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A new study published in Nature Metabolism in October 2026 offers an opportunity to explore this complexity. Researchers in the United States wanted to understand whether the degree of food processing could influence metabolism and brain activity independently of the nutritional composition of a meal. They designed an experiment in which participants consumed two meals containing approximately 300 calories each, carefully matched for several nutritional characteristics, including carbohydrates, protein, fat, fibre and sodium. One meal consisted primarily of minimally processed foods, while the other contained a selection of ultra-processed products. The researchers then followed what happened inside the participants’ bodies over the following three hours, measuring changes in blood glucose, insulin, energy expenditure and the way different nutrients were used for energy. They also investigated how the brain responded to images of food.

The results raise questions that extend beyond the familiar debate about whether ultra-processed foods are healthy or unhealthy. Despite the meals being nutritionally comparable, the researchers observed differences in insulin responses, glucose regulation and energy metabolism, alongside differences in brain activity associated with food processing. For those of us interested in lipedema, a condition involving changes in adipose tissue, these findings are worth examining, although the study itself did not include people with lipedema. At LipedemaScience, our purpose is to bring relevant research from different scientific fields into the lipedema conversation, explain the underlying biology and distinguish established evidence from hypotheses that still require investigation. Supported by readers around the world, this independent platform makes it possible to explore research in greater depth rather than reducing complex findings to another list of foods to eat or avoid. In this article, we will examine what the researchers actually discovered, why two nutritionally similar meals may produce different physiological responses, and what these findings might mean for our understanding of nutrition and lipedema.

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Although there is currently no established evidence that dietary acrylamide specifically affects lipedema, it raises interesting questions about food preparation and our overall health. I think it is important to look beyond lipedema itself and understand more about the food we eat, including how cooking can change its chemical composition.

My goal is not to create unnecessary concern or encourage more dietary restrictions, but to share some of the food science behind everyday choices so we can make informed decisions based on knowledge rather than fear.

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We know that lipedema often appears or becomes more noticeable during major hormonal changes, particularly puberty, pregnancy and menopause. But we still don’t fully understand why. I believe epigenetics is one of the most interesting areas to investigate.

To understand why, we first need to understand what epigenetics actually means.
And fortunately, the basic idea is quite simple.

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Imagine your DNA as an enormous instruction book containing all the information your cells need to function. Almost every cell in your body contains the same book, but different cells read different instructions. A fat cell needs different instructions from a muscle cell, even though they contain essentially the same DNA.

Epigenetics helps control which instructions are used. You can imagine small switches that make certain genes more or less active, without changing the DNA itself. These switches are influenced by complex biological processes, including hormonal signals and environmental conditions.

What makes this particularly interesting is that some epigenetic changes can persist over time. In other words, a cell may continue behaving differently even after the original signal has disappeared.

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What might this mean for lipedema?

We already have evidence that genetics contribute to lipedema, and many women report that their symptoms began around puberty, pregnancy or menopause. These observations make hormonal regulation an important part of understanding the condition.

But genetics and hormones may not tell the entire story.

My hypothesis is that some women may inherit a predisposition to lipedema, while epigenetic changes could contribute to when and how that predisposition becomes noticeable.

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That made me curious about what is actually happening physiologically when we walk uphill. Is steep incline walking simply a more difficult version of walking, or can it genuinely replace some of what we normally associate with running? What happens to calorie expenditure, fat oxidation, cardiovascular fitness, muscles, mitochondria, circulation and bone? And perhaps most interesting for this community, is there anything about uphill walking that makes it particularly useful if you have lipedema?

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The answer is more nuanced than “walking is good” or “running burns more calories”. At a sufficiently steep gradient, walking can become a substantial aerobic workout, while still producing considerably less impact than running. That combination makes it interesting, particularly for people who want to increase their cardiovascular fitness and energy expenditure but do not enjoy running or find repeated impact uncomfortable.

There are, however, things running does better, things resistance training does much better, and several claims about exercise and lipedema that have travelled considerably further than the research supporting them.

So let us walk uphill for a while.

A 15 percent incline is not ordinary walking

When you walk on level ground, most of the work involves moving your body forward. Once you increase the gradient, you also have to repeatedly lift your body against gravity. That sounds obvious, but metabolically it makes a surprisingly large difference.

Using the standard American College of Sports Medicine walking equation, walking at a 15 percent incline at approximately 3.5 km/h corresponds to an estimated oxygen consumption of around 25 ml/kg/min, or a little over 7 METs. At 4 to 5 km/h, the predicted demand rises toward approximately 8 to 10 METs. These calculations become somewhat less precise at very steep gradients because our gait changes, but they illustrate how quickly the workload increases.

For context, exercise above 6 METs is conventionally considered vigorous physical activity. A treadmill may therefore tell you that you are “walking”, while your cardiovascular system is dealing with a workload firmly outside what most people would describe as a leisurely stroll.

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There is also enormous individual variation. Someone with excellent endurance fitness may walk at 15 percent while having a conversation without much difficulty, while another person may reach a very high heart rate at half that gradient. This is why I would not tell everyone with lipedema to set the treadmill to exactly 15 percent. The gradient is simply a way of manipulating workload. Breathing, heart rate and perceived exertion tell you much more about how hard you are actually exercising.

What does that mean in calories?

At 15 percent incline and around 3.5 km/h, the standard prediction equation gives an energy expenditure of approximately 7.5 kcal per kilogram of body weight per hour. That works out to roughly 450 kcal for a person weighing 60 kg, about 525 kcal at 70 kg and around 675 kcal at 90 kg.

Again, these are estimates rather than laboratory measurements, but the point is not the exact number. The point is that a steep walk can create a meaningful amount of energy expenditure without requiring you to run.

We also have a useful laboratory comparison from the now rather famous 12-3-30 treadmill workout, where people walk at a 12 percent gradient at 3 mph, or approximately 4.8 km/h, for 30 minutes. Researchers compared the workout with self-paced treadmill running while matching the total amount of energy expended. Participants used roughly 308 kcal during 12-3-30 and 310 kcal during running, but the runners reached that amount faster. Running used approximately 13.1 kcal per minute compared with 10.2 kcal per minute during the incline walk.

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So yes, running remains more time-efficient. If you want to use 300 kcal as quickly as possible, running will usually get you there first. But if you prefer walking, a steep gradient can bring the metabolic cost much closer to running than flat walking ever would.

But does walking uphill burn more fat?

This is probably where incline walking receives the most enthusiastic marketing, because “fat burning” is an extremely effective phrase if you want people to click on something.

There is a physiological basis for part of the claim. During exercise, our bodies use a mixture of carbohydrate and fat to provide energy. At lower and moderate intensities, fat generally supplies a larger proportion of that energy. As exercise becomes harder, carbohydrate contributes increasingly because it can provide ATP more rapidly.

In the 12-3-30 study, fat supplied approximately 40.6 percent of the energy during incline walking compared with 33.1 percent during self-paced running. On first inspection, you might conclude that incline walking is therefore substantially better for fat loss. But the absolute difference in energy from fat was only around 20 to 25 kcal during the entire session, corresponding to only a few grams of fat. The most likely explanation for the higher fat percentage is also rather ordinary: the incline walk was performed at a lower absolute intensity than the run.

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This is where it helps to separate fat oxidation during exercise from loss of body fat over time. They are related concepts, but they are not interchangeable.

If you burn a greater proportion of fat during a workout, the body can compensate later by changing which fuels it uses. Likewise, a hard exercise session may rely heavily on carbohydrate while you are exercising but still contribute perfectly well to fat loss over weeks if your total energy expenditure exceeds your energy intake. The human metabolism is constantly shifting between substrates throughout the day.

Fun fact: a workout can therefore be excellent for fat loss even if it is not particularly impressive in the “percentage of fat burned” department. The body is annoyingly unwilling to organize its metabolism according to fitness-influencer graphics.

For long-term body-fat reduction, what matters much more is how the activity contributes to total energy expenditure, whether your diet creates an appropriate energy balance, whether you preserve muscle, and whether the exercise is something you can actually repeat consistently.

This is one reason I find incline walking useful. It can increase energy expenditure substantially without making every session a hard running session that requires considerably more recovery.

What about lipedema fat?

This question deserves more care because the old statement that “lipedema fat cannot be lost through diet or exercise” is still repeated frequently.

A 2025 study by Cifarelli and colleagues examined women with obesity and lipedema before and after approximately 9 percent diet-induced weight loss. The researchers measured body composition, insulin sensitivity and adipose-tissue biology. Leg fat decreased along with total fat mass, with broadly similar relative reductions in abdominal and leg fat. At the same time, the biological characteristics of the adipose tissue did not simply normalize: markers associated with inflammation and fibrosis remained altered.

This gives us a more sophisticated picture of lipedema adipose tissue than the idea that it is completely metabolically untouchable. Lipedema-affected regions can lose fat during negative energy balance, but losing fat does not necessarily remove the characteristic body-fat distribution or reverse the underlying tissue abnormalities.

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For incline walking specifically, we have no clinical study demonstrating that it selectively mobilizes lipedema adipose tissue. We also do not have evidence that a particular treadmill gradient, heart-rate zone, fasting state or training intensity preferentially reduces lipedema fat. It is more scientifically reasonable to treat incline walking as a way of increasing overall energy expenditure and improving fitness, rather than as a disease-specific fat-burning method.

That does not make it less useful. It simply puts the mechanism in the right place.

Your heart does not care whether the treadmill calls it “walking”

One of the reasons I wanted to write about this is that many people still associate cardiovascular fitness with running. If you cannot run, do not like running or experience discomfort when you run, it can feel as though you are choosing an inferior form of exercise.

Physiologically, that is not how the cardiovascular system works.

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Your muscles require oxygen during exercise. As that requirement increases, heart rate rises, cardiac output increases and blood flow is directed toward the working muscles. Over time, repeated aerobic training can improve stroke volume, vascular function, oxygen delivery and the muscles’ ability to extract and use oxygen. Whether you produced the workload by running, walking steeply uphill, cycling or rowing is much less important than the actual physiological demand.

A steep incline allows you to create that demand without increasing speed to the point where you have to run.

This can be especially useful if you want to accumulate a large amount of aerobic exercise each week. Running has an obvious advantage because it produces a high workload quickly, but the mechanical cost is also higher. If you can comfortably do 45 to 60 minutes of incline walking several times per week while a similar amount of running leaves your joints or lower legs unhappy, the walking may ultimately allow you to accumulate more aerobic training.

There is no prize for using the exercise mode that looks hardest if it means you do half as much of it.

The mitochondrial side of the story

Mitochondria have become fashionable enough that they occasionally seem to be blamed for, or credited with, almost everything that happens in human health. They are nevertheless genuinely important when we talk about aerobic exercise.

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Mitochondria are central to oxidative energy production inside our cells, and skeletal muscle adapts strongly to repeated endurance exercise. Research in general exercise physiology indicates that training volume is an important stimulus for increasing mitochondrial content, while higher-intensity exercise can provide additional adaptations related to mitochondrial respiratory capacity.

This is where incline walking can fit nicely into a broader fitness program. A relatively comfortable uphill walk can allow someone to accumulate 40, 50 or 60 minutes of continuous aerobic work without the same impact as running. Harder intervals, whether performed through running, fast incline walking, cycling or another activity, can then provide a separate high-intensity stimulus.

For lipedema, however, this is currently an extrapolation from general exercise physiology. The 2024 SISMeS/SIF consensus discusses mitochondrial function, lymphatic drainage and inflammation as possible mechanisms through which exercise may benefit people with lipedema, but the same consensus also acknowledges that standardized exercise prescriptions for lipedema are lacking.

That difference between plausible mechanism and demonstrated clinical effect is important throughout lipedema research. Exercise unquestionably affects mitochondria. What has not been demonstrated is that a particular form of exercise specifically corrects a mitochondrial abnormality in lipedema.

Your glutes, hamstrings and calves will notice the hill

Walking uphill also changes muscular recruitment. Compared with level walking, the hip extensors and calf muscles have to contribute more as you repeatedly propel your body upward. This is why a steep treadmill walk often produces much more noticeable work in the glutes, hamstrings and calves than a flat walk at the same speed.

For people who are sedentary or returning to exercise, this can improve muscular endurance and general lower-body capacity. For someone who already trains regularly, however, incline walking should not be confused with progressive resistance training. The muscles may work hard, but the mechanical stimulus is very different from gradually increasing loads in exercises such as squats, deadlifts, split squats, hip thrusts or calf raises.

If body recomposition is one of your goals, this is worth remembering. Incline walking can help increase energy expenditure and cardiovascular fitness, while resistance training provides the stronger signal to maintain or build muscle.

A useful way to think about the different roles is:

• Incline walking: aerobic volume, energy expenditure and muscular endurance with relatively low impact.

• Harder cardiovascular work: higher cardiorespiratory intensity and VO₂max development.

• Resistance training: muscle, strength, glucose-disposal capacity and skeletal loading.

• Yoga or mobility work: flexibility, balance, movement control, breathing and recovery.

You do not have to choose one and declare it the winner. A healthy body needs more than one type of stimulus.

Lower impact is one of incline walking’s biggest advantages

Running creates greater ground-reaction forces than walking, even when the cardiovascular workload is relatively similar. That is not automatically a disadvantage. Mechanical loading is part of how the body adapts, and impact has particular value for bone. But if repeated impact contributes to pain or limits how much exercise you can tolerate, steep walking offers an interesting alternative.

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Biomechanical studies show that uphill walking can substantially increase metabolic demand without producing the same impact profile as running. Some studies have also found reductions in particular measures of knee loading when people walk more slowly uphill compared with walking faster on level ground.

This does not mean a 15 percent incline is effortless for the musculoskeletal system. The workload is redistributed rather than disappearing. Calves and plantar flexors work considerably harder, ankle position changes and the Achilles tendon experiences repeated loading. Someone who suddenly progresses from occasional flat walking to an hour at a very steep gradient can therefore develop problems even if the cardiovascular system feels completely capable of continuing.

This is one area where enthusiasm and connective tissue may have slightly different timelines.

Increasing either duration, speed or gradient gradually gives muscles and tendons time to adapt.

Where running has the advantage: bone

If incline walking sounds extremely favourable so far, there is an important limitation.

Walking is not particularly powerful as a bone-building exercise.

Bone adapts to mechanical loading, particularly when the forces are relatively high, rapidly applied or different from the loads the skeleton experiences every day. Running creates a stronger impact stimulus than walking, while jumping and progressive resistance training can provide even more targeted skeletal loading.

Walking studies generally show relatively modest effects on bone mineral density, particularly at the spine. Some benefits are seen at the hip, especially with longer-term activity, but we currently have no evidence showing that steep incline walking suddenly behaves like running from a bone perspective.

So someone can absolutely choose incline walking instead of running for cardiovascular exercise, but I would not assume that it replaces every physiological benefit of impact.

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If bone health is important, progressive resistance training becomes even more valuable. For people who can tolerate it, smaller amounts of running, jumping, hopping or other impact activity can also complement an otherwise low-impact training routine.

This becomes particularly relevant as women age and estrogen levels change, because preserving both muscle and bone becomes increasingly important.

Hormones: more exercise is not automatically healthier

Exercise has enormous benefits for metabolic health, insulin sensitivity and cardiovascular function, but there is a point at which the conversation about “burning more calories” can become counterproductive.

Women who combine high exercise volumes with insufficient food intake can develop low energy availability. The body then has insufficient energy to support both training and normal physiological functions optimally. Reproductive signalling can change, menstrual cycles may become irregular, estrogen exposure can fall and bone health can be affected.

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The important point is that this is not unique to running.

A person who performs long incline-walking sessions every day while aggressively restricting food can create the same basic problem. If an hour of steep walking uses several hundred calories, that energy expenditure still has to be considered as part of the overall energy budget.

This is especially relevant for women who are already relatively lean but want to improve body composition. Reducing fat mass while preserving or increasing muscle is a very different goal from simply trying to make body weight as low as possible. For recomposition, resistance training, adequate protein, sufficient energy availability and gradual changes are generally much more useful than trying to maximise treadmill calories every day.

What about circulation and lymphatic flow?

Walking has another physiological feature that is particularly interesting in the context of lipedema: every step repeatedly activates the muscles of the lower leg.

The calf muscle pump plays an important role in helping venous blood return from the lower extremities toward the heart. Skeletal-muscle contractions also influence interstitial fluid movement and lymphatic flow, and human studies outside lipedema show that lymph flow can increase substantially during exercise.

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Because uphill walking increases the demand on the plantar flexors and calf muscles, it is reasonable to think that these pumping mechanisms are active during incline walking. What we cannot currently say is that a particular gradient produces a disease-specific lymphatic benefit in lipedema. No study has directly measured lymphatic transport during 15 percent treadmill walking in women with the condition.

So there is a physiologically plausible reason to be interested in walking and circulation, but the research does not support turning that into claims that incline walking specifically “drains” lipedema tissue.

And this is where the lipedema research becomes surprisingly thin

Considering how often exercise recommendations are given to women with lipedema, there are remarkably few intervention studies.

A systematic review published online in 2025 identified only six exercise-training studies including a total of 115 women with lipedema. Across those studies, exercise appeared to improve outcomes such as pain, other symptoms, quality of life, functional performance and in some cases limb volume or circumference. Effects sometimes appeared greater when exercise was combined with compression, but the authors emphasized the small sample sizes, heterogeneous interventions and need for considerably better trials.

Importantly, there is currently no published trial specifically isolating incline walking, running or conventional progressive resistance training in women with lipedema. Strength exercises have mostly appeared inside multimodal programs, often alongside aerobic exercise, stretching, compression or other conservative treatments.

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There has been an interesting NTNU feasibility study in which women with lipedema completed an eight-week treadmill HIIT program using 4 × 4-minute intervals at around 85 to 95 percent of maximal heart rate. Twenty-two women completed the program and no adverse events were reported, although formal peer-reviewed results have not yet been published. This does not prove that high-intensity exercise is optimal for lipedema, but it does make universal claims that women with lipedema must avoid vigorous exercise difficult to justify.

Atan and Bahar-Özdemir’s randomized study is another interesting example because all groups performed an exercise program containing aerobic training, strengthening and stretching. The aerobic component was not merely gentle movement. Again, the study was not designed to compare high and low intensities, so it cannot tell us which intensity is best. It does remind us how limited the evidence is behind rigid rules about how women with lipedema are “supposed” to exercise.

So, do you need to run?

No. And I think this is probably the most practical message from everything I have read.

Running is excellent cardiovascular exercise. It is time-efficient, it can provide a strong stimulus for VO₂max, and its impact contributes something useful for bone. If you enjoy running and tolerate it well, there is currently no evidence showing that having lipedema means you should automatically stop.

But running is not a requirement for becoming aerobically fit.

A steep incline can transform walking into moderate or vigorous cardiovascular exercise while maintaining a substantially lower impact profile. For someone who does not enjoy running, experiences discomfort from repeated impact or simply prefers walking, this opens up a very useful option.

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And if all you currently do is walk, increasing the incline gradually can be a way to increase the physiological stimulus without having to cross some imaginary line where “proper exercise” suddenly begins.

Walking uphill can contribute to cardiovascular fitness, mitochondrial adaptation, metabolic health, energy expenditure and lower-body muscular endurance. It can be performed gently, or it can become surprisingly hard. It can be used for longer aerobic sessions, or the gradient and speed can be manipulated to create intervals.

What it cannot do particularly well is replace progressive resistance training for muscle and bone, and there is no evidence that it selectively removes lipedema fat.

That is why I would rather think about incline walking as one very useful piece of a larger exercise picture.

For someone interested in long-term health, a combination might include regular incline walking for aerobic volume, resistance training for muscle and bone, and some harder cardiovascular work if desired. Yoga, mobility work or other forms of movement can serve completely different purposes again.

The goal does not have to be becoming a runner.

The goal can simply be becoming stronger, fitter, more metabolically healthy and more capable of moving your body in ways you actually enjoy enough to continue doing.

And if that involves spending an hour walking uphill on a treadmill instead of running, the physiology suggests that your heart is unlikely to complain that you chose the wrong verb.

Think of ultrasound as a camera beneath your skin

Ultrasound sends sound waves into your body. These waves bounce back differently depending on what they encounter, such as fat, connective tissue, or muscle. A computer turns those echoes into an image.

But what does this have to do with lipedema?

Under your skin, fat is arranged in small groups called fat lobules, held together by connective tissue. Think of it like a bunch of grapes, where the grapes represent fat and the structures holding them together represent connective tissue.

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In Dr. Vargas’s research, ultrasound revealed that this arrangement can look different in people with lipedema. Rather than simply measuring how much fat someone has, she examines how the tissue is organized.

Researchers can look for:

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• Changes in fat tissue: Whether the fat lobules appear differently arranged or the tissue looks thicker.

• Changes in connective tissue: Whether the structures separating and supporting the fat appear altered or disrupted.

• Small nodules: Localized areas that look different from the surrounding tissue. Some painful nodules investigated by Dr. Vargas contained evidence of small bleeding events and damaged fat cells.

Why is this interesting?

Because it could help us understand what is happening inside painful lipedema tissue, rather than only looking at how the legs or arms appear from the outside.

However, these findings are still being investigated. Ultrasound cannot currently diagnose lipedema on its own, and researchers need to confirm how reliably these patterns can be identified.

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Dear LipedemaScience Member

There is so much happening in the world of lipedema research, and I want to make it easier for you to explore it all! Below, I have gathered several articles that I think you might find interesting, whether you want to learn more about managing lipedema today, understand the science behind the condition, or follow the latest developments in research.

One of the things I value most about LipedemaScience is the opportunity to bring together different perspectives. I speak with researchers, healthcare professionals, experts, and people living with lipedema, all of whom contribute valuable insights. Some of our discussions focus on practical things we can do to improve our health and quality of life right now, while others explore the many unanswered questions about lipedema, its underlying mechanisms, and where future research should take us.

I believe there is enormous value in looking at lipedema from different angles, questioning what we think we know, and remaining curious about what we have yet to understand. Science is constantly evolving, and my goal is to make that knowledge accessible to you while also introducing new perspectives and nuances that are sometimes missing from the broader conversation about lipedema.

And remember, being a LipedemaScience member is about more than just reading articles! You are also invited to join our member chat, where we discuss research, exchange experiences, ask questions, and explore ideas together. I would love for you to take part and tell me what you are curious about, what you would like to understand better, and which topics you would like me to investigate and write about next.

Whether you prefer to read quietly at your own pace or actively participate in the discussions, I hope LipedemaScience will continue to be a place where you find knowledge, inspiration, and perspectives that help you better understand this complex condition.

Happy reading, and thank you for being part of LipedemaScience!

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Imagine accidentally cutting your finger while preparing dinner. Within minutes, your body begins responding to the injury. Blood vessels dilate, their permeability increases, and immune cells are recruited to the damaged tissue, where they help remove microorganisms and cellular debris while coordinating the early stages of repair. The redness, warmth, swelling, and tenderness that may develop are familiar signs of acute inflammation. Although these symptoms can be uncomfortable, the underlying response is essential for healing. Without appropriate inflammatory activity, even relatively minor wounds would become considerably more difficult to repair.

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Inflammatory processes are also involved in situations we would not ordinarily associate with inflammation. During pregnancy, for example, the immune system undergoes carefully regulated changes that support implantation, placental development, and eventually childbirth. Different stages of pregnancy require different immune environments, including periods in which inflammatory signaling plays an important physiological role. Similar interactions between immune cells and other tissues occur throughout our lives, often without producing any noticeable symptoms.

And this brings us back to eating. Researchers have observed that certain meals can temporarily influence the activity of circulating immune cells, inflammatory signaling pathways, and molecules commonly used as markers of inflammation. These responses can occur in otherwise healthy people, particularly after large meals or meals containing substantial amounts of fat or rapidly absorbed carbohydrates. However, the relationship between eating and inflammation is considerably more complicated than simply suggesting that every meal causes a little inflammation.

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To understand why, we first need to look at what inflammation actually involves, how scientists distinguish normal immune activity from harmful inflammatory processes, and what human studies have discovered about the hours following a meal.

What Is Inflammation, and Why Do We Need It?

Inflammation is a coordinated biological response involving immune cells, blood vessels, tissues, and chemical signaling molecules. It can be initiated by infections, physical injuries, damaged cells, or other disturbances that require the body to respond. The purpose of an inflammatory response depends on the circumstances, but it frequently involves eliminating harmful stimuli, removing damaged material, and creating conditions that allow tissue repair to begin.

One of the most familiar examples is acute inflammation, which develops relatively quickly after an injury or infection. When tissue is damaged, resident immune cells detect signals released by injured cells and initiate a series of responses involving inflammatory mediators, changes in local blood flow, and the recruitment of additional immune cells. Neutrophils are often among the first circulating immune cells to arrive, followed by monocytes that can develop into macrophages. These cells participate in clearing damaged tissue and microorganisms, while macrophages also help coordinate the transition from inflammation toward tissue repair.

An important part of this process is inflammation resolution, which is not simply the passive disappearance of inflammatory signals. The body actively regulates immune-cell recruitment, removes cells that are no longer needed, and produces molecules that help restore tissue function. Successful healing therefore depends on both initiating an appropriate inflammatory response and resolving it when its immediate purpose has been fulfilled.

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Problems can develop when this regulation is disrupted. Excessive acute inflammation can damage otherwise healthy tissue, while persistent inflammatory activity may contribute to chronic disease. Chronic inflammation can arise from ongoing infections, autoimmune processes, prolonged tissue injury, or metabolic disturbances, among other causes. In conditions associated with chronic low-grade inflammation, the changes may be relatively modest compared with an acute infection, but they can persist over months or years and influence tissue function.

This is one reason the distinction between acute and chronic inflammation is useful, although it is not sufficient on its own. Acute inflammation is not automatically beneficial, just as every prolonged immune response is not necessarily pathological. The consequences depend on where inflammation occurs, what initiated it, how strongly the immune system responds, and whether the response remains appropriately regulated.

There is also an important difference between inflammation and immune activity more generally. Our immune system is continuously interacting with tissues, monitoring the intestinal environment, clearing damaged cells, and participating in metabolic regulation. These activities do not necessarily represent harmful inflammation, even when some of the same immune cells and signaling molecules are involved.

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What Happens to Your Immune System After Eating?

The hours following a meal are known as the postprandial period. During this time, the digestive system breaks down food, nutrients are absorbed, and the body coordinates changes in glucose, insulin, circulating lipids, and energy metabolism. Dietary fats are packaged into particles called chylomicrons, which transport triglycerides through the lymphatic system and bloodstream, while absorbed carbohydrates influence blood glucose and insulin secretion.

These metabolic changes also involve communication with the immune system. Researchers have observed that substantial high-fat meals can temporarily increase the number of circulating neutrophils, a type of white blood cell involved in immune defense. Some studies have also reported changes in the activation of neutrophils and monocytes, suggesting that circulating immune cells respond to changes in nutrient availability and lipid metabolism.

One of the most frequently investigated molecules is interleukin-6, commonly abbreviated IL-6. This cytokine participates in inflammatory signaling but also has important metabolic functions, making it particularly interesting when studying the body’s response to food.

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In 2017, Emerson and colleagues published a systematic review in Advances in Nutrition examining inflammatory responses after high-fat meals in healthy adults. The review included 47 studies and found that IL-6 was the only one of five commonly measured inflammatory markers that increased consistently. Across the studies, IL-6 concentrations increased from approximately 1.4 pg/mL before eating to 2.9 pg/mL around six hours afterward. However, C-reactive protein (CRP) remained unchanged in 79% of the studies measuring it, while TNF-α remained unchanged in 68%.

The findings suggest that certain aspects of immune signaling may change after a meal without producing a generalized increase in the inflammatory markers commonly associated with chronic disease. However, the researchers also identified a methodological problem that complicates the interpretation of the IL-6 results.

Many studies collected repeated blood samples through an indwelling catheter, which allows researchers to obtain multiple samples without repeatedly puncturing the skin. Unfortunately, the catheter itself can stimulate local IL-6 production. Earlier experiments demonstrated that IL-6 concentrations measured through a catheter could increase substantially over several hours, while samples collected through separate venepuncture showed much smaller changes. In the systematic review, 30 of the 32 studies reporting significant increases in IL-6 had used a cannula for blood collection.

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This means that some of the apparent postprandial IL-6 response may have been caused by the measurement procedure rather than the meal. It does not invalidate the other observations, particularly the changes in circulating white blood cells, but it demonstrates why interpreting inflammatory biomarkers requires considerable care.

Larger studies have provided additional information. The PREDICT 1 study, involving approximately 1,000 adults, investigated inflammatory responses after standardized meals and found that IL-6 and GlycA, a composite marker associated with systemic inflammation, did not necessarily respond in the same way. The researchers also raised concerns about the influence of blood-sampling methods on IL-6 measurements.

The broader lesson from these studies is that inflammation cannot be adequately described by measuring one cytokine and assuming that its concentration represents the overall inflammatory state of the body.

Inflammatory Molecules Also Have Metabolic Functions

The relationship between immune signaling and metabolism has become an important area of research, often described as immunometabolism. Scientists are increasingly investigating how immune cells respond to nutrients and how immune signaling molecules influence processes such as insulin secretion, glucose regulation, and energy metabolism.

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IL-6 provides an interesting example because its effects depend on the physiological circumstances in which it is released. In a human experimental study published in Cell Metabolism in 2018, Lehrskov and colleagues found that experimentally increasing IL-6 delayed gastric emptying and reduced postprandial glucose and insulin responses. Other research has investigated how macrophage-derived IL-1β may influence insulin secretion after glucose exposure, although much of the mechanistic evidence for this pathway comes from animal experiments.

These findings do not establish that postprandial inflammation is universally beneficial. They do, however, demonstrate that molecules commonly described as inflammatory can participate in ordinary metabolic regulation. Whether their activity is protective, harmful, or physiologically neutral depends on the biological context rather than the presence of the molecule alone.

Does What We Eat Influence Inflammation?

Although certain meals can temporarily activate immune and inflammatory pathways, researchers have found that meal composition can influence these responses. The amount and type of dietary fat, the carbohydrate content, and the presence of fiber and other food components may all affect postprandial metabolism.

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Several controlled studies have compared meals containing different dietary fats. Some have reported greater activation of NF-κB, a transcription factor involved in regulating inflammatory gene expression, after butter-rich meals than after meals containing olive oil. Other experiments have investigated whether polyphenols found in virgin olive oil influence inflammatory signaling, particularly in people with metabolic dysfunction.

Researchers have also examined the effects of carbohydrates and blood glucose. In a study published in Circulation in 2002, Esposito and colleagues experimentally increased blood glucose concentrations in healthy individuals and people with impaired glucose tolerance. They observed increases in several inflammatory cytokines, including IL-6 and TNF-α, with some responses being greater or more prolonged in participants with impaired glucose tolerance. However, this experiment involved maintaining blood glucose at an unusually high concentration under controlled conditions, which differs substantially from the temporary glucose increase that normally follows a meal.

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Another proposed mechanism involves metabolic endotoxemia, the movement of small amounts of bacterial components, particularly lipopolysaccharide (LPS), from the intestine into circulation. Some studies have reported increased endotoxin measurements after high-fat meals, leading to suggestions that dietary fat absorption may facilitate the transport of bacterial products into the bloodstream. However, the hypothesis remains controversial because commonly used measurement methods have important limitations, particularly in lipid-rich blood samples. Other experiments suggest that fatty acids and metabolic factors may activate inflammatory pathways independently of bacterial endotoxins.

An additional consideration is that many postprandial studies use unusually large experimental meals, sometimes containing substantial amounts of fat or rapidly absorbed carbohydrates, to provoke measurable responses over a few hours. These experiments can provide valuable information about physiological mechanisms, but they do not necessarily reflect ordinary eating patterns. Studies also frequently involve relatively small groups of participants and measure intermediate biological markers rather than clinical health outcomes.

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Consequently, observing greater inflammatory signaling after a butter-rich meal than after an olive-oil meal does not establish that butter causes chronic inflammatory disease, just as a smaller response after a meal containing polyphenols does not demonstrate that the meal prevents disease. For long-term health, research examining overall dietary patterns, metabolic risk factors, and clinical outcomes provides a more informative foundation for nutritional recommendations.

When Does Inflammation Become a Concern?

The body is generally capable of regulating temporary metabolic and immune responses after eating, but these processes may differ in people with metabolic dysfunction. Individuals with insulin resistance or type 2 diabetes may experience larger or more prolonged increases in circulating glucose and triglycerides, while some studies have also reported greater oxidative stress and inflammatory signaling after meals.

Adipose tissue is particularly relevant because it is not simply a storage compartment for excess energy. It is a metabolically active organ containing adipocytes, immune cells, blood vessels, connective tissue, and numerous signaling molecules that participate in metabolic regulation.

In obesity-related adipose tissue dysfunction, changes in adipocyte size, immune-cell recruitment, and inflammatory signaling may contribute to insulin resistance and chronic low-grade inflammation. Researchers have proposed that repeated postprandial metabolic stress could contribute to this inflammatory environment, although the causal relationship between temporary responses after eating and the development of chronic disease remains incompletely established.

The relationship is also influenced by individual metabolic health. People with similar body mass indices may differ substantially in insulin sensitivity, fat distribution, and inflammatory activity, meaning that body weight alone cannot fully explain how someone responds to food.

What Does This Mean for People With Lipedema?

Inflammation is frequently discussed in relation to lipedema, particularly when nutritional recommendations are presented as ways to reduce inflammation in affected adipose tissue. However, the biology of lipedema is still being investigated, and findings from research on obesity-related inflammation cannot automatically be interpreted as evidence of the same processes occurring in lipedema.

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Studies examining lipedema adipose tissue have reported differences in adipocyte size, connective tissue structure, fibrosis, and immune-cell populations compared with control tissue. For example, a 2023 study by Kruppa and colleagues identified changes in adipose tissue characteristics and macrophage populations in women with lipedema. These findings suggest that the tissue environment may differ from that observed in comparison groups, although the results do not establish a uniform pattern of increased inflammation across all individuals or stages of the condition.

It is also important to recognize that lipedema and obesity can coexist. People with lipedema may have insulin resistance, obesity-related metabolic dysfunction, or type 2 diabetes, and research on postprandial responses in these conditions may therefore be relevant to their overall metabolic health. At the same time, the presence of lipedema does not necessarily imply that someone has the metabolic abnormalities commonly associated with obesity.

The studies discussed in this article do not establish whether people with lipedema experience a distinct inflammatory response after eating or whether temporary changes in postprandial immune activity directly influence lipedema symptoms. Answering those questions would require controlled human studies comparing people with lipedema and appropriately matched individuals without the condition, while accounting for metabolic health, body composition, and dietary factors.

Until such evidence is available, findings from general postprandial inflammation research should not be used on their own to justify specific food restrictions for people with lipedema.

Should We Try to Reduce Inflammation Through Our Diet?

The popularity of anti-inflammatory diets reflects a genuine scientific interest in the relationship between nutrition, immune function, and chronic disease. Dietary patterns can influence metabolic health, and several established nutritional recommendations are consistent with reducing risk factors associated with chronic low-grade inflammation.

Diets rich in vegetables, fruits, legumes, whole grains, nuts, seeds, and unsaturated fats have been associated with favorable cardiovascular and metabolic outcomes. Their benefits involve multiple physiological processes, including effects on blood lipids, insulin sensitivity, blood pressure, intestinal function, and body composition. It would therefore be an oversimplification to explain their health effects solely through changes in inflammatory markers.

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The same applies when individual foods are classified as inflammatory or anti-inflammatory. A food may influence a particular signaling pathway in a laboratory experiment without producing a clinically meaningful effect in humans. Similarly, an ingredient containing compounds with anti-inflammatory properties does not necessarily produce a measurable anti-inflammatory effect when consumed as part of an ordinary meal.

Some people may also wonder whether eating less frequently could reduce inflammation by allowing more time between postprandial responses. However, a randomized crossover trial published in The Journal of Nutrition in 2024 compared three and six eating occasions per day while keeping total energy intake and dietary composition similar. The researchers found no significant differences in the fasting inflammatory biomarkers measured between the two eating patterns. Although this does not rule out effects under other circumstances, it challenges the assumption that eating more frequently necessarily produces greater chronic inflammatory activity.

For people with lipedema, dietary choices may also need to consider individual symptoms, metabolic health, nutritional adequacy, and personal preferences. There is currently insufficient evidence to recommend avoiding particular foods solely because experimental studies have reported temporary changes in inflammatory markers after eating.

So, Is Inflammation Good or Bad?

Inflammation is one of the body’s essential biological responses, but its effects cannot be understood without considering the circumstances in which it occurs. The inflammatory response that helps a wound heal is different from persistent inflammatory activity associated with metabolic disease, and both differ from the temporary immune-metabolic changes researchers may observe after certain meals.

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We depend on carefully regulated immune responses throughout our lives, including during tissue repair, infection defense, and several aspects of normal reproductive physiology. At the same time, excessive or poorly regulated inflammation can contribute to tissue damage and disease, making the regulation and resolution of inflammatory responses just as important as their initiation.

What I find particularly relevant from a nutritional perspective is how easily changes in individual inflammatory markers can be interpreted as evidence that a food is harmful. When we hear that a meal increases inflammation, it is worth asking which marker was measured, whether the change was attributable to the meal, how long it lasted, and whether it was associated with any meaningful health outcome. A temporary increase in immune-cell activity or inflammatory signaling does not, by itself, answer those questions.

The available research supports paying attention to overall dietary quality and metabolic health, but it does not support the idea that every inflammatory response should be suppressed. Our bodies are continuously adapting to the foods we eat and the environments we encounter, and many of the processes involved in those adaptations are necessary for maintaining normal physiological function.

Rather than treating inflammation as something inherently harmful, I think we would benefit from understanding it as a complex biological process whose consequences depend on its cause, location, intensity, duration, and regulation. That understanding gives us a more useful foundation for interpreting nutrition research than simply dividing foods into those that supposedly cause inflammation and those that prevent it.

Sources:

1. Emerson SR et al. (2017). Magnitude and Timing of the Postprandial Inflammatory Response to a High-Fat Meal in Healthy Adults: A Systematic Review. Advances in Nutrition, 8(2), 213–225. https://doi.org/10.3945/an.116.014431

2. Mazidi M et al. (2021). Meal-induced inflammation: postprandial insights from the Personalised REsponses to DIetary Composition Trial (PREDICT) study in 1000 participants. American Journal of Clinical Nutrition. https://doi.org/10.1093/ajcn/nqab132

3. Fewkes JJ et al. (2022). A Single, High-Fat Meal Adversely Affects Postprandial Endothelial Function: A Systematic Review and Meta-Analysis. American Journal of Clinical Nutrition, 116(3), 699–729. https://doi.org/10.1093/ajcn/nqac153

4. Esposito K et al. (2002). Inflammatory Cytokine Concentrations Are Acutely Increased by Hyperglycemia in Humans: Role of Oxidative Stress. Circulation, 106(16), 2067–2072.

5. Erridge C et al. (2007). A High-Fat Meal Induces Low-Grade Endotoxemia: Evidence of a Novel Mechanism of Postprandial Inflammation. American Journal of Clinical Nutrition, 86(5), 1286–1292.

6. Lehrskov LL et al. (2018). Interleukin-6 Delays Gastric Emptying in Humans with Direct Effects on Glycemic Control. Cell Metabolism.

7. Dror E et al. (2017). Postprandial Macrophage-Derived IL-1β Stimulates Insulin, and Both Synergistically Promote Glucose Disposal and Inflammation. Nature Immunology.

8. Kruppa P et al. (2023). Lipedema Stage Affects Adipocyte Hypertrophy, Subcutaneous Adipose Tissue Inflammation and Interstitial Fibrosis. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2023.1223264

9. Neuhouser ML et al. (2024). No Effect of High Eating Frequency Compared with Low Eating Frequency on Appetite and Inflammation Biomarkers: Results From a Randomized Crossover Clinical Trial. The Journal of Nutrition. https://doi.org/10.1016/j.tjnut.2024.04.029

10. Thompson D and Dixon NC (2009). Measurement of Postprandial Interleukin-6 by Using a Catheter: What Does It Tell Us? American Journal of Clinical Nutrition. https://doi.org/10.3945/ajcn.2009.28460

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We are now approaching 2,000 (!!) readers from 63 (!!!) countries, which still feels a little surreal to me. When I started LipedemaScience, I wanted to create a place where people could learn about lipedema through science, research and thoughtful discussions. A place where curiosity was encouraged, questions were welcome, and information was presented in a way that people could actually understand and use. And today, I am so happy to see people from all over the world finding their way here.

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A little glimpse behind the scenes

Something you might not know is that I spend approximately four hours every day working on LipedemaScience. Sometimes more, sometimes less, but it has become a very meaningful part of my everyday life. My list of things I want to write about is getting ridiculously looong!

I have articles that I have started, articles that I am currently researching, scientific papers waiting to be read, researchers I would love to interview, and topics that I keep adding to my list because I find them so interesting.

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Sometimes I start researching one question and end up discovering five other things I want to understand better. And I absolutely love that part of the process.

With my background in human nutrition and food science, I have always enjoyed digging into research, asking questions and trying to understand how things work. Having lipedema myself has naturally made this particular field of research very personal to me.

But what makes LipedemaScience especially meaningful is knowing that I am no longer doing all this reading and learning just for myself. I get to share it with you.

We are all at different stages of life

One thing I think about quite often when planning new content is how incredibly different we all are…

Some of you are very young, perhaps trying to understand changes in your body or navigating a recent diagnosis. Others have lived with lipedema for decades and have accumulated an enormous amount of personal experience. Some are thinking about pregnancy or going through hormonal changes. Others are navigating perimenopause or menopause and wondering how these transitions might influence their symptoms.

Some of you have undergone surgery, while others are considering it or have decided that surgery is not the right path for them.

Some are living with relatively mild symptoms, while others are dealing with substantial pain, mobility limitations and daily challenges.

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We also have men living with lipedema in this community, something I think deserves more attention and understanding!

And then there are the researchers, healthcare professionals, clinicians and other experts who follow LipedemaScience because they are interested in the science and developments within the field.

I find this diversity genuinely fascinating.

We may have very different experiences, backgrounds and needs, but we share an interest in understanding lipedema better. And that is something I want to reflect in the content I create.

I know that not every article will be equally relevant to every reader. An article about pregnancy might be incredibly valuable to someone preparing to become a mother, while another reader may be much more interested in pain mechanisms, nutrition, surgery or new clinical research.

My ambition is to build a platform where, over time, everyone can find something meaningful, interesting or useful.

I would love for this to become an even more active community

Although I write most of the articles, I never wanted LipedemaScience to be a place where information only travels in one direction. I want to learn from you, too.

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I love when you leave comments, ask questions, share personal experiences or challenge something you have read. Sometimes a question from one reader gives me an idea for an entirely new article. And sometimes your experiences raise questions that science has not yet answered.

That is part of what makes this so interesting. If there is something you would like me to investigate, a study you have come across, or a topic you feel deserves more attention, please tell me!

I cannot promise to cover absolutely everything, but I do read your suggestions, and they genuinely influence what I work on.

I would also love to see more conversations between readers. With people joining us from 63 different countries, there is so much knowledge and experience within this community.

A few ways to get more out of LipedemaScience

If you are new here, I also want to make sure you know that there are several ways to enjoy the content.

You can read everything directly on LipedemaScience.com, or you can download the Substack app, which makes it easy to follow new articles, explore previous publications and participate in discussions.

You can also listen to articles in audio format through Substack, which I know can be convenient when you are walking, travelling, cooking or simply prefer listening rather than reading. And please feel free to share articles with anyone you think might benefit from them.

Whether that is a friend who has just received a diagnosis, a family member trying to understand lipedema, a healthcare professional or someone who is simply curious.

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Every time you share something from LipedemaScience, you help scientific information reach someone new. And I appreciate that more than you might realize.

Finally, a personal thank you

Building LipedemaScience has become one of the most rewarding things I have done. Not because of the number of subscribers, although watching this little community grow is certainly exciting, but because of the people I have met along the way.

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I have had conversations with researchers, surgeons, healthcare professionals and women from so many different parts of the world. Some have shared their professional knowledge, while others have trusted me with deeply personal stories about living with lipedema.

I have learned so much from these conversations. And I hope to keep learning. There is still an enormous amount we do not understand about lipedema. Research is developing, new questions are emerging, and many aspects of the condition remain uncertain.

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I want LipedemaScience to be a place where we can follow that progress together, remain curious, and be comfortable acknowledging what science has not yet established.

My list of articles is certainly not getting any shorter, so I think we have plenty to explore in the years ahead!

To everyone who reads, comments, shares, supports or simply follows along quietly, thank you!!

I am genuinely grateful that you have chosen to be here, and I hope you continue to find value in what I share. And now I would love to hear from you.

Where in the world are you reading LipedemaScience from? And is there a particular topic you would love to see me cover in a future article?
I would love to get to know more of you.

With love and curiosity,

CarinaW
Founder, LipedemaScience

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Did you know that two loaves of bread made from the same type of wheat can have different nutritional properties? Or that the microorganisms involved in fermentation can influence how certain components of the flour behave during digestion?

This is the kind of research that made me fall in love with food science. I have an academic background in both human nutrition and food science. Although these disciplines overlap, they approach food from different perspectives. Human nutrition focuses on what happens when we eat, including digestion, metabolism, nutrient absorption and the relationship between diet and health. Food science looks more closely at the food itself. What does it contain? How do its components interact? What happens when we ferment, cook or process it?

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A master’s thesis published in 2026 at the Norwegian University of Life Sciences (NMBU), where I completed my own master’s degree in Food Science, provides a fascinating example. The research comes from the same academic environment, involving researchers and professors I worked with during my studies.

The subject is something many people have probably encountered in discussions about healthy eating, although often without much explanation.

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Could ultrasound help us see changes that conventional examinations may overlook?

In this exclusive LipedemaScience interview, I speak with Dr. Deise Vargas, a Brazilian radiologist with 25 years of experience and the researcher behind the Lipedema Dermal Hypodermal Classification (LDHC). Her work explores how ultrasound imaging can reveal structural changes in the skin and subcutaneous adipose tissue, including alterations in tissue organization, fibrosis, and small, painful nodules.

Particularly interesting are her team’s investigations into microvascular changes, localized bleeding, fat necrosis, and possible mechanisms of lipedema pain. By combining ultrasound findings with tissue biopsies, the researchers are exploring whether some of these changes could help explain symptoms that have historically been difficult to assess objectively.

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Throughout our conversation, Dr. Vargas explains what her research has revealed so far, why certain ultrasound findings should not be confused with angiolipomas, and how imaging might eventually contribute to monitoring lipedema progression and treatment outcomes. We also discuss the limitations of the current evidence, including why ultrasound cannot yet replace clinical diagnosis and why independent validation remains essential.

This interview offers a fascinating look at an emerging area of lipedema research, where the goal is not simply to measure how much adipose tissue is present, but to better understand what is happening within that tissue.

1 - Could you tell us about your background as a radiologist? What first drew your attention to lipedema?

I am a Brazilian radiologist with 25 years of experience, working primarily in dermatological, musculoskeletal, and rheumatological ultrasound, with a particular focus on lipedema.

I am a researcher and the creator of the ultrasound morphological classification of lipedema, the LDHC (Lipedema Dermal Hypodermal Classification), which describes four patterns of morphological alterations in lipedema in comparison with the normal pattern.

I have published scientific articles on international platforms and in international journals, including Cureus, Radiopaedia, and SCIRP. I am also the author of the books From Unlikely to Memorable: Discovering My Purpose in Lipedema and Lipedema in Layers. I have also been a speaker at several courses and congresses throughout Brazil on lipedema ultrasound.

I am the founder and Medical and Scientific Coordinator of LIPCOR (Lipedema and Diagnostic Correlations Center), dedicated to the study of lipedema, always with a focus on ultrasound correlation.

The beginning of my journey in lipedema did not take place in a laboratory, but rather through clinical observation. It began with the leg pain experienced by my patients, who were referred to me for vascular imaging evaluation. For more than two decades, while examining women referred for venous and arterial Doppler ultrasound, I repeatedly encountered the same situation: patients with severe pain, increased limb volume, and spontaneous bruising, yet whose vascular examinations were often normal. Nevertheless, these women continued to suffer and were sometimes even referred for varicose vein surgery.

In 2024, I began to recognize that there were alterations that conventional vascular imaging methods were failing to demonstrate. Then, in early 2025, one particular patient definitively changed the way I understood lipedema. She presented with clinical manifestations associated with profound suffering, which deeply affected me. Faced with her case, I began to question whether we were truly examining the tissue responsible for her symptoms. I realized that I needed to look beyond the vascular system and investigate the hypodermis.

That was when I began identifying ultrasound alterations in the organization of the hypodermis. When these findings were grouped together, they corresponded to morphological patterns that warranted systematic investigation.

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From this observation, my journey as a lipedema researcher began, together with the purpose of developing an ultrasound methodology capable of documenting these alterations, reducing subjectivity in their assessment, and contributing to the monitoring and follow-up of these patients.

Therefore, my research was born from a very simple question:

“How can an examination be considered normal when the patient continues to experience so much pain?”

2 - Was there a particular patient, ultrasound finding, or unanswered question that led you to begin researching the tissue changes associated with lipedema?

Yes. She was exactly the patient I mentioned earlier. She represented a turning point in my scientific journey because it was during her examination that I began to understand that we had been evaluating patients in an incomplete way.

Until then, the ultrasound assessment of lipedema described in the literature had focused primarily on quantitative parameters, particularly the measurement of subcutaneous tissue thickness, an approach widely disseminated by Dr. Alexandre Amato, a Brazilian physician and researcher and a recognized reference in the field of lipedema.

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However, in that patient, I realized that there was a need to understand the architecture of all layers of the dermis and hypodermis.

During the examination, I observed a constellation of morphological alterations that immediately caught my attention. I observed changes in tissue thickness, as previously described by Dr. Amato, but also alterations in the echogenicity of the hypodermis, associated with changes in the organization of the septa and fascial structures located between the adipose lobules.

I began to systematically assess five morphological aspects: tissue thickness, echogenicity, septal organization, alterations of the interfaces and fascial structures, and the presence of focal alterations in the architecture of the hypodermis and at the dermal–hypodermal junction.

As I began evaluating other patients with lipedema, I realized that these findings were not isolated observations. Rather, they represented recurring morphological patterns, although with different degrees of expression and tissue disorganization.

Within this context, I identified a “hyperechoic nodule” within the hypodermis. It was not clinically palpable, yet it was associated with marked pain upon digital pressure.

These observations led me to identify four distinct ultrasound patterns, which subsequently provided the foundation for the development of the LDHC (Lipedema Dermal Hypodermal Classification).

3 - You developed the LDHC ultrasound classification. What gap were you trying to address, and how would you explain the classification to someone without a medical background?

The research gap emerged from the absence of a standardized ultrasound methodology capable of identifying, characterizing, and classifying the morphological alterations of adipose tissue in patients with lipedema.

Imaging methods such as magnetic resonance imaging, computed tomography, and DEXA were already capable of providing important information about the distribution and quantity of adipose tissue. However, I was looking for something different: I wanted to understand and demonstrate the alterations in the tissue architecture itself through ultrasound, and to give the disease an imaging representation.

It was from this need that the LDHC (Lipedema Dermal Hypodermal Classification) was developed.

The proposal was to establish morphological criteria that would allow the assessment of alterations from the skin surface through the different compartments of the hypodermis. Measuring hypodermal thickness as a diagnostic parameter may produce false-positive results, for example, in patients with obesity or edema. The distinction is that we do not want to know only how much adipose tissue is present, but rather how that tissue is organized.

The LDHC also opens the possibility of monitoring these patients, including their tissue alterations, clinical evolution, and responses to different treatments.

It is important to clarify that the LDHC was developed as a complementary morphological classification. Its diagnostic application and prognostic value still require validation in larger populations and by independent research groups.

My purpose was to provide lipedema with an ultrasound representation of its tissue architecture, so that we could not only measure the tissue, but also begin to understand and objectively document its alterations.

4 - What first made you suspect that some painful nodules in lipedema might be mistaken for angiolipomas?

During the development of the LDHC classification, hyperechoic nodules were observed exclusively in LDHC Type 3. These nodules are small, generally less than 1 cm in diameter, not clinically palpable, and markedly painful. They are distributed within adipose tissue that already exhibits structural alterations.

To investigate the etiology of these nodules, we performed an excisional biopsy for histopathological analysis. Microscopy demonstrated that the nodules represented areas of hemorrhage associated with fat necrosis, hemosiderin deposition, and immature neoangiogenesis. These findings were interpreted as evidence of a hemorrhagic process occurring within a hypoxic–ischemic tissue environment.

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It is essential to clarify that these nodules are not pathognomonic of lipedema. However, they are frequently observed in patients with lipedema.

Angiolipoma is a benign tumor composed of adipose tissue and a vascular component and may also present with pain. Therefore, these clinical characteristics could potentially lead to confusion between an angiolipoma and the LDHC Type 3 nodule.

Because I have extensive experience in dermatological ultrasound, using high-frequency, high-resolution transducers, I began to investigate the morphological characteristics of the LDHC Type 3 nodules in greater detail. I recognized that these nodules displayed characteristics that differed from those I typically observed in angiolipomas.

The most important insight was realizing that our objective was no longer simply to identify the hyperechoic nodule on ultrasound. Instead, we began to ask what this finding might reveal about the underlying processes occurring within the hypodermis of patients with lipedema.

This observation may represent a shift in the way we understand the pathophysiology of lipedema. Traditionally regarded primarily as an inflammatory condition, lipedema may also involve ischemic changes within the tissue, particularly in the context of the LDHC Type 3 pattern.

Thus, the hyperechoic nodule may be more than an isolated ultrasound finding. It may represent an imaging marker of underlying tissue injury and provide a window into the microvascular and hypoxic–ischemic processes occurring within the hypodermis.

5 - In your recent case series, what were the clearest differences between the nodules on ultrasound? What did the tissue samples add to your understanding?

The decision to perform biopsies arose from the need to differentiate structures that may exhibit similar ultrasound appearances when the nodules are analyzed in isolation, but that have different origins and require different therapeutic approaches.

The hyperechogenicity of the nodule does not determine the diagnosis. Both angiolipomas and the hemorrhagic processes observed in LDHC Type 3 can produce echogenic ultrasound appearances. Therefore, it is essential to evaluate the architecture of the surrounding tissue, particularly the degree of hypodermal disorganization.

The main contribution of our series was to establish a correlation among three elements: what we identify on ultrasound, what the patient experiences, and what is found on biopsy.

6 - The lipedema samples showed evidence of bleeding, fibrosis, and fat necrosis. What can we reasonably infer from these findings about how the nodules develop, and what remains uncertain?

The nodules are hemorrhagic lesions; this is already established. The other microscopic findings helped us develop a proposed pathophysiological mechanism, which is described in greater detail in our publication.

Briefly, expansion of the hypodermis may lead to tissue compression and increased demand for nutrients and oxygen, resulting in ischemia and a compensatory need for increased blood supply. This increased supply may occur through neoangiogenesis. However, due to increased pressure within the subcutaneous tissue—as demonstrated by Doppler, which showed increased resistance to blood flow in the region compared with controls—the neoangiogenesis may remain immature and predispose the vessels to rupture, leading to hemorrhage.

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These hemorrhagic events may further increase pressure within the hypodermis, creating a vicious cycle. In addition, fat necrosis may occur as a consequence of ischemia affecting adipocytes located farther from the vascular supply.

Hemorrhagic events may also trigger histamine release, resulting in increased edema and further elevation of pressure within the hypodermis. The release of heparin may additionally contribute to maintaining an increased susceptibility to bleeding.

To arrive at this hypothesis, we biopsied eight LDHC Type 3 lesions, all of which demonstrated similar histopathological findings. The consistency of these findings led us to discontinue further biopsies and to consider the LDHC Type 3 finding as a “virtual biopsy” of tissue exhibiting hypoxic–ischemic alterations associated with lipedema.

To confirm this hypothesis, however, we still need to better understand the origin of the microvascular alterations and demonstrate the specific contribution of hypoxia and ischemia to this process.

This discovery does not conclude the investigation. Rather, it opens the door to a new question: Could these nodules serve as ultrasound markers of microvascular, hemorrhagic, and fat-necrosis processes occurring within lipedematous tissue?

When we reassessed these nodules in the same patients at different time points—including 30 days, 60 days, 6 months, and 9 months—we observed changes in their ultrasound appearance. The nodules had lost their initial configuration; some had decreased in size and developed signs of involution, suggesting partial resorption of the hemorrhagic component.

This behavior reinforced the hypothesis that we were observing a dynamic tissue process rather than a stable tumor formation.

Based on these observations, we also described different ultrasound presentations of LDHC Type 3 nodules, including poorly defined hyperechoic nodules, well-defined hyperechoic nodules, nodules with a central anechoic area, and nodules associated with posterior acoustic shadowing.

Our hypothesis is that this diversity of ultrasound appearances may represent different stages in the evolution of hemorrhagic and reparative processes within lipedematous tissue.

7 - Many people with lipedema can feel painful lumps beneath their skin. Do we know whether these are the same kinds of nodules you studied?

No, the clinically palpable nodules are not the same lesions identified as LDHC Type 3.

We believe that the nodules palpated by patients may correspond to LDHC Type 2, which is characterized on ultrasound by expansion and disorganization of the hypodermis, particularly involving the deep hypodermis, and by more pronounced inflammatory changes within the LDHC classification.

LDHC Type 2 is characterized by bulging of the hypodermis, predominantly in its deeper portion, with rounded septa and septal disruption occurring in approximately 50% of cases.

We should also consider angiolipomas as an important differential diagnosis in patients presenting with painful palpable subcutaneous nodules. However, in these cases, the surrounding tissue is expected to appear completely normal on ultrasound, without the diffuse architectural alterations observed in lipedematous tissue.

Nevertheless, we cannot exclude the possibility that different nodular pathologies may coexist in the same patient. Therefore, the clinical and ultrasound assessment of the nodule should always be performed in conjunction with careful evaluation of the surrounding tissue architecture.

8 - Could these tissue changes help explain pain in lipedema, or is it too early to establish that connection?

In a recently published review, we described the possible pathways involved in pain in lipedema, addressing different mechanisms that may contribute to its pathophysiology, including inflammatory processes, hypoxic–ischemic alterations, microvascular impairment, neural compression mechanisms, and fascial and myofascial changes. These mechanisms may coexist and interact with one another, contributing to different manifestations of pain.

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The investigation of hyperechoic nodules added a particularly interesting perspective to this model: the possibility of identifying, through ultrasound, focal tissue alterations with a precise anatomical correlation to specific sites of pain.

Histopathological analysis demonstrated interlobular hemorrhage, hemosiderin deposition, inflammatory changes, and fat necrosis. These findings support the hypothesis that hemorrhagic processes and adipose tissue injury may contribute to the generation and persistence of localized pain.

Hemosiderin is a marker of blood degradation and previous hemorrhage. Its presence, together with inflammatory and reparative processes, suggests a tissue environment that may promote sensitization of nerve endings.

One of the most interesting clinical observations was not included in the original publication because it was made after the study had already been published: there was a dramatic reduction in pain at the sites that underwent excisional biopsy for histopathological analysis.

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This observation raises an intriguing possibility: perhaps the pain associated with LDHC Type 3 nodules is more intense than pain related to predominantly inflammatory processes, and by excising the nodule, we may have removed the anatomical focus responsible for the pain. But what exactly was removed—the hemorrhagic focus, the ischemic tissue, or both?

Ischemic pain is recognized as one of the most severe forms of pain that a human being can experience. Could ischemia therefore be one of the mechanisms underlying the intense pain associated with these nodules?

There is another possible explanation. In addition to removing the focus of hemorrhage and potentially ischemic tissue, excision also decompressed the hypodermis. This decompression could theoretically improve local tissue perfusion and alter the mechanical environment surrounding the microvasculature and sensory nerve endings.

Therefore, there is no shortage of hypotheses to explain this observation. What we need now is to illuminate this pathway further so that we can better understand the relationship between hemorrhage, ischemia, tissue pressure, microvascular dysfunction, and pain in lipedema.

Perhaps the most important lesson is that the LDHC Type 3 nodule may not simply be an ultrasound finding. It may represent a visible point of convergence between the microvascular, ischemic, inflammatory, and nociceptive mechanisms that contribute to pain in lipedema.

9 - How do you decide when ultrasound provides enough information to monitor a nodule and when a biopsy or further investigation is needed?

At first, an LDHC Type 3 nodule, when identified within a typical ultrasound pattern of lipedema and accompanied by the other findings that characterize the classification, does not necessarily require biopsy, given the robust scientific correlation suggesting that these lesions represent hemorrhagic foci associated with hypoxic–ischemic tissue alterations. Follow-up of these nodules over time represents an additional and important component of their assessment, particularly when accompanied by clinical improvement.

If the nodule demonstrates growth or other features suggestive of a neoplastic process, surgical excision with histopathological analysis should be considered. This approach is consistent with international recommendations for the evaluation of soft-tissue lesions.

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The central aspect of our proposal is to use ultrasound not only to identify the nodule, but also to monitor its biological behavior over time, potentially avoiding unnecessary invasive surgical procedures.

However, following our observation of significant pain improvement after excision, a new possibility emerges: could removal of LDHC Type 3 nodules become a therapeutic approach for patients with severe localized pain?

Perhaps this could be achieved through a less traumatic technique than conventional excisional biopsy. In our cases, the excisional biopsy involved both the skin and subcutaneous tissue. An intriguing possibility for future investigation would therefore be whether these lesions could be selectively removed through ultrasound-guided mini-liposuction, potentially allowing targeted removal of the hemorrhagic focus while minimizing tissue trauma.

This is, however, only a hypothesis at this stage and would require dedicated clinical studies to determine its feasibility, safety, and therapeutic efficacy. The possibility is particularly interesting because it could transform an ultrasound finding currently regarded primarily as a morphological marker into a potential therapeutic target for localized pain in lipedema.

10 - What evidence is still needed before the ultrasound patterns you describe can be used reliably by clinicians outside your research group?

The central issue is reproducibility: are other physicians able to see and identify the same findings that our group has been observing?

From the very beginning of the development of the LDHC classification, our goal has been to establish objective morphological criteria that could be recognized and reproduced by physicians anywhere in the world using an ultrasound system.

Another important aspect is access to ultrasound equipment. To make the technique more accessible and facilitate its widespread adoption, we use conventional linear transducers, similar to those routinely used for vascular Doppler examinations, with frequencies ranging from 12 to 15 MHz. These transducers are sufficient to identify the morphological alterations described, provided that they are used with appropriate technique, proper equipment settings, and adequate knowledge of the anatomical structures that need to be assessed.

Higher-frequency transducers could provide additional detail, particularly in the evaluation of the dermal–hypodermal junction. However, relying on specialized high-frequency equipment could limit the technical reproducibility and accessibility of the method.

We are already in the process of training physicians in Brazil specifically to assess the reproducibility of the classification, and the results so far are encouraging. A research group in Mallorca, Spain, is also willing to participate remotely in this process and help demonstrate scientifically that the methodology can be reproduced internationally.

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For this reason, we consider multicenter studies essential, involving physicians with different levels of experience and using ultrasound equipment from different manufacturers. These studies should assess both interobserver and intraobserver agreement, demonstrating whether different physicians can consistently identify and classify the same morphological findings.

The learning curve should also be taken into consideration. In our preliminary experience, approximately 10 cases from each LDHC category may be sufficient for physicians to begin reproducing the method consistently, although this needs to be formally evaluated in prospective studies.

Our intention is for the LDHC classification to become a universal ultrasound language—accessible, objective, and reproducible, regardless of who performs the examination or which ultrasound system is used.

After all, a scientific discovery reaches its true purpose when it can be reproduced and applied anywhere in the world.

11 - Beyond this case series, which of your studies would you most like our readers to know about, and why?

I would especially like readers to become familiar with the LDHC (Lipedema Dermal Hypodermal Classification), which I consider the central work of my scientific journey in the ultrasound study of lipedema. This publication provides the foundation for understanding the subsequent studies that followed.

I would also highlight our study of the hyperechoic nodules identified in the LDHC Type 3 pattern and their etiology. This publication opens an important paradox regarding their origin and raises new questions about the pathophysiological mechanisms underlying lipedema.

Another important contribution is the observation that not every echogenic nodule identified on ultrasound represents an angiolipoma, particularly when it occurs in a patient with lipedema. In these cases, evaluation of the surrounding tissue architecture may provide important clues for differentiation.

We have also published two reviews: one addressing the possible mechanisms involved in pain in lipedema, and another focusing on microvascular alterations in lipedema and the limitations of conventional Doppler ultrasound.

However, if I had to highlight only two contributions, I would undoubtedly choose the LDHC classification and the histopathological investigation of hyperechoic nodules associated with the LDHC Type 3 pattern.

But, without a doubt, in the mind of a researcher, the next publication is always the one that feels most important. It carries forward everything we have learned from the previous work and connects that accumulated knowledge with the next question we are trying to answer.

And perhaps that is the most fascinating part of scientific research:

What will the next publication be?

12 - Are there findings from other researchers that have changed how you think about lipedema or influenced your own work?

Yes. There are several publications that have influenced my thinking and helped me understand the findings I was encountering in my clinical practice.

Lipedema should not be considered simply as an increase in adipose tissue volume. We need to evaluate the organization of the skin and subcutaneous tissue, its vascular components, supporting structures, and their possible relationships with pain.

I consider the work of several researchers particularly influential in shaping the lines of research I have developed, including Dr. Alexandre Amato, Dr. Karen Herbst, Dr. Carla Pirri, Dr. Antonio Stecco, and Dr. Philipp Kruppa.

I see significant potential for ultrasound, particularly through the LDHC classification, not only as a tool for diagnostic assessment, but especially for the longitudinal monitoring of patients throughout clinical and surgical treatment, including preoperative and postoperative assessment of liposuction.

This perspective also raises an important question in the context of the current widespread use of GLP-1 receptor agonists. Perhaps LDHC could contribute to monitoring patients undergoing these treatments. These therapies may substantially modify body composition, but we still need to determine whether these changes correlate with alterations in the architecture of lipedematous tissue.

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This may become another important area of research: understanding whether changes in body composition are accompanied by measurable changes in the ultrasound morphology and organization of the lipedematous tissue.

Ultimately, ultrasound may allow us not only to observe whether the tissue becomes smaller, but to investigate how the tissue itself changes over time.

13 - What are you and your colleagues investigating now? If you could design the next study without practical constraints, what question would you most want it to answer?

Currently, we are deepening our investigation of the ultrasound features of lipedema. In this new phase, we are developing a classification of myofascial alterations associated with lipedema and investigating their possible relationship with sarcopenia.

This project represents a natural evolution of the LDHC research line, moving beyond the superficial tissues to explore structures that may affect mobility and the development of future orthopedic conditions associated with lipedema.

The literature already includes studies addressing alterations in muscle strength, dynapenia, and possible associations between lipedema and muscle impairment. However, important gaps remain regarding how these changes manifest structurally and whether they can be identified before clinically evident functional impairment occurs.

Our goal is therefore to investigate whether ultrasound can detect early structural changes in the muscle–fascia complex, potentially providing a means of identifying patients at risk of future functional decline before significant clinical manifestations become apparent.

14 - What do you hope ultrasound will eventually contribute to lipedema care, and what should patients be cautious about expecting from it today?

The scientific purpose of my work is to contribute to establishing ultrasound as an accessible, affordable, and reliable reference method for the morphological assessment of lipedema, making it a valuable tool for diagnosis, longitudinal monitoring, and evaluation of therapeutic outcomes.

Beyond its potential role in monitoring clinical and surgical treatments, ultrasound may also have applications in preoperative planning and postoperative follow-up of liposuction.

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Regarding patients’ expectations, I consider it essential to emphasize that the diagnosis of lipedema remains primarily clinical. Ultrasound examination alone should not determine the diagnosis, clinical severity, or indication for a specific treatment.

We also need to expand multicenter ultrasound studies, establish reference values, and demonstrate the reproducibility of ultrasound findings across different populations, ultrasound systems, and physicians. The goal is not to replace clinical assessment with imaging, but rather to allow both approaches to complement each other and help physicians individualize the most appropriate treatment for each patient.

My hope is that, in the future, patients with lipedema will be able to monitor their condition in a safe, objective, and reliable way, while ultrasound provides additional evidence to support clinical decision-making.

This, to me, is the true meaning of the research we have developed: to transform clinical observations into scientific evidence and use that knowledge to improve the care of patients with lipedema.

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Published articles:

https://www.scirp.org/journal/paperinformation?paperid=142155

https://scirp.org/journal/paperinformation?paperid=144979

https://share.google/zXqY3OaQx9JOCdRF7

https://share.google/BQT0HB8WYcrRyDTTy

https://www.scirp.org/journal/paperinformation?paperid=151472

https://share.google/l2vP4FUVJCRGPHTFB

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Each of the professionals mentioned below represents an important part of this journey, because, after all, walking alone makes the journey much more difficult.

As the Medical and Scientific Coordinator of the LIPCOR Center, I feel deeply grateful to all the professionals who believed in the potential of our discoveries and supported the development of this research.

I would also like to express my sincere gratitude to LipedemaScience for the opportunity to present the results of our research to the international community.

Scientific dissemination plays a fundamental role in this process. It is through scientific communication that our observations can reach the world, stimulate new questions and new research, and contribute to ensuring that knowledge can be reproduced, challenged, refined, and improved.

My greatest wish is for the ultrasound morphological mapping of lipedema to continue advancing and become increasingly accessible, allowing physicians around the world to learn about, study, and apply this methodology responsibly and on an evidence-based foundation.

I am grateful to LipedemaScience for helping us share this story.

Because a discovery reaches its true value when it ceases to belong solely to the person who created it and begins to contribute to the knowledge of everyone.

Website: https://dradeisevargas.com

CRM-SP: 234.484 | RQE-SP:105.713

E-mail: deisevargas1808@gmail.com

Dr. Deise Vargas
Radiologist
CRM-SP: 234.484 | RQE-SP: 105.713
Lipedema Researcher
Medical and Scientific Coordinator, Lipedema and Diagnostic Correlations Center (LIPCOR)

São Paulo, Brazil

Dr. Anderson Nadiak Bueno
Vascular Surgeon and Vascular Ultrasound Specialist
CRM-SP: 122.105 | RQE: 46.614 and 46.614-1
Researcher
Vascular Ultrasound Residency Supervisor, FMABC
Scientific Director, LIPCOR

São Paulo, Brazil

Dr. Thais Oliveira Foureaux
Radiologist
CRM-SP: 222.354 | RQE: 100.849
Researcher
Director of Scientific Production, LIPCOR

São Paulo, Brazil

Dr. Dayana Ornelas
Radiologist
CRM-BA: 15.043 | RQE: 12.880 / 17.975
Researcher
Director of Scientific Integration, LIPCOR

Salvador, Brazil

Dr. Alexandre Sacchetti Bezerra
Vascular and Endovascular Surgeon
CRM-SP: 112.815 | RQE: 28.114 / 28.115
Researcher
Professor of Vascular Surgery, FMABC
Full Member of the Brazilian Society of Angiology and Vascular Surgery (SBACV)

São Paulo, Brazil

Dr. Alexandre Campos Moraes Amato, MD, PhD
Vascular and Endovascular Surgeon
CRM-SP: 108.651 | RQE: 29.069
Researcher
Amato Duo
São Paulo, Brazil

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I don’t count carbs. I don’t meticulously calculate how much of everything I’m eating. I don’t have a long list of foods I’m not allowed to eat. A large portion of what I eat is based on relatively unprocessed foods, and I tend to eat fewer refined carbs without actively trying to follow a low-carb diet. I probably eat something close to an 80/20 split when I look at my overall diet. A large portion of what I eat contributes to my health, but there’s also enough flexibility for eating out, travel, holidays, and simply eating something because I enjoy it. It took me many years to get here. And, having tried other approaches myself, I’m wary of judging those who choose a more restrictive diet.

Why can clear rules sometimes be easier to implement than monitoring what people do?

Often, we assume that it is easier to follow an average diet than to follow a very strict diet. However, this is not necessarily true when considering behavior.

“Eat this, but only occasionally” requires making repeated decisions. How often is “occasionally”? How much is “advisable”? Does today count? What about tomorrow? If a particular food is strongly associated with the habit in question, allowing a small amount of it may cause some people to think about it more, rather than less. A strict rule eliminates some of these decisions.

The ketogenic diet is a good example. The restrictions can be significant, but they are relatively clear. For an individual who previously struggled with hunger or certain eating habits, meals that are rich in protein and fat can also be enjoyable. Therefore, an individual may experience a very restrictive diet as psychologically simpler than constantly negotiating with themselves about moderation. This does not automatically make a restrictive diet biologically better. It simply makes it easier for that individual to adhere to it.

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This analysis sparks my interest, as there is often talk about nutrition as if adhering to a planned diet is unpleasant and hinders “real” biological interventions. In reality, following the diet is part of the intervention. Although a diet may be a great idea, it has limited benefit for an individual if they cannot adhere to it.

Restrictions and adherence to them are not the same.
A diet can be restrictive, but still easier for certain individuals to follow. Clear rules reduce the number of food decisions that need to be made repeatedly. Whether this helps or hinders depends on the individual and the circumstances.

We are not starting from the same place.

There is another problem with general dietary advice: people differ in their metabolism and health.

Someone with insulin resistance or type 2 diabetes may not necessarily make dietary decisions based on the same assumptions as someone with normal glucose control. Someone with celiac disease needs restrictions that would be completely unnecessary for most people. Lactose intolerance changes which types of foods are tolerable. Symptoms related to histamine may require individualized assessment. Gastrointestinal issues can change an individual’s attitude toward fiber, fermentable carbohydrates, and certain food groups.

Even among people who have not been diagnosed with any disease, glucose metabolism, appetite, energy expenditure, body composition, physical activity, medication, genetics, age, and hormone levels vary.

It doesn’t mean that everyone needs a completely personalized diet plan, nor does it mean that the basic principles of nutrition no longer apply. It simply means that the same advice can have different effects on different individuals.

The same applies to medical treatment. Some people can achieve significant and positive changes in their metabolism simply by changing their diet and behavior. Other people may need medication, including drugs based on GLP-1 or other treatments. The need for medication is not proof that an individual is not disciplined enough, and being able to live without medication does not make a person’s lifestyle morally superior.

Different doesn’t mean everything is permissible
Individual variability is real, but that doesn’t mean all dietary claims are equally credible. A personalized approach should still be based on biology, nutritional value, medical needs, and the quality of the available information.

What exactly is a “low-carb diet”?

Even the information on food packaging can provide more certainty than science allows. I remember being shown food from a Norwegian study on low-carbohydrate diets, and I was struck by how familiar it seemed. The participants had achieved ketosis, but even so, the diet was not as strict as the “keto” diet I had come to associate with the term. When I looked at the food itself, I remember thinking:“This is quite similar to what I usually eat.”

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This highlights a larger problem in nutrition. “Low-carb craze” describes a broad range. Keto describes a metabolic state. “Keto craze,” meanwhile, has evolved and now has a much narrower cultural meaning, especially online. These terms have converged, but they are not necessarily interchangeable.

We often categorize common biological phenomena into different groups, as categories make it easier to communicate information. Over time, a category can gradually become a self-image: keto, carnivore, vegetarian, low-carb, anti-inflammatory...

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When that happens, defending this dietary habit can become almost as important as questioning what it actually does.

I understand that inclination to seek certainty, because I have experienced it myself.

One example that comes to mind is from before I formally started studying nutrition. When my father was diagnosed with cancer in 2011, I desperately wanted to be able to do something helpful with food. His cancer was very serious, and we knew that his prognosis was extremely poor. He only lived for a few months after the diagnosis.

At that time, I was very concerned that sugar was “feeding” the cancer. I wanted him to stop consuming sugar and he followed a very strict diet based on whole, unprocessed foods, with foods like cauliflower being a focus. At the same time, he was receiving cancer treatment within the Norwegian healthcare system, and he was offered cake and sugary drinks. At the time, I found this almost incomprehensible. When someone you love is dying and there is little you can control, strict rules can provide something incredibly powerful – something to do.I think we sometimes underestimate this when we talk about extreme health behaviors.

It is not always unconsciousness that drives them forward. Sometimes it is fear, hope, desperation, a need to make a difference, or simply a desire to take an active part in their own health.

The feeling of being in control of one’s life can be powerful.
Decisions about health are not based solely on biological information. Uncertainty, fear, hope, past experiences, and the desire to regain control of one’s life can all influence which treatments seem most appealing.

It doesn’t have to be the case that seeking solutions in this way leads to a permanent self-image.

This is where my thinking has changed significantly. Previously, I viewed dieting as something I needed to find the right one for. Today, I don’t believe there is necessarily one diet that an individual needs to find and then follow without changes for the rest of their life.

There may be times when a structured approach is beneficial. Someone might follow a fairly strict diet while trying to improve their health metrics or change ingrained habits. Someone suffering from digestive symptoms might temporarily limit certain types of food while trying to figure out what they can tolerate. Someone might find that a low-carb diet helps them achieve certain goals and then gradually add more carbs while continuing to improve their condition.

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There can also be times when one’s own health requires flexibility. Grief is a good example. A serious illness in the family is another. The same goes for fatigue, fertility treatments, major life changes, caregiving, and periods of mental difficulty. Sometimes, one has the capacity to maximize performance. Sometimes, it’s enough just to get through the day. I don’t think these periods reflect moral success or failure. They reflect life.

This will be especially important when dealing with a chronic condition, such as lipedema. If you know that you may need to manage the condition for many years, it will be important to be able to maintain it. But that doesn’t necessarily mean you need to do exactly the same thing every day for many years. It may mean that you need to develop enough self-awareness to know when you benefit from more structure and when you need more flexibility.

What works in extreme cases might work, but we should still ask ourselves why.

I believe that what matters is not simply whether a particular approach “works.” Rather, I want to know why it works. Did reducing carbohydrates help improve glucose control in an individual with significant insulin resistance? Did increasing protein intake help increase the feeling of fullness? Did eliminating a specific food eliminate symptoms because the individual was actually intolerant? Did the diet indirectly reduce overall calorie intake? Did reducing highly processed foods affect the overall nutritional value of the diet? Or did a simple rule at the end make it possible to control changed behavior?

Many of these systems can lead to the same outcome, but they still provide us with very different information about what the individual actually needs in the long run.

This difference will be particularly important when personal success is transformed into general advice.

If someone loses a significant amount of body weight through a ketogenic diet, that experience is real for them. However, it doesn’t mean that everyone needs to be in ketosis. If someone feels much better after eliminating gluten from their diet because they have celiac disease, it doesn’t mean that gluten is harmful to everyone. If someone needs medication to manage their appetite or metabolism, it doesn’t mean that everyone who is overweight needs the same treatment. And even if I have success with the 80/20 method, that doesn’t mean that everyone else should eat the same way I do.

The results do not always reveal what the effects are.
If people feel better after eliminating a particular food, it suggests that something has changed. But it doesn’t automatically tell us why. Energy intake, nutrient composition, symptoms, expectations, other changes that occur at the same time, and underlying health conditions can all have an impact.

Maybe we should stop trying to find the one right way to eat.

After having an interest in nutrition for about 20 years, including the years I formally studied nutrition and dietetics, I have decreased my interest in categorizing food into different groups, but rather become more interested in what is more than just food. That doesn’t mean I think nutrition is irrelevant. Quite the opposite. Food is one of the things that matters most to me. But I have become increasingly interested in the bigger picture, the context, and the person sitting in front of me.

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Today, I’m all about simple food, good ingredients, nutrient-rich and varied meals, and something versatile enough that my diet doesn’t dictate my entire life. I want my food to support my metabolic health, gut health, overall health, and help me manage my lipedema. I also want to eat dinner with my partner, eat with friends, travel, and experience food as more than just a biological necessity. This balance works well for me now. It might not have worked for me at all times in my life. And maybe that’s what I want to convey with this article. Why are we so eager to change what has helped us into something that everyone should be doing?

Sometimes, certain measures can be effective. Sometimes, it is difficult to find a middle ground, but it is easier to set limits. Sometimes, it is necessary to use medication. Sometimes, an individual’s illness requires a truly specific diet that would not be necessary for others. And sometimes, the measure that helps us in one phase of life does not need to follow us into the next.

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We can learn from each other’s experiences without turning them into universal truths. And perhaps we could become a little less interested in asking what dietary ideology a person adheres to and a little more interested in asking what they need, what they can sustain, what their health requires right now, and what kind of life they ultimately want to live.

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My personal approach is actually quite holistic. I do not think about my body as a collection of separate problems, and I do not organize my life around lipedema alone. I have lived with lipedema for around two decades, so managing it is naturally part of my everyday decisions. At the same time, I care about my cardiovascular and metabolic health, my gut, my physical strength, my mental health, my sleep, my stress levels and my ability to function well as I get older. I also care about relationships, meaningful work, social connection, enjoyment, travel and having enough space in my life to recover from periods of high demand. These things are not secondary to health. They are part of what health means to me.

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This is particularly important because the human body does not experience food, exercise, sleep, psychological stress and social life as completely independent exposures. These systems interact. Sleep affects metabolic and neuroendocrine regulation. Psychological stress involves autonomic and endocrine responses with downstream effects throughout the body. Physical activity influences cardiovascular function, skeletal muscle, metabolism and mental well-being. Diet interacts with metabolism, the gastrointestinal system and the gut microbiome. Social relationships and psychological well-being also have measurable associations with health. None of this means that every symptom can be explained by “stress” or fixed through lifestyle. It means that reducing health to a single diagnosis or intervention gives us an incomplete picture of human physiology.

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When I worked as a laboratory manager, my team was responsible for microbiological testing. As a food scientist, microbiology is also a major part of what we study. We learn about bacteria from many different perspectives, like how microorganisms can be used to produce foods such as cheese and fermented products, how pathogenic bacteria can cause foodborne illness, and how other microorganisms and parasites can affect human health.

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For four years, I was also a co-author on a scientific research project together with a food safety research group at a veterinary university. We studied Bacillus cereus, a bacterium with some particularly interesting and potentially dangerous characteristics. Part of the work involved whole-genome sequencing, which allowed us to study the bacterium at a much deeper level and better understand the genetic features behind its behaviour.

My master’s research brought me even closer to the intestine itself. I worked with intestinal cell models and studied how peptides could be transported across the intestinal barrier. That experience gave me a much deeper interest in what happens at the interface between food, the gut and the rest of the body.

Gut health is therefore something I care about both scientifically and personally. The gut is closely connected with immune function, metabolism and communication between the gut and the brain. But one important thing to understand is that there is no single scientific definition of a “healthy gut.” Researchers instead look at features such as microbial diversity and resilience, the production of compounds such as short-chain fatty acids, the intestinal barrier and how the immune system interacts with the microbiome.

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The gut microbiome has also been linked to inflammation, metabolic disease and aspects of mental health. However, this is an area where popular claims often go much further than the human evidence. Much of what we know about the underlying mechanisms comes from animal and cell studies, while the effects demonstrated in humans are generally more modest.

This is particularly important when we talk about lipedema. At the moment, we do not have evidence showing that an unhealthy gut causes lipedema or that changing the microbiome can treat it. There has only been very limited human research on the microbiome in lipedema, so the gut–lipedema connection should currently be considered a hypothesis rather than an established finding.

Still, I think gut health matters. Not because I believe that every disease starts in the gut, but because the gut is one important part of our overall health. Supporting good gastrointestinal, metabolic and nutritional health makes sense regardless, and for people with lipedema, taking care of the whole body is an important part of long-term health and disease management.

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So in this article, I want to look at what we actually know about gut health, the microbiome and the intestinal barrier, what is still uncertain, and what may be relevant for people living with lipedema.

What do we actually mean by gut health?

“Gut health” is a term we hear everywhere, but scientifically, there is no single definition of what a healthy gut looks like. There is also no one test that can tell you whether your gut is “healthy” or “unhealthy.” Researchers instead look at several different features, including the microorganisms living in the intestine, how stable that microbial community is, what those microbes produce, and how well the intestinal barrier and immune system are functioning.

Our gut contains a huge community of microorganisms, mainly bacteria, but also viruses, fungi and other microbes. Together, they are often referred to as the gut microbiome. These microorganisms are not simply passengers. They interact with the food we eat, produce substances that our own cells can use, and communicate with both the immune system and the intestinal lining.

One example is dietary fiber. Some gut bacteria ferment fibers that we cannot digest ourselves and produce short-chain fatty acids, including butyrate, acetate and propionate. Butyrate is particularly interesting because it is used as an energy source by cells in the colon and is involved in maintaining the intestinal barrier and regulating immune activity. Much of the detailed biological evidence comes from animal and laboratory research, while the effects in humans are more complex and generally more modest.

The intestinal barrier is another important part of gut health. The intestine has to perform two almost opposite jobs at the same time. It has to allow nutrients to pass into the body while helping to keep potentially harmful microorganisms and substances where they belong. A mucus layer, intestinal cells and the connections between those cells all contribute to this barrier.

This is also why gut health should not be reduced to having as many different bacteria as possible. Diversity is often discussed as a positive feature, but a high diversity score does not automatically mean that someone is healthy. Two people can have very different microbiomes and still both be healthy. What seems to matter is not only which bacteria are present, but also what they are doing and how resilient the whole system is when it is disturbed.

So when I use the term gut health in this article, I am not referring to a perfect microbiome or a specific bacterial composition. I mean a gastrointestinal system that functions well.. digestion works, the intestinal barrier is maintained, the microbial ecosystem is reasonably stable, and the gut and immune system are able to interact without unnecessary disruption.

That distinction is important, because the science of the microbiome is fascinating, but it is also still developing. There is much more individual variation than many commercial “gut health” claims suggest, and we should be careful about turning interesting biological mechanisms into conclusions that have not yet been demonstrated in humans.

What I hope you take away from this article

Gut health is important, but it is also an area where the science is often simplified too much.

What I hope you take away from this article is not that there is one perfect microbiome, one food, one probiotic or one test that can tell you whether your gut is healthy. The reality is much more complex.

I want you to remember that:

• There is no single definition of a “healthy gut.” Researchers look at several features, including microbial diversity, stability, function, the intestinal barrier and immune regulation.

• Your gut microbiome is highly individual. Two healthy people can have very different combinations of gut bacteria.

• Function may matter more than individual bacteria. Different microorganisms can perform similar jobs, including producing short-chain fatty acids such as butyrate.

• The gut and the immune system are closely connected. The intestinal barrier and the microorganisms living in the gut constantly interact with immune cells and influence how the body responds to its environment.

• Diet can influence the gut microbiome, but the effects are not always dramatic. Fiber-rich foods, minimally processed foods, Mediterranean-style eating patterns and fermented foods have some of the better human evidence, but they are not magic treatments.

• “Leaky gut” is often oversimplified online. Increased intestinal permeability is a real biological phenomenon, but many commercial tests marketed to measure it are not clinically validated.

• A microbiome association does not automatically mean causation. Diet, medications, body weight, bowel habits and disease itself can all change the microbiome.

• For lipedema, the gut connection is still a hypothesis. We currently do not have evidence showing that an altered gut microbiome causes lipedema or that treating the gut can treat the disease.

• Supporting gut health can still be valuable for overall health. Good nutrition, metabolic health, cardiovascular health and gastrointestinal function matter regardless of whether they directly change lipedema tissue.

For me, that is the most important perspective. We can take gut health seriously without exaggerating what we know. The microbiome is an exciting and rapidly developing field, but good science also means being comfortable with what we do not yet know.

And when it comes to lipedema, that distinction matters. We should remain curious about the possible connection between the gut, immune system, metabolism and adipose tissue, while being equally careful not to turn an interesting hypothesis into a proven explanation before the research is there.

Personally, I think a lot about my own gut health. I know how complex the gut microbiome is, and I also know that there are many things I cannot control. Genetics, medications, previous infections, stress, hormones and countless other factors can all influence what happens in the gut.

But there are also things I can influence.

That is why I try to do what I can to support my gut health through the choices that are actually within my control. I try to eat in a way that supports a diverse and well-functioning gut microbiome, take care of my overall health, stay active, manage stress as well as I can and pay attention to how my body responds.

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I do not expect that this gives me a “perfect” microbiome, because I do not think such a thing exists. I also know that I cannot control every biological process taking place in my body.

For me, it is more about doing what I realistically can, while accepting that there is a great deal I cannot control.

I cannot guarantee the outcome, but I can influence some of the conditions. And personally, doing what is within my control feels important. I do what I can, and then I hope that those choices contribute positively to my health over time.

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The studies are not equally strong. LIPLEG is a large randomized multicentre trial. Several of the other papers are small observational studies, case series or early diagnostic work. I have therefore kept the interpretation close to what the studies actually measured.

4 October, orthorexic eating and body-shape concern

A study in the Journal of Clinical Medicine compared 44 women with lipedema with 44 women without it. The researchers used questionnaires on orthorexic eating, body-shape concern, anxiety and depression. Orthorexic eating refers to an unhealthy preoccupation with eating in a way that is considered healthy, pure or correct.

Women with lipedema scored higher on all four measures. However, when the researchers adjusted the analysis, body-shape concern remained associated with orthorexic eating while lipedema itself did not.

The study therefore does not show that lipedema causes orthorexia. It points instead towards body image as one factor that may be relevant when strict dietary approaches are discussed in this population.

2 October, lipedema reported in an adolescent male

A case report in the Journal of Rehabilitation Medicine described lipedema in an adolescent male after discontinuation of valproate.

Male lipedema is very rarely reported. The authors discuss valproate because the drug can affect weight, lipid metabolism and reproductive hormones, but a single case cannot establish whether the medication, its discontinuation or another factor contributed to the development of lipedema. Puberty and other hormonal changes are also difficult to separate from the timing.

For now, the paper adds another documented male case to a very small literature.

1 October, KU Leuven starts the BIO-LIP project

KU Leuven has launched BIO-LIP, a new project led by Nele Devoogdt. The study plans to include 100 people with lipedema, 50 people with obesity without lipedema and 50 non-obese controls.

Researchers will examine body composition, sensory characteristics, blood markers, physical function and psychological function. The inclusion of an obesity control group is one of the more useful parts of the design. Many early diagnostic studies compare people with lipedema with healthy controls, but a clinically useful marker would also need to distinguish lipedema from obesity.

There are no results yet.

28 September, five blood markers do not distinguish lipedema from controls

Esra Şahingöz Bakırcı and colleagues compared 40 women with lipedema with 36 healthy controls matched for age and BMI. They measured irisin, leptin, adiponectin, resistin and galectin-3 in blood, together with subcutaneous fat thickness on ultrasound.

The women with lipedema had thicker subcutaneous fat, but none of the five blood markers differed significantly between the groups.

This does not rule out biological differences in lipedema tissue. It does show that these five markers, measured in blood, did not provide a simple biochemical signature for the condition.

28 September, French patient organisation challenges the classification of surgery

The Association Maladie du Lipœdème France reported that its president had written to Thomas Fatôme, director-general of the French national health insurance fund CNAM.

The organisation objected to patient information describing liposuction and dermolipectomy for lipedema as aesthetic procedures outside reimbursement while also stating that liposuction may reduce pain and tissue tension. It asked for the wording to reflect the therapeutic purpose of surgery.

No response or policy change had been published by 4 October.

25 September, three lipedema studies presented in Valencia

Three lipedema-related presentations appeared in the programme of the European Society of Lymphology congress in Valencia.

Juan Vázquez and Isabel Forner presented a comparison of flat-knit and circular-knit compression garments. Daniel A. Cespedes, Fátima Sirvent and Isabel Forner presented a prospective cohort study on comorbidities in lipedema. A third presentation, by Isabel Muñoz, Cespedes and Forner, reviewed psychiatric conditions and psychosocial burden in lymphoedema and lipedema.

The programme confirms that the studies were presented, but the abstracts and numerical results were not publicly available at the time of writing. There is therefore not enough information yet to judge the findings.

24 September, small randomized trial of shock-wave therapy

A randomized study in the American Journal of Physical Medicine & Rehabilitation compared extracorporeal shock-wave therapy, complex decongestive therapy and a combination of the two.

Thirty-three people were divided equally between the three groups. After six sessions, all groups improved in leg volume, pain, pressure-pain threshold and quality of life. There were no significant differences between them.

Fat mass decreased within the groups receiving shock waves, but the between-group comparison did not show an advantage over decongestive therapy. With around 11 participants per group and follow-up only two weeks after treatment, the study is too small and too short to establish whether shock-wave therapy offers any additional clinical benefit.

24 September, first clinical observations involving gestrinone

A retrospective case series described women with lipedema who had received gestrinone for endometriosis or fibroids.

The drug was not prescribed to treat lipedema, and the information came from existing medical records. Earlier reviews had found no direct human clinical data on gestrinone in lipedema, so this paper adds the first published clinical observations.

It is still very early evidence. There are no controlled data showing that gestrinone improves lipedema.

23 September, tirzepatide and body composition

A Brazilian retrospective study examined 100 women with lipedema who received compounded tirzepatide for 12 weeks. Fifty followed a lower-dose titration and 50 a standard regimen.

Both groups lost weight and fat mass. Muscle mass, estimated with bioimpedance, fell by 0.7 kg in the lower-dose group and 2.0 kg in the standard group. The researchers also created an exploratory responder definition based on losing at least 5 percent fat mass while keeping muscle loss below 5 percent. Sixty-eight percent of the lower-dose group met that definition compared with 22 percent of the standard group.

The study was not randomized, total drug exposure differed between the groups, and muscle mass was estimated with a method that is sensitive to hydration and other factors. More importantly, the researchers did not measure pain, bruising, heaviness or tenderness.

The study therefore provides body-composition data in women with lipedema, but it does not show that tirzepatide treats lipedema itself.

23 September, AI chatbots tested on lipedema questions

A study in Phlebology gave 25 common lipedema questions to ChatGPT, DeepSeek and Gemini. Three experts then rated the answers.

DeepSeek had the highest proportion rated comprehensive and correct, at 72 percent, followed by Gemini at 64 percent and ChatGPT at 56 percent. Treatment, follow-up and maintenance were among the weaker areas, and the answers varied between sessions.

The study says little about lipedema itself, but it is relevant because patients increasingly use AI systems to interpret medical information. The results show that performance is still inconsistent, especially once questions move from general information into treatment.

21 September, small study proposes preliminary diagnostic thresholds

Erika Mendoza and Felix Amsler examined whether history, pressure-pain testing, ultrasound and skin measurements could distinguish women with lipedema from controls.

The study included 14 women with lipedema and 12 controls. The researchers proposed preliminary thresholds for several measures, including pain at lower cuff pressures, lateral-thigh skin thickness and ankle subcutaneous fat thickness.

The sample is very small. The control group also did not include women with obesity, lipohypertrophy or lymphoedema, which are among the conditions most relevant to differential diagnosis. The proposed thresholds should therefore be treated as candidates for future testing rather than diagnostic criteria.

21 September, review questions the use of BMI alone

A narrative review in Clinical Obesity discusses the limitations of using BMI as the main way of classifying women with lipedema.

BMI reflects weight relative to height but says nothing about where fat is stored. A large amount of fat around the hips and legs can raise BMI without necessarily corresponding to the same amount of visceral fat seen in central obesity.

The reverse is also important. Having lipedema does not protect against visceral obesity, insulin resistance or cardiometabolic disease.

The authors recommend looking at waist distribution, metabolic markers, body composition and muscle mass alongside BMI. The paper is a review and does not contain new patient data.

18 September, Australian study on living with lipedema

Researchers at Macquarie University interviewed 16 people with diagnosed lipedema.

Four broad themes emerged from the interviews. Participants described the constant work involved in managing the condition, restrictions in everyday life, the tension between self-acceptance and social judgement, and the experience of navigating healthcare largely alone.

The researchers also identified 21 subthemes covering symptoms, psychological wellbeing, healthcare experiences and weight stigma.

With 16 participants, the study cannot tell us how common these experiences are. Its contribution is mainly descriptive. It captures parts of living with lipedema that are easily missed when studies focus only on circumference, pain scales and general quality-of-life scores.

15 September, insulin changes do not explain the low-carbohydrate pain result

Julianne Lundanes and colleagues published a secondary analysis of a Norwegian randomized diet trial involving 70 women with lipedema and obesity.

One group followed a low-carbohydrate diet with around 75 grams of carbohydrate per day. The other followed a low-fat diet with around 180 grams. Both diets provided approximately 1,200 kcal per day.

Both groups improved several measures of glucose and insulin metabolism, and the low-carbohydrate group lost more weight. However, changes in glucose and insulin were not associated with changes in pain.

This is useful because improved insulin sensitivity had been suggested as one explanation for the greater pain reduction previously seen in the low-carbohydrate group. The new analysis does not support that explanation.

It does not tell us what caused the difference in pain.

12 September, altered pain processing in lipedema

A study in Pain Medicine compared 59 women with lipedema with 59 women of the same age without it.

A score of 40 or more on the Central Sensitization Inventory was found in 78 percent of the women with lipedema and 8.5 percent of controls. The women with lipedema also had lower pressure-pain thresholds, poorer sleep and poorer quality of life.

Central sensitization refers to increased responsiveness of the nervous system to pain-related input. The findings therefore support the idea that pain processing may be altered in lipedema.

The study cannot show whether this altered pain processing contributes to lipedema pain from the beginning or develops after living with pain over time. The Central Sensitization Inventory is also a questionnaire, not a direct physiological measurement.

10 to 12 September, first national lipedema conference in Canada

The Lipedema Canada Conference took place in Winnipeg and was developed together with the University of Manitoba’s continuing professional development programme.

The conference offered accredited education for clinicians. A separate programme, Doctor Is In, allowed physicians and nurse practitioners to examine people with lipedema alongside experienced clinicians. Organisers reported that all 58 appointments were filled within two hours.

This was not a research study, but it is relevant to clinical education and diagnostic capacity in Canada.

10 September, arm liposuction and shoulder function

Agostino Bruno and Riccardo Foti followed women who underwent circumferential liposuction for lipedema of the arms.

Sixty-eight women completed six months of follow-up. Average shoulder abduction increased from 132.4 degrees before surgery to 154.7 degrees after six months and remained at about that level at 12 months. Pain, heaviness, disability scores and arm circumference also improved.

There was no control group. The study therefore shows improvement after surgery but cannot separate the effect of surgery from rehabilitation and other changes during recovery.

10 September, International Lipoedema Association endorses Lipalgia Syndrome

The board of the International Lipoedema Association voted unanimously to endorse the term Lipalgia Syndrome in place of lipoedema.

The argument is that the traditional name places too much emphasis on oedema and lymphatic dysfunction, while pain is a more consistent clinical feature. Lymphoedema Wales, the Földi Clinic and Klose Training had already adopted the term.

This is an organisational position, not a formal international change in diagnosis. Diagnostic coding and access to treatment remain unchanged.

The association also states that lipedema is not a lymphatic disorder. That claim is stronger than the research literature currently allows, since lymphatic findings vary between studies and between patients.

5 September, Lancet Comment argues for calling liposuction curative

The same issue of The Lancet that published LIPLEG included a Comment by Erich Brenner and Francesca Bonomini arguing for liposuction as a curative treatment.

This was an opinion article, not a second trial.

LIPLEG measured pain, quality of life and safety over 12 months. It did not test whether the underlying disease process had been eliminated, and 12 months is too short to establish whether symptoms can recur later.

The term curative therefore goes beyond what the trial itself showed.

5 September, LIPLEG published in The Lancet

The LIPLEG trial is the strongest study in this month’s update.

Podda, Cornely and colleagues randomized 410 women with stage I to III lipedema at 11 German centres. All had already undergone a period of conservative treatment before being assigned either to liposuction or to continued conservative treatment.

The main outcome was a reduction of at least two points in leg pain after 12 months. This was achieved by 190 of 278 women in the liposuction group, or 68 percent, compared with 10 of 132 women in the conservative group, or 8 percent. Quality of life also favoured surgery.

The study also recorded more adverse events after surgery. Adverse events occurred in 47 percent of the liposuction group and 21 percent of the conservative group. Serious adverse events occurred in 8 percent and 3 percent respectively.

Pain was self-reported and participants knew which treatment they received, which is relevant when interpreting the size of the effect. Still, the difference between the groups was large, and this is the first major randomized multicentre trial to provide this level of evidence for liposuction in lipedema.

Follow-up continues to 36 months. Those results will be important because the current paper tells us what happened after one year, not how durable the effect is over several years.

What changed this month

The main change is the evidence for liposuction. LIPLEG moves the field beyond reliance on observational studies and shows a large difference in pain at 12 months, alongside a higher rate of adverse events.

The drug studies are much less developed. The tirzepatide paper reports changes in weight and body composition, but not in lipedema symptoms. Gestrinone now has published clinical observations, but no controlled evidence as a treatment for lipedema.

The pain literature continues to point towards altered pain processing, although it is still unclear whether this is part of the early disease process or develops after years of chronic pain.

The Norwegian diet analysis is also useful because it removes one proposed explanation. Improved insulin handling does not appear to explain the pain difference previously seen with the low-carbohydrate diet.

Diagnostic research remains early. The five blood markers tested in September did not distinguish lipedema from matched controls, and the small diagnostic measurement study is not ready for clinical use. The BIO-LIP project may provide better data because it includes a proper obesity comparison group.

We still do not have a validated biomarker, a blood test or a clear biological explanation for lipedema. But this month did add stronger evidence in some areas and close off a few weaker assumptions in others.

This distinction matters in lipedema because nutrition advice can quickly become a search for individual foods to add or remove. Turmeric is added because of curcumin, berries because of polyphenols, oily fish because of EPA and DHA. At the same time, sleep, stress, pain, physical activity, other illnesses and the broader dietary pattern may receive much less attention.

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I find it more useful to separate the subject into three levels. The first is the individual food or compound. The second is the dietary pattern repeated over time. The third is the wider lifestyle and living conditions surrounding both. The levels overlap, but the evidence behind them is not interchangeable.

Anti-inflammatory foods are only the first level

Individual foods can contain compounds that influence inflammatory biology. Oily fish provides the long-chain omega-3 fatty acids EPA and DHA. Extra virgin olive oil contains phenolic compounds. Berries contain several classes of polyphenols, while turmeric provides curcuminoids.

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The strength of the human evidence differs considerably between them. EPA and DHA have been studied extensively in humans. For many plant and spice compounds, a larger part of the literature comes from laboratory experiments, small clinical studies or concentrated preparations that bear little resemblance to the amount normally eaten in food.

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That difference matters to me because of my own laboratory background. My master’s research in food science covered inflammation, bioactive peptides and gut health, using simulated gastrointestinal digestion, human intestinal Caco-2 cell models and IL-8 ELISA measurements. Working with these models makes the distance between a biological mechanism and a human health outcome very tangible.

A compound can alter inflammatory signalling in cultured cells without demonstrating that a normal serving of the food containing it reduces pain, improves physical function or changes the course of a disease. Mechanistic evidence can help explain how something might work. It does not automatically establish that it works in everyday life.

This is why I see individual anti-inflammatory foods as inputs into a larger dietary pattern rather than as treatments in themselves.

What the evidence says about an anti-inflammatory diet

The evidence becomes different when researchers study entire dietary patterns.

Mediterranean-style diets are one of the better studied examples. A systematic review and meta-analysis published online in 2025 and in the September 2026 issue of Nutrition Reviews included 33 randomized controlled trials with 3,476 participants. Mediterranean-style interventions reduced hs-CRP, IL-6 and IL-17 compared with control diets, while conventional CRP, IL-10, TNF-alpha and total antioxidant capacity did not change significantly. Subgroup results also varied according to characteristics such as age, intervention duration and cardiovascular disease status.

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Those findings are more informative than simply calling the Mediterranean diet “anti-inflammatory.” Some inflammatory markers changed while others did not, and the effects were not identical across participants.

A smaller randomized trial provides another example. In the AUSMED Heart Trial, people with coronary heart disease were assigned to a Mediterranean or low-fat dietary intervention for six months. Among the 56 participants who completed the trial, the Mediterranean diet produced a significantly lower Dietary Inflammatory Index score than the low-fat diet, but the differences in hs-IL-6 and hs-CRP were not statistically significant.

A related analysis of the same trial found that greater improvement in the Dietary Inflammatory Index correlated with a larger reduction in hs-IL-6, although the sample was small.

Taken together, these studies support the idea that dietary patterns can influence some inflammatory measures. They also show why the word anti-inflammatory should not be treated as an on-off switch.

What you replace matters too

Dietary research has another complication that is often missing from social-media discussions. Changing a diet rarely means adding one food while everything else remains untouched.

If someone begins eating more whole grains, refined grains may decrease. If fish appears more often, it replaces another main course. Increasing legumes, vegetables or nuts changes the proportion of other foods in the diet.

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This means that part of an observed effect may come from what is removed or displaced rather than from the food being added in isolation.

A 2020 systematic review and meta-analysis of randomized trials compared whole grains with refined grains or placebo. The pooled result suggested a small reduction in CRP, with the confidence interval reaching the boundary of no effect. The authors found some additional cardiometabolic differences but did not consider the evidence strong enough to support broad treatment claims for cardiovascular disease. The comparison is informative precisely because it is a replacement comparison, not a study of simply adding one “healthy” food.

That replacement effect is one reason I am cautious when a particular ingredient is credited with the effect of an entire dietary pattern.

What about inflammatory foods?

The same caution is needed when foods are placed on the opposite list and described as inflammatory.

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Ultra-processed food is a useful example. A 2025 cross-sectional analysis of 9,254 adults in NHANES examined ultra-processed food intake as a proportion of total energy intake. Compared with the lowest intake category, some higher categories had a greater adjusted likelihood of elevated hs-CRP, but the association was not a simple stepwise dose-response. Because the study was cross-sectional, it cannot establish that ultra-processed food caused the higher inflammatory marker. Other characteristics associated with the overall dietary pattern may still contribute.

The distinction is important. A habitual diet in which a large proportion of energy comes from ultra-processed food is one research question. Whether eating one processed food on Saturday afternoon causes a meaningful inflammatory state is another.

The same logic works in both directions. A serving of blueberries does not make an otherwise poor dietary pattern anti-inflammatory, and one ice cream does not define an otherwise nutritious diet.

Sleep shows why the wider context matters

Food is consumed by a body that has also slept, moved, recovered and experienced stress. Those factors do not sit in separate biological compartments.

Sleep research provides a particularly useful example because pain and inflammation do not always move together.

In a 2025 randomized crossover study, 39 healthy adults shortened their sleep substantially for two nights. Participants rated some experimental heat and cold pain as more painful after sleep restriction, while the inflammatory plasma markers measured in the study did not significantly change. The authors also noted poor adherence to the intended sleep-restriction condition, which is an important limitation.

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A broader meta-analysis adds a different time scale. It included 35 experimental studies and 887 participants and found that multiple nights of partial sleep deprivation, around 4.3 hours of sleep for at least three nights, were associated with increases in circulating IL-6 and CRP. A single night of total or partial sleep deprivation was not associated with the same inflammatory changes. The paper was published online in 2025 and appears in the 2026 volume of the Journal of Sleep Research.

These findings help illustrate why “I hurt more today” and “my systemic inflammation increased today” are not equivalent statements. Duration, outcome and context matter.

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Stress is relevant, but the evidence has limits

Psychological stress can also affect inflammatory signalling, although it is easy to overextend this literature.

A meta-analysis of 34 laboratory studies found increases in circulating IL-1 beta, IL-6, IL-10 and TNF-alpha following acute psychological stress. CRP did not significantly increase in that analysis.

These were acute experimental stressors. They cannot simply be translated into claims about months of grief, job pressure or caregiving, and they do not establish a lipedema-specific mechanism.

They do, however, reinforce a broader point. Food is only one exposure occurring within a much larger physiological context.

What my own history has made me question

My interest in this subject is also personal.

My lipedema symptoms began around the age of 15, and the physical changes were documented by my general practitioner. My late teens and early twenties also included a serious illness at 18 and a major family bereavement at 20. Around that broader period, my pain became severe enough that I repeatedly sought help from my GP.

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In 2018, while completing my master’s degree in food science, I experienced another particularly difficult period. My stress level was high, and my legs became substantially more swollen and painful.

Between 2021 and 2022, I had four lipedema surgeries involving my legs and arms. The procedures improved important aspects of my condition, particularly pain and mobility, but they did not remove the fact that I continue to live with lipedema through both easier and more demanding periods of life.

Looking backwards, I cannot separate all the variables involved in those changes. Hormones, illness, grief, sleep, activity, diet, pain and stress overlapped. My history cannot demonstrate which factor caused which symptom.

What it did allow me to do was notice patterns.

The factors I repeatedly noticed most strongly in my own body were hormonal changes, high sugar intake and stress. I treat those as observations from one person rather than evidence that the same triggers apply to everyone with lipedema.

My tolerance hypothesis

One observation has become particularly interesting to me.

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When I sleep well, move regularly, eat well, recover and experience relatively little stress, I often seem to tolerate more. I can have chocolate, cake or ice cream without noticing an obvious flare in my symptoms.

During periods of greater stress, grief, illness or poor recovery, the same foods can appear to bother me more.

Before turning that into a biological theory, several simpler explanations have to be considered. Poor sleep can increase pain sensitivity. Stress can change appetite, eating behaviour and pain perception. Menstrual phase, portion size, earlier meals, physical activity and expectations may differ between occasions.

After those explanations are considered, I think one further question is reasonable. Could the total physiological load a person is carrying alter the threshold at which another exposure becomes noticeable?

At present, I regard that as a personal hypothesis. It has not been demonstrated as a mechanism in lipedema.

That distinction allows lived experience to generate questions without allowing it to become proof.

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Is lipedema itself an inflammatory disease?

This is where the discussion becomes more complicated.

Inflammation is frequently mentioned in lipedema, sometimes as though the condition has already been established as a uniform systemic inflammatory disease. The available research does not support such a simple conclusion.

A 2023 tissue study examined subcutaneous adipose tissue from 32 women with lipedema and 14 age- and BMI-matched controls. The researchers found larger adipocytes in affected thigh tissue and a trend toward increasing fibrosis with stage. Macrophage markers were increased in affected thigh tissue, and the macrophage profile showed a transient shift toward an M2-like phenotype. Later stages showed features consistent with a more pro-inflammatory profile.

This is a local tissue finding. It does not automatically tell us what is happening systemically.

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Blood studies provide another perspective. A 2026 retrospective study compared 78 women with lipedema, 76 women with obesity without lipedema and 75 normal-weight controls. CRP and erythrocyte sedimentation rate were higher in both the lipedema and obesity groups than in normal-weight controls, while there was no significant difference between the lipedema and obesity groups for those measures. BMI was substantially higher in both groups than in the normal-weight controls, which makes adiposity an important confounder.

A much smaller study comparing 13 women with lipedema with 13 age- and BMI-matched controls also found differences in circulating inflammatory and oxidative-stress-related proteins, alongside metabolic differences.

The tissue findings and blood findings therefore answer different questions. They also show why it is premature to describe every person with lipedema as being in one uniform systemic inflammatory state.

Nothing in these studies demonstrates that eating individual anti-inflammatory foods treats lipedema.

Testing my own assumption about lipedema and obesity

I also think it is important to test the assumptions we bring into a subject.

I started with the belief that lipedema is biologically distinct from ordinary obesity. There are good clinical reasons to distinguish them, and reducing lipedema to excess weight has contributed to misunderstanding and weight stigma.

At the same time, that starting position cannot be protected from evidence.

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Lipedema and obesity can coexist. Some local tissue findings appear different from patterns commonly described in obesity, while some systemic inflammatory measurements overlap considerably. BMI, adiposity, disease stage and tissue location can all influence what researchers measure.

The more useful research question is therefore which biological features are genuinely specific to lipedema, which overlap with obesity and which are influenced by other characteristics of the people being studied.

Current evidence does not settle that question.

Why the pyramid has three levels

The pyramid accompanying this article is intentionally not a ranking of which factor has the largest biological effect.

At the top are single foods, where evidence varies by compound, dose and outcome.

The middle represents the dietary pattern, including the foods eaten repeatedly and what those foods replace.

The broad base represents lifestyle and living conditions. This includes sleep, stress, movement, pain, other illnesses, finances and access to care.

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The base is wider because it covers more of the environment in which a person lives, not because I am claiming that lifestyle has a mathematically larger effect than diet. Studies of sleep, diet, stress and other exposures use different populations and outcomes and cannot simply be placed on one common effect-size scale.

Time runs underneath the entire pyramid because these exposures are repeated over months and years.

I also include the tolerance idea separately and label it as my observation rather than an established mechanism.

Sustainability matters more than collecting anti-inflammatory ingredients

This broader model also changes what an anti-inflammatory lifestyle means.

Lifestyle is not only a collection of personal decisions. Pain can limit movement. Another illness can disrupt sleep and recovery. Financial circumstances shape access to food, treatment and exercise. Work and caregiving can reduce the time available for rest. Access to healthcare differs greatly between people and countries.

For someone with lipedema, a sustainable approach therefore has to fit inside a real life rather than an idealized health routine.

Needs can also change. A period of grief, illness or prolonged sleep loss may require more recovery and fewer additional demands than a stable period. The same person may have different capacity at different points in life.

This does not make one piece of cake a failure, and it does not make a spoonful of turmeric a treatment.

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Individual foods can contribute useful nutrients and bioactive compounds. Dietary patterns provide a broader nutritional exposure over time. Sleep, stress, movement, pain, other illnesses and living conditions add further context. In lipedema, the role of inflammation itself remains an evolving research question, which makes it especially important to distinguish mechanistic plausibility, personal experience and evidence from human studies.

That wider view is the reason I no longer think “Which anti-inflammatory food should I add?” is the most useful question on its own.

About the author

CarinaW is the founder of LipedemaScience. She has a bachelor’s degree in Human Nutrition and a master’s degree in Food Science from the Norwegian University of Life Sciences. Her laboratory background includes research on inflammation, bioactive peptides and gut health, using simulated gastrointestinal digestion, human intestinal Caco-2 cell models and IL-8 ELISA measurements. She has also worked with food microbiology and whole-genome sequencing, including as a laboratory manager, and is a co-author of peer-reviewed research. Diagnosed with lipedema in 2012, she combines scientific training with long-term lived experience while keeping personal observations separate from research evidence.

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Because lipedema does not exist in isolation. It affects adipose tissue, but the symptoms you experience are influenced by the condition of the whole body.

Pain, swelling, heaviness and tissue sensitivity can vary considerably even when the amount of lipedema tissue has not changed. That tells us that symptoms are shaped by more than fat mass alone. Hormonal changes, sleep, stress, physical activity, metabolic health, inflammation, circulation, lymphatic function and other health conditions can all influence how the body feels and responds.

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Caring for your overall health therefore matters for several reasons:

• Your inflammatory environment matters. Lipedema tissue shows changes involving adipocytes, immune signalling, blood vessels and extracellular matrix. Conditions elsewhere in the body that increase systemic inflammatory signalling may affect how symptomatic you feel.

• The nervous system influences pain. Stress does not mean lipedema is psychological. But the nervous system can amplify or dampen pain signals, and prolonged stress can influence immune, hormonal and metabolic processes.

• Muscle and movement support function. Maintaining muscle strength, cardiovascular fitness and mobility can make everyday movement easier and support long-term metabolic and vascular health.

• Metabolic health still matters. Having lipedema does not protect someone from insulin resistance, obesity, cardiovascular disease or other metabolic conditions. Improving those factors may benefit health even if some lipedema tissue remains disproportionately distributed.

• Sleep affects almost everything. Poor sleep changes appetite regulation, pain sensitivity, glucose metabolism, stress hormones and immune signalling.

• Hormones can influence symptoms. Many women describe symptom changes around puberty, pregnancy, the menstrual cycle or menopause, although the mechanisms are still being investigated.

• Nutrition supports the whole system. Food is not a cure for lipedema, but adequate energy, protein, micronutrients, fibre and an overall nutritious dietary pattern support muscle, immune function, metabolic health and recovery.

• Your body is dynamic. The same person may tolerate heat, exercise, certain foods, long periods of standing or hormonal changes differently from one month to another. The surrounding physiological state matters.

This is also why I think it can be limiting to ask only, “How do I treat my lipedema?” A broader question is often more useful:

“How can I make the rest of my body as healthy, resilient and well-functioning as possible while living with lipedema?”

That does not mean blaming yourself for symptoms, and it does not mean that lifestyle can eliminate lipedema. It means recognising that the affected tissue is part of a much larger biological system. Supporting that system can improve health, function and potentially symptom burden, even when the underlying predisposition remains.

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Remember, you can listen to all my articles as podcasts. Just open the Substack app on your phone, go to the LipedemaScience article you want to listen to, and tap the play button in the top-right.

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That probably sounds contradictory. Refined sugar, for example, is something I identified as a personal trigger very early, around the time I was diagnosed in 2012. I noticed that there were occasions when eating a lot of refined sugar seemed to be followed by more pain and sensitivity in my tissue. I did not learn this from a lipedema community, because I did not have one at the time. It was simply something I noticed by paying attention to my own body.

Yet even something I consider a relatively consistent trigger does not affect me identically every time. There are periods when my body seems more sensitive and I notice relatively small deviations from my usual habits. There are other periods when I am sleeping well, eating well, exercising, feeling happy and experiencing little psychological stress, and I seem able to tolerate considerably more without noticing the same increase in symptoms.

For years I thought about this mainly as a personal observation. Now, with what we know about stress physiology, pain, immunology and neuroendocrinology, I think there is a much more interesting way of looking at it. Perhaps we should stop thinking about our bodies as static systems in which one input reliably produces one output.

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The chocolate cake is approximately the same chocolate cake. The body eating it is not necessarily in the same physiological state.

This distinction matters when we talk about lipedema triggers because people with lipedema are exposed to an enormous number of claims about what causes inflammation. Sugar causes inflammation. Carbohydrates cause inflammation. Stress causes inflammation. Estrogen causes inflammation. A certain food causes swelling. Another food causes pain. Sometimes these claims are based on research, sometimes they are extrapolated far beyond the research, and sometimes they are based almost entirely on personal experience.

I think there is another possibility worth discussing. A trigger may not operate independently of everything else happening in the body. Its effect may depend partly on the physiological environment into which it arrives.

We can see this dynamic biology in other conditions

This idea becomes easier to understand when we temporarily leave lipedema behind.

Consider herpes simplex. After someone becomes infected with herpes simplex virus, the virus can remain latent in sensory neurons. During the months or years when that person has no outbreak, the virus has not disappeared. The underlying susceptibility remains, but its clinical expression changes.

Psychological stress has been studied as one factor associated with herpes recurrence. A meta-analysis of prospective studies found a statistically significant, although relatively small, association between psychosocial stress and subsequent symptomatic HSV recurrence. Importantly, the authors also found that psychological distress appeared more strongly associated with recurrence than exposure to stressful events themselves.

This does not make herpes a psychological disease. Stress does not create HSV, and relaxation does not eliminate a latent viral infection. What it illustrates is that an existing biological vulnerability can behave differently depending on the environment in which it exists.

Psoriasis gives us another, more complicated example. It is an immune-mediated disease involving genetic susceptibility and dysregulated immune signaling. People with psoriasis commonly report stress as relevant to their disease, but the research is less definitive than this is sometimes presented. A systematic review and meta-analysis including 39 studies and more than 32,000 patients found that many people reported preceding stressful events, but much of the evidence was retrospective and methodologically limited. The authors concluded that convincing evidence for a strong relationship between preceding stress and psoriasis onset or exacerbation was lacking.

I actually think this uncertainty makes psoriasis a more useful comparison, not a less useful one. Biology does not require us to choose between “stress causes psoriasis” and “stress has absolutely nothing to do with psoriasis.” A disease can have a clearly biological pathology while its expression may still interact with sleep, stress physiology, immune regulation, treatment, infection and many other factors.

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Alopecia areata provides another example of this type of interaction. It is an autoimmune disease involving disruption of the immune privilege of the hair follicle. Researchers have investigated how stress-associated mediators, including corticotropin-releasing hormone and substance P, might interact with immune and follicular biology. That does not establish emotional stress as the cause of alopecia areata, but it illustrates how closely the nervous, endocrine and immune systems can communicate.

The skin itself provides particularly interesting evidence. An evidence-based review of 21 studies found that psychological stress can affect epidermal barrier function through HPA-axis activation and local and systemic stress-hormone signaling, with changes including reduced epidermal lipid production, lower stratum-corneum hydration and increased transepidermal water loss. An earlier human experiment followed students through periods of lower stress and final examinations and found that worsening perceived stress occurred alongside impaired recovery of the skin permeability barrier. When stress subsequently declined, barrier recovery improved again.

These examples involve very different biological processes. Herpes is not psoriasis. Psoriasis is not alopecia. Alopecia is not lipedema. We should therefore not borrow mechanisms from one disease and pretend they have been demonstrated in another.

What they do show is something more fundamental: disease expression takes place inside a changing biological system.

Your body is constantly adapting

One useful scientific concept for understanding this is allostasis.

Homeostasis is often described as the body’s tendency to maintain internal stability. Allostasis expands that idea by recognizing that maintaining stability often requires change. Heart rate changes when we exercise. Cortisol follows a daily rhythm and responds to challenges. Immune activity changes when we encounter an infection. Energy metabolism changes depending on whether we have eaten, fasted, exercised or slept.

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The body survives precisely because it is able to adapt.

The neuroscientist Bruce McEwen described allostasis as “stability through change.” He also developed the concept of allostatic load, the physiological burden that can arise when adaptive systems are activated repeatedly, fail to switch off efficiently, or become poorly coordinated over time. These adaptive systems involve the nervous, endocrine and immune systems rather than one isolated “stress pathway.”

I find this framework much more useful than the language of being either “inflamed” or “not inflamed.”

At any particular moment, your physiology reflects what has been happening before that moment. How did you sleep last night? What phase of your menstrual cycle are you in? Have you recently been ill? Are you recovering from hard exercise? Have you eaten enough? Are you under sustained psychological pressure? Are you experiencing pain? Has that pain been present for years?

None of these questions gives us a single measurement of “inflammation.” Together, however, they illustrate why the physiological background against which we experience a potential lipedema trigger is continuously changing.

Why the same lipedema trigger may feel different

Imagine the same woman during two different weeks.

During the first, she has been sleeping well, moving regularly, eating normally and feeling psychologically well. Her life is relatively calm and her body is recovering adequately between periods of activity.

Several weeks later, she has slept badly for five nights. Work is unusually stressful. She is worried about something in her personal life. Her normal exercise routine has disappeared because she is exhausted. She happens to be in a different hormonal phase and may also be fighting a minor infection without realizing it.

On Saturday evening during both periods, she eats the same meal she personally associates with increased lipedema symptoms.

It is tempting to think of the meal as the experiment and everything else as background noise. Physiologically, everything else may be part of the experiment.

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This is where I think the idea of a response threshold becomes more useful than thinking about triggers as switches. The nervous system, HPA axis, endocrine system, immune system, metabolism and pain-processing systems are continuously interacting. A stimulus arriving when several of these systems are already being challenged may not necessarily be experienced in the same way as that stimulus arriving during a period of recovery and relative stability.

That does not mean that we can say someone has accumulated a “cytokine overload” until a piece of cake pushes them over an inflammatory threshold. Cytines do not behave like water filling a bucket. Inflammation is an extraordinarily complicated network involving immune cells, cytokines, chemokines, vascular signaling, lipid mediators, endocrine signaling and neural regulation. Different inflammatory conditions also involve different pathways. The IL-17-dominated biology relevant to psoriasis cannot simply be transferred to lipedema, just as antiviral immune surveillance in herpes cannot be treated as equivalent to inflammation in adipose tissue.

This distinction is particularly important because the inflammatory phenotype of lipedema itself remains incompletely characterized. We do not currently have evidence demonstrating that stress creates a particular inflammatory state in lipedema tissue that subsequently makes sugar, salt or another proposed trigger more inflammatory.

The threshold model is therefore a framework for thinking, not an established lipedema mechanism.

Sometimes what changes may be pain, not inflammation

There is another possibility that I think is particularly important for lipedema.

When my tissue becomes more painful after a stressful period, my intuitive interpretation may be that my lipedema has become more inflamed. But pain cannot tell me how much inflammation is present in my adipose tissue.

Pain is also influenced by the nervous system, and pain sensitivity itself is dynamic. Sleep deprivation, psychological stress, previous pain and central sensitization can influence how sensory information is processed. The same peripheral stimulus does not necessarily produce the same subjective experience under every physiological condition.

This has become especially interesting because new lipedema research published in 2026 has begun examining central sensitization directly. A cross-sectional study published this summer compared women with lipedema with healthy controls and investigated central sensitization, pressure-pain thresholds and psychosocial variables. A second case-control study published in Pain Medicine in September 2026 similarly examined central sensitization alongside pain, sleep and quality of life in women with lipedema.

These studies do not show that the nervous system causes lipedema, nor do they establish the direction of the relationship. Years of painful peripheral input could potentially influence central pain processing, altered processing could contribute to symptom severity, or several processes could coexist.

But they make one point increasingly difficult to ignore: variation in lipedema pain does not necessarily mean that the adipose tissue itself has undergone an equivalent change in inflammation.

That is important when interpreting our own triggers. If something appears to produce more pain during a difficult month than during a good month, several things could have changed. Inflammation is one possibility. Pain sensitivity is another. Sleep, hormonal state, physical activity and psychological stress may be interacting with both.

The body works through feedback loops, not isolated pathways

The more I learn about physiology, the less useful I find the traditional separation between the “physical” and the “mental.”

This does not mean that disease is created by our thoughts. It means that thoughts, emotions and psychological experiences occur within a biological organism.

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A stressful experience can activate the sympathetic nervous system and HPA axis. Hormones released through those systems can interact with immune cells. Immune mediators can signal back toward the brain. Pain can disturb sleep. Poor sleep can increase pain sensitivity. Persistent symptoms can create psychological stress, which can then alter sleep and behavior further.

The direction is therefore rarely simply brain to body or body to brain. It is reciprocal.

This is why chronic disease can create feedback loops. Someone with psoriasis may become psychologically distressed because their skin disease is worsening, while stress-related physiology may simultaneously interact with processes relevant to their skin. Someone experiencing recurrent herpes may become anxious about another outbreak, while stress itself is associated with recurrence. Chronic pain can interfere with sleep, and insufficient sleep can subsequently increase pain sensitivity.

None of this means the original disease was caused by the person’s psychological state.

And this distinction matters enormously to me, because otherwise the conversation about stress and chronic disease can become surprisingly cruel.

This is what holistic means at LipedemaScience

LipedemaScience has an academic approach. When I read a paper, I want to know what was actually measured. I want to know how many participants were included, whether there was a control group, whether the study was observational or experimental, whether researchers measured inflammation or merely asked about symptoms, and whether an association is being quietly transformed into causation.

I also think holistically.

Those positions are not contradictory.

For me, holistic medicine does not mean abandoning biology for intuition or accepting every alternative explanation because it sounds plausible. It means recognizing that lipedema does not exist inside an isolated pair of legs.

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Lipedema tissue exists inside a human being with a nervous system, immune system, endocrine system, lymphatic system, cardiovascular system, muscles, gastrointestinal tract and brain. That person sleeps, eats, exercises, menstruates, ages, becomes ill, recovers, experiences relationships, goes through grief and excitement, changes jobs, travels, worries, laughs and adapts continuously to the environment around her.

All of those systems communicate.

This is also why I am interested when two people with lipedema report completely different experiences rather than assuming that one of them must be wrong. One woman may eat carbohydrates without noticing any difference in her symptoms, while another consistently believes that certain carbohydrate-rich foods affect her. One woman may thrive on high-intensity exercise while another finds that the same type of training temporarily aggravates her symptoms.

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Even the same woman may respond differently at different times.

That does not mean every perceived trigger has a biological mechanism. Human beings are exceptionally good at finding patterns, including patterns that are not really there. But personal observations can still generate useful questions. The scientific task is then to investigate whether those observations correspond to measurable biology.

Why this changes how I think about lipedema management

For me, this perspective has gradually changed the question from What should I eliminate? to Under what conditions does my body function well?

Those are very different approaches.

The first can easily lead to an increasingly narrow life. If every episode of pain requires us to identify something we ate, did or failed to do, the list of potential enemies becomes enormous. Food becomes dangerous. Exercise becomes something we worry about doing incorrectly. A stressful week becomes evidence that we have failed to regulate our nervous system.

The second approach creates curiosity.

If my lipedema symptoms increase, I can look at the broader context. Have I been sleeping badly? Has something hormonal changed? Am I unusually stressed? Have I changed my training? Have I recently been ill? Have several things changed simultaneously?

Sometimes I may identify a useful pattern. Sometimes there will be no obvious explanation.

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That uncertainty is part of living in a biological system rather than a laboratory.

It is also why I promote well-being over guilt at LipedemaScience. Understanding that stress can affect physiology should never become another instruction telling women with lipedema that they need to be perfectly calm. Nobody chooses every stressor in their life. A psoriasis flare does not mean someone failed to meditate. A herpes outbreak is not evidence of poor nervous-system regulation. Alopecia is not caused by insufficient positive thinking. And an increase in lipedema pain during a difficult period does not mean you have failed to manage your disease.

There will be periods when you exercise less than you wanted. There will be nights when you sleep badly. There will be foods you eat because you enjoy them, even if they are not nutritionally perfect. There will be difficult relationships, demanding jobs, illness, travel, celebrations and periods when simply getting through the week takes priority over optimizing every aspect of your health.

That is life, not failure.

I will therefore never tell you exactly how you have to live with lipedema. My role with LipedemaScience is different. I want to give you enough knowledge to understand the biology, distinguish evidence from speculation and recognize where the science still has enormous gaps. I will share my own experiences as one person who has lived with lipedema for almost 15 years, but I do not expect your body to behave exactly like mine.

Your journey is yours.

What I hope the science gives us is a better way of interpreting that journey. The body is not a machine waiting for one wrong food or one stressful day to break it. It is a dynamic biological system, continuously adapting to what came before and what is happening now.

Perhaps that is one reason our triggers sometimes seem so inconsistent. The trigger may look the same.

The biological context in which it arrives is not.

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If you have seen the headlines, you may be wondering which findings could change care and which are still early clues. That is the question I want to answer in this September 2026 research roundup. I have brought the developments together in one place, explained what each study actually found, and looked at what remains uncertain. Some results are genuinely encouraging. Others are reminders that an interesting observation is the beginning of a research question, not its answer.

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The first is very personal: I simply don’t think it would be sustainable for me. I’m a foodie. I love discovering different cultures through their cuisines. Going to restaurants is genuinely one of my hobbies. Food is pleasure, curiosity, tradition and social connection for me, and I don’t want to build a way of eating that makes me feel restricted from participating in those things.

But there is also a nutritional reason.

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Animal foods can be extraordinarily nutritious. Fish, eggs, meat and dairy can provide high-quality protein and important vitamins, minerals and fatty acids. I eat animal foods myself, and this is not an argument against them.

But plants bring things to the table that meat simply does not.

Plants provide an enormous variety of polyphenols, carotenoids and other bioactive compounds. They are also where we get something I think deserves much more attention when we talk about nutrition and lipedema:

Fiber.

And fiber is fascinating, because it reminds us that food is much more complicated than calories, protein, carbohydrates, fat, vitamins and minerals.

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As a food scientist, this is something I find particularly interesting. When you work with food in the laboratory, you quickly realise that foods are incredibly complex biological matrices. We often reduce nutrition to numbers because numbers are easy to communicate: 30 grams of protein, 500 calories, 10 grams of carbohydrate. But there are many components in food that influence physiology without fitting neatly into the usual macro- and micronutrient conversation.

Fiber is one of them.

Fiber is not just something that makes you poop

Dietary fiber is essentially a collection of carbohydrates and related compounds that resist digestion in the small intestine. Instead of being completely broken down and absorbed there, they continue into the large intestine.

And this is where things become interesting.

Some fibers contribute bulk and water to the stool. Others form viscous gels. Some are readily fermented by our intestinal microbes, while others are fermented much less. Different fibers therefore have different physiological effects.

This is why I don’t particularly like talking about “fiber” as though it were one single substance.

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Cellulose, pectins, beta-glucans, resistant starches, inulin and psyllium are not physiologically identical. In the same way that we wouldn’t describe all fats as having exactly the same biological effects, we shouldn’t assume that all fibers behave identically either.

That is also one reason I prefer thinking about diversity of fiber-containing foods rather than simply trying to hit a number on a nutrition app.

Your bacteria can eat what you cannot

One of the coolest things about fiber happens after it reaches the colon.

We cannot digest certain fibers ourselves, but some of the microorganisms living in our intestine can.

When gut bacteria ferment these carbohydrates, they produce metabolites including the short-chain fatty acids acetate, propionate and butyrate. Butyrate is particularly interesting because colon cells can use it as an important energy source, and short-chain fatty acids are involved in intestinal barrier function, immune signalling and metabolic regulation.

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Human intervention studies show that dietary fibers can modify the gut microbial ecosystem and influence short-chain fatty-acid production, although the response depends considerably on the type of fiber and the individual microbiome.

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The lipedema landscape was completely different then. I did not know anyone else with the condition, and social media was not filled with lipedema accounts telling me what to eat, which supplements to take, how to exercise, or which symptoms were supposedly caused by which mechanism. That was isolating, but looking back, I think there was also an advantage to it. I had to pay attention to my own body rather than learning what I was supposed to experience from other people.

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I started recognizing patterns quite quickly. Hormones were already considered relevant to lipedema, and my GP changed my contraception to one without estrogen. I also noticed that refined sugar seemed to trigger my symptoms. I still have old messages to family and friends where I described these reactions, long before I knew whether anyone else with lipedema experienced the same thing. I did not have a theory about glucose, insulin, inflammation or adipose tissue. I simply knew that when I ate certain foods, my body sometimes felt different afterward.

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Over the following years, stress became another pattern that was difficult for me to ignore. Some of the periods when my lipedema seemed to progress, and some of the periods when I experienced more symptoms, were also periods of considerable psychological stress. At other times, when I was sleeping well and life felt relatively calm, my body seemed less reactive. I could tolerate more, including some of the things I otherwise regarded as triggers.

I want to be careful with that observation because this is exactly where personal experience can easily become pseudoscience. I cannot look back at a stressful period of my life and know that my inflammatory cytokines increased. I cannot know whether stress caused my lipedema to progress, whether it increased pain without changing the underlying tissue, or whether several things were happening at the same time. Pain is not a measurement of inflammation, and feeling swollen or sensitive does not tell me what happened to IL-6, TNF-α or CRP.

What I can say is that stress has consistently mattered to how I experience my condition. It matters enough that today I consider stress management part of my own lipedema management, together with food, exercise, sleep and paying attention to hormonal changes. I have also changed what stress management means to me. It is less about doing a particular breathing exercise and more about how I structure my life.

I say no much more often than I used to. I pay attention to which people and activities leave me depleted and which give me energy. I care considerably less about satisfying other people’s expectations. If something repeatedly creates unnecessary stress, I am much more willing to remove myself from it rather than continually asking myself to cope better with it. LipedemaScience is an interesting example of the opposite. I can spend hours reading papers and working on this platform without experiencing it as draining. It gives me energy, and I want to keep it that way. I want LipedemaScience to fit into my life sustainably rather than becoming another source of chronic pressure.

For years, I did not have the scientific language for any of this. Now that “nervous system regulation” has become such a popular subject online, however, I wanted to understand whether there is actually biology behind what I have experienced. There is, but it is considerably more specific and considerably less magical than social media often makes it sound.

The nervous and immune systems are connected

The nervous system does not sit separately from the immune system. Communication between the two is a well-established area of physiology, and one of the best characterized examples is the inflammatory reflex and the cholinergic anti-inflammatory pathway associated particularly with the work of Kevin Tracey and colleagues.

Early experiments showed that electrical stimulation of the vagus nerve could inhibit production of pro-inflammatory cytokines, including TNF, during an inflammatory challenge. Subsequent research helped establish a more complicated neuroimmune circuit involving vagal signaling, the splenic nerve and immune cells. Acetylcholine signaling through the α7 nicotinic acetylcholine receptor is an important component of this pathway and can inhibit intracellular inflammatory signaling and cytokine production.

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This work matters because it demonstrates something fundamental: neural activity can influence immune activity. The brain can receive information about inflammation, and neural circuits can participate in regulating the inflammatory response.

This is no longer purely animal physiology. Vagus nerve stimulation has subsequently been investigated in people with inflammatory diseases, including rheumatoid arthritis. Implantable devices provide controlled electrical stimulation to the vagus nerve, allowing researchers to test whether manipulating this pathway can influence inflammatory disease activity in humans.

But this is also where we need to make the first important distinction. Evidence that an implanted medical device delivering calibrated electrical impulses to the vagus nerve can influence an inflammatory pathway does not mean that meditation, slow breathing, cold exposure or a “vagus nerve exercise” has the same effect. The existence of the biological pathway establishes the mechanism. Each proposed method of manipulating that pathway still needs its own evidence.

Chronic stress can influence inflammatory regulation through another route

The vagus nerve is not the only connection between psychological state and immune function. Chronic stress also interacts with the immune system through the hypothalamic-pituitary-adrenal axis, or HPA axis.

Cortisol is often discussed online as though it were simply an inflammatory stress hormone that we should try to lower. Physiologically, that is an oversimplification. Cortisol is an important regulator of the immune response and normally has substantial anti-inflammatory activity. One of the more interesting findings from stress research is that prolonged psychological stress may alter how effectively immune cells respond to cortisol.

Research by Sheldon Cohen, Gregory Miller and colleagues has investigated what is often described as glucocorticoid resistance. With prolonged stress exposure, immune cells can become less sensitive to glucocorticoid signaling. The important consequence is not simply “more cortisol equals more inflammation.” Rather, one of the body’s mechanisms for controlling an inflammatory response may become less effective.

This relationship has been studied using experimental viral-challenge models, not simply questionnaires asking people whether they feel stressed. In these studies, participants were deliberately exposed to respiratory viruses and subsequently monitored. Chronic stress and impaired glucocorticoid sensitivity were associated with a less well-controlled inflammatory response.

This provides a biologically plausible explanation for something many people intuitively recognize: prolonged stress is not simply an unpleasant psychological experience. It can have physiological consequences. What it does not establish is that chronic stress specifically increases inflammation within lipedema tissue or causes lipedema to progress. We do not currently have the lipedema-specific experiments required to make that conclusion.

Lipedema adds another nervous-system question: pain

The nervous system becomes particularly relevant to lipedema when we move from inflammation to pain. Pain is one of the defining clinical characteristics of lipedema, yet the biological explanation for that pain remains incomplete.

Historically, several mechanisms have been proposed, including pressure within expanding tissue, altered microvasculature, inflammation and nerve abnormalities. Small-fiber neuropathy has also been discussed, although the evidence has not consistently supported it as the primary explanation. In 2017, Erich Brenner argued that the pain characteristics of lipedema were more compatible with mechanical allodynia involving Aβ fibers and potentially tactile C fibers than with direct small-fiber nerve damage.

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More recent research has shifted some of the attention toward central pain processing. A case-control study published in Pain Medicine in September 2026 compared 59 women with lipedema with 59 age-matched healthy controls. The researchers assessed several dimensions of pain rather than simply asking whether participants experienced painful tissue. Women with lipedema had higher pain intensity and Central Sensitization Inventory scores, more neuropathic pain characteristics and lower pressure-pain thresholds.

This is important because central sensitization describes increased responsiveness within the central nervous system to sensory input. In practical terms, the nervous system can become more sensitive to signals arriving from the body, contributing to amplification or persistence of pain.

It is equally important not to reverse the direction of the evidence. These studies do not demonstrate that central sensitization causes lipedema. If painful peripheral tissue repeatedly sends nociceptive signals to the nervous system over many years, altered central pain processing could potentially develop as a consequence of persistent pain. Alternatively, differences in pain processing might contribute to the severity of symptoms. Both processes could also occur simultaneously.

We therefore have increasingly interesting evidence that the nervous system is involved in the experience and processing of lipedema pain. That is different from demonstrating that nervous-system dysfunction produces the abnormal adipose tissue, vascular changes or other underlying characteristics of lipedema.

What does this mean for inflammation in lipedema?

This is the point at which I think the language needs to become particularly careful.

There is good evidence that the nervous system can regulate inflammatory processes. There is evidence that chronic psychological stress can alter immune regulation. There is evidence connecting sleep disturbance with inflammatory markers such as CRP and IL-6. There is also emerging lipedema-specific evidence that pain processing may be altered.

What we do not yet have is a study showing that psychological stress increases inflammatory activity specifically within lipedema tissue. Nor do we have a clinical trial demonstrating that reducing stress or increasing vagal activity lowers lipedema-specific inflammation or slows progression of the disease.

Those missing experiments matter.

If I experience more pain during a stressful month, there are several possible explanations. Inflammatory signaling could have changed. My pain-processing system could have become more sensitive. Poorer sleep could have affected pain thresholds and immune function. My physical activity might have changed. Hormonal or metabolic factors might also be involved. Most likely, biology does not respect the neat categories we use to describe it, and several systems interact.

This is why I am comfortable saying that the nervous system matters to the inflammatory environment of the body, including in someone who happens to have lipedema, while remaining much more cautious about saying that “nervous-system dysregulation causes lipedema inflammation.” The first statement rests on established human physiology. The second requires lipedema-specific evidence that we do not yet have.

Can we actually change this through “nervous system regulation”?

One of the most interesting experiments in this area was published by Paul Lehrer and colleagues in 2010. Researchers induced a temporary inflammatory response in healthy volunteers using bacterial endotoxin and examined whether heart-rate-variability biofeedback could alter the response.

The study was tiny, involving only 11 participants, but its findings are useful because they illustrate how easily different physiological outcomes can be confused. Participants trained in HRV biofeedback were better able to maintain heart-rate variability during the inflammatory challenge. In other words, they altered part of their autonomic response.

What they did not do was suppress the inflammatory cytokine response. The intervention affected autonomic physiology during experimentally induced inflammation, but the measured increase in pro-inflammatory cytokines remained.

That distinction is central to understanding the current evidence. Increasing HRV is not synonymous with reducing inflammation, and neither is synonymous with improving lipedema.

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Another controlled study in young athletes provides a similarly useful caution. Focused breathing and HRV-biofeedback training did not produce the expected significant improvement in measured vagally mediated HRV. An intervention can make someone feel calmer or provide other psychological benefits without necessarily creating the physiological change that is being claimed for it.

Meditation and yoga have somewhat broader research literatures. Meta-analyses have reported changes in some inflammatory markers, particularly CRP, but results for IL-6, TNF-α and other cytokines are less consistent. Studies also differ substantially in population, duration, intervention and methodological quality. These practices may have value for stress, sleep, mobility, pain coping and quality of life without requiring us to claim that they are directly switching off inflammation through the vagus nerve.

Cold exposure is further down the evidence hierarchy. There are interesting experimental findings, including studies combining breathing, meditation and cold exposure, but the evidence is nowhere near sufficient to recommend cold exposure as a treatment for lipedema inflammation.

What I actually take from the science

After reading this literature, I have not changed my mind about stress being important in my own lipedema management. If anything, I take it more seriously. What has changed is how precisely I think about it.

I no longer need to explain every improvement I experience as “lower inflammation.” Stress can influence sleep, pain sensitivity, autonomic activity, endocrine signaling, immune regulation, food choices, movement and recovery. All of those can affect how I feel. Trying to reduce that entire network to a single cytokine or to the state of my vagus nerve probably makes the biology less accurate rather than more understandable.

It also changes what I prioritize. If the objective is to support health and reduce chronic inflammatory burden, some of the strongest evidence still belongs to interventions that are far less fashionable than nervous-system hacks: adequate sleep, regular physical activity, good metabolic health, nutritious food, avoiding smoking, and addressing persistent psychological stress when it becomes a problem. If meditation, slow breathing, yoga or HRV biofeedback helps someone sleep better, manage pain or reduce perceived stress, that can be valuable without pretending that we know it is reversing lipedema inflammation.

For me personally, stress management has become even broader than that. It means recognizing when something is repeatedly draining me and deciding whether it needs to remain in my life. It means not automatically saying yes. It means spending more of my time on work and people that give me something back. It means taking the signals from my body seriously without automatically assuming that I know the molecular explanation for them.

In some ways, that takes me back to being 20 years old in 2012. I did not have a community, an algorithm or a list of recommended lipedema protocols. I had a diagnosis and a body that was giving me information. Over the following 15 years, I learned to pay attention to that information.

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Today we have something I did not have then: a rapidly expanding scientific literature and a community capable of sharing it almost immediately. That is an enormous advantage, provided we do not allow the amount of information available to create more certainty than the research justifies.

My own experience tells me that stress matters to my lipedema. Science tells me there are credible biological reasons why stress, the nervous system, immune regulation and pain can interact. Emerging lipedema research tells us that altered pain processing may be part of the condition’s symptom biology.

The part that remains unknown is just as important. We cannot yet say that nervous-system dysregulation causes lipedema, that stress directly drives inflammation in lipedema tissue, or that “regulating” the nervous system can stop disease progression.

For me, that uncertainty does not make stress management less important. It simply means I can listen to what my body has been telling me for 15 years without turning my personal experience into a mechanism that science has not yet demonstrated.