[JessOBX]

Great show last night!!! Wayyy over my head but Betsy and the docs did a wonderful job clarifying and simplifying the biology/molecular information making it easier to understand. Thank you for all you do!!

[kmorros]

Yeah it was. It was very helpful for our clinician followers.

[K.]

Hi, I’m requesting more information about shedding exposure for people who are more susceptible to shedding. I know 2 people in remission from cancer for over 10 yrs, they did not get the mRNA Injections but once exposed to their daily office environment 5 days a week ( surrounded by an environment of multiple mRNA vaccinated coworkers) – the cancer in remission without any health issues for over 12 years came back and so aggressive that it can’t be successfully treated. There are so many unknown variables but with someone who has a predisposed history to cancers that have been more impacted by the mRNA injections and with shedding now known to cause microclots… is it better for those who are in that category of high risk susceptibility to try and arrange a remote work environment and avoid the highly mRNA injected surroundings as much as possible to protect their health and the increased susceptibility of their cancer returning after many years in remission. Theses cancers that have been more susceptible are returning with the more aggressive “ turbo cancer” and due to our limited blood supply without mRNA – needing repeated blood transfusions in those types of cancers is another added risk. These cancers returning are breast cancer, leukemia AML. There are some oncologists acknowledging the mRNA causing these cancers to return aggressively- the shedding exposure can also impact that higher risk group if they are repeatedly exposed to high levels of mRNA shedding?

Any ideas? Thoughts? Advice?

[kmorros]

Hey, I would just encourage them to speak with a provider who treats long COVID/vax injury. They can explore individually the risk factors and options with these patients and what is the best decision.

[MariaDL]

Hi Everyone – In the Feb 21 webinar, Scott Marsland recommended using a micro-current device (can be wrapped around the ankle) in treatment for long covid fatigue symptoms.

I’d like to try it but not sure what to buy – does anyone know which one he recommends?

Thanks!

[kmorros]

Hey Maria, it is mentioned in the I-RECOVER post-vaccine treatment guide.

[kgg12003]

Thank you for this post as I had a follow up question on collagen. I am confused. I heard Scott Marsland FNP-C say not to use it last week. Something about clotting. And then last night someone asked and your reply was, it is OK to use unless your physician says otherwise.

Is what he was referring to last week, are people who have been vaccinated and already have clotting problems? Which would not apply to me as I already had a vaccine injury from the HepB series, so I did not get the covid shot.

The reason I ask is I take it in my morning coffee in an effort to heal my gut. I do not want to encourage clotting, but I like using it.

Thank you for any further clarification.

[healnaturally]

What I have learned about collagen is NOT to trust it. It will be high in Prions (ALS/Creutzfeldt-Jacob Disease) & it proliferates and exasperates an underlying Lyme (especially those not aware they are presenting with this systemic issue).

There are much better ways to heal the GI.

[kmorros]

HI, do you have a study that shows this to share? We actually also saw in the studies this was not the case with Lyme either. @ysaleeby would you like to weigh in here?

The organism that causes Lyme disease, Borrelia, is not fed by oral collagen peptide supplements. Conversely, by aiding in the process of collagen rebuilding, oral collagen peptide supplements may potentially support the healing

process associated with Lyme disease.

Borrelia burgdorferi can degrade both soluble and insoluble ground substances in the

extracellular matrix and to trigger metalloprotease activity. As a result, the collagen

dissolves and B. burgdorferi can start colonizing the collagen fibers. Interestingly,

because Borrelia prevents fibronectin from generating new collagen, it can also impede

the repair of tissue. (1-3)

Our bodies depend on type II collagen and extracellular matrix materials like hyaluronic

acid and other polysaccharides for connective tissue repair and regeneration. To

optimize strength, mobility, and elasticity, these constituents aid in the aggregation,

organization, and healing of connective tissue fiber. In the absence of these elements,

type III collagen can become weak, immature, and irregularly oriented during healing.

Giving patients the right nutritional support will speed up their recovery and encourage

the production of collagen, which will relieve their joint discomfort. (1)

Supplemental collagen may be beneficial for patients in addition to nutrient-dense diets,

stress management, sleep optimization, and avoidance of pollutants as ways to protect

collagen. Patients can readily add powder formulations to beverages to support their

bodies while they keep up with collagen repair, even though some forms of

supplemental collagen are accessible in pill form. (1,3)

Take-home point: First, our bodies cannot absorb collagen in its whole form. To enter

the bloodstream, it must be broken down into peptides so it can be absorbed through

the gut. (5,6) Hence, it cannot be extrapolated that the oral collagen peptide

supplementation is the same as those intrinsic collagens exist in human tissue.

Second, the interaction between platelet and collagen is a complex multistep

mechanism. VWF found in plasma will bind to exposed collagens prior to a platelet and

collagen coming into direct contact with each other. (4,7) Platelet receptor complex

GPIb/V/IX can then interact with the immobilized VWF to initiate the first platelet

contact. (4,8) The circulating platelets attach themselves to the vessel wall because of

this contact. (4,9) Platelets are propelled by shear pressures and roll over VWF-coated

surfaces in the direction of flow. The rolling process is sustained by the ongoing loss of

GPIb–VWF contacts on one side of the platelet and the creation of new interactions on

the opposite side. (4,10) When the rolling platelets are activated, the "classic" collagen

receptor α2β1 becomes available and participates in the process, which finally leads to

firm attachment. Firm adherence to collagen is mediated by integrin α2β1, which

permits platelets to engage with the low-affinity receptor GPVI, which is primarily

responsible for collagen-induced platelet activation. (4,11)

Therefore, the idea that consuming oral collagen supplementation aggravates platelet

activation and clot formation cannot be substantiated by existing literature.

In mammals, collagens are the most prevalent type of proteins. There are twenty-eight

members in the collagen family that have at least one triple-helical domain. Most

collagens form supramolecular assemblages in the extracellular matrix, where they are

deposited. Type II membrane proteins called collagens also exist in a soluble form that

is expelled by shedding from the cell surface. Collagens have structural functions and

influence the mechanical characteristics, structure, and form of tissues. They govern the

proliferation, migration, and differentiation of cells by interacting with them through a

variety of receptor families. Certain collagens have biological activities due to their

limited tissue distribution. (1)

Blood vessel wall cell function is also significantly regulated by collagen. By preserving

the stability and integrity of the arterial wall, collagens mediate vital hemostasis. Fibrosis

and other pathologic diseases may arise from an imbalanced turnover of collagens due

to unregulated creation and/or breakdown. Arterial occlusion or thrombosis may result

from thickening of the artery wall caused by collagen buildup. Aneurysms or vessel wall

rupture may result from the wall's thinning due to collagen insufficiency or degradation.

Collagen-mediated mechanisms are essential for preventing excessive bleeding or

thrombosis. Collagen can be bound by clotting factors, von Willebrand factor, integrins,

and glycoprotein VI to help restore normal hemostasis following damage. (2)

The vascular endothelium, circulating platelets, and coagulation proteins must

communicate in a well-regulated manner for the hemostatic system to function. Under

physiological conditions, anticoagulant and antiplatelet mechanisms prevent

thrombosis, and the commencement of clot formation at the site of injury restores

arterial integrity. Excessive thrombosis or bleeding may occur when the equilibrium

between procoagulant and anticoagulant systems is upset due to hereditary or acquired

malfunction, which can have adverse effects. When the vascular endothelium is

damaged, the vascular wall's underlying extracellular matrix (ECM) is exposed, and

protein-derived fragments might be released. Hemostasis must be maintained by the

clotting mechanism involving the extracellular matrix, specifically collagens. (2)

The vascular wall's mechanical strength is derived from collagens, the most common

proteins in the extracellular matrix (ECM), which are normally concealed underneath the

blood vessel's endothelial layer. Collagens that have been exposed to the bloodstream

following vascular wall injury bind to platelet receptors, causing the platelets to stick

together and aggregate, initiating the coagulation process. To the best of our

knowledge, collagens are the only extracellular matrix proteins that can facilitate

complete platelet activation in addition to promoting platelet adhesion and synthesis.

(2,4)

Under both biochemically treated and shear flow conditions, an integrated analysis of

the data revealed a strong correlation between clot stiffness, clot contractile force, and

the degree of clot retraction (volume shrinkage). This suggests that these two stimulants

have an equally strong, independent effect on clot remodeling and stiffening. (3)

It was later determined that the initial theory that collagen was also directly in charge of

initiating the intrinsic coagulation cascade (4,13) was false. (4,14) However, negatively

charged phospholipids like phosphatidylserine become exposed on platelets' surface

after interacting with collagen, forming the catalytic surface for the assembly of active

coagulation complexes and thrombin generation. This is how collagen indirectly

regulates the formation of thrombin. (4,15)

Platelet interaction with collagen under shear should be seen as a dual process

involving adhesion and activation. (4, 12) VWF found in plasma will bind to exposed

collagens prior to a platelet and collagen coming into direct contact with each other.

(4,7) Platelet receptor complex GPIb/V/IX can then interact with the immobilized VWF to

initiate the first platelet contact. (4,8) The circulating platelets attach themselves to the

vessel wall because of this contact. (4,9) Platelets are propelled by shear pressures and

roll over VWF-coated surfaces in the direction of flow. The rolling process is sustained

by the ongoing loss of GPIb–VWF contacts on one side of the platelet and the creation

of new interactions on the opposite side. (4,10) When the rolling platelets are activated,

the "classic" collagen receptor α2β1 becomes available and participates in the process,

which finally leads to firm attachment. Firm adherence to collagen is mediated by

integrin α2β1, which permits platelets to engage with the low-affinity receptor GPVI,

which is primarily responsible for collagen-induced platelet activation. (4,11)

Our bodies cannot absorb collagen in its whole form. To enter the bloodstream, it must

be broken down into peptides so it can be absorbed through the gut. These peptides

may be broken down further into the building blocks that make proteins like keratin that

help form skin, hair, and nails. (5,6)

[kgg12003]

Wow! Thank you

[kmorros]

We will be releasing a post that is a more lay person version friendly- if you are a lay person.🤣 I know that was a lot.