To be honest his story has massive gaps without being connected by any type of measurements. So the results of Herpesviruses producing miRNA and the results of decreased nIgM-FN1 are completely independent if one doesn't try to construct a hypothesis to connect the two. One could even argue that a disconnection of these results is more supported than a connection given the low nIgM-FN1 results of people who recently had Covid without developing LC (let's not forget that there were no differences between IgM-FN1 of HC vs ME/CFS and both HC & ME/CFS patients had higher levels of IgM-FN1 than patients that had Covid independently of whether they developed LC or not).
Prusty talks about his upcoming research on a podcast
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The Scientific findings are in the paper Bhupesh Prusty and his co-authors produced and which he constanty evolves as more knowedge/data appears month by month - as is the nature of science.
Professor Carmen Scheibenbogen, a co-author, is very experienced and knowledeable in immunology and wouldn't associated herself with a ''story'' without ''any type of measurements''.
Research 1st
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Everything is fitting into place nicely by various biomedical researchers that ME/CFS can be an outcome of SARS-COV-2, which makes perfect sense as ME is a post viral illness. NB: It's the CDC who took out viral association with Fukuda/CDC criteria CFS alongisde PEM - both hallmarks of ME. ME and PVFS (Post Viral Fatigue Syndromw) are instead, linked to a viral trigger.
Exciting research to follow:
CFS Mitochondrial dysfunction evidence. Prusty et al.
CFS Autoimmunity evidence. Scheibenbogen et al.
CFS microclots and CFS vascular damage(endothelial debris). Pretorius et al.
Immune cell invasion into the brain using novel PET tracer. Younger et al.
+ Many others..
Once the long awaited 'Long Covid' ELISA microclot assays and the novel autoimmune markers (Bhupesh Prusty's team discovered) are available to the patient community, things will move forward over the next few years.
In my opinion, things are looking positive.
Exciting research to follow:
CFS Mitochondrial dysfunction evidence. Prusty et al.
CFS Autoimmunity evidence. Scheibenbogen et al.
CFS microclots and CFS vascular damage(endothelial debris). Pretorius et al.
Immune cell invasion into the brain using novel PET tracer. Younger et al.
+ Many others..
Once the long awaited 'Long Covid' ELISA microclot assays and the novel autoimmune markers (Bhupesh Prusty's team discovered) are available to the patient community, things will move forward over the next few years.
In my opinion, things are looking positive.
They are, and he is not claiming otherwise.
His paper is sort of a brain dump of his current research, but if you listen to his interviews and talks, he explains why they wanted to get it out ASAP. He feels that nIgM-FN1 and fibronectin discovery may have immediate clinical application. He calls for further research into this and for clinical trials.
Forummember9922
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Heres an image with a slide from a recent Prusty Interview.
The dark purple portion of the bar is LC and CFS groups with zero antibodies for the specific herpesvirus.
The question I would like to know is can someone have CFS with the same features - yet have zero antibodies to all three of these viruses examined? (Hsv1, Ebv, Hhv6)? Or is one of these lurking in every CFS patient?
Also if such a patient exists- lets say severe but zero aabs to any of these 3 herpesviruses- how is their fibronectin? Do they have high aabs to another virus?
This helps to answer if all the herpes stuff is moreso downstream or upstream.
I realize he never said ‘CFS is from a herpesvirus’ but he’s seemed to paint a compelling tale of how much can be explained by them - Mitchondrial dysfunction from HERV's causing fatigue, brain fog. Older thoughts about CFS after mono. Why CFS patients don't catch colds as much (herpesviruses claim the turf). And the simple trend he is showing here to begin with.
From the TLC podcast interview it sounded like his theories about herpesviruses/CFS are all about where the viruses get. Hints of bone marrow etc.
Also maybe I dont understand the type of test being talked about here, IE the difference between Dutpases and just ‘having’ hsv1.
The dark purple portion of the bar is LC and CFS groups with zero antibodies for the specific herpesvirus.
The question I would like to know is can someone have CFS with the same features - yet have zero antibodies to all three of these viruses examined? (Hsv1, Ebv, Hhv6)? Or is one of these lurking in every CFS patient?
Also if such a patient exists- lets say severe but zero aabs to any of these 3 herpesviruses- how is their fibronectin? Do they have high aabs to another virus?
This helps to answer if all the herpes stuff is moreso downstream or upstream.
I realize he never said ‘CFS is from a herpesvirus’ but he’s seemed to paint a compelling tale of how much can be explained by them - Mitchondrial dysfunction from HERV's causing fatigue, brain fog. Older thoughts about CFS after mono. Why CFS patients don't catch colds as much (herpesviruses claim the turf). And the simple trend he is showing here to begin with.
From the TLC podcast interview it sounded like his theories about herpesviruses/CFS are all about where the viruses get. Hints of bone marrow etc.
Also maybe I dont understand the type of test being talked about here, IE the difference between Dutpases and just ‘having’ hsv1.
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Do you think a test for Fibronectin might help people that are unsure if they have ME/CFS or have been misdiagnosed and actually have a different / treatable disease ? any idea how much such a test might cost and whether it would be available across most of the usual countries ?
Forummember9922
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In keeping with Prusty theme of herpesviruses and fibronectin here are some GPT thoughts on any relationship
Fibronectin plays a role in the interaction between herpesviruses and host cells. Herpesviruses are a family of viruses that include several human pathogens, such as herpes simplex virus (HSV) types 1 and 2, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV). Here are some relationships between fibronectin and herpesviruses:
1. Viral Attachment and Entry: Fibronectin can act as an extracellular matrix component that facilitates the attachment of herpesviruses to host cells. Herpesviruses often utilize cell surface receptors that interact with fibronectin to bind to and gain entry into host cells. For example, HSV-1 and HSV-2 can attach to cell surface heparan sulfate proteoglycans, which can interact with fibronectin, enabling viral entry.
2. Cell-to-Cell Spread: Fibronectin can also contribute to the cell-to-cell spread of herpesviruses. After initial entry into host cells, herpesviruses can move from one cell to another by directly spreading across cell junctions. Fibronectin and its interactions with cellular receptors may play a role in promoting this cell-to-cell spread of the virus.
3. Modulation of Immune Responses: Fibronectin can influence the immune responses to herpesvirus infection. It can interact with immune cells and modulate their functions, such as cell adhesion, migration, and activation. Fibronectin can affect the recruitment and activation of immune cells at the site of infection, thereby influencing the immune response against herpesviruses.
4. Pathogenesis and Tissue Tropism: Fibronectin may contribute to the pathogenesis of herpesvirus infections by affecting tissue tropism and viral dissemination. The expression and distribution of fibronectin in various tissues can influence the ability of herpesviruses to infect and spread within the host. Fibronectin interactions can promote viral attachment and dissemination to different tissues, contributing to the systemic spread of infection.
Different herpesviruses have evolved specific strategies to interact with fibronectin and exploit its functions to facilitate their replication and dissemination within the host.
Fibronectin plays a role in the interaction between herpesviruses and host cells. Herpesviruses are a family of viruses that include several human pathogens, such as herpes simplex virus (HSV) types 1 and 2, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV). Here are some relationships between fibronectin and herpesviruses:
1. Viral Attachment and Entry: Fibronectin can act as an extracellular matrix component that facilitates the attachment of herpesviruses to host cells. Herpesviruses often utilize cell surface receptors that interact with fibronectin to bind to and gain entry into host cells. For example, HSV-1 and HSV-2 can attach to cell surface heparan sulfate proteoglycans, which can interact with fibronectin, enabling viral entry.
2. Cell-to-Cell Spread: Fibronectin can also contribute to the cell-to-cell spread of herpesviruses. After initial entry into host cells, herpesviruses can move from one cell to another by directly spreading across cell junctions. Fibronectin and its interactions with cellular receptors may play a role in promoting this cell-to-cell spread of the virus.
3. Modulation of Immune Responses: Fibronectin can influence the immune responses to herpesvirus infection. It can interact with immune cells and modulate their functions, such as cell adhesion, migration, and activation. Fibronectin can affect the recruitment and activation of immune cells at the site of infection, thereby influencing the immune response against herpesviruses.
4. Pathogenesis and Tissue Tropism: Fibronectin may contribute to the pathogenesis of herpesvirus infections by affecting tissue tropism and viral dissemination. The expression and distribution of fibronectin in various tissues can influence the ability of herpesviruses to infect and spread within the host. Fibronectin interactions can promote viral attachment and dissemination to different tissues, contributing to the systemic spread of infection.
Different herpesviruses have evolved specific strategies to interact with fibronectin and exploit its functions to facilitate their replication and dissemination within the host.
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Firstly it's important to mention that the currently presented Fibronectin levels in the study are not statistically significant and there's some slightly unusual statistical representation happening. Assuming that GPT didn't make up a lot of things, which is a big if, here are some more details.
1. Only is relevant to cFN. No clear connection to Prustys study can be seen since pFN seems to be the major contributor to his examined levels. Perhaps further studies can examine the levels he observered in terms of cFn and pFn.
2. Also only seems to be relevant to cFN?
3. Based on what Prusty said about Fibronectin not being incorporated into the immune complex this seems like the most relevant point to his hypothesis.
4. More relevant to cFN?
To examine how valuable what ChatGPT said I also asked it "what is the relationship between fibronectin and acute Covid", "what is the relationship between fibronectin and Ebola", "what is the relationship between fibronectin and Herpesviruses" and "what is the relationship between fibronectin and Hepatitis C". In all cases it gave me a 4 point list very similar to the above. So this is really just a representation of what ChatGPT predicts Fibronectin to do, independent of the specifics of Herpesviruses. ChatGPT is a LLM and so simplified it just predicts the next word in a sentence, meaning that sentences that require reasoning pretty much are always answered wrong.
Perhaps one can ask for more details to get better responses, but I suspect at that point it's more valuable to consult the literature. Unfortunately, concerning the literature, there doesn't seem to be too much material that Prusty or this forum itself didn't already discuss.
Forummember9922
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Thanks very much for your thoughts. I think it's great to propose ideas and then shred them up to see what nuggets of truth may remain in a socratic fashion. Agreed not a good idea to take GPT as gospel. Herpesviruses being the culprit for fibronectin issue would be convenient and yeild more actionability, but convenience does not make it true or false.
EDIT: Not to beat a dead horse about this subject but just realized they do actually claim this in the preprint "Here we show antibody response to herpesvirus dUTPases, particularly to that of Epstein-Barr virus (EBV) and HSV-1, increased circulating fibronectin (FN1) levels in serum"
EDIT: Not to beat a dead horse about this subject but just realized they do actually claim this in the preprint "Here we show antibody response to herpesvirus dUTPases, particularly to that of Epstein-Barr virus (EBV) and HSV-1, increased circulating fibronectin (FN1) levels in serum"
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Looks we can add the re-activation of human adenovirus (HAdV) to the list
https://www.frontiersin.org/articles/10.3389/fmed.2023.1208181/full
"We found a significantly elevated anti-adenovirus IgG titer in saliva of patients with ME/CFS after SARS-CoV-2 infection. This was not observed in healthy donors. We propose that this indicates an exhausted dysfunctional antiviral immune response in ME/CFS, allowing reactivation of adenovirus upon stress encounter such as COVID-19"
Including using the antiviral brincidofovir (BCV) as an option
https://www.frontiersin.org/articles/10.3389/fmed.2023.1208181/full
"We found a significantly elevated anti-adenovirus IgG titer in saliva of patients with ME/CFS after SARS-CoV-2 infection. This was not observed in healthy donors. We propose that this indicates an exhausted dysfunctional antiviral immune response in ME/CFS, allowing reactivation of adenovirus upon stress encounter such as COVID-19"
Including using the antiviral brincidofovir (BCV) as an option
More antibodies does not necessarily mean reactivation.
What I find unusual is that they never reproduce their similar past findings for other viruses. Are they just slicing and dicing data until they find something or what is going on here? These authors have a similar paper in similar directions (https://www.frontiersin.org/articles/10.3389/fimmu.2022.949787/full) and there's work of other groups in a similar direction (https://www.medrxiv.org/content/10.1101/2021.01.06.20248486v1) but there never seems to be a reproduction of older results which would be really significant.
Some of the findings seem significant to a layman like me, but perhaps an immunologist like Iwasaki would think differently.
Forummember9922
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Ok thats my brain fog. I was operating under the belief that only a preview was availble. Thank you.
datadragon
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the reactivation of multiple herpesviruses (EBV, HHV-6) and their production of dUTPase can elicit both humoral and cellular immune responses, including the hyperactivation of Th1 and Th17 in some patients with ME/CSF which has been in the literature for awhile. It does not appear to be the cause of the problem but is instead another downstream effect if immune function is compromised or stressed and viruses are allowed to reactivate adding additional fuel to the fire of the existing problem.
EBV and HHV-6 are actually the most common immunotropic viruses which use latency after infection to hide from the immune system. EBV has infected more than 90% of the world’s population and more than 95% of healthy adults. HHV-6 is the collective name for the double-stranded DNA viruses HHV-6A and HHV-6B. More than 90% of humans are infected with HHV-6B within the first three years of life.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9967513/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142679/
The complement component 1q (or simply C1q) is a protein complex involved in the complement system, which is part of the innate immune system. Complement activation then elicits secretion of both IL-1β and IL-18 via activation of the NLRP3 inflammasome https://pubmed.ncbi.nlm.nih.gov/23817414/ again adding to the inflammation cascade as I've been mentioning https://forums.phoenixrising.me/thr...ed-abnormalities-in-me-cfs.90173/post-2439526
A bit more from that article for those who want more detail: TLR2 is a type of receptor that is localized on the surface of immune cells and can form complexes with TLR1 or TLR6. A significant binding affinity exists between viral dUTPases (PAMPs) and TLR2. Although TLR2 is part of the innate immune response and is vital for the defense against viruses, its activation has been shown to be involved in various autoimmune diseases, including RA, Sjögren’s syndrome, MS, systemic sclerosis and systemic lupus erythematosus (SLE). This is because once engaged, TLR2 activates a signaling cascade that results in the production of proinflammatory cytokines that contribute to the development and progression of many disorders. For example, Ariza et al. demonstrated that through the engagement of the TLR2 homodimer, EBV-dUTPase induces the activation of NF-κB, which is a very strong proinflammatory mediator. Interestingly, HSV-2 and HHV-6A dUTPases also activated NF-κB after ligation with TKR2/1 heterodimer. Furthermore Ariza et al. showed that EBV, HHV-6 and other viral dUTPases are capable of activating different lymphocyte subpopulations and inducing the production of T-helper-1 (Th1), T-helper-17 (Th17), and other inflammatory cytokines such as IL-1β, IL-6, IL-8 and TNF-α
EBV and HHV-6 are actually the most common immunotropic viruses which use latency after infection to hide from the immune system. EBV has infected more than 90% of the world’s population and more than 95% of healthy adults. HHV-6 is the collective name for the double-stranded DNA viruses HHV-6A and HHV-6B. More than 90% of humans are infected with HHV-6B within the first three years of life.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9967513/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3142679/
The complement component 1q (or simply C1q) is a protein complex involved in the complement system, which is part of the innate immune system. Complement activation then elicits secretion of both IL-1β and IL-18 via activation of the NLRP3 inflammasome https://pubmed.ncbi.nlm.nih.gov/23817414/ again adding to the inflammation cascade as I've been mentioning https://forums.phoenixrising.me/thr...ed-abnormalities-in-me-cfs.90173/post-2439526
A bit more from that article for those who want more detail: TLR2 is a type of receptor that is localized on the surface of immune cells and can form complexes with TLR1 or TLR6. A significant binding affinity exists between viral dUTPases (PAMPs) and TLR2. Although TLR2 is part of the innate immune response and is vital for the defense against viruses, its activation has been shown to be involved in various autoimmune diseases, including RA, Sjögren’s syndrome, MS, systemic sclerosis and systemic lupus erythematosus (SLE). This is because once engaged, TLR2 activates a signaling cascade that results in the production of proinflammatory cytokines that contribute to the development and progression of many disorders. For example, Ariza et al. demonstrated that through the engagement of the TLR2 homodimer, EBV-dUTPase induces the activation of NF-κB, which is a very strong proinflammatory mediator. Interestingly, HSV-2 and HHV-6A dUTPases also activated NF-κB after ligation with TKR2/1 heterodimer. Furthermore Ariza et al. showed that EBV, HHV-6 and other viral dUTPases are capable of activating different lymphocyte subpopulations and inducing the production of T-helper-1 (Th1), T-helper-17 (Th17), and other inflammatory cytokines such as IL-1β, IL-6, IL-8 and TNF-α
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Sorry for my delayed response, been working on something big with my NPO team at Solving MS,
Immediate Release: July 25, 2023
SOLVING MS ANNOUNCES FUNDING FOR GROUNDBREAKING HARVARD EBV CLINICAL TRIAL
Solving MS, a patient-led nonprofit organization dedicated to advancing research and finding effective treatments that have restorative effects and neuroprotection for Multiple Sclerosis, is proud to announce its collaboration with Harvard Medical School/Massachusetts General Hospital in funding a groundbreaking biomarker Clinical Trial (NCT05957913) focused on utilizing TDF (Tenofovir Disoproxil Fumarate) to possibly reduce EBV (Epstein-Barr Virus) viral load as evidenced in the saliva of Multiple Sclerosis patients.
We believe that through innovative research and collaboration, tangible progress can be made in the fight against EBV as a cause of Multiple Sclerosis. By supporting this groundbreaking Clinical Trial, Solving MS remains committed to improving the lives of MS patients and bringing us closer to a future free from the burden of this chronic disease.
Link for the full Press Release https://www.solvingms.org/news
SolvingMS.org
Facebook MS Research Study Group: https://www.facebook.com/groups/solvingms
Facebook Business Page: https://www.facebook.com/solvingms/
Twitter: https://twitter.com/SolvingMS
----------------------------------------------
Dr. Levy's 4 month biomarker trial is simple and inexpensive, It should set an example for all the other illnesses like ME/CFS and Long Covid, which like MS, are suspected if being driven by latent/lytic EBV. It will answer the question if the Tenofovir TDF (Truvada) antiretroviral has an effect or not on the EBV measured in blood and saliva tests. They included a fatigue test to capture an efficacy effect. This trial is to provide support for the larger phase 2 trial of Tenofovir TAF (Vemlidy) trial was turned down for funding citing insufficeint preclinical evidence.
Aceptance of Alberto Asherio's study of 10 million servis members over 20 years is hard to refute, but acceptance among MS neurologists is still mixed.
MS Australia has partnered with Australian research teams in five successful bids for government funding for research into the Epstein-Barr virus (EBV) in MS, totalling almost $10 million.
This could change the minds of those who reject the EBV causes MS idea. It will also add replication to the Harvard EBV antiviral trials, because Australi is ALso going to trial 2 antivirals. Which ones will be announced soon.
There are some EBV-aware MS neurologists who have given scripts to MS patients for the more potent TAF (Vemlidy). I know 6 whom I'm tracking and are showing improvement; most notable a long term progressive MS patient who at 2 months has quit her wheelchair and gone back to a walker in the house, and quit taking Tylenol and 4 gabapentin a day beecause her neuropathic pain is gone! Some of these neurologists will write case studies.
The current mABs used for MS like Ocrevus and Rituxan are effective because they reduce EBV to some extent when they deplete B cells where the laten EBV is. But the Rituxan trial failed for ME/CFS, right? What is the concensus now on EBV in ME/CFS? It seems the reports on Tenofovir have died down in this forum, is it not working? There is a new therapy that just completed phase 2 trial for EBV in MS with very good results, Frexalimab . And Kesimpta is getting rave reviewes on effectiveness from MS patients, It's already approved, a gentler B cell depletor that spares the B cells in the spleen so less infection risk. It is a monthly sub q injection instead of every 6 month infusion like Rituxan.
For when the MS therapies in trials will get approved, see the Solving MS database.
Click the link or picture on this page to go to the database. On the bottom click Trial Finder tab and look at column 7 Prescribe Phase 4. That the year it could reach patients. Soonest at the top by 2026 is Immunic's Vidofludimus Calcium which has a stong antiviral effect of EBV and has stopped prgression in interim results. So yes everythin is 3-10 years away. In the profile I wrote for Antivirals for EBV in MS, I suggest that Tenofovir could serve as an off-label stop gap medication that would hold us over until these others get here. Some of these trials are for remyelination, but the details like modality, method of action etc are on the All Therapies tab bottom of page. Temelimab hasn't progressed, not sure why.
It's not too hard to setup a tracking database like I did, It would be a good way to track all the therapies ME/CFS and long covid patients are trying, even if not in tirals yet. I was relational database designer for 15 years before MS left me disabled at 37. But for this with a short record set and no need for extensive searching other than Ctrl+F for keywords, I just used google sheets. Then for the profile documents just link to google docs. This was the best thing I could come up with, to keep my brain from exploding trying to keep track of all the research and trials.
I hope this gives y'all some ideas on how to advance the situation for everyonesuffering from these fatiguing diseases. If EBV is the culprit, the antiviral trials for MS should translate.
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So sad it took 50 years to arrive at Dr. Asherios's paper proving EBV causes MS Jan. 2022.
I made this meme about 2 weeks ago and today it's up to 886 papers.
(Multiple Sclerosis) AND (EBV) 886
(Long Covid) AND (EBV) 45
(ME/CFS) AND (EBV) 25 (some are Long Covid that mention fatigue)
And here's a new paper pertinent to our conversation about the fact there should be cross-discipline research efforts comparing EBV in MS and ME/CFS.
Association analysis between symptomology and herpesvirus IgG antibody concentrations in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and multiple sclerosis
Tiago Dias Domingues et al.
Heliyon 2023 Jul 13;9(7):e18250. doi: 10.1016/j.heliyon.2023.e18250.
EBV and HHV6 infections are thought to be at the origin and a risk factor for both conditions,
Has tables of all herpes antibodies, and the percent occurence in ME/CFS vs MS.
Compares 48 symptoms between the 2 conditions, and found 13 had strong overlap between both.
Shows association between symptoms and antibodies.
Forummember9922
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In case it is fruitful I would like to bump the concept in Prustys paper of Hyperpolarized Mitochondria
Anyone have any thoughts on some of these concepts:
How is hyperpolarized mitochondria different from mitochondrial fragmentation?
Would a treatment approach be different from the former to latter? Do we want a drug that accomplishes depolarized mitochondria? Does that even exist?
Is the phenomenon of hyperpolarized mitochondria that special to CFS?
From paper The appearance was similar to the stress-induced mitochondrial hyperfusion (SIMH) phenotype that is seen with exposure to certain environmental chemicals8, nutrient depletion, viral infections, and in certain chronic disease states9.
Even in the presence of reactivated herpesviruses in a Prusty vision of CFS, would this (hyper mito) be caused from something other than herpesviruses ?
Or any thoughts someone else might have?
Hope everyone's doing alright cheers
Anyone have any thoughts on some of these concepts:
How is hyperpolarized mitochondria different from mitochondrial fragmentation?
Would a treatment approach be different from the former to latter? Do we want a drug that accomplishes depolarized mitochondria? Does that even exist?
Is the phenomenon of hyperpolarized mitochondria that special to CFS?
From paper The appearance was similar to the stress-induced mitochondrial hyperfusion (SIMH) phenotype that is seen with exposure to certain environmental chemicals8, nutrient depletion, viral infections, and in certain chronic disease states9.
Even in the presence of reactivated herpesviruses in a Prusty vision of CFS, would this (hyper mito) be caused from something other than herpesviruses ?
Or any thoughts someone else might have?
Hope everyone's doing alright cheers
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I’m sure many have probably already seen this. Cort J. shared it on an FB group I’m on. I was just doing a search here on PR for mitochondria, which brought me to your post. I’m still figuring out PR and how to look around on here using my phone. Anyway thought i would share this.
https://www.healthrising.org/blog/2023/08/16/nih-mitochondria-chronic-fatigue-syndrome/
https://www.healthrising.org/blog/2023/08/16/nih-mitochondria-chronic-fatigue-syndrome/
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Has anyone else tried Pentaglobin to try and treat the IGM deficiency that the Paper Found? I recently got the opportunity to try Pentaglobin, and I know a few people have said they have gone into remission on it, but I think both of them were Parvo patients which makes me worried it could be a Parvo specific treatment. The theory is that it'll address the low natural Igm that was identified in the Prusty Preprint, but I was wondering if there was any merit to this theory? It's high risk for me as I'm severe and would have to travel 20+ hrs to get the treatment, its also pricey and I have limited resources. Is this a treatment anyone else is looking into trying, or is it quackery?