugar could make my legs flare. I did not understand why estrogen containing birth control seemed to make everything worse. I did not understand why my legs could feel so painful even when the rest of my body looked healthy.

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That is one of the reasons I started LipedemaScience. Because a diagnosis is not always the end of confusion. Sometimes it is the beginning of finally learning how to understand your own body.

I want to get to know you a little better

So many of us arrive here with different stories. Some were diagnosed early. Many spent years being told it was just weight, hormones, aging, or something they were doing wrong. Some have had surgery. Some are still searching for answers. Some are newly diagnosed and still trying to understand what this disease means for their body and their life.

I would love to hear your lipedema story in the comments.

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• When did you first notice symptoms?

• How long did it take before you found the word lipedema?

• What has helped you, and what do you wish more people understood?

Share as much or as little as feels right. I read your stories with care, and they help shape what I write about here.

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I believe Substack has already made it possible to translate comments and notes, so feel free to write your story in your own language.

• A new review suggests that lipedema may involve vascular dysfunction, including leaky and fragile blood vessels, not only abnormal fat accumulation.

• These vascular changes may help explain symptoms such as swelling, heaviness, easy bruising, pain, inflammation, and progressive tissue stiffness.

• The review does not prove what causes lipedema, but it supports a more complex disease model involving fat tissue, blood vessels, lymphatics, immune activity, and connective tissue.

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LipedemaScience started from a very personal place, but it has grown into something bigger than my own story. I created it because I know how difficult it can be to live with symptoms that are often misunderstood, while the scientific information is hard to access or written in a way that patients cannot easily use. My goal is to help bridge research and lived experience by reading the studies carefully, explaining what they show, and being honest about what we still do not know. Paid memberships make this work possible. Every subscription gives me more time to follow the research, write deeper articles, and build a space where lipedema is taken seriously as a biological disease. Your support means so much, not only for this article, but for helping LipedemaScience continue to grow into a knowledge platform for patients, families, and health professionals.

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For me, the timing was very clear. It happened after I started hormonal birth control. My body changed quickly, in a way that felt different from normal teenage weight gain. The fat on my legs did not behave like ordinary fat. It felt heavy, painful and out of proportion. At the time, I did not have the language for what was happening. I did not know that lipedema often appears around major hormonal transitions such as puberty, pregnancy, menopause or sometimes after hormonal contraception. I only knew that something had changed in my body, and that I could not control it in the way I thought I should be able to.

Today, after many years of reading, studying, living with lipedema and writing about it, I no longer see lipedema as simply a problem of fat storage. I see it as a disorder of tissue biology. Lipedema involves subcutaneous fat, but also blood vessels, connective tissue, pain pathways, immune cells, fluid handling, hormones and possibly lymphatic function. It is not only about size. It is about how the tissue behaves. That distinction matters, because it changes how I understand the rest of my life.

LipedemaScience is where I share deeper reflections on lipedema, biology, hormones, inflammation, pain, nutrition, surgery, and the lived experience of having this condition. My goal is to make complex science understandable without oversimplifying it. If you want thoughtful, research-informed writing that connects evidence with real life, I would love to have you here.

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After my lipedema started, my body went through several major forms of trauma. Some were physical. Some were emotional. Some were both. But the more I learn about the body, the less meaningful that distinction becomes.

When I was 18, I developed severe sepsis caused by Fusobacterium necrophorum. In my case, it became Lemierre’s syndrome, a rare but life threatening condition where an infection can spread into the bloodstream and cause thrombosis, septic emboli and abscesses. My lungs were severely affected. I was frighteningly close to death.

Because the infection was so rare, the doctors did not immediately know what they were dealing with. The situation was critical, and I was given several extremely strong courses of antibiotics. At that point, the priority was survival. No one was thinking about long term immune effects, endothelial damage, microbiome disruption or how a near fatal infection might affect a young body.

And of course, why would they? I was 18. I just needed to survive.

But when I look back now, I cannot separate that event from the rest of my body story. Sepsis is not just an infection. It is a systemic immune crisis. It affects inflammation, blood vessels, coagulation, metabolism, mitochondria and immune regulation. For some people, the body does not simply return to its previous state after sepsis. Research on post sepsis syndrome suggests that some survivors may experience long term immune dysregulation, low grade inflammation, metabolic changes and increased vulnerability after the acute infection is over.

My lipedema had already started. And I do wonder whether such a severe inflammatory and vascular event changed the internal environment in which my lipedema existed.

That is the question I keep returning to. Not what caused everything. But what turned up the volume.

When I was 20, my father died suddenly of cancer. I went into deep grief and depression. Losing a parent that young is not only an emotional experience. It changes the whole body. It changes sleep, appetite, breathing, energy, hormones, stress responses and immune function. Grief is often spoken about as something that happens in the mind, but that has never made sense to me. I felt grief in my body. I felt it in my nervous system. I felt it in my fatigue, my heaviness and my ability to function.

Bereavement research supports this more embodied view of grief. Severe grief can be associated with changes in inflammatory signaling, cortisol patterns, immune function and sympathetic nervous system activity. Again, this does not mean grief causes lipedema. That would be too simple, and in my own timeline it would be wrong. But grief can change the biological terrain. A body in grief may become more inflamed, more exhausted, more pain sensitive and less resilient. For someone with lipedema, that may matter.

Lipedema tissue is already sensitive. Many of us live with tenderness, pressure pain, swelling, easy bruising and a feeling that the tissue becomes angry under certain conditions. If grief increases inflammatory tone, disrupts sleep and changes stress biology, then it is biologically plausible that symptoms may feel more intense during or after periods of deep loss. The disease may already be there. But the body carrying the disease is not static.

Between the ages of 25 and 27, I went through another kind of stress. I was doing my master’s degree in food science after studying nutrition. At the time, it was possible in Norway to move from nutrition into food science, but it was not an easy transition. The two fields are very different. Nutrition had taught me about the human body, metabolism and health. Food science demanded microbiology, chemistry, processing, laboratory methods, technology and a completely different scientific language.

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The year between those two studies was intense. My study friends and I had to learn laboratory techniques in one year that food science students had spent years building. Then we continued into two more years of demanding food science. I spent so much time in the lab, writing lab reports, studying and trying to catch up. That was the period when my lipedema became its worst.

I do not think this was a coincidence, but I also do not want to turn my story into a simplistic claim. Chronic stress is not a magic explanation for lipedema. It does not explain why lipedema has such a strong female pattern, why onset clusters around hormonal transitions, why the tissue is distributed in specific areas, or why the fat behaves differently from ordinary weight gain.

But chronic stress does affect systems that are relevant to lipedema. It activates the HPA axis, cortisol signaling, the sympathetic nervous system, inflammatory cytokines, sleep disruption, insulin sensitivity, mast cells, pain pathways and sometimes movement patterns. Acute stress can be adaptive. Chronic stress is different. It keeps the body in a prolonged state of biological vigilance. During those years, my body was not only studying. It was surviving.

I was mentally stretched, but I was also physically inflamed, tired and under pressure. I had less capacity for recovery. I had more heaviness. My pain and swelling felt worse. My body felt harder to regulate.

This is one of the reasons I find the phrase “mental health” too narrow. It makes it sound as if stress lives only in thoughts and emotions. But chronic stress also lives in cortisol rhythms, immune cells, blood sugar regulation, gut function, vascular tone, muscle tension, sleep architecture and pain sensitivity. The body does not divide our experiences into neat categories.

Then, when I was 30 and 31, I went through lipedema surgery. I had four surgeries between 2021 and 2022. Surgery helped me enormously. It gave me back mobility, freedom and a body that felt much easier to live in. I can walk for hours now. I can travel. I can exercise. I have far less pain than before. But surgery was also trauma.

Not emotional trauma in the usual sense, although it can be that too. I mean biological trauma. Lipedema surgery is not a small intervention. It is a major physical event. The body has to respond to tissue injury, inflammation, swelling, bruising, fluid shifts, wound healing and pain. The nervous system is involved. The immune system is involved. The endocrine system is involved. And this is where the story becomes more interesting.

Surgery is an acute inflammatory insult, yet for many people with lipedema, including me, it can reduce long term pain and heaviness by removing diseased tissue. That is not a contradiction. It shows how dynamic the body is. Sometimes a short term physical burden can lower the long term burden if it removes a source of pressure, inflammation, fibrosis or pain signaling.

This is also why lipedema surgery should not be framed as cosmetic. It is not simply about appearance. For many of us, it is about function, pain, pressure, mobility and the ability to live in the body with less daily struggle.

Still, even successful surgery does not erase the larger biology. It does not remove the nervous system. It does not remove hormonal sensitivity. It does not remove the immune system. It does not remove the life a body has lived. And my body had lived a lot before lipedema ever appeared.

When I was 7 years old, my brother died in a car accident. Soon after, my mother developed ME/CFS. For many years of my childhood, she was severely ill. She often lay on the sofa, in a dark room, with very little energy. As a child, I carried grief, fear and confusion inside me. I also had a lot of stomach pain.

At the time, that pain may have looked like a purely physical symptom. But now I understand it differently. Children often express distress through the body. The gut and the nervous system are deeply connected. Early life stress can shape stress responses, pain sensitivity, immune tone and the gut brain axis. My stomach pain was not imaginary. It was my body speaking a language I did not yet understand. This is one of the most important lessons my life has taught me. Pain can be physical and emotional at the same time because those are not separate systems.

My mother’s journey also shaped me. After many years of illness, she started exploring food, health and lifestyle. Her recovery process inspired me deeply. It is one of the reasons I became interested in nutrition, food science, biology and the possibility that food can support the body in meaningful ways.

I know the phrase “food as medicine” can become too simplistic. Food is not a cure for everything. Diet culture can be harmful. People with chronic illness are often blamed for not finding the right lifestyle solution. I do not want to contribute to that.

But I also cannot deny what I have seen in my own life. Food can affect inflammation, blood sugar, gut function, energy, symptoms and well being. It can become one way of communicating with the body. Not as punishment. Not as control. Not as ideology. But as support.

Lipedema is still misunderstood, and many people are left trying to connect the dots on their own. Through LipedemaScience, I want to build a place where science, personal experience, and careful reflection can meet. Subscribe if you want to follow that journey and be part of a more informed conversation about lipedema.

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This is especially relevant when thinking about lipedema. Lipedema is not caused by eating the wrong food. But many people with lipedema experience that their symptoms change depending on sleep, stress, infections, hormones, inflammation, movement and diet. That does not mean the disease is our fault. It means the tissue is responsive to the internal environment.

For me, this is the bridge between personal experience and science. Lipedema may begin with a combination of genetic, hormonal, vascular, immune and adipose tissue mechanisms. In my case, the hormonal timing around puberty and birth control feels central. But once lipedema exists, the disease does not live in isolation. It lives inside a whole person.

That person may go through sepsis.

That person may go through grief.

That person may live with chronic stress.

That person may undergo surgery.

That person may carry early childhood trauma.

That person may sleep poorly, lose movement, experience depression, have gut symptoms, live in fear, recover, relapse, adapt and rebuild.

All of this matters because all of it happens inside the same biological system.

This is why I believe the separation between physical health and mental health is outdated. It may be useful administratively. It may help organize medical specialties. But biologically, it is too limited. The immune system talks to the brain. The nervous system talks to the gut. Hormones affect inflammation. Stress affects pain. Grief affects sleep and immune function. Infection affects metabolism and blood vessels. Surgery affects the nervous system and inflammatory response. Adipose tissue is not passive storage. It is an active endocrine and immune organ.

Nothing about this means lipedema is “in the mind.” That is the exact opposite of what I am saying. Lipedema is real tissue disease. It involves real biological changes. It is not caused by weakness, imagination or unresolved emotion. But the body that carries lipedema is influenced by every major biological stressor it has lived through.

To me, the most honest framing is this. Chronic stress, grief, sepsis, surgery and early life adversity should not be presented as proven causes of lipedema. We do not have the research to say that. But they are plausible modifiers of lipedema expression. They may influence symptom intensity, pain sensitivity, swelling, inflammation, recovery capacity, hormonal balance, immune tone and the body’s ability to regulate itself. They may not write the disease. But they may turn up the volume.

And sometimes, when I look at my own timeline, that is exactly how it feels. Lipedema began at puberty, after hormonal contraception. Then my body moved through near fatal infection, deep grief, chronic academic stress, major surgery and the earlier wounds of childhood loss. Each event left something behind. Not always something visible. Not always something measurable in a standard blood test. But something biological nevertheless.

I think many people with chronic illness understand this intuitively. We know that our symptoms are not separate from our lives. We know that a stressful year can change the body. We know that grief can make pain louder. We know that infection can leave us altered. We know that surgery can both help and hurt. We know that childhood experiences can live in the gut, in the nervous system, in the breath, in the muscles and in the way the body protects itself.

Science is beginning to give language to what many patients have felt for years. The body remembers. Not in a mystical way. In an immune way. In an endocrine way. In a nervous system way. In a vascular way. In an inflammatory way. In a cellular way.

For me, understanding lipedema means understanding that whole system. Not just the fat. Not just the hormones. Not just inflammation. Not just mental health. Not just trauma. The whole body.

Because there was never one part of me that was physical and another part that was emotional.

It was always the same body.

Trying to survive.

Trying to adapt.

Trying to protect me.

Trying to heal.

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During the years around surgery, the role of lymphatic support felt relatively clear to me. I used compression garments. I used a lymphatic press. I went to manual lymphatic drainage with a physiotherapist. These were not small additions to my life at the time. They were part of the structure around surgery, recovery and tissue healing. My body was swollen, sensitive and changing, and I wanted to give it every reasonable form of support I could.

That phase had its own logic. The phase I am in now feels different.

I am several years post-surgical, and I would describe my current situation as maintenance rather than active recovery. I travel frequently, and my life is not organised around being in one place with access to all the tools I used before. I cannot bring a lymphatic press with me everywhere. I cannot always plan physiotherapy appointments. I do not want my health routine to become so elaborate that it only works under perfect conditions.

At the same time, I notice a familiar question returning in the background:
am I doing enough for my lymphatic system?

It is a difficult question, because the lymphatic system occupies a strange place in lipedema. It is often mentioned in patient communities, treatment protocols and commercial messaging, but the scientific picture is still more nuanced than many explanations suggest. Lipedema is not simply lymphedema. The legs may feel swollen, heavy and pressurised, but that does not necessarily mean the primary problem is failed lymphatic drainage. Several studies suggest that pure lipedema is not characterised by the same fluid accumulation seen in lymphedema, and some imaging studies indicate that the lymphatic vessels may still be functioning, at least in earlier stages.

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That does not mean the lymphatics are irrelevant. It means the question is more complicated.

One model I keep returning to is that the lymphatic system may not be the first thing that breaks. It may be the system that is asked to compensate. If the small blood vessels in lipedema tissue are more fragile or more permeable, if the fat tissue is inflamed, if the interstitial matrix becomes more fibrotic or altered, then the lymphatics may be handed more work than they would receive in a normal limb. In that case, the lymphatic system is involved, but perhaps not as the original cause. It may be carrying part of the burden created by the adipose and microvascular environment.

This distinction matters, because it changes how I think about treatment.

If lymphatic support mainly helps symptoms, then it may still be valuable. Compression may reduce heaviness, pain, bruising or swelling sensations. Pneumatic compression may be useful when fluid or pressure builds up. Manual lymphatic drainage may feel calming and supportive, especially in periods of recovery or flare. Water may offer a gentle form of hydrostatic compression that also supports movement and circulation. These things may improve comfort and quality of life.

But are they modifying the disease itself? Are they changing the altered fat tissue? Are they reducing fibrosis? Are they preventing progression? Are they protecting the lymphatic system over decades? I do not think we can answer those questions with confidence yet.

This is where I find myself with more questions than conclusions.

In my own life, I have shifted my focus toward the things I can sustain consistently: sleep, stress regulation, less alcohol, nutrient-dense food, running and strength training. These do not look like classic lymphatic treatments, but I increasingly wonder whether they may be central to maintenance. Muscle contraction supports venous and lymphatic return. Strength protects function. Cardiovascular fitness supports circulation. Sleep and stress regulation influence inflammation, recovery and hormonal signalling. Food quality affects metabolic health and perhaps the inflammatory environment in which the tissue exists.

None of this is specific enough to call it a lipedema treatment in the narrow sense. But perhaps maintenance after surgery is not only about targeting the lymphatic system directly. Perhaps it is also about supporting the broader biological environment that the lymphatic system has to operate within.

That is something I want to understand better.

I also try to be in water as often as I can. This is partly because it feels good, but also because the mechanism makes sense to me. Immersion creates external pressure around the limbs. The deeper the body is submerged, the greater the hydrostatic pressure. Combined with movement, water can support circulation, muscle activity and fluid return in a way that feels far less burdensome than compression garments. For someone who travels, water is also more accessible than many devices. A pool, the sea or even gentle movement in water can become a form of care that does not require carrying equipment.

Recently, I also bought a dry brush.

I did not buy it because I believe it will cure lipedema. I do not expect it to break down fat tissue or meaningfully change the disease. I bought it because I was curious. It is simple, portable and inexpensive, and I wanted to see whether gentle skin stimulation might feel beneficial in my body.

But dry brushing is also exactly the type of intervention that makes me cautious.

It is often described as “stimulating the lymphatic system,” but I have not seen good evidence that it improves lipedema symptoms, reduces limb volume or changes lymphatic function. The proposed mechanism is not impossible. The superficial lymphatics sit close to the skin, and mechanical stimulation may plausibly create some sensory or local circulatory effect. But plausible is not the same as proven. This is where the boundary between physiological possibility and wellness marketing becomes difficult to navigate.

I do not want to dismiss every practice simply because the evidence is incomplete. Many parts of conservative care in lipedema are under-researched, and lived experience can sometimes point toward questions that science has not yet studied properly. At the same time, I do not want to present low-evidence practices as if they have stronger support than they do.

So I am treating dry brushing as a small personal experiment, not as a medical intervention.

If it feels calming, improves my relationship with my skin, or gives me a few minutes of quiet body awareness, that may be reason enough to continue. If it irritates my skin or becomes another task on an already long list of things women with lipedema are told to do, I will stop.

This, I think, is one of the hardest parts of living with lipedema in the current evidence landscape. There are many recommendations, but not always enough data to separate what is essential, what is optional, what is helpful for some, and what is mostly commercial enthusiasm. The field contains real science, clinical experience, patient knowledge and marketing claims, often mixed together in the same conversation.

I find myself asking more and more questions..

• How much lymphatic support is actually needed after surgery?

• Does that need change depending on whether someone has pure lipedema or lipolymphedema?

• Are some people more dependent on compression and drainage than others because of venous disease, fibrosis, stage, surgery history or inflammation?

• Can strength training and aquatic exercise reduce the need for more passive lymphatic treatments?

• Does the lymphatic system recover some capacity after the fat load is reduced surgically?

• Could certain maintenance routines protect against secondary lymphatic overload, or is that still an assumption?

• And how do we design care plans that women can actually live with for decades?

I do not have clear answers to these questions. But I think they are important questions, because they move the conversation away from guilt and toward individualised care.

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My own maintenance routine is not perfect, and perhaps that is the point. It is not designed to be perfect. It is designed to be livable. I use compression when it makes sense, especially during flights or situations where I know my legs may react. I prioritise movement, strength, food quality, sleep and stress regulation. I seek water when I can. I remain open to tools like dry brushing, but I hold them lightly.

I am still trying to understand what my body needs now compared with what it needed during surgery recovery.

I am also curious how other women experience this shift.

• For those who have had lipedema surgery, did your need for compression, manual drainage or pneumatic compression change over time?

• Did you feel able to reduce some of these supports, or did you continue needing them?

• Have you found water, strength training or other forms of movement to be enough for maintenance?

• Has dry brushing done anything noticeable for you, or does it feel more like a pleasant ritual than a treatment?

I would especially like to hear from people in different stages: those with early lipedema, those who are post-surgical, and those who have lipolymphedema or clear fluid accumulation. My suspicion is that “lymphatic care” is not one thing, and that the right level of support may depend heavily on the person, the stage, the tissue, the comorbidities and the phase of life.

For now, I am trying to stay in the space between certainty and dismissal.

I do not believe my lymphatic system is simply broken. I also do not believe it is irrelevant. I think it may be carrying part of the load created by a more complex tissue environment involving fat, vessels, inflammation, fibrosis and mechanical pressure. That is the part I want to learn more about.

And perhaps this is where I currently land: maintenance after surgery is not necessarily about doing every lymphatic intervention forever. It may be about understanding which forms of support still give something back, which ones belong to a previous phase, and which ones are simply not worth the energy anymore.

That answer will probably not be the same for everyone. And I think that is exactly why we need more honest conversations about it.

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If you spend any amount of time in nutrition communities, it quickly becomes clear that almost every food imaginable has become controversial. Red meat is a perfect example. Some people see it as one of the most nutrient-dense foods available and believe it should form the foundation of a healthy diet. Others view it as something inherently harmful and avoid it entirely. The same pattern exists with vegetables, fruit, dairy products, eggs, grains, nuts, seeds, fish, soy, coffee, saturated fat, carbohydrates, and oils. It is remarkable how two people can look at exactly the same food and come away with completely opposite conclusions. One person looks at fruit and sees vitamins, minerals, fiber, polyphenols, and health benefits. Another sees fructose and sugar. One person sees dairy as a rich source of protein, calcium, and beneficial fermentation products, while another sees hormones, inflammation, and digestive problems. One person views bread as a staple food that humans have consumed for thousands of years, while another sees it as a major contributor to modern disease.

Become a member of LipedemaScience if you want thoughtful, science-based writing about lipedema, nutrition, hormones, metabolism, and the complexity of the human body. My background in nutrition and food science shapes how I write, with curiosity rather than dogma. I do not believe in simple answers where the biology is complex. Subscribe now if you want to explore these questions with more nuance.

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What fascinates me most is not necessarily that these disagreements exist. Science has always evolved through disagreement and debate. What fascinates me is how absolute many of these beliefs have become. There is often very little room for uncertainty. Very little room for nuance. Very little room for the possibility that two people can have different experiences with the same food and both be telling the truth. Food discussions can sometimes resemble religious debates more than scientific discussions. People are not simply sharing what works for them. They are defending entire worldviews. If someone questions those worldviews, it can feel almost personal.

Perhaps this happens because food is one of the few things we interact with every single day. We eat multiple times per day for our entire lives. Unlike many other health interventions, food produces immediate experiences. We can feel energized after a meal, sluggish after another, satisfied by one food and hungry after another. We build stories around these experiences. Over time, those stories become beliefs, and those beliefs can become identities. The person who feels dramatically better after removing carbohydrates may naturally begin to view carbohydrates as the problem. The person who experiences improvements after adopting a plant-based diet may naturally begin to view plants as the solution. The challenge is that human biology is rarely that simple.

One of the things I learned during my education is that food is incredibly difficult to study. Many people imagine that nutrition science should provide straightforward answers, but the reality is often much messier. Human beings are not laboratory mice living in controlled environments. We have different genetics, different hormone levels, different gut microbiomes, different lifestyles, different stress exposures, different sleep patterns, different health conditions, and different life histories. Even when researchers try to isolate specific variables, the complexity of human biology creates enormous challenges. During my own studies, I worked with food components on a cellular level and saw firsthand how difficult it can be to interpret biological responses even under highly controlled conditions. Once you move from isolated cells to entire human beings living real lives, the complexity increases exponentially.

Subscribe to LipedemaScience if you are tired of black-and-white nutrition advice. I write from both personal experience with lipedema and a professional background in nutrition, food science, food safety, microbiology, and human metabolism. The goal is not to tell you what to eat, but to help you understand why bodies respond differently. Become a member if you want deeper, more reflective science writing.

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This complexity becomes particularly relevant when discussing lipedema. One of the reasons I have become cautious about making broad dietary recommendations is because I have spent years observing how differently people with lipedema respond to food. Some people report significant improvements when reducing carbohydrates. Others do not. Some feel noticeably better when avoiding dairy. Others consume dairy daily without any apparent issues. Some find seed oils problematic. Others notice no difference whatsoever. Some thrive on higher-fat diets. Others feel better with more carbohydrates. The more people I speak with, the more convinced I become that there is no single dietary approach that explains every experience within the lipedema community.

My own experience reflects this reality. Over the years, I have learned that refined sugar is one of the clearest triggers for my symptoms. That relationship has been remarkably consistent. I have also found that I generally feel better when I minimize heavily fried foods, highly processed meat products, large amounts of candy, and certain ultra-processed foods. At the same time, I do not have major food intolerances or allergies. I eat fish, meat, vegetables, fruit, dairy products, nuts, seeds, eggs, and many other foods. I do not feel compelled to eliminate entire food groups because I have never seen convincing evidence in my own body that doing so improves my health. What I have learned is not that certain foods are universally good or bad. What I have learned is that my body has specific triggers, and those triggers may not be identical to someone else’s.

This is one of the reasons I have become increasingly uncomfortable with extreme certainty in nutrition discussions. The older I get, the more I realize how much we still do not know. Food is not simply calories, protein, fat, and carbohydrates. Food contains thousands of biologically active compounds. As a food scientist, I am aware of considerations that rarely enter mainstream nutrition discussions. Acrylamide, polycyclic aromatic hydrocarbons, mycotoxins such as aflatoxin B1, oxidation products, food processing contaminants, naturally occurring plant defense compounds, bioavailability, food matrices, and countless other factors all influence how food interacts with the body. If I wanted to focus exclusively on potential risks, I could probably make almost every food sound frightening. But I do not believe that would help anyone.

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In fact, one of my biggest concerns about modern nutrition culture is the amount of fear it creates. I have seen people become so overwhelmed by conflicting dietary advice that they lose trust in their ability to eat normally. Every meal becomes a source of anxiety. Every ingredient becomes something to investigate. Every restaurant menu becomes a puzzle. Food gradually transforms from something enjoyable and social into something stressful and exhausting. For people already navigating a chronic condition such as lipedema, that burden can become particularly heavy. Many are already managing pain, swelling, frustration, uncertainty, and years of feeling misunderstood. Adding another layer of fear around food is rarely productive.

That does not mean nutrition is unimportant. Quite the opposite. I believe nutrition matters enormously. I believe food can influence metabolic health, inflammation, satiety, energy levels, blood sugar regulation, and overall wellbeing. I believe some dietary patterns may genuinely help certain people with lipedema manage symptoms more effectively. But I also believe that the healthiest relationship with food often exists somewhere between obsession and indifference. It involves paying attention to your body without becoming consumed by every dietary trend. It involves learning from science without treating every new study as absolute truth. It involves remaining curious rather than dogmatic.

At LipedemaScience, I write for people who want more than quick answers and diet rules. Food, lipedema, hormones, inflammation, and metabolism are complex, and they deserve to be explored with honesty and depth. My aim is to make the science understandable without pretending it is simpler than it is. Subscribe now to support this work and become part of a more thoughtful conversation.

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Perhaps that is why I have gradually moved toward a philosophy of dietary flexibility. I prefer diversity over restriction whenever possible. I prefer observing patterns over following rigid rules. I prefer asking questions over defending ideologies. Rather than searching for a perfect diet, I focus on understanding how my own body responds while recognizing that those observations remain incomplete. There are things I know with reasonable confidence, such as my response to refined sugar. There are many other things where uncertainty remains, and I am comfortable with that uncertainty.

The longer I study nutrition, the more I find myself returning to a surprisingly simple conclusion. Human beings are different. Our biology is different. Our experiences are different. Our responses to food are different. That reality may not provide the satisfying certainty that many people are looking for, but it is probably closer to the truth. Food does not need to become a religion. It does not need to become an identity. It does not need to divide people into competing camps. Sometimes it is enough to acknowledge that nutrition is complex, that our understanding remains incomplete, and that two people can eat very differently while both making choices that are right for them.

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That perspective has brought me a great deal of peace, both as someone who studied food professionally and as someone living with lipedema. Instead of constantly searching for dietary perfection, I focus on building a way of eating that supports my health, respects my individual triggers, allows flexibility, and still leaves room for enjoyment. Because at the end of the day, food is not only biology. It is culture, tradition, pleasure, connection, family, celebration, and everyday life. When we reduce it to a list of rules, we risk losing sight of everything that makes it meaningful in the first place.

At LipedemaScience, I believe nutrition deserves both curiosity and humility. Food influences health, but human biology is rarely black and white. My goal is not to tell you what to eat, but to explore the science, uncertainty, and individuality that make both nutrition and lipedema such fascinating subjects. Because sometimes the most honest answer is not certainty. It is complexity.

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I had four lipedema surgeries between 2021 and 2022. The first surgery was in September 2021, the second in November 2021, the third in February 2022 and the fourth in October 2022. These were not small procedures for my body. They were major surgeries in tissue that was already painful, swollen and affected by disease after many years. Before surgery, my legs had gradually become heavier and more fluid filled. In the last years before surgery, they almost felt like two large balloons, with constant pressure, swelling and that characteristic feeling of lactic acid in the legs. It was not an aesthetic problem. It was a physical limitation in everyday life.

When I was first diagnosed in 2012, I was 20 years old, had a BMI of 19 and was in an early stage. At that time, the toothache like pain in my legs was the most obvious symptom, and I experienced it as being linked to hormonal birth control. Over the years, my lipedema progressed. The pain, heaviness and swelling became more dominant. That is why surgery eventually became a choice I made because the disease had already taken up too much space in my life. I did not want surgery because I thought it was an easy solution, but because I needed a real reduction in tissue pressure and symptoms.

Still, I think it is important to be honest that lipedema surgery is not the same as walking into a cosmetic treatment and coming out with a new life without risk. It is surgery. It is invasive. The body is exposed to trauma, tissue is loosened, fat is removed, fluid is moved, blood vessels and lymphatic structures are affected, and the nervous system needs a long time to calm down and repair itself. For some people, this may be relatively uncomplicated. For me, it was not.

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After one of the surgeries, I developed a large seroma in my thigh. A seroma is a collection of fluid under the skin, often consisting of clear or yellowish wound fluid, serum and lymphatic fluid. After liposuction, it can occur because a hollow space forms in the tissue where fat has been removed, while the body produces fluid as part of the healing process. If the fluid is not drained well enough, it can collect like a pocket under the skin. For me, this was not just a small technical complication. It was something I could feel in my body, something that made recovery more demanding and reminded me of how much the tissue had actually been through.

I have previously described it as a large seroma in my thigh, especially connected to the area at the front of my thigh. It gave the tissue an uncomfortable and unfamiliar feeling. Even long afterwards, the thigh could still feel different. These are exactly the kinds of things you do not always fully understand before you experience them yourself. You can read about seroma as a known complication, but it is something else to have it in your own body after an operation you have already spent so much courage, money, hope and energy on.

After the last surgery in October 2022, I also developed internal bleeding in both hands. That was a tough complication, and it still stays with me as an important part of my surgery story. My hands were affected in a way I had not expected. When you prepare for lipedema surgery, you naturally think mostly about the areas that are going to be operated on. You think about the legs, the thighs, the arms or the specific fat tissue involved. You may think about pain, swelling, compression, drainage and scars. But the body is a whole, and complications can also happen in ways you did not imagine.

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For me, the internal bleeding in my hands was a reminder that even though lipedema surgery can be life changing, it is not risk free. I have also experienced some altered sensation and nerve damage or nerve irritation afterwards, including in the palms of my hands. These symptoms are minor compared with the pain I lived with before surgery, but they are still real. They are part of my body now. They are part of the price I paid to get better.

This is perhaps the most difficult part of speaking about lipedema surgery in a nuanced way. On one hand, I am incredibly grateful for the result. The surgeries have given me a life with far less pain, less swelling and much more freedom. I can walk around Lisbon for days without the constant lactic acid feeling in my legs. I can move in a way that would have cost me much more before. I can live more normally. That means an enormous amount.

On the other hand, I will never present surgery as a simple cure. Surgery does not cure lipedema. It does not necessarily remove all lipedema affected fat tissue, and it does not remove the underlying biological predisposition that makes the body develop lipedema. It can reduce volume, pressure, pain and functional limitations. For many, it can lead to a dramatic improvement. But that is not the same as the disease being gone, or the body never again being vulnerable to hormonal, metabolic, inflammatory or lymphatic triggers.

I think it is important that we are able to hold two thoughts at the same time. Lipedema surgery can be one of the most effective things some patients can do to reduce symptoms. At the same time, surgery can be demanding, expensive, physically exhausting and associated with complications. Both can be true at the same time. For me, surgery was completely worth it. I would choose it again. But I would never tell anyone that it was easy.

When I talk about the seroma and the internal bleeding, it is not to scare other women away from surgery. It is because I believe we need more honest conversations about what lipedema surgery actually involves. Many of us come to surgery after years of pain, disbelief, failed dieting, lack of help and the feeling of not being taken seriously. In that context, it is understandable that surgery can seem like the rescue. For some, it is also exactly what gives life back. But even when the result is good, the road there can be brutal.

My recovery was not a polished before and after story. It was long, painful and physically demanding. I travelled and lived my life along the way, but my body was working hard. I had complications. I had fluid accumulation. I had bleeding. I had strange sensations in the tissue. I had nerve involvement. I had to accept that healing is not linear, and that the body does not always follow the timeline you hope for.

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At the same time, it is precisely because I have experienced both the benefit and the complications that I feel so strongly about speaking about lipedema surgery in a more knowledge based way. We do not need to glorify surgery in order to acknowledge that it can help. We also do not need to reject surgery because it can cause complications. What we need is more precise information, better follow up, better research, better patient selection and more realistic expectations.

For me, this is not about being for or against surgery. It is about being honest. Today, I live in a body that functions much better than it did before surgery. The pain that once controlled large parts of my everyday life has been greatly reduced. I have regained freedom of movement, and I have regained a kind of trust in my body. But I also live with the experience that the road there involved major procedures, complications and residual damage.

That is why I always say that surgery helped me enormously, but that it did not cure my lipedema. It reduced a large part of the disease burden. It removed much of the pressure. It made my life bigger. But my body still has a lipedema history, and I still need to understand the body I live in. For me, saying that is not a defeat. It is simply the truth.

I think many people need to hear exactly this. Not a romanticised story about surgery as a miracle cure, and not a fear based story about surgery being dangerous. But a real story from a real body. My experience is that lipedema surgery can change your life, but it can also require much more from you than you expect. I am grateful for the result. I am also honest about the complications. Both are part of my story.

Lipedema is not simply ordinary fat that sits in the wrong place, and it is not the same as obesity. It is a chronic connective and adipose tissue disorder, most often affecting women, where the fat tissue develops in a disproportionate and painful pattern, usually on the legs, hips, buttocks and sometimes the arms, while the hands and feet are often spared. The tissue can be tender, heavy, swollen, easy to bruise and resistant to ordinary weight loss. Many patients describe a deep aching, pressure sensitivity, burning, heaviness or a feeling of lactic acid in the limbs. Research increasingly suggests that lipedema tissue is biologically different from ordinary adipose tissue, involving changes in fat cell size, microcirculation, lymphatic function, immune activity, extracellular matrix remodelling, fibrosis and pain signalling. This is why lipedema cannot be reduced to a question of body weight or discipline.

The exact cause of lipedema is still not known, but the disease appears to involve a combination of genetic susceptibility, hormonal influence, vascular and lymphatic dysfunction, inflammation, fibrosis and altered adipose tissue biology. It often begins or worsens during hormonal transitions such as puberty, pregnancy, perimenopause or menopause, which is one reason hormonal signalling is considered an important part of the picture. Liposuction can remove a significant amount of affected fat tissue and may reduce pain, pressure, swelling and mobility problems for many patients, but it does not remove the underlying biological tendency that allowed the disease to develop in the first place. That is why surgery can be life changing without being a cure. It can reduce the burden of the disease, but the body still needs to be understood and cared for as a body with a lipedema history.

LipedemaScience exists for readers who want the real story: the personal experience, the biology, the uncertainty and the emerging research. You can subscribe for free to stay connected, or become a member if you want full access to the longer science essays. Either way, your presence helps build a place where lipedema is taken seriously.

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1. Safety and Effectiveness of Liposuction Modalities in Managing Lipedema: Systematic Review and Meta-analysis (DOI: 10.1055/a-2334-9260)

2. Comparing the safety and effectiveness of different liposuction techniques for lipedema (DOI: 10.1016/j.bjps.2024.07.038)

3. Effects of diet-induced weight loss on adipose tissue biology, body composition and metabolic health in women with obesity and lipedema, Obese-LIP (DOI: 10.2337/db24-0890)

4. Adipose tissue hypertrophy, an aberrant biochemical profile and distinct gene expression in lipedema (DOI: 10.1016/j.jss.2020.03.055)

5. Improvements in patients with lipedema 4, 8 and 12 years after liposuction (DOI: 10.1177/0268355520949775)

6. Long-term benefit of liposuction in patients with lipoedema: follow-up after an average of 4 and 8 years (DOI: 10.1111/bjd.14289)

7. Standardized Treatment Protocol for Water-Jet-Assisted Liposuction in Lipedema (DOI: 10.1016/j.bjps.2020.04.030)

8. Liposuction reduces the severity of symptoms and the need for conservative treatment in lipedema patients (DOI: 10.1097/PRS.0000000000008885)

9. A retrospective comparative study of patient-reported outcome measures pre- and 12 months post tumescent liposuction for lower-limb lipoedema (DOI: 10.1016/j.jpra.2024.05.007)

10. Liposuction in the Treatment of Lipedema: A Longitudinal Study (DOI: 10.5999/aps.2017.44.4.324)

11. Outcomes of liposuction techniques for management of lipedema: a case series and narrative review (DOI: 10.21037/atm-24-165)

12. Lipedema: What we don’t know (DOI: 10.1016/j.bjps.2023.05.056)

13. Lipedema and adipose tissue: current understanding, controversies, and future directions (DOI: 10.3389/fcell.2025.1691161)

14. Current Mechanistic Understandings of Lymphedema and Lipedema: Tales of Fluid, Fat, and Fibrosis (DOI: 10.3390/ijms23126621)

As a food scientist and nutritionist, I have always been interested in how food interacts with the body. Not only in the simple sense of calories, protein, carbohydrates and fat, but in the deeper biological sense. How does food change hormones. How does it affect inflammation. How does it influence the gut microbiome, the immune system, the blood vessels and the way our cells communicate with each other.

When I studied human nutrition, much of the focus was on lifestyle related diseases. We learned about type 1 diabetes, type 2 diabetes and gestational diabetes. We learned about blood sugar regulation, insulin treatment, pregnancy related glucose intolerance and the long term complications of diabetes. But I do not remember insulin resistance being explained to me as its own important state in the body.

That is why I still remember the first time one of my readers asked me about insulin resistance and lipedema. This was a couple of years ago, and I had to admit that I did not really know what to answer. It was not because I had never studied metabolism. I had. It was not because I did not understand glucose or diabetes. I did. But insulin resistance as a separate, quiet, early metabolic dysfunction was not something I had spent much time thinking about in relation to lipedema.

To be honest, I love getting questions like that from this community. They make me grow. They force me to go back to the biology, read more, think more and sometimes admit that I do not know enough yet. Even with a background in human nutrition and food science, you never become an expert on everything. The body is too complex for that. And in lipedema, there are still so many unanswered questions.

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That curiosity is one of the reasons I started looking more closely at insulin resistance. I wanted to understand how it differs from type 1 diabetes, type 2 diabetes and gestational diabetes. I wanted to understand what actually happens inside the cells when insulin works normally, and what happens when the cells stop responding properly.

This also became personal in a different way because two of my close friends from university have lived experience with different forms of disturbed glucose metabolism. One of my very good friends has type 1 diabetes. She needs insulin and tracks her blood sugar every day. Another friend, who also has a background in both human nutrition and food science, developed gestational diabetes during pregnancy, even though she was healthy, active and highly knowledgeable about nutrition. In her case, it was not a story of poor lifestyle. It was a story of biological vulnerability meeting the metabolic stress test of pregnancy.

We have spent many hours discussing how blood sugar behaves in real life. Not only in theory, but in actual bodies. Both of them have told me how certain foods that are often considered healthy can still give surprisingly high blood sugar responses. Oatmeal is one example. In theory, oatmeal should usually give a slower rise in blood sugar than refined white bread or sugary cereal. But in real people, the response can vary a lot. When oatmeal is eaten alone, it may spike blood sugar more than expected. When it is combined with protein or fat, the response can look quite different, because protein and fat slow down how quickly the carbohydrate is absorbed. The protein and fat are doing the real work.

That was also something we saw when I studied nutrition. In one class, we were divided into groups and tested how different meals affected our bodies. My group had to eat white bread with jam. I still remember how awful I felt afterwards. It was not my kind of breakfast or lunch at all. Another group ate eggs and bacon, a very old style low carbohydrate meal. Another had whole grain bread with ham, cheese and vegetables. Another had a smoothie. The point was not that one meal is universally good and another is universally bad. The point was that food is not only food. Food is information. The body reads it through glucose, insulin, gut hormones, satiety signals, inflammatory responses and energy metabolism.

This is why insulin resistance has become such an interesting topic for me in relation to lipedema. Not because I believe every woman with lipedema has insulin resistance. I do not. The evidence is not that simple, and the lipedema population is not metabolically identical from person to person. Some women with lipedema are insulin resistant. Some are not. Some have normal blood sugar for years. Some have PCOS, gestational diabetes, type 2 diabetes or a family history that makes the picture more complicated. Some have clear symptoms after certain foods, while others do not.

But I do think insulin resistance is something many of us should at least understand. Not as a diagnosis we give ourselves, but as a possible layer in the larger lipedema picture.

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In my own case, I once asked my GP to check whether I could have signs of insulin resistance. We tested glucose and other markers. There were some signs that made me wonder, but not enough to clearly confirm it. That is part of the challenge. Insulin resistance can be tricky to detect in a regular doctor’s appointment, especially if fasting glucose and HbA1c are still normal. The body can compensate for a long time by producing more insulin. From the outside, everything may look fine, while the pancreas is working harder in the background.

Because of that, I keep it in the back of my mind. I may have some degree of insulin resistance. I may not. But if the lifestyle measures that support insulin sensitivity also support inflammation, energy levels, hormonal balance and long term metabolic health, then I would rather take them seriously than ignore them completely.

This article is my attempt to explain the basics clearly. What insulin normally does. What happens in type 1 diabetes. What insulin resistance means. How type 2 diabetes develops. Why gestational diabetes can happen even in healthy women. And finally, why this matters for lipedema.

At the center of all of this is one hormone.

Insulin.

Insulin is often described as the hormone that lowers blood sugar, but that is only part of the story. Insulin is really one of the body’s main storage signals. It tells cells that energy is available. It tells muscle and fat cells to take up glucose. It tells the liver to stop producing glucose and start storing energy. It tells fat tissue to reduce the release of fatty acids. In other words, insulin helps move the body from a fasting state into a fed state.

After we eat carbohydrates, glucose rises in the blood. The pancreas senses this and releases insulin from the beta cells in the islets of Langerhans. Insulin then travels through the bloodstream and binds to insulin receptors on target cells, especially in muscle, fat tissue and the liver.

On the cell surface, the insulin receptor works like a molecular switch. When insulin binds, the receptor becomes activated and starts a chain reaction inside the cell. This involves proteins such as IRS, PI3K and Akt. The names are technical, but the concept is not. Insulin knocks on the door, the receptor hears the knock, and the cell starts moving glucose transporters toward the surface.

In muscle and fat cells, one of the most important results is that GLUT4 transporters move from storage vesicles inside the cell to the cell membrane. These GLUT4 transporters act like doors for glucose. When they reach the membrane, glucose can enter the cell more efficiently. In muscle, that glucose can be used for energy or stored as glycogen. In fat tissue, insulin promotes storage and reduces the release of fatty acids. In the liver, insulin suppresses glucose production and promotes glycogen synthesis and fat production.

When this system works well, blood sugar rises after a meal and then comes back down in a controlled way. The pancreas releases insulin, the cells respond, glucose is taken up, and the body returns toward balance.

But when this system fails, it can fail in different ways.

The first way is that the body does not produce enough insulin.
This is the core problem in type 1 diabetes.

Type 1 diabetes is an autoimmune disease. The immune system attacks and destroys the insulin producing beta cells in the pancreas. This can happen gradually, and autoantibodies may be detectable before symptoms appear. Eventually, the body loses the ability to make enough insulin.

The key point is that type 1 diabetes is not primarily a problem of the cells ignoring insulin. It is a problem of insulin being absent or severely deficient. The signal is missing.

Without insulin, muscle and fat cells cannot take up glucose normally. At the same time, the liver behaves as if the body is fasting, even when blood sugar is already high. It continues to release glucose into the bloodstream. This creates the strange and dangerous situation where there is too much glucose in the blood, but many cells cannot access it properly.

Because insulin normally suppresses fat breakdown, lack of insulin also allows fat tissue to release large amounts of fatty acids. The liver converts some of these fatty acids into ketones. In untreated type 1 diabetes, ketones can accumulate and cause diabetic ketoacidosis, a life threatening acidification of the blood.

This is why people with type 1 diabetes need insulin. Not as a lifestyle tool, not as a temporary support, but as a life sustaining treatment.

Insulin resistance is different.

In insulin resistance, insulin is present. Often, especially in the early stages, there is a lot of it. The problem is that the cells do not respond properly. The signal is there, but the cells are less sensitive to it.

This can happen in muscle, liver and fat tissue. In muscle, glucose uptake becomes less efficient. In the liver, insulin fails to suppress glucose production properly. In fat tissue, insulin’s ability to regulate fat storage and fat release becomes disturbed. The pancreas tries to compensate by producing more insulin. For a while, this can keep blood sugar normal.

This is one reason insulin resistance can be silent. If a doctor only checks fasting glucose or HbA1c, everything may look acceptable for a long time. But behind the scenes, the body may be maintaining normal glucose by producing more insulin than it should need.

At the cellular level, insulin resistance involves problems in the insulin signaling pathway. Instead of a clean signal from the insulin receptor through IRS, PI3K and Akt, the signal becomes weaker or disrupted. Lipid molecules can accumulate in places where they do not belong, especially in muscle and liver. Inflammatory signals can interfere with insulin signaling. Mitochondrial dysfunction may also play a role. Adipose tissue inflammation can contribute through cytokines and immune cell activity.

This is where things become interesting for lipedema.

Lipedema is not simply obesity. It is a disease of abnormal, painful, often fibrotic adipose tissue, with vascular, lymphatic, inflammatory and hormonal features. The affected tissue does not behave like ordinary fat tissue. Many women describe swelling, heaviness, pain, easy bruising and a disproportionate fat distribution that behaves stubbornly. When women with lipedema lose weight, the affected areas, usually the legs and hips, often shrink far less than the rest of the body, so the disproportion tends to remain. This does not mean weight loss is pointless. It still reduces fat, it can ease pain and it may slow progression. It simply means you usually cannot slim the affected areas selectively in the way diet culture promises. Research increasingly points toward altered microcirculation, connective tissue remodeling, immune activity and adipose tissue dysfunction.

Because insulin is one of the most important hormones acting on fat tissue, it makes sense to ask whether insulin resistance could matter in lipedema. But we have to ask that question carefully.

It would be too simplistic to say that lipedema is caused by insulin resistance. I do not believe the evidence supports that. In fact, some of the most careful studies suggest something that surprises people: when researchers compare women with lipedema to women of the same body size without lipedema, the women with lipedema often have better insulin sensitivity, not worse. I think that is a genuinely important point, because it pushes back against the lazy assumption that larger legs must mean a broken metabolism. It would also be too simplistic, though, to say that insulin resistance is irrelevant. The more reasonable position is that insulin resistance may be one contributing factor in some women with lipedema, especially when lipedema overlaps with weight gain, PCOS, a history of gestational diabetes, central adiposity, inflammatory symptoms or metabolic syndrome markers.

This distinction matters because women with lipedema are often told two opposite but equally unhelpful things. One is that everything is their fault and they should simply eat less. The other is that metabolism does not matter at all because lipedema fat is different. I think both positions are too flat.

Lipedema fat is different. That does not mean the rest of metabolism becomes irrelevant.

The body is one connected system. Fat tissue communicates with immune cells, blood vessels, hormones, the gut, the liver, skeletal muscle and the brain. If insulin resistance is present, it may influence inflammation, fluid retention, energy levels, hunger signals, fat storage, lipid metabolism and vascular function. It may not explain lipedema itself, but it could influence how the disease feels and progresses in some women.

Type 2 diabetes develops when insulin resistance and beta cell failure come together.

In the early phase, the pancreas compensates by producing more insulin. This can work for years. But over time, the beta cells may no longer keep up. Chronic high glucose, high fatty acids, inflammation and stress inside the beta cells can reduce their function. When insulin production is no longer enough to overcome the resistance, blood sugar rises. That is when prediabetes or type 2 diabetes becomes visible through standard tests.

The important difference between insulin resistance and type 2 diabetes is therefore compensation. In insulin resistance, the pancreas may still be able to compensate. In type 2 diabetes, compensation is no longer sufficient.

This also means that type 2 diabetes usually develops gradually. It is not one sudden switch. It is often a long process where the body works harder and harder to maintain normal glucose until it no longer can.

Gestational diabetes is another version of this story, but with pregnancy as the stress test.

During pregnancy, the placenta produces hormones that naturally make the mother more insulin resistant. This is not a mistake. It is part of normal pregnancy physiology. By making the mother’s tissues slightly more insulin resistant, more glucose remains available for the growing fetus.

Most women compensate by producing more insulin. Gestational diabetes occurs when the beta cells cannot compensate enough for the pregnancy induced insulin resistance. This can happen even in women who are active, healthy and knowledgeable about food. Pregnancy reveals a metabolic vulnerability that may not have been obvious before.

That is why I think gestational diabetes is often misunderstood. It is not simply a sign that someone did something wrong. It can be a sign that the body was pushed into a state where its insulin producing capacity was not enough for the demand.

For women with lipedema, this is relevant because many report that lipedema begins or worsens around hormonal transitions such as puberty, pregnancy, perimenopause or menopause. These are also times when insulin sensitivity, sex hormones, inflammation and fat distribution can change. We do not yet have all the answers, but the overlap is biologically interesting. The current thinking is not that women with lipedema have abnormal hormone levels in their blood, but that the affected tissue itself seems unusually sensitive to normal hormonal shifts.

So what can we actually do with this knowledge.

First, I think we need to stop seeing blood sugar as only a diabetes issue. Blood sugar regulation is part of metabolic health. Insulin sensitivity is part of metabolic health. And metabolic health may matter in lipedema even when a person is not diabetic.

Second, I think we need to become more curious about individual responses. One woman may tolerate oatmeal well. Another may get a strong glucose response unless she combines it with protein and fat. One woman may feel better on a Mediterranean style diet with legumes, whole grains, fish, olive oil and vegetables. Another may need a lower carbohydrate approach to reduce symptoms. One may react strongly to refined sugar with swelling or pain. Another may not notice an immediate effect.

This does not mean everything is random. It means human metabolism is individual. In practice, the lifestyle measures that improve insulin sensitivity are not extreme. Strength training is one of the most powerful tools because skeletal muscle is a major site of glucose disposal. Walking after meals can reduce post meal glucose rises. Protein and fiber can slow digestion and improve satiety. Replacing refined carbohydrates with less processed foods can reduce glucose peaks. Sleep matters. Stress matters. Alcohol can matter. Omega 3 rich fish, colorful plants, fermented foods and anti inflammatory dietary patterns may support the broader inflammatory environment. None of this means that lifestyle cures lipedema. It does not. I am very clear about that. But lifestyle can still matter.

For me, the most useful mindset is not control. It is support. I am not trying to punish my body into behaving. I am trying to understand what kind of environment gives my body the best chance to function well.

This is also why I have decided to use more of my own background in human nutrition and food science in LipedemaScience going forward. I have worked with the gut microbiome at DNA level and molecular level. I have worked with inflammation, intestinal permeability and what people often call leaky gut. I have spent years in laboratories. I have worked as a nutrition coach. I have worked with lifestyle related diseases. I know enough to see that lipedema cannot be reduced to nutrition, but I also know enough to see that nutrition should not be excluded from the conversation.

We need a more mature discussion..

• A discussion where we can say that lipedema is a real disease, not a failure of willpower.

• A discussion where we can say that surgery can reduce diseased tissue and improve symptoms, but it is not a metabolic reset button for everyone.

• A discussion where we can say that insulin resistance may be relevant for some women, without turning it into another thing women are blamed for.

• A discussion where we can say that food can be powerful, without pretending it is magic.

If you are reading this and wondering whether you might have insulin resistance, the best next step is not to panic or self diagnose. It is to talk to a healthcare professional and ask about appropriate testing. Fasting glucose and HbA1c can be useful, but they may not always show early insulin resistance. Depending on the situation, fasting insulin, C peptide, lipid profile, waist measures, blood pressure, oral glucose tolerance testing or HOMA IR may be discussed. These are screening tools rather than a single definitive test, and what they mean depends on the whole picture. The right tests depend on your history, symptoms and risk factors.

And if everything looks normal, that is still useful information. Not every woman with lipedema is insulin resistant. We need to allow for that too.

The main thing I hope you take from this article is that insulin is not only about diabetes. It is about how the body handles energy. It is about communication between the pancreas, liver, muscle, fat tissue and blood vessels. It is about whether the cells hear the signal they are supposed to hear.

• In type 1 diabetes, the insulin signal is missing.

• In insulin resistance, the signal is present, but the cells respond poorly.

• In type 2 diabetes, insulin resistance is combined with beta cells that can no longer compensate enough.

• In gestational diabetes, pregnancy creates a natural insulin resistant state, and diabetes appears when the body cannot compensate sufficiently.

For lipedema, the question is not whether insulin resistance explains everything. It does not. The question is whether insulin resistance may be one important metabolic layer for some of us. I think that question deserves more attention, more research and more careful discussion.

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And I think many women with lipedema deserve to understand this biology before they are told that everything is either their fault or completely outside their influence. Neither is true. The body is more complex than that.

LipedemaScience exists because women with lipedema deserve access to deep, serious and understandable science about their own bodies. My goal is to translate research and physiology into articles that make you feel more informed, not more confused, and more respected, not blamed. If you want to keep learning about lipedema through a scientific but human lens, including metabolism, hormones, inflammation, pain, surgery, nutrition, fibrosis, lymphatics and the lived reality of this disease, you can subscribe to LipedemaScience. Paid subscriptions make it possible for me to spend the time needed to read the research properly, connect the dots carefully and build a knowledge platform that treats lipedema with the seriousness it deserves.

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My partner and I rented a house outside Peniche and spent more than two weeks there before meeting friends in Lisbon. We both work a lot, perhaps more than most people would consider healthy. We genuinely enjoy building things, learning, creating, and solving problems, but being driven also comes with a responsibility. If work is allowed to consume everything, life eventually becomes very small. For us, travel is one of the ways we create balance. We need new impressions, new cultures, different food, beautiful surroundings, and experiences that stimulate us in ways that work never can. Portugal turned out to be exactly what we needed.

I had never visited Portugal before, and I quickly understood why so many people fall in love with the country. During our stay we explored Porto, Nazaré, Óbidos, Sintra, Lisbon, and countless smaller places in between. What struck me most was how much history seemed to be woven into everyday life. Ancient buildings stood next to local cafés. Narrow streets opened into beautiful squares. Fishermen worked along the coastline while tourists wandered through medieval towns. There was a calmness to Portugal that I found incredibly appealing. It felt authentic rather than curated.

Food is always an important part of travel for me. As both a nutritionist and a food scientist, I have always been fascinated by how food reflects culture, geography, history, and lifestyle. Portugal was a dream in that regard. Fresh seafood was available everywhere. Fish, shellfish, vegetables, fruit, olive oil, and locally produced ingredients formed the foundation of many meals. This aligns closely with how I naturally prefer to eat. Even when I am travelling, I tend to gravitate towards simple meals built around fresh ingredients rather than heavily processed foods. Breakfast might consist of salmon, avocado, poached eggs, fruit, and a green smoothie. Dinner might be fresh sardines caught locally. At wine bars, oysters often accompanied a glass of Portuguese wine. For me, this is not dieting. It is simply food that makes me feel good.

At the same time, I no longer believe that perfect eating is the goal of lipedema management. That is probably one of the biggest lessons I have learned since receiving my diagnosis 14 years ago. When I was first diagnosed, I approached lipedema much like many people do. I wanted to find the perfect solution. The perfect diet. The perfect strategy. The perfect way to eliminate symptoms. What I eventually learned was that life becomes very small when every decision revolves around avoiding potential triggers. Today I think very differently.

LipedemaScience was created because I wished something like it had existed when I was first diagnosed. Over the past 14 years, I have spent countless hours reading research papers, speaking with clinicians, testing different management strategies, and trying to understand what lipedema actually is. Through LipedemaScience, I share that journey by connecting the latest research with real-life experiences, reflections, and practical questions that many women living with lipedema face every day.

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When my friends arrived in Lisbon, I found myself standing in a local grocery store preparing for a weekend together. I filled the basket with things I knew they would enjoy. Chips, snacks, sweet treats, and foods associated with celebration and social gatherings. At the same time, I bought blueberries, raspberries, walnuts, Brazil nuts, olives, and other foods that I personally enjoy and know make my body feel good. Looking back, that grocery basket was probably the perfect illustration of how I think about lipedema today. It was not about restriction. It was about balance.

For me, sustainable lipedema management has become an 80-20 approach. Most of the time I focus on habits that support my health. I prioritise exercise, sleep, recovery, nutritious food, and stress management. However, I also make room for experiences. Sitting at a small wine bar in Lisbon with close friends while sharing oysters and Portuguese wine is part of life. Trying a local pastry that generations of Portuguese families have enjoyed is part of life. Laughing with friends until midnight in a city you have never visited before is part of life. Those moments matter too.

One reason I can approach travel this way today is that I know my body extremely well. I have lived with lipedema symptoms since my teenage years. I was diagnosed when I was 20 years old, and I am turning 35 next month. That means I have spent almost 15 years actively learning how my body responds to different foods, stressors, hormones, environments, and lifestyle choices. I know many of my triggers. I know which choices tend to increase pain, heaviness, swelling, or fatigue. Equally important, I know which choices make me feel strong, energetic, and resilient.

My body also responds very differently today than it did before surgery. Before lipedema surgery, certain foods could trigger immediate reactions. The relationship between sugar and my symptoms was particularly obvious. Today many of those reactions are significantly reduced. However, surgery did not cure my lipedema. The disease is still present. I simply have less affected tissue than before. That distinction is important because it influences how I think about long-term management. I do not live as though lipedema disappeared. I still wear compression garments during long flights. I still pay attention to recovery. I still prioritise movement. I still think carefully about nutrition. The difference is that I no longer allow lipedema to become the centre of every decision.

This past year has added another layer to that equation. Alongside managing lipedema, I have been going through multiple egg retrieval cycles. Anyone who has undergone fertility treatment understands how profoundly hormones can influence the body. I have seen very clearly that my lipedema tissue responds to hormonal changes. The effects are not necessarily immediate, but they are noticeable. Looking back, I think it has often taken two or three months after treatment cycles before I feel that my body has returned to its previous baseline. The experience has reinforced something that many women with lipedema already suspect. Hormones matter.

Interestingly, fertility treatment has also introduced me to concepts that may be relevant for lipedema in ways I had not previously considered. During fertility treatment, you quickly learn that the eggs retrieved several months from now are influenced by the choices you make today. Exercise, nutrition, sleep, stress, and metabolic health all contribute to the environment in which those eggs mature. That has led me down a fascinating path of learning about mitochondria, energy production, and cellular health. Resistance training has become an increasingly important part of my routine, not only because of its benefits for overall health but because of its potential influence on mitochondrial function. The more I learn, the more interested I become in the possible connections between mitochondrial health, fertility, and lipedema. It is a topic I plan to explore in a future article.

Perhaps the most important thing I want readers to take away from this story is that my journey is exactly that. My journey. One of the challenges within the lipedema community is the temptation to compare ourselves with others. Someone reads about a person who improved on a particular diet, underwent surgery, started a specific exercise programme, or lost weight, and immediately begins comparing their own experience. I understand that instinct because I have done the same thing myself. However, after almost 15 years with this diagnosis, I have become increasingly convinced that comparison is often unhelpful.

We share a diagnosis, but we do not share identical bodies. We do not share identical hormones, genetics, lifestyles, stress levels, medical histories, or symptom profiles. What works beautifully for one person may be ineffective for another. What feels sustainable for one person may feel impossible for someone else. There is no single lipedema journey. There are thousands of individual journeys unfolding simultaneously.

As I flew home from Lisbon today wearing my compression garments, I found myself reflecting on how much my relationship with lipedema has changed over the years. When I was younger, I often felt as though life would begin once I had solved the problem. Once I had found the right treatment. Once my symptoms improved. Once my body changed. What I eventually realised is that life does not wait for those things to happen. Life is happening now.

It is happening during fertility treatment. It is happening while living with a chronic disease. It is happening while trying to build a career, maintain relationships, travel, exercise, and pursue goals. Portugal reminded me of that. It reminded me that good health is not the same thing as perfect health. It reminded me that balance is often more sustainable than perfection. Most importantly, it reminded me that while lipedema will always be part of my story, it does not have to be the entire story.

For now, Portugal is behind me, but only temporarily. I already know I will return. Next, I will spend some time in Norway before heading towards Italy, where another chapter of this journey awaits. There will be new places to explore, new foods to taste, new experiences to collect, and undoubtedly new lessons to learn along the way. Wherever those adventures take me, one thing remains unchanged. Lipedema comes with me. But it does not decide where I go.

If you enjoy articles like this, I would love for you to become a subscriber to LipedemaScience. When I was diagnosed with lipedema at the age of 20, reliable information was incredibly difficult to find. Much of what existed was fragmented, anecdotal, or focused solely on symptoms and treatment options. Over the years, I developed a habit of reading scientific papers myself, trying to understand the biology behind the condition and how new discoveries might translate into everyday life. LipedemaScience grew out of that curiosity.

Today, LipedemaScience is where I share both the science and the lived experience of lipedema. Some articles explore newly published research on topics such as hormones, inflammation, lymphatic function, adipose tissue biology, pain, surgery, and genetics. Others, like this one, explore what it actually means to live with a chronic condition while building a career, travelling, exercising, navigating fertility treatment, maintaining relationships, and trying to live a full and meaningful life. My goal is not only to explain the science, but also to place it into a real-world context that readers can relate to.

By subscribing, you support independent science communication dedicated entirely to lipedema. More importantly, you become part of a community of curious, thoughtful women who want to understand their condition more deeply and make informed decisions about their own health. Whether you are newly diagnosed or have been living with lipedema for decades, my hope is that these articles help you feel both better informed and a little less alone on your journey.

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Before my lipedema surgeries, refined sugar was one of the clearest and most immediate symptom triggers I had. I could eat many foods without dramatic reactions, but white, refined sugar was different. It could trigger a very specific kind of pain and swelling in my legs. The pain felt deep, aching and inflammatory, almost like a toothache inside the tissue. The swelling could come quickly, and at its worst, my legs felt as if they changed size within a short time.

What made this especially interesting to me was that the reaction was not simply “carbohydrates are bad”. I did not experience white flour in exactly the same way. The strongest reaction was linked to refined sugar and rapid sugar exposure. Before surgery, it felt as if the lipedema tissue itself was reacting acutely.

After my liposuction surgeries, this changed. I am not saying that diet no longer matters, or that sugar is suddenly biologically neutral. But the dramatic acute reaction I used to experience in the lipedema tissue is no longer the same. The intense swelling and pain response that I associated with refined sugar largely disappeared after a substantial amount of diseased fat tissue had been removed.

That observation has made me think about lipedema in a very concrete way. What if the reaction was not only about sugar itself, but about sugar entering a tissue environment that was already inflamed, fluid sensitive, microvascularly fragile and pain sensitized?

This is where my personal experience meets the mechanistic theory.

Lipedema tissue is increasingly described as more than enlarged fat tissue. Studies have reported adipocyte hypertrophy, immune cell activity, microvascular changes, increased capillary fragility, extracellular matrix remodeling, fibrosis, pain sensitivity and signs of altered lymphatic or fluid handling. The exact biology is still debated, and not every study finds the same inflammatory pattern, but the overall picture suggests that lipedema tissue can be biologically reactive.

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If a tissue is already close to a threshold, it may not take much to push it into a symptomatic state. A high sugar load can create a rapid postprandial response. Blood glucose rises, insulin rises, oxidative stress can increase, inflammatory signaling can be activated, and the vascular endothelium can become more permeable. In general physiology, acute hyperglycemia has been linked to endothelial dysfunction and damage to the endothelial glycocalyx, the protective layer that helps regulate vascular permeability. Insulin can also promote sodium retention, and sodium draws water with it.

In normal tissue, this may not be felt as pain. But in lipedema tissue, the situation may be different. If the microvasculature is already fragile, if lymphatic drainage is already less efficient, if the extracellular matrix already binds fluid, and if the nerves are already sensitized, then a postprandial sugar response could theoretically become a local swelling and pain event.

In that model, sugar is not “creating lipedema”. It is exposing the vulnerability of the tissue.

The acute reaction could be understood as a kind of perfect storm. A rapid glucose and insulin response may increase sodium and water retention. Endothelial stress may increase leakage from the capillaries. Low grade inflammatory signaling may lower the pain threshold. Fluid moves into a tissue that already struggles with fluid handling. The tissue pressure rises. Pain nerves that are already sensitized respond more strongly.

This could explain why the pain felt so deep and immediate. It may not have been ordinary “diet discomfort”. It may have been a local tissue reaction in a pathological fat compartment.

This is also why the change after liposuction is so interesting. Liposuction for lipedema does not only change body shape. It removes a large volume of the pathological fat tissue that may be driving pain, fluid retention and inflammatory signaling. In several surgical studies, patients report long lasting reductions in pain, tenderness, bruising, edema and mobility limitations after liposuction. The mechanism is still not fully understood, but the simplest explanation is that removing diseased, reactive tissue reduces the biological substrate that can generate symptoms.

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In my case, this is exactly what it felt like. The same body, the same person, but with much less reactive lipedema tissue. After surgery, there was simply less tissue available to swell, retain fluid, produce inflammatory signals and amplify pain.

I think this is a more plausible explanation than the idea that surgery works mainly by “cutting nerves”. That theory is sometimes mentioned informally, but it is not well established in the lipedema literature. Modern lipedema liposuction techniques are designed to be tissue sparing, especially toward lymphatic structures, vessels and nerves. Temporary sensory changes can happen after surgery, but that is not the same as saying that long term pain relief is caused by intentional denervation.

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To me, the more convincing explanation is substrate reduction. Less pathological tissue means less inflammatory capacity, less fluid binding capacity, less mechanical pressure and less nociceptive input. If sugar previously triggered an acute reaction in that tissue, then removing much of the tissue could logically reduce or stop the reaction.

There is also some dietary research that makes this question even more relevant. Small studies on low carbohydrate or ketogenic diets in lipedema suggest that pain may improve independently of weight loss, and that pain can return when carbohydrates are reintroduced. These studies are still small and should not be overinterpreted, but they support the idea that carbohydrate metabolism may influence lipedema pain in ways that are not only about body weight.

Still, there are important limitations. To my knowledge, no study has directly measured acute sugar induced swelling in lipedema tissue before and after a glucose or sugar challenge. No study has taken patients like me, measured tissue water, tissue sodium, inflammatory markers and pain response after sugar intake, and then repeated the same measurements after liposuction. That is the study I wish existed.

So this remains a theory. A biologically plausible theory, but still a theory.

My personal interpretation is this: before surgery, refined sugar triggered a rapid inflammatory and fluid related response in my lipedema tissue. The tissue was already vulnerable. It was probably more prone to fluid retention, vascular leakage, pressure and pain signaling. After surgery, much of that reactive tissue was removed, and the acute sugar reaction largely disappeared.

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That does not mean everyone with lipedema will experience the same thing. Lipedema is not identical from person to person. Some people may react strongly to sugar. Others may not. Some may respond to low carbohydrate diets. Others may do better with a different nutritional strategy. Surgery may reduce symptoms dramatically for some, while others still need compression, movement, lymphatic support and careful symptom management.

But I do think these personal observations matter. They can help generate better research questions. Why do some patients report acute swelling and pain after sugar? Is it linked to insulin, sodium, endothelial permeability, inflammation, lymphatic load, nerve sensitization or all of these at once? Does liposuction change this response because it removes the pathological tissue substrate? Could tissue sodium MRI, water imaging or postprandial inflammatory markers help us understand this better?

For me, the experience changed how I think about lipedema. It made the disease feel less mysterious and more biological. The pain was not imagined. The swelling was not random. The sugar reaction was not a moral failure or a lack of discipline. It felt like a measurable tissue response that science has simply not studied properly yet.

And that is where I think we need to go next. Not toward simplistic diet rules, but toward mechanisms. Not toward blaming patients for what they eat, but toward understanding why some lipedema tissue reacts so strongly in the first place.

Have you experienced something similar? Did sugar or other high-carbohydrate foods trigger pain, heaviness, swelling, or tenderness in your lipedema tissue before surgery? And if you have undergone liposuction, did those reactions change afterward?

I would love to hear about your experience in the comments. Personal observations are not scientific proof, but they can help identify patterns and generate important research questions.

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Lipedema management is not one-to-one. The same intervention will not necessarily make sense for every person with lipedema, because lipedema itself is not experienced in exactly the same way by everyone. Some people have clear metabolic complications. Some do not. Some have insulin resistance, obesity, or metabolic syndrome alongside lipedema. Others have a relatively stable weight, normal metabolic markers, and still experience pain, heaviness, swelling, fibrosis, and disproportionate fat accumulation.

Personally, I do not use GLP-1 medication. But I find this area of research very interesting to follow, because it may become relevant for certain patients with lipedema, especially where metabolic dysfunction, inflammation, fibrosis, or obesity coexist. At the same time, the current evidence does not support presenting GLP-1 receptor agonists as a proven lipedema treatment.

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The study is titled Targeting Inflammation and Fibrosis in Lipedema: The Potential Role of Glucagon-like Peptide-1 Receptor Agonist Therapies. It was written by Yasmine Mohseni, Aria Vazirnia, Ardalan Minokadeh, David M. Amron, and William P. Coleman III, and published in Dermatologic Surgery.

The central question of the paper is whether GLP-1-based therapies could have a role in lipedema management.

This is a timely question because lipedema remains a condition with very limited medical treatment options. Conservative management may help symptoms for some patients, and liposuction remains the main intervention with lasting evidence for limb volume reduction. But there is still no established pharmacological therapy that directly treats the underlying lipedema tissue.

The authors describe lipedema as a chronic disorder characterized by disproportionate subcutaneous fat accumulation, most commonly affecting the extremities, and associated with pain, inflammation, and fibrosis. This is important, because it frames lipedema as more than a question of body size or weight. The paper also emphasizes that lipedema tissue shows changes such as enlarged adipocytes, extracellular matrix remodeling, fibrosis, chronic inflammation, microvascular dysfunction, and impaired lymphatic vessel formation.

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This is where GLP-1 receptor agonists become scientifically interesting.

GLP-1 receptor agonists are best known for their role in obesity and diabetes treatment. They affect appetite regulation, glucose metabolism, insulin sensitivity, and body weight. But research outside lipedema has also suggested that these therapies may influence inflammatory and fibrotic pathways. The newer dual GLP-1 and GIP receptor agonist tirzepatide is of particular interest because the paper discusses its potential effects on fat oxidation, mitochondrial function, inflammatory signaling, macrophage behavior, and fibrosis.

However, this is where we need to be careful. A biological rationale is not the same as clinical proof.

The paper does not show that GLP-1 medications cure lipedema. It does not show that they reverse lipedema progression. It does not establish them as a disease-modifying treatment for lipedema. What it does show is that there is a plausible scientific reason to study them further, especially in patients where lipedema overlaps with insulin resistance, obesity, metabolic syndrome, or inflammatory burden.

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That is an important distinction. For me, this study is not a reason to say that everyone with lipedema should consider GLP-1 medication. It is a reason to say that lipedema research is beginning to move into more targeted biological questions. Instead of only asking whether weight loss changes lipedema, researchers are beginning to ask whether specific pathways such as inflammation, fibrosis, insulin signaling, macrophage activity, and tissue remodeling could be clinically relevant. That is the part I find most interesting.

The rest of this article looks more closely at what the study actually found, what the current evidence is, and why the results should be interpreted with both interest and caution.

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