Along with fatigue and nausea, pain has been one of the defining symptoms of my daughter’s illness. After she was diagnosed in 2018-2019 at age 14-15 with hypermobile Ehlers-Danlos syndrome (EDS), chronic fatigue syndrome (ME/CFS), craniocervical instability, Chiari malformation, occult tethered cord syndrome, postural orthostatic tachycardia syndrome (POTS), and mast cell activation syndrome (MCAS), we learned of treatments that have helped to reduce her pain. Low-Dose naltrexone has reduced the pain in her back and ribs. After starting mast cell stabilizers, her joints have become less likely to pop out of place, reducing pain from joint dislocations.
But certain forms of pain persisted and even worsened over time. In particular, many parts of her body, including her abdomen and upper arms, were painful when touched. She also had pain in her chest, lower back near her coccyx, and face, among other locations. One doctor suggested the pain was caused by central sensitization, potentially related to her MCAS or craniocervical instability.
These factors may well be contributing to her pain, but I have come to believe that the most proximate and important cause of the pain in her abdomen, chest, upper arms, and lower back has been the build-up of lymphatic fluid and the resulting formation and fibrosis of adipose tissue. I believe this because we have made dramatic gains in treating this pain through a combination of manual lymphatic drainage and massage techniques designed to break up fibrotic tissue and reduce the build-up of fluid in her tissues.
Her arms and abdominal areas are no longer painful when touched. The coccyx pain is also largely gone and the pain in the chest and face is more manageable. The treatments, which we do regularly, have also helped reduce problems with swallowing, breathing, and sitting up as well as swelling and pain around previously engorged lymph nodes. In the abdomen and thighs, the treatment has eliminated bubbles that could previously be felt under the skin; in these locations and on the upper arms, the skin now has a smoother texture. The treatment also helps to reduce the feeling of heaviness in her arms and legs.
I cannot say whether my daughter’s experience is generalizable to others with her conditions, but as I have done more research into the lymphatic system, adipose tissue fibrosis, and the related disorder of lipedema, I have become convinced these are important topics that merit further exploration in the context of EDS, fibromyalgia and ME/CFS. At a minimum, I would encourage broader awareness of lipedema, a condition involving the build-up and fibrosis of adipose tissue, which may be an important comorbid condition in some people with EDS, fibromyalgia, and ME/CFS. More broadly, I would encourage researchers to investigate whether the build-up of lymphatic fluid and the fibrosis of adipose tissue play an important part in the disease cycle of one or more of these conditions, even in the absence of noticeable weight gain.
As described in a recent article on the standard of care for lipedema in the United State:
“Lipedema is a disease of fibrotic loose connective (adipose) tissue . . . on the lower abdomen, hips, buttocks, and limbs of females, sparing the trunk, hands, and feet. Lipedema is rare in men. A trigger for the development of lipedema tissue may be an increase in fluid and connective tissue remodeling that occurs alongside body changes during puberty, childbirth, menopause, stress associated with lifestyle change, or by altering tissue structure after surgery or trauma. A hallmark of lipedema tissue is inflammation, resulting in tissue fibrosis and pain, and in some cases, the tissue may become numb.”
The literature suggests lipedema is quite common: “Prevalence estimates for lipedema range from 6.5% in children in the US, 6%–8% in women in Germany, and 15%–19% in vascular clinics.” These estimates are based on small samples, so they could overstate the incidence of lipedema. But even if the prevalence of lipedema were only a fraction of the stated estimates, it would be a fairly common disorder. Moreover, a large percentage of women with lipedema are hypermobile. One study of 160 patients with lipedema found that 58 percent had a Beighton score of 5 or more, a marker of hypermobility.
The most widely recognized symptom of lipedema is weight gain in specific areas of the body, but lipedema can be difficult to detect in the early stages when it is most easily treated. There are five types of lipedema, which describe different patterns of affected areas, which can include the buttocks, hips, thighs, calves, and arms. Lipedema can also affect the abdomen. Other areas may be affected in some patients. For example, a study of 160 women with lipedema found nodular fat, fibrosis or edema to be present in the mid-back (76 percent of the sample), chest/breast (43 percent), and hands and feet (33 percent).
There are three main stages of lipedema:
- “In Stage 1, the skin is smooth but there are pearl-sized nodules in the fat underneath.
- In Stage 2, there is retraction of the skin due to fibrosis of connective tissue fibers surrounding fat lobules and pearl-sized and larger masses in the fat tissue.
- In Stage 3, there are pearl-sized nodules, larger masses, and lobules of the skin and fat.”
Lymphedema, which is sometimes classified as a fourth stage of lipedema, can occur at any of the first three stages but is more common in stage 3 than stages 1 or 2. In lymphedema, the lymphatic system is blocked or damaged, leading to the noticeable swelling of the affected tissue.
Early-stage lipedema in adolescents can be difficult to detect given the many changes occurring during puberty. In our daughter’s case, the pain in her abdomen, arms, and coccyx area was present before we noticed any unusual weight gain. Eventually, she experienced more noticeable weight gain and we observed nodules under her skin, but we would not have recognized them as problematic had her physical therapist not suggested they may be related to the build-up of lymphatic fluid.
According to consensus guidelines, conservative treatment for lipedema includes compression garments that help lymphatic fluid move through the lymphatic system and “manual therapy [that] . . . includes soft tissue mobilization to reduce pain, inflammation and musculoskeletal restrictions, and manual lymphatic drainage as part of an individualized comprehensive therapy program to stimulate lymphatic flow and reduce edema.” Conservative treatment also includes nutritional guidance, sequential pneumatic compression pumps, and exercise.
While there are no medications approved specifically for lipedema, the consensus guidelines mention sympathomimetic amines, metformin, diosmin, and vitamin D supplementation as possible therapies. The guidelines also recommend against the use of thiazolidinediones, which increase subcutaneous adipose tissue, treatments that lead to weight gain, and the long-term use of diuretics, which can concentrate protein in the lymphatic fluid, obstructing the flow and contributing to fibrosis.
Dr. Karen Louise Herbst, a leading expert on lipedema, also recommends supplementation with selenium and avoidance of oral corticosteroids and medications that promote fluid retention, including NSAIDS, sex hormones, calcium channel blockers, beta-blockers, clonidine, and gabapentin.
Lipedema can also be successfully treated with surgery, utilizing a specialized form of “liposuction, excision and manual extraction that spares blood and lymphatic vessels.”
Applicability to EDS, Fibromyalgia and ME/CFS
I am unaware of any research documenting the incidence of lipedema in people with EDS, fibromyalgia, and ME/CFS, but if lipedema is anywhere near as common as estimated, the overlap is likely to be significant. Hypermobility is common in lipedema, EDS, fibromyalgia, and ME/CFS. Overlapping symptoms have also widely been observed – for example, between lipedema and fibromyalgia and between EDS and fibromyalgia. One study found that “symptomatic hypermobility predict[ed] symptom severity in pain and fatigue conditions” in a sample of people with ME/CFS and fibromyalgia.
I am not by any means suggesting these disorders are the same. But the high incidence of hypermobility in all four disorders suggests that connective tissue problems may play a role in each one, at least for a cohort of affected individuals. (Since some connective tissue disorders are not marked by hypermobility, it is possible the overlap would be even greater once these other connective tissue disorders were factored in.) The common thread of connective tissue problems raises the possibility that a significant share of patients with EDS, fibromyalgia, and ME/CFS may also have or be susceptible to lipedema.
- Lipedema is a disorder characterized by the build-up of lymphatic fluid and the resulting formation of subcutaneous adipose tissue, which then becomes fibrotic and painful.
- Given high rates of hypermobility across all four conditions, lipedema may be a fairly common, yet underappreciated, comorbid condition of Ehlers-Danlos Syndrome (EDS), fibromyalgia, and ME/CFS.
- The author has found some of the treatments for lipedema – including manual lymphatic drainage and the break-up of fibrotic adipose tissue – to be helpful in treating the pain experienced by his teenage daughter, who has EDS, ME/CFS, MCAS, and POTS. Further research is needed to assess the potential of these and other lipedema therapies to help individuals with EDS, Fibromyalgia, and ME/CFS.
- Research is also needed to explore the possibility that the build-up of lymphatic and interstitial fluid and the formation and fibrosis of adipose tissue play important roles in the disease cycles of EDS, fibromyalgia, and ME/CFS. For example, these processes may be contributing to widespread pain, inflammation, and MCAS.
- The author also hypothesizes that leakage from microangiopathic blood vessels in people with connective tissue disorders may play a central role in post-exertional malaise, at least for some individuals with ME/CFS, leading to excess lymphatic/interstitial fluid that floods tissues, leading to hypoxia and inflammation.
- The author urges researchers working on EDS, fibromyalgia, ME/CFS, and lipedema to work collaboratively to identify opportunities for learning across these different domains.
While there are suggestions in the lipedema literature of a connection between EDS and lipedema, I have found little formal research exploring this connection, with only one case study of an individual with both conditions and no articles examining the use of manual lymphatic drainage in individuals with EDS. While there is a paucity of formal research on the connection between EDS and lipedema, patients are certainly discussing it. See, for example, this article by Oh TWIST and the comments on the article from individuals experiencing both conditions. There are also a number of articles on the overlap in the informal literature, such as this article by functional medical doctor Jill Carnahan.
A number of small studies have found manual lymphatic drainage to be helpful in reducing pain in people with fibromyalgia. One pilot study of 17 women with fibromyalgia (and no controls) found that “[p]ain, stiffness, sleep, sleepiness, and well-being all improved during” treatment with manual lymphatic drainage, and that the benefits in these areas (except for sleep) were still apparent two months after cessation of treatment. Another study of 50 women with primary fibromyalgia compared the effectiveness of manual lymphatic drainage and connective tissue massage (with no control group), finding that both approaches were helpful in reducing pain but that manual lymphatic drainage may have been somewhat more effective. A recent article found strong similarities in the symptoms experienced by patients diagnosed with lipedema and fibromyalgia and notes the possibility of overlap in individual cases. The article does not explore the extent to which individuals experience both conditions, however, as patients with fibromyalgia in the study were not systematically evaluated for lipedema.
Manual lymphatic drainage is, of course, central to the Perrin Technique for treating ME/CFS, but it’s not clear how widely manual lymphatic drainage is being applied outside of the practitioners certified in the Perrin technique. A search for “lymphatic drainage” and “chronic fatigue” on PubMed and Google Scholar revealed two articles by Dr. Perrin and a case study, but nothing that would suggest a broader formal evaluation of lymphatic drainage in ME/CFS. I have found no formal articles exphttps://theperrintechnique.com/loring the connection between lipedema and ME/CFS in-depth, though one recent preprint on a UK cohort of lipedema patients lists chronic fatigue as a comorbid condition and another article notes that myopathy (muscle weakness) has been observed in both people with lipedema and those with chronic fatigue.
To sum up: there is reason to believe that lipedema may be an important comorbid condition for some people with EDS, fibromyalgia, and ME/CFS, but only minimal exploration of this potential comorbidity has occurred. A lynchpin of lipedema treatment, manual lymphatic drainage, is being used to a limited extent to treat ME/CFS and fibromyalgia, but more research is needed to formally assess its benefits.
Recommendations for Research and Practice
The intersections of these conditions with lipedema merit further exploration through research and practice. I have five recommendations for making progress in this area.
I. Explore the extent to which individuals with EDS, fibromyalgia, and ME/CFS have lipedema
Research is needed on the prevalence of lipedema in individuals with EDS, fibromyalgia, and ME/CFS. A good place to start would be to look at women with EDS whose illness took a dramatic turn for the worse during adolescence, as lipedema appears to be associated with hormonal changes during puberty. The incorporation of protocols to screen for lipedema in studies of women with long-term fibromyalgia and ME/CFS would also help shed light on the prevalence of lipedema in these patient groups.
Screening for lipedema may also be helpful in the care of individuals with EDS, fibromyalgia, and ME/CFS. The Lipedema Foundation has a number of helpful diagnostic resources for doctors and patients. An online diagnostic questionnaire is available from the Lipedema Project. There are also any number of self-assessment guides available on the Internet, such as this one from a physiotherapist in Toronto.
While there is no cure for lipedema, the literature suggests that early detection and treatment can help prevent the condition from becoming worse. There are also a number of treatments that can help reduce the associated pain, several of which I discuss in this article.
2. Explore whether manual lymphatic drainage and other massage techniques adapted from the lipedema literature may be helpful for individuals with Ehlers-Danlos Syndrome, fibromyalgia, and ME/CFS
I am not a physician and cannot provide medical advice. But given the reported benefits of manual lymphatic drainage for people with fibromyalgia and ME/CFS, it may make sense for people with one of these conditions or EDS to consider this treatment option whether or not one meets the formal diagnostic criteria for lipedema. If manual lymphatic drainage proves helpful and there are signs of adipose tissue fibrosis, a next step might be techniques that work to smooth or break up the fibrotic tissue. As with all potential treatment options, it makes sense to seek advice from knowledgeable doctors, physical therapists, or other trained practitioners to ensure the treatment makes sense and is safe for you. While the exact process by which manual manipulation remodels fibrotic tissue is not fully understood, we have found it to be enormously helpful in reducing pain, discomfort, and fluid accumulation.
If you are well enough to travel in a car, I would encourage a consultation and treatment session with a certified lipedema specialist or another individual trained in manual lymphatic drainage. If you are not well enough to travel, remote consultations with specialists can be helpful for getting started and implementing the guidance available on the web. My daughter’s physical therapist emphasized the importance of activating the lymph nodes before starting each area and showed us the location of additional lymph nodes that we were not aware of. (We have found that areas around the major lymph nodes can become engorged and painful; regular massaging of these areas has helped to substantially reduce that pain.) A good place to start is with manual lymphatic drainage of the neck/throat and face. We now do a modified version of lymphatic drainage regularly on pretty much the entire body as well as a scalp massage. It is possible to do manual lymphatic drainage on yourself, though a partner will be needed for the back.
It is more difficult to find online materials on how to smooth or break up fibrotic tissue and reduce the accumulation of interstitial fluid in tissues. I would strongly encourage reaching out to a trained physical therapist/physio to have them help with this. Getting treatment from a trained therapist can both provide an indication of whether these techniques are helpful for you and provide guidance on whether, and if so how, these techniques might be safely used at home.
The manual manipulation of subcutaneous adipose tissue to treat fibrosis can be quite painful, but my daughter reports that it provides lasting relief from pain and discomfort; she says it feels like stale fluid has been released. There are a number of techniques for treating fibrosis apart from manual therapy, including vibration and elastic taping. Given its potential for remodeling tissue, it seems plausible that Frequency Specific Microcurrent (FSM) also may be helpful in treating fibrosis, but I have not seen any formal literature on its use for lipedema and have no personal experience with it.
3. Develop clear medication guidelines for patients with these comorbid conditions
As summarized above, the lipedema literature describes a number of medications that might be helpful, as well as a long list of medications to avoid. Readers will note, however, that the list of medications to avoid includes numerous medications and supplements that are commonly used in treating people with EDS, fibromyalgia, and ME/CFS. Fluid enhancers, for example, are a mainstay of treatment for POTS, a common complication of all three conditions. Gabapentin and NSAIDs are used for pain and aspirin (an NSAID) is used to treat MCAS.
The carbonic anhydrase inhibitor and diuretic acetazolamide is used to treat intracranial hypertension, a common problem in people with ME/CFS and the neurological complications of EDS. As I discussed in two earlier Health Rising posts, many people with ME/CFS, fibromyalgia, and Ehlers-Danlos report benefitting from high-dose thiamine, but an in vitro study suggests it also functions as a carbonic anhydrase inhibitor and is thus likely also a diuretic. Quercetin and Luteolin, bioflavonoids used to treat MCAS, also inhibit carbonic anhydrase isoenzymes and thus presumably have diuretic properties. Many herbal supplements are also diuretics.
Given the potential of individuals with EDS, fibromyalgia, and ME/CFS to also have lipedema, it will be important to provide guidance on how to safely treat these conditions without exacerbating lipedema. It will also be helpful to better understand if regular manual lymphatic drainage or other compensatory strategies can help people with lipedema tolerate moderate doses of these medications and supplements.
In my survey of high-dose thiamine, many individuals reported benefitting from doses well below the levels evaluated in prior studies. In my view, the potential of diuretics to aggravate lipedema underscores the importance of formal research to confirm whether these lower doses are effective.
4. Develop creative and practical solutions to help increase the movement of lymphatic fluid in people with severe EDS and ME/CFS
It seems clear to me that physical inactivity was not the initial cause of my daughter’s lipedema or build-up of lymphatic fluid and fibrosis of adipose tissue. (To the contrary, the initial crash that made her disease evident appears to have been prompted by physical exertion.) But conventional wisdom suggests there is a risk that prolonged physical inactivity following a crash could exacerbate these problems by inhibiting the movement of lymphatic fluid through the system.
Assuming this widely held belief is true, we need creative and practical ways to increase the movement of lymphatic fluid in people whose severe EDS or ME/CFS inhibits their ability to get out of bed. This could involve the use of pneumatic compression pumps, for example, or simple exercises that could be done in bed without aggravating patients’ symptoms. These approaches need to be introduced with sensitivity and respect, in a manner that carefully avoids blaming patients for health problems they did not create. It seems to me that timing matters here – introducing these approaches soon after a crash may help to ward off further problems while avoiding an insinuation that inactivity is somehow responsible for the patients’ symptoms.
5. Explore whether the build-up of lymphatic fluid and the formation and fibrosis of adipose tissue play important roles in the disease cycles of Ehlers-Danlos Syndrome, fibromyalgia, and ME/CFS
In addition to studying the formal overlap with lipedema, research is needed on whether the build-up of lymphatic fluid and the fibrosis of adipose tissue might play important roles in the disease cycles of people with EDS, fibromyalgia, and ME/CFS. This topic merits a column of its own, but I briefly describe below five questions to consider in future research.
A. Could the build-up of lymphatic fluid be contributing to intracranial hypertension? The lymphatic system of the brain is called the glymphatic system and was only discovered in 2012. A recent study found that patients with idiopathic intracranial hypertension have impaired glymphatic function. The exact mechanism for the impaired flow of lymphatic fluid in the brain is unclear. The authors “suggest that in IIH pathological alterations at the glia-neuro-vascular interface may restrict transport of fluid and solutes along perivascular pathways and to and from interstitial tissue via astrocytic inter-end feet gaps.”
Peter Wostyn hypothesizes that impaired drainage of cerebrospinal fluid plays a central role in both ME/CFS and Long COVID. In Long COVID, he suggests this may be due to damage to olfactory sensory neurons and infection of lymph endothelial cells.
Since we know that adipose tissue fibrosis obstructs the lymphatic flow in other parts of the body, this seems like a mechanism worth exploring for the glymphatic system as well. Our personal experience suggests that the bridge of the nose may be one area to focus on; massaging of this area has led to reductions in the symptoms of intracranial pressure in my daughter (as well as fluid draining down the spine and throat). The cribriform plate, which is behind the bridge of the nose, plays an important role in the drainage of cerebrospinal fluid. Could the blockage or impairment of drainage at the cribriform plate contribute to increased intracranial pressure?
B. Could fibrotic adipose tissue be contributing to some of the inflammation and MCAS experienced by people with ME/CFS and EDS? Researchers have found that people with lipedema have excess interstitial fluid, possibly related to dysfunctional microangiopathic blood vessels, which may be a consequence of a connective tissue disorder like EDS. As described by researchers, this excess fluid generates hypoxic conditions at the cellular level, which leads to inflammation: “When excess fluid is present, [loose connective tissue] becomes compliant, allowing more fluid to collect, stimulating proteoglycan synthesis. Excess fluid limits cell access to oxygen resulting in hypoxia, inflammation, and fibrosis.” This book chapter provides a more complete description of the process by which lipedema may lead to hypoxia.
Could the hypoxia from fluid inundation be a significant contributor to the inflammation and MCAS experienced by people with EDS, ME/CFS, and fibromyalgia? Among other evidence that is consistent with this hypothesis is the finding that adipose tissue leads to increased levels of IL-6 cytokines in people with impaired lymphatic function. IL-6 levels also tend to be elevated in people with ME/CFS and fibromyalgia.
C. Could the build-up of lymphatic fluid be contributing both to widespread pain and some of the neurological symptoms attributable to median arcuate ligament syndrome (MALS) and thoracic outlook syndrome (TOS)? Earlier in this article, I describe how the use of manual techniques adapted from lipedema treatment has substantially reduced my daughter’s pain in areas that were painful when touched. While the precise “etiology of pain in lipedema is unclear,” I would propose, based on my daughter’s experience, that there could be at least two distinct mechanisms at work: the first is the build-up of lymphatic fluid that causes nerves to be impacted when touched; the second is pain from fibrotic adipose tissue.
Is it possible that some of the pain currently associated with central sensitization or small fiber neuropathy is due to the build-up of lymphatic fluid or the fibrosis of adipose tissue? Similarly, could the build-up of lymphatic fluid be contributing to the compression of nerves seen in the neurological manifestations of MALS and TOS? We had reached the point of researching surgeons for these conditions before we discovered techniques to drain lymphatic fluid, which have helped to significantly ameliorate the symptoms prompting this investigation. Notably, MALS occurs near the cysterna chyli (largest lymph node in the body) and TOS occurs near the point where all lymph travels to drain.
D. Could excess lymphatic or interstitial fluid be responsible for some of the symptoms associated with post-exertional malaise (PEM)? In July 2020, following a trip to the hospital to get an MRI, my daughter experienced a major crash from which she has still not fully recovered. The incident left her with a feeling of “awfulness” throughout her entire body that was incredibly debilitating – one of the worst sensations she has ever experienced. We have since come to recognize that this sensation is related to the presence of excess lymphatic/interstitial fluid in her tissues that responds to manual lymphatic drainage and squeezing, which leads to substantial improvement.
For a long time, we thought her experience was anomalous, but as I have read more about PEM, I have come to believe that at least some other people with ME/CFS are going through similar experiences. For example, I have seen descriptions of PEM by people with ME/CFS on Twitter as feeling like every cell in your body is poisoned – a description my daughter strongly identifies with. Similarly, the literature on PEM notes that there is often a delay of hours between exertion and the onset of the horrible feelings associated with PEM, which my daughter also experienced. The whole-body shaking my daughter experienced after the delay has apparently also been reported by others. And of course, the increased discomfort that my daughter experiences with exercise is widely reported by people with ME/CFS.
Could some of the symptoms of PEM for some individuals with ME/CFS be related to excess lymphatic or interstitial fluid that literally drowns the affected tissue, resulting in hypoxia and inflammation? This could happen through several potential mechanisms. One possibility is that exercise causes an increase in the leakage from microangiopathic blood vessels that occurs in people with connective tissue disorders, perhaps through a short-term increase in blood pressure; as one study notes, “[s]ystolic blood pressure (BP) normally rises with exercise as cardiac output increases during exercise in responses to the increased demand of oxygen from working muscles via increased sympathetic tone.” (Could this tendency for leakage be related to the reduced endothelial function observed in people with ME-CFS?). Increased fluid volume from elevated estrogen, cortisol or medication/supplements could potentially exacerbate the problem by increasing blood volume and pressure (leading to increased leakage from blood vessels) and by increasing the overall amount of lymphatic and interstitial fluid. Exercise could also cause joint dislocations that lead to the release of additional interstitial fluid.
Another, more dramatic possibility, is that a mast cell reaction causes the release of inflammatory mediators that increase the permeability of blood vessel walls (increasing the leakage of fluid) and possibly impair the functioning of lymphatic vessels as well (inhibiting the uptake of fluid). This could happen for any number of reasons, including mast cell reactions to perfumes or mold or dislocation in the spine that increases intracranial pressure. A biphasic mast cell reaction could explain the delay that is often seen before the onset of severe PEM.
(More speculatively, could a virus or other pathogen cause endothelial damage / dysfunction in blood vessel walls and lymphatic vessels – either directly, as in the case of COVID-19 or indirectly, through a cytokine storm or other overactive inflammatory response—in people with a connective tissue disorder, laying the groundwork for the leakage of lymphatic fluid and resulting experience of PEM at the onset of post-viral ME/CFS?)
E. Could some of the benefits attributed to vagus nerve stimulation stem from stimulation of the lymphatic system? Like many others, my daughter derives benefit from some of the techniques that are said to stimulate the vagus nerve, such as deep breathing, singing, and stimulating conversation. We have begun to wonder, however, if some of these benefits may be due to stimulating the lymphatic system to more efficiently remove excess fluid, rather than, or in addition to, stimulating the vagus nerve.
For the most part, these are unproven hypotheses that need evaluation through further research. My point in raising them is not to suggest they are all fully accurate or to suggest that the lymphatic system or adipose tissue fibrosis explains all the pathologies of EDS, fibromyalgia, and ME/CFS. Rather, I seek simply to suggest that these are additional avenues that merit exploration – in addition to and in conjunction with other inflammatory processes and abnormalities related to the spine, mitochondria, and blood.
As connective tissue disorders like EDS affect every system of the body, it should be unsurprising that they affect the lymphatic system as well.
Acknowledgements: This article benefited from review and comments by a number of reviewers, including Danielle Ayers; Elke Christ; and Karen Ashforth, MS, OTR, CLT-LANA, Board Certified Lymphedema Therapist; Clinician, Consultant, Educator. In addition, the article benefitted from research citations shared by Elizabeth Swope.
 Jeffrey Lubell is the parent of a teenager with chronic illness. He is not a doctor and does not have medical training.
Health Rising’s BIG (little) Donation Drive Update
Thanks to the over 160 people who have contributed to Health Rising’s year-end donation drive!
Health Rising has probably left some bruised egos out there. We’re constantly getting requests for guest blogs but we turn almost all of them down. Why? Because we’re looking for well-researched blogs that open up new areas of ME/CFS, fibromyalgia, long COVID, and other diseases – and those don’t come often. When they do, though, they can be inspiring, informative, and sometimes hard-hitting.
Over 70 people have contributed blogs to Health Rising over time. Guest blogs from the last year included: Jeffrey Lubell (Could High Dose B-1 Help?, this lipedema blog, Brendan (The Coronavirus Vaccine: Is There a Better Way?), Amber Ella (Are We Failing People with Extreme ME/CFS?), Jeff Wood (Is ME/CFS be a Chronic, Ongoing Brain and Spinal Cord Injury Exacerbated by Exertion?), Michael Sieverts (A Science Insider Takes an Inside Look Nath’s Long Covid Study), Art Mirin (The Education of an ME/CFS Advocate), and Dorothy Wall (Review of “Sick and Tired: Intimate History of Fatigue“)
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