The Hidden Link Between Hypermobility and Vaccine Injuries

How ligamentous laxity predisposes sensitive patients to vaccine induced microstrokes

Note: over the last month, individuals who’ve been injured by the COVID vaccine reached out to me to share the earlier version of this article was very insightful for them. As such, I felt it was important to revise it so more could learn about this concept (likewise why I recently published another article discussing what creates fluid motion in the body).

Frequently, a treatment which works very well for one patient will fail to help (or harm) a patient with a very similar issue. In turn, a critical aspect of medicine is being able to recognize the unique differences between patients so you can best determine what treatment fits best for each patient and what dose is the most appropriate for each patient. Unfortunately, in “standardized medicine” (where everyone follows treatment algorithms) there is no single approach which helps all patients, and as such, protocols and dose are decided upon which will overall fit the most number of people, but simultaneously fail many others (which is a major reason individuals quit conventional care and seek out alternatives). Thriving Beyond Fifty ... Harlow MSc MCSP, Will Best Price: $20.25 Buy New $16.10 (as of 06:46 UTC - Details)

Note: the art of selecting the correct dose (and the perils of our current approach to it) are discussed here.

Constitutional Archetypes

Fortunately, while this task seems impossible (as the basics of medicine are complicated enough), there are a variety of tricks that make the process much easier. One is a recognition of “constitutional archetypes” where individuals share a cluster of similar traits. This concept (discussed further here) is very useful, as once you become familiar with an archetype and you spot indicators of it in someone, it then becomes possible to identify to predict many other characteristics of that individual.

In medicine, I find one of the most helpful archetypal frameworks to be the three Gunas (from Hinduism), which posits that three primordial energies exist that individuals can be composed from:

Sattva, which has qualities including “goodness, calmness, harmonious.”

Rajas, which has qualities including “passion, activity, and movement.”

Tamas, which has many qualities including “ignorance, inertia, laziness.”

Note: Sattva in many ways mirrors Vatta, and to a lesser extent the ectomorph type. Rajas in turn pairs with Pitta and mesomorphs while Tamas pairs with Kapha and endomorphs.

From a medical standpoint, Tamasic patients tend to have a general thickness, heaviness and solidity to them, while Sattvic patients tend to have a more light and ephemeral quality to them. Each in turn has a very different response to medical therapies. Tamasics typically tolerate and often only respond to forceful interventions (e.g., many of the standard medical therapies) whereas Sattvic’s respond very poorly to aggressive therapies and instead need gentle ones to coax their health back (which are often energetic in nature like acupuncture)—something which often does virtually nothing for Tamasic patients.

Put differently, Sattvics are often recognized as being much more sensitive to environmental toxins and harmful medications (e.g., many of them refer to themselves as canaries in reference to the birds miners used to monitor for toxic gases in coal miners as they would be affected much sooner than the miners and that we should be taking their medical injuries as a warning sign many of the substances we are being exposed to are not safe). Likewise, Sattvics frequently need much lower doses of medications, but unfortunately often instead are overdosed because standardized medicine only uses the dose that best fits the entire population (which as I discuss here, is inevitably the wrong dose for many).

Note: COVID vaccine injuries disproportionately affected the Sattvic archetype.

Throughout my life, I’ve known more Sattvics than I can count, and one of the things I’ve always found immensely unfair is that most people cannot relate to the struggles they face (e.g., many, including some of their doctors, think they are “crazy” or “hypochondriacs”) or how sensitive they are to many things around them most never even notice.

As such, I’ve made one of the missions of this Substack to bring attention to their situation. At the same time however, I’ve always wondered “why is this constitution so sensitive?

Ligamentous Laxity

At this point, I often immediately recognize the sensitive patients by their presence, their psychological demeanor and their body shape. For instance, one of the frequent physical traits I associate with this archetype is a distinct pattern of movement (which is often graceful) that I believe results from laxity in their ligaments.

Since the ligaments stabilize the joints of the body by constraining their maximum range of motion, once the ligaments weaken, their laxity (looseness) frequently causes the maximum range of motion of the joint to increase.

Individuals with ligamentous laxity have certain advantages. For example, they are normally much more flexible (e.g., they can stretch their body much further), and often become dancers because of the mobility afforded to their body.

Conversely, ligamentous laxity also creates a variety of issues for those patients. The most common one is that since their body uses the ligaments to stabilize itself when a force enters it, once the ligaments weaken, things will frequently shift inside the individual more than they should in response to those forces.

For example, individuals with ligamentous laxity tend to be more susceptible to developing chronic injuries from car accidents or other physical traumas. Likewise, their joints “pop” easily, but if they get forceful adjustments to reset the position of their bones, the bones will often go back out of place (since the stability which would otherwise maintain that structure is lacking).
Note: I have seen numerous patients with ligamentous laxity that had far too many forceful adjustments that eventually created issues for them. This normally occurs either because the repeated adjustments (performed due to the patient’s pain rapidly returning after each adjustment) further weakened their ligaments or because the weakened joint exceeded its expected range of motion during a thrust and the bones of the joint ended up in a position which created other issues for the body.

Similarly, individuals with ligamentous laxity (especially when it is significant) tend to develop a variety of issues that are ultimately treated with surgery. Unfortunately, due to being more “sensitive” and having an impaired ability to heal following the surgery, they frequently suffer significant complications from those surgeries—which sadly leads to even more surgeries (e.g., there are many stories of this in the Ehlers-Danlos syndromes [EDS] support groups).
Note: since ligaments are composed of collagen, impaired collagen production often gives rise to ligamentous laxity. Likewise, since collagen production is needed to heal from surgeries, individuals with impaired collagen production have greater difficulty recovering from surgery.

Ligamentous laxity can also create a variety of other issues throughout the body (e.g., all sorts of gastorintestinal problems). One of the least appreciated consequences of hypermobility is that the body depends upon ligamentous tension for proprioceptive feedback (knowing where the body is in space), and as a result, once the ligaments become lax, hypermobile patients lose some of the general awareness that allows us to subconsciously navigate through the world.

For example, EDS is known to be associated with impaired balance and an increased likelihood of falling. However, it’s much less appreciated that this lack of proprioceptive feedback can give rise to a general sense of anxiety because the ground does not feel as stable below one’s feet—something which is difficult to appreciate unless one has experienced it directly (e.g., I’ve met people who easily survived a major earthquake but were psychologically disturbed for years after as a result of them briefly losing their sense of the ground which they had always previously taken for granted).

What Causes Ligamentous Laxity?

A variety of processes can cause ligamentous laxity. Frequently, a combination of these are at work (e.g., someone with a pre-existing weakness in a ligament is more likely to have something injurious to a ligament create a chronically lax ligament).

Physical Injuries

Ligamentous weakness is frequently caused by a chronic injury to a ligament (or an injury which did not properly heal). For example, when the ankle is injured from a sprain, the ligament that keeps the ankle from turning inwards gets damaged, predisposing us to an unstable ankle and future ankle injuries until the ligament is repaired and strengthened.

Pharmaceutical Injuries

In addition to physical injuries, biochemical injuries can also occur. This is best known to occur following the use of anti-inflammatory medications. For example, NSAIDS like Ibuprofen (which are typically the go to for “treating” sports injuries) in addition to reducing the discomfort of an ankle injury also weaken the ligaments (as by suppressing the inflammatory process it also suppresses the healing process).

This results in sprains that are treated with NSAIDs often being predisposed to future injuries (since the stability given to the joint by those ligaments is partially lost until something like a regenerative therapy is given to repair that ligament)—which in the case of ankle sprains is something I and colleagues frequently see in our patients.

One of the most common therapies given to treat joint pain are injected steroids, which, by being powerful anti-inflammatories, are often initially effective in making the patient feel better. Unfortunately, injected steroids are also weaken ligaments at the site where they are injected, particularly when they are given multiple times. Since joint inflammation (and pain) often is a result of improper joint stabilization by a ligament (leading to the joint being worn down by inappropriate pressures), this treatment approach results in patients needing more and more injections as their ligaments further weaken.
Note: this is also a common issue for those with chronic neck or back pain and unfortunately often results in them often “needing” to get a surgery to stabilize the spine—which often makes things even worse (that subject and alternative approaches to treating spinal pain are discussed here and here). One of the particularly frustrating things about this situation is that DMSO can be used for many of the same injuries and chronic pains the ligamentous destroying drugs are used for, but rather than further weaken them, DMSO often repairs the ligaments (along with often being far more effective at resolving the patient’s condition).

Additionally certain more toxic pharmaceuticals can also weaken the ligaments. For instance, beyond steroids, I have also frequently observed this after the someone suffers an injury from a more toxic pharmaceutical (e.g., this is well known to occur from fluoroquinolone antibiotic like ciprofloxacin but I’ve also seen it after an accutane injury).

This I believe results from the fact that the body is continually rebuilding and remodeling its structural tissues to meet the needs of the environment. For example, the bones depend on the weight of gravity to signal growth, so when astronauts are in space for prolonged periods of time, their bones significantly weaken (and may break once they return to Earth’s gravity) unless the astronauts also do special exercises in space.

In addition to bones, the collagen of the body also continually rebuilds and remodels itself. Since collagen production is an energy intensive process, if the mitochondria get injured (which fluoroquinolone antibiotics are notorious for doing), over time the connective tissue in the body will also weaken until it fails as a result of it no longer being able to accommodate a previously manageable force input (e.g., sudden tendon ruptures are very common after fluoroquinolone usage).

Constitutional Predispositions.

EDS and Marfan Syndrome are the two classic medical conditions that are associated with ligamentous laxity. Both of these conditions are considered to be rare diseases, with EDS being estimated to affect between 1 in 5000 to 1 in 100,000 patients (depending on its severity and the source of the estimate), while Marfan Syndrome is estimated to affect 1 in 5000 patients.
Note: One recent paper found that the prevalence of diagnosed EDS was 1 in 500 and many believe it is even more common (e.g., I’ve met dozens of people who have appear to have EDS or an EDS-like syndrome).

In addition to EDS, there is also a self-explanatory condition known as “generalized joint hypermobility,” (GJH) which is found to affect around 12.5% of the population and predisposes them to musculoskeletal pain and injury. At this point I suspect that both this condition and EDS are under-diagnosed and that a spectrum exists between overt EDS and GJH.

Functional Predispositions

It some cases you can watch a ligamentous laxity rapidly onset within the body. The most classic example results from the hormone relaxin (released during pregnancy), which weakens the ligaments of the body so that the pelvis becomes able to stretch and accommodate the birthing process. Because of this increased hypermobility, pregnant women become more predisposed to physical injuries (and developing musculoskeletal pain from the weight their baby).
Note: other hormones the female body secretes counteract the effects of relaxin, especially once the pregnancy is complete, and in turn, those with pre-existing hormonal imbalances are significantly more susceptible to musculoskeletal issues both during and after a pregnancy. Likewise, having pre-existing hormonal imbalances (due to the ligamentous weakness they create) can make women much more susceptible to musculoskeletal issuesparticularly after menopause.

In my eyes the most important functional predisposition of ligamentous integrity is nutritional status. While a variety of things can affect ligamentous integrity, we’ve found the often forgotten metal manganese (Mn) plays one of the most important roles. In turn, it is extremely common to find people who:

•Live in areas with lower manganese levels in the soil also appear to have higher rates of ligamentous laxity.

•Have ligamentous laxity that gradually improves when they appropriately take manganese for a prolonged period.

•Have a predisposition to ligamentous laxity (e.g., EDS or a hypermobility syndrome) be tipped over the edge by a manganese deficiency, and likewise have patients with existing hypermobility significantly improve from manganese supplementation.

Since manganese deficiency is such a common issue now, we’ve put a lot of thought into why we see it so frequently. Presently, we have four leading explanations:

•First, the topsoil has been heavily depleted of essential minerals by our modern farming practices. This creates a variety of issues (and likewise significant improvements are seen in the plants grown in remineralized soil and in the humans who consume those plants).

•Glyphosate (Roundup), a toxic but widely used herbicide, has a high affinity for chelating (trapping) certain minerals, once of which is manganese. Because of this, I believe the continually increasing levels of glyphosate in the environment have contributed to the current widespread deficiency of manganese.

•Bacteria require iron for their metabolism (and in turn one of the defensive mechanisms the body has to stop an infection is to sequester iron so bacteria cannot reproduce). The bacteria which causes Lyme disease has an unusual adaptation, which to my knowledge is unique in nature (which raises interesting questions about where Lyme came from). It uses manganese instead of iron, which thereby protects it from that defense mechanism, and we have long suspected it also causes individuals infected with the bacteria (including those with “silent” infections) to become manganese deficient. Indoctrinating Our Chi... Newman, Alex Best Price: $11.11 Buy New $17.76 (as of 06:16 UTC - Details)

•Mineral absorption is intrinsically linked to the acidity of the stomach (as acid is needed to chelate minerals that are tightly bound to plants), so deficient stomach acid (especially in the setting of nutritionally depleted soil) may predispose one to a manganese deficiency and hypermobility.
Note: in many cases, hypermobile patients have a variety of emotional sensitivities and varying degrees of psychiatric instability. Some of these patients have remarkable responses to targeted trace mineral supplementation (particularly for anxiety or feeling “ungrounded”). This observation in turn has led me to suspect an inability to obtain sufficient minerals from the diet (e.g., manganese) plays a key role in hypermobility.

Lastly, the relationship between manganese levels and hypermobility can also be seen in animals. For example, a study (inspired by the observation manganese deficiency correlated with weak antlers that were more likely to break) supplemented half of the deer with manganese and showed those deer had thicker and stronger antlers compared to the ones which did not receive manganese.

Note: manganese is often considered to be a toxic element (as it is associated with the neurological issues that follow chronic exposure to welding gas). I always thought this was strange as manganese is a necessary cofactor for numerous critical enzymes in the body (e.g., some of those within the mitochondria). Presently, I believe this is because the toxic form of manganese (e.g., that found in welding gas) is Mn³⁺, whereas the form that helps people found in the dietary supplements (and that typically tests well for patients) is Mn²⁺. In turn, I suspect that for some reason, Mn³⁺ impairs the function of essential enzymes that depend upon Mn²⁺. Alternatively, a hypothesis has been put forward (with data to support it) that manganese, while essential, also becomes toxic at high doses.

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