Lipoedema: a paradigm shift and consensus
2020; Mark Allen Group; Volume: 29; Issue: Sup11b Linguagem: Inglês
10.12968/jowc.2020.29.sup11b.1
ISSN2052-2916
AutoresTobias Bertsch, Gabriele Erbacher, Rebecca Elwell, H Partsch,
Tópico(s)Sympathectomy and Hyperhidrosis Treatments
ResumoJournal of Wound CareVol. 29, No. Sup11b International Consensus DocumentFree AccessLipoedema: a paradigm shift and consensusTobias Bertsch, Gabriele Erbacher, Rebecca Elwell, Hugo PartschTobias BertschFöldi Clinic, Hinterzarten–European Center of Lymphology, GermanySearch for more papers by this author, Gabriele ErbacherFöldi Clinic, Hinterzarten–European Center of Lymphology, GermanySearch for more papers by this author, Rebecca ElwellUniversity Hospitals of North Midlands NHS Trust, UKSearch for more papers by this author, Hugo PartschDivision of General Dermatology, Medical University of Vienna, AustriaSearch for more papers by this authorTobias Bertsch; Gabriele Erbacher; Rebecca Elwell; Hugo PartschPublished Online:10 Nov 2020https://doi.org/10.12968/jowc.2020.29.Sup11b.1AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail Consensus groupTobias Bertsch, Gabriele Erbacher, Thomas Zähringer: Földi Clinic, Hinterzarten–European Center of Lymphology, GermanyDomenico Corda: Polimedica San Lanfranco, Pavia, ItalyRobert J. Damstra, Kirsten van Duinen, Jose van Esch-Smeenge, Ad Hendrickx, Bea Koet: Center of Expertise in Lymphovascular Medicine, Nij Smellinghe, Drachten, The NetherlandsJoanna Dudek: SWPS University of Social Sciences and Humanties, Warsaw, PolandRebecca Elwell: University Hospitals of North Midlands NHS Trust, UKGabriele Faerber: Centre for Vascular Medicine, Hamburg, GermanyJodok Fink: Department of General and Visceral Surgery at the Medical Center, University of Freiburg, GermanyAnnemarieke Fleming: Rehabilitation-Centre Reade, Amsterdam, The NetherlandsKristiana Gordon: St. George's Hospital, UKDenise Hardy: Kendal Lymphology Centre, UKTobias Hirsch: Practice for Internal Medicine and Vascular Disease, Halle, GermanyPeter Mallinger: Klagenfurt Clinic, AustriaAnya Miller: Practice for Dermatology, Berlin, GermanyChristine Moffatt: Nottingham Trent University, UKNestor Torio-Padron: Practice Clinic for Plastic Surgery, Freiburg, GermanyChristian Ure: Lymphology Clinic, Wolfsberg, AustriaStephan Wagner: RehaClinic, Bad Zurzach, SwitzerlandOther KOLs supporting the consensusHakan Brorson: Department of Clinical Sciences, Lund University, Plastic and Reconstructive Surgery, Skåne University Hospital, Malmö, SwedenLeif Perbeck: Karolinska University Hospital, SwedenNele Devoogdt: Department of Rehabilitation Sciences, Katholieke Universiteit Leuven, BelgiumSarah Thomis: University Hospitals Leuven, BelgiumStéphane Vignes: Lymphology Service, Reference Centre for Rare Vascular Diseases, Hôpital Cognacq-Jay, Paris, FranceMichael Oberlin: Földi Clinic–European Center of Lymphology, Hinterzarten, GermanyRené Hägerling: Researcher at Charité, University of Berlin, GermanyKatja S. Mühlberg: University of Leipzig, GermanyErika Mendoza: Practice for Venous Diseases, Wunstorf, GemanyAndrzej Szuba: Department of Angiology, Hypertension and Diabetology, Wroclaw Medical University, PolandNote: The individuals listed as part of the consensus group do not necessarily endorse all the views proposed in the document.ForewordLipoedema is a chronic condition characterised by a disproportionate increase in adipose tissue and pain in the legs and, sometimes, the arms of women. Its prevalence is largely unknown. The disproportionate increase in weight around the legs usually starts in phases of weight gain that are mostly connected to hormonal changes, such as puberty, pregnancy and menopause. Years later and mostly after further weight gain, pain or the feeling of severe heavy legs may occur, at which point the condition meets the diagnostic criteria for lipoedema. Research on lipoedema is limited and there is a lack of diagnostic testing; therefore, clinicians lack a strong enough evidence base for their practice. This, in turn, hampers patient care.Lipoedema often is confused with lymphedema; as a consequence, many doctors prescribe decongestive lymphatic therapy. As the authors convincingly demonstrate in this supplement, lipoedema neither includes oedema nor is there any scientific evidence for lymphatic insufficiency. For this reason, decongestive lymphatic therapy is an inadequate treatment for patients with pure lipoedema. There is also considerable variation in how clinicians approach lipoedema among different countries. This lack of homogeneity naturally affects patients, who are already distressed by the pain their condition causes as well as their legs not meeting the standards of the current beauty ideal. Overall, there seems to be an urgent need for standardisation of lipoedema management, based on scientific evidence.The time has come to establish the diagnosis of lipoedema by eliminating old, never proven concepts from the field. In this supplement, the authors disprove with a high level of scrutiny, several unproven dogmas related to lipoedema. Further, they clarify the clinical situation of this ailment and describe the need to adopt new approaches on handling it, taking into consideration new facts regarding its pathophysiology, which are rather complex. Thus far, the scene has been dominated by case reports, rather than scientifically validated information.In 2018 and 2019, a group of lymphology experts from seven European countries met in Hamburg to discuss a consensus regarding lipoedema. This group was led by Tobias Bertsch, who is a senior consultant at the Földi Clinic in Hinterzarten, Germany. The consensus proposed by the group attempts to dispel some of the rampant myths surrounding lipoedema and introduces a paradigm shift in the pathophysiology of lipoedema, as it states that lipoedema is not an oedematous condition at all.The authors of this work should be congratulated for recruiting this outstanding group of international experts as supporters of this work—the number of European countries represented has now grown to ten. It may be hoped that these experts will also be willing to offer opinions on holistic treatment modalities for ‘lipalgia syndrome’—which ‘lipoedema’ should be called henceforth, according to the authors.Hugo Partsch, Emeritus Professor of Dermatology, Medical University of Vienna, Austria2. The paradigm shift: there is no oedema in lipoedemaThe idea that lipoedema is an oedematous condition seems to be lymphological dogma, and this naturally affects how the condition is managed. This false perception of lipoedema seems to stem from the name given to the condition by Allen and Hines when they first described it in 1940. However, the concept of oedema does not feature prominently in their first two publications.1, 2 In their second publication in 1951, they wrote: ‘Particularly at the end of the day, there may be some evidence of [o] edema, although the evidence is not great enough to explain the patient's statement relative to the degree of swelling which has occurred as a result of orthostatic activity’.2 In both publications, the mental health of the patients with lipoedema seemed more a point of interest, but was explored very briefly. In fact, only 24% of the 119 participants in their first study on lipoedema actually had orthostatic oedema (‘minimal to mild pitting oedema’), while 29% reported had an ‘associated neurosis’.2By definition, oedema is an accumulation of fluid that manifests the classic pitting appearance of the soft tissues on clinical examination. However, the authors have found no relevant fluid accumulation in their patients with lipoedema who are examined using a high-resolution ultrasound scan (with a 18.6-MH transducer and a Moisture Meter to measure the amount of moisture). Additionally, the findings on clinical inspection and ultrasound scan appear to be identical in patients with lipoedema and those with pure lipohypertrophy (which is painless disproportionate increase in adipose tissue). Figure 2.1 shows a patient with lipoedema, while Figure 2.2 is the ultrasound scan of her thighs (the left and right thighs were identical). There are no abnormalities apart from widening of the subcutaneous tissue; in particular, there is no evidence of fluid. Figure 2.3 shows a patient with lipohypertrophy, Figure 2.4 is the ultrasound scan of her thighs (here, again, the left and right thighs were identical). As can be seen from Figures 2.1 and 2.2, the clinical picture and ultrasound images are virtually identical between a patient with lipoedema and one with lipohypertrophy. Figure 2.5 shows a patient manifesting three clinical conditions: lymphoedema of the distal lower leg and forefoot; lipoedema that is restricted to proximal lower leg; and morbid obesity (body mass index (BMI) of 48 kg/m2). Figure 2.6 shows the sustained pitting present in lymphoedema (lower circle) and the non-pitting nature of the soft tissues in lipoedema (upper circle) in the same patient. Figure 2.7 shows an ultrasound scan of the distal right lower leg depicting stage 2 lymphoedema with partial separation of the soft tissue structures, thickened dermis and fluid in the tissues (small arrows). Figure 2.8 (proximal lower leg) shows the typical ultrasound appearance of lipoedema, that is, an unremarkable dermis, thickening of the subcutaneous tissues, and no evidence of fluid in the soft tissues.Fig 2.1. A patient with lipoedema. 2.2. Ultrasound scan of the thigh of a patient with lipoedema, showing no evidence of fluidFig 2.3. A patient with lipohyertrophy. 2.4. Ultrasound scan of the thigh of a patient with lipohypertrophyFig 2.5. A patient with lymphoedema of the lower leg and forefoot, lipoedema of the thigh and proximal lower leg and obesity. 2.6. Upper circle: non-pitting lipoedema tissue; lower circle: pitting lymphoedema tissueFig 2.7. Ultrasound scan of the distal right lower leg of the patient in Fig 2.5 showing stage 2 lymphoedema with fluid (small arrows). 2.8. Ultrasound scan of the proximal lower leg showing the typical ultrasound appearance of lipoedema, with no signs of fluidAfter lipoedema was first described by Allen and Hines,1 the condition received very limited attention until 1980. There were only a few individual case reports on lipoedema or painful adipose tissue in the 1960s and 70s.3,4 Then, in 1980, Schmitz published an article entitled ‘Lipoedema – the fat leg in the healthy woman’ in the journal Gynäkologie.5 However, oedema, that is, fluid accumulation, did not feature in this report, nor did it in Brunner's 1982 study, which described the patients' condition as a disorder in the distribution pattern of the subcutaneous fat, stating ‘The fat layer has a soft consistency and does not allow pitting even over the tibia’.6 Gregl described lipoedema as a ‘mucoid pseudo-oedema’ and stated that, unlike what happened with cardiac and dystrophic oedema, pressing over lipoedema did not cause pitting.7 Using the American oedema classification, Rudkin reported only 1/4 + oedema in the pretibial area of those with lipoedema (1/4 + means hardly pitting).8It is clear from the existing literature that oedema does not play a relevant role in the development of lipoedema. Despite this, oedema often forms the basis for the treatment of lipoedema. The two most popular treatments under consideration here are liposuction and manual lymphatic drainage. In one study, structural drainage insufficiency was considered the basis of the need for lymphological liposculpture (that is, liposuction) in patients with lipoedema.9 The researchers believed that lipoedema leads to overproduction of lymphatic fluid in the arms and legs, which manifests as tenderness; further, they claimed that the adipose tissue is flooded with lymph, and this increases the tension in the thickened extremities.10 However, these notions are not supported by any scientific evidence. Specifically, the flooding of adipose tissue by lymph cannot be demonstrated clinically or ultrasonographically, nor by other imaging procedures, such as computed tomography and lymphoscintigraphy.11,12,13,14 In a recent publication, researchers examined patients with lipoedema using magnetic resonance lymphography of the lower extremities. They concluded that the fat tissue was homogenous and showed no signs of oedema in pure lipoedema patients.15 Histological evidence of oedema in the adipose tissue in lipoedema patients is also lacking. Histological examination of the adipose tissue in patients with lipoedema has shown a localised increase in adipose tissue, isolated foci of fat necrosis and increased numbers of anti-CD68+ macrophages in the interstitial tissue.16 The latter two findings support the hypothesis that inflammatory and hypoxic processes are responsible for the pain in lipoedema. Laboratory tests on patients with lipoedema also argue in favour of this interpretation. The glutathione status in red blood cells (RBCs) and malondialdehyde (MDA) in the plasma have been studied as biomarkers of oxidative stress, and the levels of both markers in patients with lipoedema were found to be higher than those in healthy patients.17 Surprisingly, oedema has been cited as the cause of lipoedema symptoms by several researchers.18,19,20 However, the question then arises: if oedema is the cause of pain in patients with lipoedema, why do patients with cardiogenic oedema or lymphoedema have no pain at all or only very mild discomfort?21 In these last two types of oedema, both clinical and ultrasound examinations clearly demonstrate fluid in the tissues. A similarly critical approach to the ‘oedema’ in lipoedema has been taken in both the UK and the Netherlands. The authors of the 2014 Dutch lipoedema guidelines stated that ‘Lip[o] edema is an unfortunate term, as it evokes the idea of swelling due to fluid accumulation. However, it refers to swelling—in a sense of an increase in volume—due to increased fat tissue’.22 Further, the authors of the current Dutch guidelines have not listed ‘oedema’ in the criteria for lipoedema definition. Similarly, the UK guidelines for lipoedema from 2017 reflect this paradigm shift by defining lipoedema as ‘fat swelling’, with no reference to a fluid component.23, 24Many national and international publications consider regular manual lymphatic drainage to be the standard treatment for lipoedema.25,26,27,28,29 This recommendation is based on the belief that oedema is responsible for the pain experienced in lipoedema. However, if no relevant oedema can be demonstrated in patients with lipoedema, the rationale for prescribing manual lymphatic drainage is shaky. Two questions need to be answered in this scenario: (1) Is there any scientific evidence that oedema is the cause of the patient's symptoms? (2) Is there any scientific evidence that manual lymphatic drainage improves the symptoms of patients with lipoedema by its drainage effects? The answer to both these questions is no. At the lead authors' lymphology outpatient department, many attending women with lipoedema request manual lymphatic drainage, and they often encounter patients with lipoedema who have been prescribed manual lymphatic drainage (MLD) twice or even three times a week for many years. Many of these patients report that they benefit from lymphatic drainage, but whether it is medically necessary remains debatable. It is likely that patients find MLD pleasant, which has little to do with its decongestive effect. Many patients with lipoedema have mental health issues that require treatment, such as depressive disorders, anxiety and eating disorders.30 There could be other aspects of MLD that benefit patients, such as the massage itself reducing stress and exhaustion. Massage therapy is well-known to alleviate psychological symptoms, such as anxiety and depression.31,32,33 Further, the touch and personal attention corresponding to MLD also produce positive effects. Last, but not least, for any patient, having treatment prescribed means that their condition is recognised as a disease. Patients with lipoedema often report very long durations between when they first experience symptoms and when their symptoms are finally taken seriously and addressed, with the subsequent diagnosis and treatment of lipoedema. Psychological, psychosocial and societal factors have a considerable impact on the symptoms of patients with lipoedema.30, 34Lipoedema always develops from lipohypertrophy, but only in a small percentage of women.35 It remains unclear why some women develop pain in the adipose tissue, and the underlying pathology of this symptom is still subject to speculation. Apart from the oedema hypothesis presented above, there are several ideas about the cause of lipoedema-related pain in the scientific literature.36 There is, however, a consensus that the pain is located in the subcutaneous adipose tissue of the limbs.28 As patients have usually experienced pain for more than 6 months at the time of diagnosis, it can be considered chronic. The causes of chronic pain are usually degenerative processes in the musculoskeletal system (e.g. osteoarthritis), ischaemia (e.g. peripheral arterial disease), neuropathies (e.g. after a stroke, diabetic polyneuropathy), cancer and inflammatory conditions (e.g. rheumatoid arthritis). The literature on expanding subcutaneous fat mentions two main processes: inflammation and hypoxia.16, 37, 38 In their recent work, Crescenzi et al compared the adipose tissue between patients with lipoedema and a control group of women without lipoedema. They found an increase in the sodium content of the skin in patients with lipoedema, an emerging hallmark of inflammatory disease.39 To date, a chronic low-grade state of inflammation40 and tissue hypoxia are the most plausible explanations for the pain in lipoedema patients; unlike those with lymphoedema, patients with lipoedema do not have a higher risk of cellulitis. Furthermore, the experience of pain is a multifactorial phenomenon involving not only sensory but also cognitive, affective, motivational and behavioral dimensions. Therefore, therapeutic approaches to lipoedema should focus on these causes of pain.30ConclusionThere is no evidence that oedema plays a relevant role in lipoedema, and it is certainly not the cause of the pain experienced by lipoedema patients. Lipoedema is a more complex condition than simply painful, fat legs. Comprehensive treatment of lipoedema should take into account all those aspects that are less apparent than the observable changes and reported symptoms. In addition to alleviating somatic symptoms, lipoedema therapy must also focus on the other aspects of this complex condition and include a thorough work-up, pain management, addressing the psychological vulnerability of women with lipoedema, managing any weight gain and encouraging self-acceptance in an era where skinny is considered aesthetically appealing.3. Myth: Lipoedema makes patients fatThere are two popular concepts in the field of lipoedema and its common comorbidity—obesity. The first is that lipoedema makes the patient fat and the second is that weight loss has no effect on lipoedema. To the authors' knowledge, there is no evidence to support either of these statements. However, there is also no evidence to support the corollary—that is, that lipoedema does not lead to weight gain and that weight loss does lead to an improvement in lipoedema. It is obvious that there is a close correlation between being overweight or obese and having lipoedema. Of the 2344 women diagnosed with lipoedema at the authors' lymphology clinic in 2015, only 3% were of normal weight; 9% were overweight (BMI=25–30 kg/m2) and 88% were obese (BMI>30 kg/m2).41 Their patient cohort appears largely representative in this regard. For example, Bosman reported that up to 80% of the lipoedema patients in a centre in the Netherlands were overweight and/or obese.42 In 2011, a British research group reported that only 4% of their lipoedema patients were of normal weight, while 11% were overweight and 85% were obese.43 In a study by Herbst et al44 from the US, 76% of the lipoedema patients were obese, and, in another investigation by Dudek in Poland, this number was 80%. Around 50% of the patients in the latter study were morbidly obese, which means they had a BMI of over 40 kg/m².30,43,45 In short, a lipoedema patient of normal weight is a rarity.In this context, BMI has only limited value in lipoedema patients who are overweight (BMI=25–30 kg/m2). There is the rare group of patients with a largely slim upper body and marked increase in fat in the extremities. However, in such patients, overweight is an illusion because the fat distribution is uneven, given the lipohypertrophy of the legs. The waist-to-height ratio (WHtR) is the more suitable measure for these patients, as it provides a better indication of the distribution of body fat. At the authors' clinic, both BMI and WHtR are measured in all patients with lipoedema.So how can this apparent relationship between lipoedema and obesity be explained? Patients as well as the media are keen to explain the connection between lipoedema and obesity as lipoedema being responsible for the weight gain in women with lipoedema.46,47,48,49 This notion is even more widespread in the US, where there is a coalition of doctors and patients who explain their weight gain by the disease lipoedema.50,51 However, there is no scientific evidence for this view. There is also no conclusive pathophysiological construct to explain how lipoedema leads to weight gain. There is general agreement that a disproportionate increase in fat in the legs (and sometimes the arms) is an important criterion for a lipoedema diagnosis. This initial, often only slight, disproportionality is frequently seen even during puberty, at which point the patients are largely without complaints in the soft tissues; at most, there is mild lipohypertrophy of the legs. The risk of symptoms and, hence, the development of lipoedema usually starts when the weight progresses and the associated disproportionate increase in fat in the lower half of the body occurs. Therefore, the notion that weight gain (often obesity) can, in the case of the relevant (genetic) disposition, result in lipoedema, seems more likely.The causes of obesity are varied and highly complex, but there is scientific evidence for genetic and especially epigenetic influences.52,53,54,55 Biological factors such as stress or addictive behaviour can also affect weight,56,57 as can psychological conditions such as depression and eating disorders.58 Finally, sociocultural changes also play a considerable role in the development of obesity: for example, changes in eating habits, the regular consumption of sugar (particularly in soft drinks) and a sedentary lifestyle, in addition to lack of confidence regarding wearing and being seen in exercise clothing; for example, in the 2016 Lipoedema UK survey, 95% respondents reported difficulty in buying clothes, and 59% stated that embarrassment stopped them exercising in water.59 Added to these is the beauty ideal that skinny is aesthetically pleasing, and this is closely connected with a diet culture, which often begins in adolescence and whose long-term course does not lead to weight loss but, in fact, to weight increase.60,61,62,63,64 In Germany, roughly 25% of the population is now obese (BMI > 30 kg/m2),65 and, in the US, this figure had already reached 40% in 2017.66If lipoedema does not make one fat, how can the broad support for this position be explained? The essential basis for the popularity of this view of lipoedema is the stigmatisation of the disease of obesity, which is frequently considered to be the result of incorrect behaviour, a weak will or lack of discipline. Even among medical professionals, and particularly among doctors, weight-related discrimination and stigmatisation is especially marked.67,68,69 Stigmatising attitudes towards obese patients can also be found among medical specialists in obesity and dieticians.70, 71 The causes of obesity are complex, as also recognised by the World Health Organization (WHO). Simultaneously, data concerning the poor prognosis of conservative weight reduction are extensive. Between 80% and 99% of all patients who lose weight conservatively will put it on again in the long term.72,73,74,75,76,77,78,79 Particularly in women, attempts to lose weight that were started during adolescence lead to a decades-long dieting spiral, with a resultant continuous increase in weight.64The advice to reduce weight is especially concerning in lipoedema. Studies have shown that women (in contrast to men) regain weight after weight loss disproportionately in the lower half of the body,80 and, as stated above, most who diet regain any lost weight. In other words, any recommendation by a doctor to female lipoedema patients to lose weight actually increases the risk of a further increase in fatty tissue in the leg region and, hence, also increases the risk of their symptoms increasing. In the authors' opinion, the ‘boom’ in lipoedema is due to the way the obesity has been handled. On the part of patients, lipoedema has developed into an ‘excuse’ or explanation of sorts for weight gain and overweight. Many lipoedema self-help groups as well as the media have proposed that patients are not fat, but have lipoedema.81,82,83 Women believe the lipoedema is responsible for their long history of progressive weight gain. It is laborious and time-consuming to convince patients that they are misinformed and that there are other factors that lead to an increase in weight, and it is certainly not due to lipoedema. It is also challenging to convince patients that the frequently desired treatment options—manual lymphatic drainage or liposuction—will in no way result in a substantial, permanent or even only approximately satisfactory weight loss.ConclusionThere is no evidence that lipoedema leads to weight gain, although weight gain does exacerbate lipoedema symptoms. Given the right genetic disposition for lipoedema, weight gain appears to be a trigger for lipoedema development. From the authors' observations, there certainly are women with normal weight or those who are slightly overweight with highly disproportional fat distribution and soft tissue symptoms, but in view of the overwhelming majority of obese and morbidly obese women with lipoedema, these individuals form a very small minority.4. Myth: Weight loss has no effect on lipoedemaIt is a matter of grave concern that medical professionals often confuse lipoedema with obesity or lymphoedema.84,85 Cornely and Gensior stated that lipoedema is rarely diagnosed quickly and accurately.86 Karen Herbst, endocrinologist and protagonist in the American lipoedema scene entitled her article that mainly discussed lipoedema ‘Rare adipose disorders (RADs) masquerading as obesity’. She said that one of the most common misconceptions about lipoedema is that the condition is lifestyle- or diet-induced obesity.25 Unfortunately, this view is perpetuated by patients and the media, lipoedema self-help groups and internet fora.87,88,89 What complicates matters further—and what needs to be highlighted—is that most women with lipoedema are actually also obese; the statistical details have been mentioned in Chapter 3. In fact, a woman of normal weight with lipoedema is very rare. Thus, most women concurrently have two conditions: obesity and lipoedema. Focusing only on lipoedema in a woman with a BMI of 35 kg/m2 or more seems pointless, as clearly the obesity is a more pressing concern. In the authors' experience, the vast majority of female patients with lipoedema more often complain of a progressive weight increase rather than pain in the legs.Many self-proclaimed lipoedema experts and, consequently, patients believe that weight loss has no effect on lipoedema, only on obesity. Herbst mentioned that, although lifestyle changes and bariatric surgery are effective interventions to address the obesity component, these treatments do not routinely reduce the abnormal subcutaneous adipose tissue seen in lipoedema.25 Similarly, Schmeller reported that weight loss helps only in the case of concomitant obesity, and it merely reduces truncal circumference. As a result, however, the disproportionality between the trunk and extremities worsens, since lipoedema-specific fat accumulations cannot reduce through weight loss.84 Stutz argued that the fat pads on the legs are not the same as stored reserve fat in obesity, declaring that this fat has a different structure and, cannot be lost through dieting and exercise.90 This view is also frequently adopted by patients and lipoedema self-help groups.91The lead authors of this supplement sought to identify the basic pathophysiological construct for the assumption that weight reduction in obese lipoedema patients does not also lead to substantial loss of fat in the extremities, as well as reduction of lipoedema symptoms. The self-proclaimed experts mentioned above provide no explanatory model in their publications that justifies the published statements. What has been propagated is just the myths, ones that have been passed on and adopted by women with lipoedema for years. The fact that mostly the doctors practising liposuction play a considerable role in propagating these myths gives pause for thought. These myths certainly contradict the publications of Allen and Hines, the first people to describe lipoedema in 1940 and 1951, who wrote that, in cases of generalised obesity, a sharp reduction in weight may help alleviate symptoms.1,2 In the lead authors' experience as well, weight loss through conservative therapy has helped reduce the volume of fat in the region of the extremities of women with lipoedema, but this reduction is only temporary, because of weight gain after weight loss. Through the clinic's multimodal obesity programme, in which lymphoedema and also lipoedema patients with a BMI upwards of 40 kg/m2 are prepared for surgical obesity treatment, pa
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