Ehlers-Danlos Syndrome, referred to as EDS, is a congenital connective tissue disorder that often presents with numerous complications. EDS is diagnosed as a genetic condition that affects different types of collagen, and connective tissue constituents. Joint hypermobility is a common characteristic finding of most forms of EDS. Aberrant and deficient connective tissue can lead to several complications that can impair: organ function, joint stability, immunological mechanisms, and neurological function. Over the past 7 years we have worked with a good number of individuals who have been diagnosed with EDS. We have accumulated a fair amount of knowledge regarding EDS, including the therapeutics that we have seen work. This article will discuss some of the therapeutics we’ve seen work in EDS, as well as touch upon the need to differentiate between congenital forms of EDS and environmentally-acquired joint hypermobility.
Ehlers-Danlos Syndrome consists of a group of 13 different conditions, which adversely affect the connective tissue. Although all forms of EDS are believed to be genetic in origin, the most common form, hEDS, has no known genetic association. Diagnosis of EDS is typically done through a geneticist, or a physician versed in diagnostics. While genetic testing is often used, this is not always the case. Many patients are diagnosed with EDS simply by evaluating family and patient history. When genetic testing is performed, and no known association is found, but the patient still exhibits hereditary characteristics, they are usually diagnosed with hEDS (hypermobile EDS).
While all forms of EDS usually feature some degree of joint hypermobility, the fact that the most commonly diagnosed form has no known genetic association, poses problems. One of these problems is the chance of misdiagnosis.
Differentiating Congenital EDS from Environmentally Acquired Hypermobility
It is my contention based upon clinical observations that there are many patients diagnosed with EDS who rather have environmentally- acquired joint hypermobility. In 2019, We released this article calling attention to the fact that certain stealth infections, namely Borrelia (the bacteria that causes Lyme disease) and Bartonella are capable of producing symptoms that resemble EDS, in some patients. In that article I cited a study which involved a veterinarian who was misdiagnosed with Vascular EDS (Type 3 EDS), when in fact she was infected with Bartonella, by exposure to fleas. She presented with many of the same clinical manifestations of EDS, including joint hypermobility and joint pain. Upon being given Bartonella-specific antibiotics (azithromycin, rifampin, and minocycline), the patient’s symptoms (including joint hypermobility) resolved (1).
Since that time, we have encountered several patients diagnosed with EDS, who upon more careful review of their history, reveal that their loss of connective tissue function and joint hypermobility were actually acquired following illness. Having trialed various EDS-specific protocols with this group of patients, we have yet to see any connective tissue symptoms improve.
At the 2019 TFIM Conference (The Forum For Integrative Medicine) in Seattle, Washington, during my presentation on EDS and Joint Hypermobility, I specifically called attention to this important clinical distinction and the necessity to treat patients with Environmentally Acquired Hypermobility differently. The environmental factors must be sought and addressed as a matter of primary importance. From what I’ve seen, this is more often than not caused by one or more stealth infections such as Bartonella or Borrelia. It is now increasingly more understood that these types of bacteria are able to invade and damage the host’s connective tissue through numerous mechanisms (4). Why the patient’s connective tissue system or extracellular matrix can go into a free fall of dysfunction is a matter of contention. In my presentation at TFIM, I cited Dr. Naviaux’s Cell Danger Response as the most probable mechanism of how matrix-generating fibroblast cells may undergo a cell danger response, given that these cell types contain purinergic receptors, and are capable of effluxing ATP. Consequently, as a result of cell danger, fibroblast mitochondria likely will go quiescent, and the continual turnover of matrix constituents slows drastically.
Environmentally-Acquired Joint Hypermobility may also be caused by the use of fluoroquinolone antibiotics. As an important rule, I educate and urge physicians that under no circumstances should they use this class of antibiotics with patients who have EDS or joint hypermobility. This is because of the known risks of fluoroquinolones damaging Type 1 collagen and ß integrin receptors, as well as the risks of mitochondrial DNA damage, tendon rupture, retinal detachment and aortic aneurism. There is also the possibility that Environmentally-Acquired Joint Hypermobility can be caused by mercury toxicity because mercury inhibits collagen, and can lead to the increase in metalloproteinases, which causes collagen damage.
Before we get into EDS therapeutics, I want to summarize that there’s a clear need to distinguish between congenital hypermobility (EDS) and Environmentally-Acquired Joint Hypermobility. Further complicating matters is there are some people with congenital EDS who also have stealth infections such as Lyme or Bartonella. This makes matters even more complex, given the double hit on the connective tissue. While the subject of this article doesn’t involve this highly complex type of EDS patient, it should be noted that under these circumstances, special care should be taken to not acquire these types of infections, and to address these immediately if infected.
EDS Therapeutics That We’ve Seen Improve Symptoms
***Disclaimer: The information below should not to be taken as advice for anyone. These represent the author’s own statements and opinions from experience, and should not be construed as advice.
Approximately 50% of actual EDS patients (those with a congenitally acquired form) have favorably responded to one or more types of polysaccharides. This typically includes vapor distilled aloe vera, maitake mushroom, and/or red algae. Polysaccharides are complex sugar molecules, which are in fact the basis of all glycosaminoglycans. I’ve previously referred to polysaccharides as “the basic food stuff of the extracellular matrix”. When polysaccharides have worked favorably in EDS, I’ve observed improvements in the following symptoms. Note that these improvements are seen across the board, and are not necessarily for each person:
- Reduced joint subluxation and/or dislocation
- Reduced connective tissue or joint pain
- Reports of holding chiropractic adjustments better
- Reports of greater tolerance to and benefits from exercise and physical therapy
- Improved bowel function
- Improved circulation
PQQ: As an adjunct to polysaccharides, I usually trial PQQ (pyrroloquinoline quinone), which is a common antioxidant and electron donor. Perhaps 30-40% of EDS patients have shown some benefit when 20mg or more of PQQ is added. The benefits, if obtained seem similar to those produced by polysaccharides, but less pronounced. Several years ago I found literature that reveals that PQQ is the carbonyl redox cofactor of the collagen synthesizing enzyme Lysyl oxidase, which is a biochemical target in many forms of EDS (2). Perhaps PQQ would work better if copper was added to a regimen, because lysyl oxidase is a cupric enzyme. More research is needed.
CoQ10 and Vitamin B-2: For migraines, ocular migraines and recurrent migraines, in 50% or more of patients I’ve seen a combination of higher daily doses of CoQ10 and Vitamin B-2 work. There have been a good number of studies in non-EDS patients showing the benefit of CoQ10 and Riboflavin (B-2) for reducing the occurrence, intensity and frequency of migraine. In some cases I’ve seen this combination resolve migraines entirely. The fact that B-2 and CoQ10 can improve migraine calls to attention the likelihood that oxidative stress is involved in migraine, and particularly mitochondrial stress, and aberrant oxygen respiration. This is simply because B-2 and CoQ10 act specifically in mitochondria. It should be noted that migraines discussed here are not the same as headaches, or head or neck pain that is related to a structural component. Often, EDS patients have both migraines and general head/neck pain, as well.
Amino Acids – I’ve used MAP (master pattern amino acids), which boasts a more than 90% utilization and low nitrogen waste. MAP contains a variety of amino acids, including BCAA’s, tryptophan, methionine, phenylalanine and others. There have been a number of hypermobility cases where this product definitely was useful when higher protein and amino acid intake was needed. Some reports of benefit include reduction in inflammatory flares, and less episodes of hypermobile intensity. Some of the benefits associated with MAP may be attributed to enhanced utilization of the branch chain amino acids (BCAA’s) in the product. It’s known that the BCAA leucine is necessary for regulating cell growth via mTOR signaling, and this includes extracellular matrix-generating fibroblast cells.
Hormone Therapies – When called for, modulation of steroid hormones through different means has shown useful. Often, joint subluxation, and intensification of EDS-related symptoms are more pronounced in one of the phases of the menstrual cycle. I’ve found it important to look for that aspect, because it could highlight the critical involvement of steroid hormones, cytokines and growth factors on the neuro-endocrine-immune axis. The first research that I became aware of that elucidated the relationship between cytokines, steroid hormones and the extracellular matrix were from Pischinger (in his book Matrix and Matrix Regulation) and Heine (regarding Homotoxicology and the ECM). Progesterone modulation may be useful if intensification of symptoms occurs in the luteal phase, and/or if estrogen is higher. In aging, DHEA is often useful if osteoporosis is involved, because plenty of clinical studies have shown that DHEA can modulate osteogenesis and related mechanisms via IgF-1 and estrogen signaling. In post menopause, all sex steroids tend to decline. DHEA could be useful for both estrogen and androgen signaling in women.
Growth factors are a huge piece of the EDS puzzle, as many different growth factors can interact with and induce collagen biosynthesis. For example, IgF-1 can induce the activation of COL1 (type 1 collagen) and COL3 (type 3 collagen), and IgF-1 induces lysyl oxidase. Platelet-derived growth factor induces COL2 (type 2 collagen), COL4 (type 4 collagen) and COL5 (type 5 collagen). DHEA acts in part to increase IgF-1 signaling, and this is partly responsible for DHEA’s beneficial role in osteoporosis (5). IgF-1 is necessary for mTOR-mediated cell growth. Perhaps some combination of mTOR-specific amino acids (namely Leucine, Methionine, Arginine, Glutamine) and DHEA along with copper and PQQ could benefit some group of EDS patients.
EDS Therapies That Should Be Trialed But Not Enough Data Yet to Know If They Work
More serious EDS complications that include cervical cranial instability, cerebrospinal fluid leaks, chiari malformation and tethered cord often require more specific medical attention because these cases often present with multi-system involvement and are exceedingly complex. What else could possibly work in these complex cases? There are some isolated reports of benefit attributed to the GHK-Cu peptide, as well as frequency specific microcurrent, BPC-157 peptide, and some people who are trialing the Lifewave X39 patch, which purportedly increases GHK-Cu levels. GHK-copper is an endogenously produced peptide with known actions on tissue remodeling. It is often used as a peptide by injection. Whereas the photon wave patch from LifeWave known as X39 has been shown in a few small trial studies to raise levels of GHK-Cu, even though the patch is not transdermal and only involves the use of photon interaction (3). The use of GHK copper peptide gained attention in 2020 when a blog post was written, providing anecdotal testimony to its efficacy in EDS/tethered cord/ME/CFS (4). There has also been at least 1 report that the X39 patch produced more pain and was associated with adverse symptoms. More research is needed.
Energy Medicine & EDS
It must be candidly stated that work going back several decades has identified that collagen operates as a piezoelectric semiconductor. This research was pioneered by orthopedic surgeon Robert Becker, and was the subject of the groundbreaking 1985 book ‘The Body Electric’. Energy medicine constitutes a vastly under-explored range of therapies for EDS, in my opinion. Energy medicine comprises anything that encompasses the utilization of electro-therapies, or therapies that effect the body’s electric fields. The history of electricity, biology and medicine goes back a long time, and has undergone many separations, transformations and reunions. Some of the greatest molecular biologists became heavily invested in studying the role of electricity, subtle electromagnetic fields and the nature of biology (for example Nobel Laureate Albert Szent-Gyorgi). Because we now live in a literal sea of non-native EMF’s, it is nearly impossible to understand how electricity on all scales is positively and negatively affecting EDS patients. For now, we can appreciate the fact that collagen possesses semi-conductive properties, that EDS patients have disruptions to collagen, and likely, electricity in different forms could be both a powerful therapeutic treatment, as well as a toxin, capable of causing harm.
My experience, observations and research has led me to discover that people with joint hypermobility often possess certain “gifts” which seem to be related to enhanced mechanisms of the nervous system and higher brain function. These enhanced functions are possibly due to differences of charge distribution within connective tissue and collagen matrices. Information processing is often higher, and this suggests that electrical conductivity and charge distributions in their tissues will exhibit unique characteristics. I have been told by countless numbers of EDS patients that they possess the ability to talk to spirits, possess psychic abilities, have extrasensory perceptive abilities, can astral travel at will, are often attacked by spirit entities, are highly empathic, and don’t ordinarily talk about any of these things. Indeed it has remained taboo for many.
I became highly invested in experimenting with energy medicine when I purchased a Theraphi device in 2021. This is a type of Cold Atmospheric Plasma (CAP) light technology. Plasma in this context refers to ionized gas, the 4th phase of matter. When high voltage charges noble gasses, an electromagnetic field is created, which is measurable. Furthermore, when frequencies are used to modulate these charge dynamics, very interesting effects often occur. While the type of physics involved in these processes are far outside of the scope of this article, it is worth noting that a plethora of medical literature already exists with respect to cold atmospheric plasma as used for: inactivating pathogens, modulating wound healing, inducing collagen synthesis, activating certain immune cells, inducing apoptosis in cancer cells via ROS/RNS, just to name a few. My experience with a limited number of EDS clients using the Theraphi have been very interesting, to say the least. I’ve had reported to me, immediate subjective improvements in vascular tone and venous circulation, reduction of pain and neuropathic symptoms (the effects of which have shown to last for 3-4 weeks in some instances), as well as enhancement of brain-related functions, and also effects related to interacting with various “gifts”.
Frequency Specific Microcurrent (FSM) has been around a long time, and was resurrected by a number of now well known people, including Dr. Carol McMakin. The successful use of FSM in EDS-related complications was highlighted by this story by a patient. Dr. McMakin reported at the 2019 TFIM conference, a 14% increase in collagen synthesis in a rabbit study using FSM. There’s no question that frequency modulated microcurrent improves tissue healing. This was proven several decades ago. What needs to be trialed is how FSM is synergistic with other related EDS therapies. I will say that there have been a few isolated reports that FSM backfired in EDS. Perhaps the correct frequency wasn’t used, or the duration needed to be altered. More research is needed. For more information on FSM, and to locate a trained practitioner go here.
There must be more attention to non-pharmacological therapies for EDS. While pharmacological and biochemical-related therapies can be important, there is a lot more to learn and unpack with respect to how the connective tissue, brain and nervous system of EDS patients is unique, and I would argue, often highly evolved. The use of different energy medicine technologies, including but not limited to PEMF (pulse electromagnetic field therapy), Beemer, FSM, Theraphi/cold plasma, pulsed sound waves and various frequency applications may yield important results for EDS patients going forward. Additionally, I would like to learn how many EDS patients have heightened sensitivities to non-native EMF and electric fields.
Somatic Experiencing & Related Therapies – Somatic experiencing is a type of therapy developed by Peter Levine that involves integrating body and mind with the attempt to modulate the limbic brain, cognitive processes and the autonomic nervous system. From my experience, EDS patients frequently have heightened sensory processing functions. Several years ago, research carried out by Jessica Eccles in the U.K. found patients with joint hypermobility tend to have anxiety disorders, and this is associated with hypertrophic limbic brain structures (amygdala and hippocampus). Somatic therapies can entrain new neural patterns and lessen overactive limbic responses.
Limbic Brain Training – The limbic brain processes emotional information and shapes autonomic responses. A variety of different limbic retraining programs now exist. These hold promise because research has now established the relationship between joint hypermobility, anxiety and amygdala hypertrophy (6). Limbic retraining holds promise for reducing anxiety, pain, pain perception, stress response, and improving interoceptive abilities.