Jamie Deckoff Jones on the Naviaux paper

Remy

Administrator
There is a lot more to be found on her blog...I encourage everyone to read it. She's making a lot of sense to me.

My reaction to the Naviaux et al paper, Metabolic features of chronic fatigue syndrome, was dismay that the damage is so extensive and widespread. So many broken pathways. Finding a specific drug target seems very unlikely. There won’t be an answer anytime soon. They, and everyone else, including Lipkin and Hanson, are studying downstream effects, without attempting to identify the root cause.

It’s a good thing that people are thinking and looking, but hibernation and dauer are not disease states and being compared to larval worms isn’t exactly the image change we are after;-). Even if they’re right and a handful of common abnormalities in this very heterogeneous group is accepted as validating real disease, my guess is that the findings will be similar in other diseases, e.g. GWI, fibromyalgia, maybe even chronic depression. GWI patients have PEM and often meet criteria for ME/CFS.

As I said five years ago, I think all of these diseases of modern civilization are related and there is a family factor that confers risk to partners and offspring. There are even a few patients who believe themselves to be contagious by casual contact.

So what lies in wait to be activated by heterogeneous triggers and once activated causes immune dysfunction, neurological disease and opportunistic infections? The most likely explanation lives in the realm between retrovirology and genomics, the difference between the fields being as small as a single mutation. We have been injecting retroviruses and pieces of retroviruses into people for over a century. What are the chances that nothing bad happened from that? XMRV apparently doesn’t infect people, but injected into monkeys, it sets up a low level infection.

Retroviruses recombine and rescue each other. Environmental toxins activate retroelements (HERVs and retrotransposons) which can recombine with each other or new incoming retroviral sequences and fully replicative retroviruses from vaccinations, biologics and lab workers. XMRV was created in a lab. The Paprotka paper said the odds of the recombination event that produced XMRV happening twice are infinitesimal. On the other hand, the odds of similar events having happened many times is very high I would think, since there have been so many chances.

In the last few years it has been found that many cell lines produce viruses like XMRV which are capable of infecting human cells in tissue culture. Lipkin said in a press conference that 85% of Montoya’s samples contained retroviral sequences and in the XMRV study, 6% of patients and controls were positive for an antibody to SFFV, a very nasty murine retrovirus, but everybody is choosing to ignore those clues because that well is poisoned. Nobody wants to be the next Judy Mikovits. Lo and Alter both dropped it like a hot potato, returning to other research, never mind the question of how all these labs, Mikovits, Ruscetti, Silverman and Lo/Alter had managed to consistently contaminate the patient samples at a higher rate than the controls.
 

Strike me lucky

Well-Known Member
Hibernation Consternation
Posted on September 19, 2016
7


My muse left on extended vacation when the Lipkin XMRV study and subsequent press conference succeeded in discrediting retroviruses as a possible explanation for ME/CFS, with lots of important questions still left unanswered. The discussion reverted to whether or not it is a real disease and which set of diagnostic criteria are best, so there hasn’t been much to inspire me. It got pretty depressing. The IOM report was a joke: “The term ‘myalgic encephalomyelitis’ is not appropriate because there is a lack of evidence for encephalomyelitis (brain inflammation) in patients with this disease…”. Fail. I don’t know what to make of the Lipkin cytokine paper, because I take with a grain of salt results from a debunker on call for the government. XMRV wasn’t the first time: Lack of association between measles virus vaccine and autism with enteropathy: a case-control study. Nothing worth blogging about there. Certainly nothing hopeful. But recently, the Naviaux study was published and a couple of proposals posted by NIH have been making the rounds of Facebook, so I’ve had an uptick in email, some asking what I think about the paper and some telling me about successes with antiretrovirals in Europe, as well as encouragement to blog again. So, feeling very rusty, I’m going to give it a go.

My reaction to the Naviaux et al paper, Metabolic features of chronic fatigue syndrome, was dismay that the damage is so extensive and widespread. So many broken pathways. Finding a specific drug target seems very unlikely. There won’t be an answer anytime soon. They, and everyone else, including Lipkin and Hanson, are studying downstream effects, without attempting to identify the root cause. It’s a good thing that people are thinking and looking, but hibernation and dauer are not disease states and being compared to larval worms isn’t exactly the image change we need ;-). Even if they’re right and a handful of common abnormalities in this very heterogeneous group is accepted as validating real disease, my guess is that the findings will be similar in other diseases, e.g. GWI, fibromyalgia, ASD, maybe even chronic depression. GWI patients have PEM and often meet criteria for ME/CFS. As I said five years ago, I think all of these diseases of modern civilization are related and there is a family factor that confers risk to partners and offspring. There are even a few patients who believe themselves to be contagious by casual contact.

So what lies in wait to be activated by heterogeneous triggers and once activated causes immune dysfunction, neurological disease and opportunistic infections? The most likely explanation lives in the realm between retrovirology and genomics, the difference between the fields being as small as a single mutation. We have been injecting retroviruses and pieces of retroviruses into people for over a century. What are the chances that nothing bad happened from that? XMRV apparently doesn’t infect people, but injected into monkeys, it sets up a low level infection. Retroviruses recombine and rescue each other. Environmental toxins activate retroelements (HERVs and retrotransposons) which can recombine with each other or new incoming retroviral sequences and fully replicative retroviruses from vaccinations, biologics and lab workers. XMRV was created in a lab. The Paprotka paper said the odds of the recombination event that produced XMRV happening twice are infinitesimal. On the other hand, the odds of similar events having happened many times is very high I would think, since there have been so many chances. In the last few years it has been found that many cell lines produce viruses like XMRV which are capable of infecting human cells in tissue culture. Lipkin said in a press conference that 85% of Montoya’s samples contained retroviral sequences and in the XMRV study, 6% of patients and controls were positive for an antibody to SFFV, a very nasty murine retrovirus, but everybody is choosing to ignore those clues because that well is poisoned. Nobody wants to be the next Judy Mikovits. Lo and Alter both dropped it like a hot potato, returning to other research, never mind the question of how all these labs, Mikovits, Ruscetti, Silverman and Lo/Alter had managed to consistently contaminate the patient samples at a higher rate than the controls.

Take a look at this paper: Are human endogenous retroviruses triggers of autoimmune diseases? Unveiling associations of three diseases and viral loci by Bjørn et al. “We speculate the possibility that recombinants or mixed viral particles are formed and that the resulting viruses stimulate the innate immune system, thereby initiating the autoimmune response.” They looked at multiple sclerosis, type 1 diabetes mellitus, and rheumatoid arthritis. It is one of several recent papers heading in this direction.

I hypothesized way back when that ME/CFS is related to MS. There are case reports of MS improving when patients take antiretrovirals, Multiple sclerosis patient walks after taking HIV drugs, and new cases of MS are rare or nonexistent in patients taking AIDS drugs, HIV and lower risk of multiple sclerosis: beginning to unravel a mystery using a record-linked database study.

Our very own Gerwyn Morris published an excellent paper on the subject of ME and MS being related diseases. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. I’d like to take this opportunity to acknowledge Gerwyn’s extraordinary achievement. If you search “Morris Gerwyn” on PubMed, his name appears as an author on 23 papers since 2013, usually as first author.

Lots of evidence has been published about the MS retrovirus, MSRV. Viral particles have clearly been detected, but it is less clear if these particles are ever infectious. There are several new papers reporting findings similar to this one, Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Which brings us back to where this blog began. Are retroviruses at the bottom of ME/CFS? Might antiretrovirals be effective for ME/CFS and other diseases? Despite the thorough trashing of retroviruses in our disease and the intense ongoing fear mongering about how dangerous antiretroviral drugs are, apparently people are still trying it in Europe. The experience five years ago, when maybe a hundred people tried various regimens in a completely uncontrolled fashion, was some subjective improvement in about half, and no complete recoveries, except for one notable exception. The exception was a teenager who had only been sick for eight months. His mother wrote in the comments on this blog. He recovered fully, took the drugs for 6 months, stopped and as far as I know, didn’t relapse. I still find it upsetting that the prescribing physician was too cowardly to come forward and write a case report. How many teenagers could have been treated acutely since then? There were no injuries that I ever heard of. I was in touch with many of the doctors who were prescribing and there was lots of sharing, doctors and patients together, the only time I’ve ever seen that happen. One doctor I knew prescribed for 50 patients and concluded that it was better than placebo, but not worth the risk of prescribing it.

However encouraging the Naviaux paper may be with respect to advancing the case that ME/CFS is, in fact, a real and dreadful disease, it is discouraging with respect to finding treatment. A viable drug target seems unlikely. We are left with global strategies, hoping for synergy between therapies that don’t stand alone, same as now. But just as I was feeling dour about dauer…

The NIH compilation of responses to their request for proposals was published here. Read bottom of page 3 to top of page 4. I’m not going to mention any names for Google, because I don’t want to increase the risk of regulatory repercussions against a doctor brave enough to report successes with antiretrovirals. Also please read pages 9-12.

Then I heard from a patient in Europe who is having success with antiretrovirals after 20+ years of illness. In his own words:

I have been ill with ME since my mid-teens in 1994. Onset was in two stages. Firstly a gradual onset, whereby I was feeling increasingly more tested after the combined measleas/rubella vaccine, followed a few weeks later by the polio booster. And then secondly once that prodrome had got its hold, the downward cascade was always inevitable, and just waiting for me around the corner. 1994-2014 were harsh and brutal years. I hovered around 55% on the Bell scale and it was torture enough.

From September 2014 to July 2015 I took tenofovir 245mg. Improvement was an upward curve, albeit with some turbulence. Sometimes taking half- week, or full-week, or month-long breaks when I felt my body needed a rest from it so as to hold its own for a while. From August 2015 to September 2016 I added raltegravir to tenofovir and initially at full dose daily which sent me to sleep almost in the first few days. During this period I toggled around until I found the right balance for me. I got it right in the end around about June/July 2016 and the past two/three months have been great. My current regimen is tenofovir 245mg Tuesday through Friday, and on Tuesday and Thursday I also take raltegravir 400mg x 2. My original baseline was about 55% on the Bell scale for the twenty or so years when I was sick. I am now 95-100% and can go to the gym once weekly thanks to the antiretrovirals where I can build up quite a healthy sweat and recuperate normally. My VO2 max continues to increase substantially and my CD3-4-8 counts are x2.5 to 3 fold what they were before I started the antiretrovirals. Life is very good. I also take celebrex and multivitamin/antioxidant supplements and I am monitored closely.

This year I feel more confident about the winter than I did in 2014 on just tenofovir and than in 2015 when I was grappling with adding raltegravir. They were bad winters even though the arv’s did help me through better I guess. Winter 2016 can throw at me what it wants however. Now that I have hit the perfect treatment regimen with the antiretrovirals I am sure it will be a better winter. It was worth sticking it out and learning. I thank Dr Judy Mikovits and my physician over in Germany, along with the continued support of a rare and dedicated French doctor over there in Paris. Finally I thank two doctors over there in the UK for listening. I salute them all as men and women of true honour.

Several people wrote to ask what happened with antiretrovirals for my daughter and me. Ali and I plateaued without recovering fully. After the initial improvement, there was really no way to know what was happening. We both had a very mild flare of symptoms for the first six weeks and then a noticeable increase in energy and resilience. We started with AZT and Isentress, then switched the AZT to Viread a year later. Ali stayed on the two drugs for three years, not wanting to rock the boat, as she was doing relatively well. I stopped the Isentress after about a year and half and took Viread alone after that. We both improved during the three years we took antiretrovirals, but we were doing lots of other things documented on this blog. Since there was always the possibility that we might do better without them, eventually we decided we should find out. As it turned out, we didn’t decline when we stopped. I had some trouble coming off Viread, because my always labile blood pressure went crazy when I stopped, twice. Go figure. In the end, I weaned without any sort of noticeable decline. When we started, we were all so hopeful. Judy believed we’d be able to monitor viral load in a year, but it wasn’t to be. Our combined copays were breaking the bank and after three years, with no way to monitor and able to stop, it just didn’t make sense to continue. I would consider antiretroviral drugs again if either of us crashed completely.

My experience treating six very informed patients was similar to what other doctors have reported, 50% improved subjectively. Two had adverse reactions to Viread, including one who had responded initially; both resolved quickly when the drugs were stopped. Two patients continued long term, one on two drugs and one who opted for Viread monotherapy. I didn’t see anything dramatic enough to make me very encouraged though. I had successes with other things that were similar in scale with less risk to the patient and the doctor. However, it’s possible that tinkering with lower doses and less than every day regimens would make the drugs we have more useful for ME/CFS, even if they were designed for a virus we don’t have. Although we do not want to encourage resistance to the drugs, it’s possible that a small dose of a reverse transcriptase inhibitor would work for us. I heard from a doctor in Europe who reported complete recovery in 2011 after nine months on micro dose AZT (20-30mg/day). I don’t know how it turned out long term, but will write to him and ask.

Dr. Michael Snyderman is still doing remarkably well, still able to work in his hematology oncology practice at 75, controlling his cancer like a chronic disease, specifically like AIDS. He has been taking HAART for over 6 years, having twice passed his median survival, meaning there was less than a 25% chance that he’d still be alive by now. I will share his data here in the near future. He is still hoping to collaborate with Roswell Park Cancer Center in his hometown of Buffalo, NY to help patients who have cancer and who have a poor prognosis. The same viruses that infect cancers infect the immune system. If cancer patients benefit as he expects they will, initiatives can be made with the neuroinflammatory disorders including ME/CFS. There is now a reliable virus detection methodology, ViroCap invented by the Wylies at Washington University and the Wylies are interested in collaborating with this research.

These are leads, the only leads we have. If drugs developed for a completely different retrovirus have some activity against a disease, think what could happen with some attention to the process that is actually occurring. The technology, next generation sequencing, already exists to begin to answer our questions, but the various software platforms that analyze the data are still in their infancy. The metabolomics studies are happening because there is a new toy. There are going to be lots of new toys in the near future. It already didn’t happen by random doctors prescribing off label. Since it wasn’t a slam dunk, it needs to be formally and properly studied.

It is possible that the metabolites that Naviaux et al have identified as a potential diagnostic panel might be useful for monitoring success with antiretrovirals. Dr. Naviaux has answered questions here, stating that he thinks the use of antibiotics and antivirals aren’t indicated and I mostly agree with him, planning to share my thoughts on treatment in a future blog.

I continued to go slowly uphill after I last blogged about ME/CFS almost two years ago, but nothing like a full recovery. I was able to work a little and I was able to ride on the back of a tandem, close to a thousand miles in two years according to Strava, half of it on dirt. Still lots of symptoms, but a life, where once there wasn’t one, plus a way to get endorphins. My recovery was slow after exercise; I felt drained the next day, but nothing like full blown PEM. I was still maintaining the fantasy that someday I would recover fully. But a year ago, while hiking, I twisted my ankle and broke my distal fibula. It was a minor fracture that should have healed without problems in 6 weeks. Instead I got RSD/CRPS (reflex sympathetic dystrophy/complex regional pain syndrome), a very challenging and painful condition. It takes most of my energy just to cope and I’ve been out of commission since it started, able to attend only to my own treatment (HBOT).

After 5 years of managing patients, I had to retire completely. I only worked with a very small number of patients, scattered all over the country, who saw me in person once a year in Hawaii or Arizona, but I got to know them very well, because most of the contact was electronic, day to day, moment to moment even, and that works well for ME/CFS patients. It was enough to learn quite a bit about the spectrum of disease, what works and what doesn’t, especially given that almost everyone I saw had been around the block and came with voluminous records, having failed treatment with the best. I’d like to share my impressions while still fresh, so intend to keep blogging, if I don’t get too beat up over this one ;-).

http://www.x-rx.net/blog
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
There won’t be an answer anytime soon. They, and everyone else, including Lipkin and Hanson, are studying downstream effects, without attempting to identify the root cause.
This is just the wildest statement; it's exact opposite of what Ron Davis thinks they're doing. He thinks most everyone else is not looking for the answer but he is.

By looking for the molecular roots of the disease by examining genetics, genomics, metabolomics and doing intense searches for pathogens, etc. Davis thinks he's going for the cause.

Jones says look at retroviruses and genomics but Davis is doing those studies and more.

The thing about Deckoff-Jones IMHO is that while in general she makes sense and has interesting ideas I don't think she's very rigorous with her words.

I stopped trusting her after she bananas on Suzanne Vernon because Vernon had worked at the CDC at one time. This was after I asked whether Vernon's history at the CDC (all biological stuff) or afterwards at the SMCI (all biological stuff) mattered? She said not it didn't - if she ever worked at the CDC Vernon was basically dead meat - and she publicly went off on her.

I couldn't believe that coming from Deckoff-Jones. I expected other people to feel that way but not a doctor.

I should probably get over that incident :)
 
Last edited:

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I d
Hibernation Consternation
Posted on September 19, 2016
7


My muse left on extended vacation when the Lipkin XMRV study and subsequent press conference succeeded in discrediting retroviruses as a possible explanation for ME/CFS, with lots of important questions still left unanswered. The discussion reverted to whether or not it is a real disease and which set of diagnostic criteria are best, so there hasn’t been much to inspire me. It got pretty depressing. The IOM report was a joke: “The term ‘myalgic encephalomyelitis’ is not appropriate because there is a lack of evidence for encephalomyelitis (brain inflammation) in patients with this disease…”. Fail. I don’t know what to make of the Lipkin cytokine paper, because I take with a grain of salt results from a debunker on call for the government. XMRV wasn’t the first time: Lack of association between measles virus vaccine and autism with enteropathy: a case-control study. Nothing worth blogging about there. Certainly nothing hopeful. But recently, the Naviaux study was published and a couple of proposals posted by NIH have been making the rounds of Facebook, so I’ve had an uptick in email, some asking what I think about the paper and some telling me about successes with antiretrovirals in Europe, as well as encouragement to blog again. So, feeling very rusty, I’m going to give it a go.

My reaction to the Naviaux et al paper, Metabolic features of chronic fatigue syndrome, was dismay that the damage is so extensive and widespread. So many broken pathways. Finding a specific drug target seems very unlikely. There won’t be an answer anytime soon. They, and everyone else, including Lipkin and Hanson, are studying downstream effects, without attempting to identify the root cause. It’s a good thing that people are thinking and looking, but hibernation and dauer are not disease states and being compared to larval worms isn’t exactly the image change we need ;-). Even if they’re right and a handful of common abnormalities in this very heterogeneous group is accepted as validating real disease, my guess is that the findings will be similar in other diseases, e.g. GWI, fibromyalgia, ASD, maybe even chronic depression. GWI patients have PEM and often meet criteria for ME/CFS. As I said five years ago, I think all of these diseases of modern civilization are related and there is a family factor that confers risk to partners and offspring. There are even a few patients who believe themselves to be contagious by casual contact.

So what lies in wait to be activated by heterogeneous triggers and once activated causes immune dysfunction, neurological disease and opportunistic infections? The most likely explanation lives in the realm between retrovirology and genomics, the difference between the fields being as small as a single mutation. We have been injecting retroviruses and pieces of retroviruses into people for over a century. What are the chances that nothing bad happened from that? XMRV apparently doesn’t infect people, but injected into monkeys, it sets up a low level infection. Retroviruses recombine and rescue each other. Environmental toxins activate retroelements (HERVs and retrotransposons) which can recombine with each other or new incoming retroviral sequences and fully replicative retroviruses from vaccinations, biologics and lab workers. XMRV was created in a lab. The Paprotka paper said the odds of the recombination event that produced XMRV happening twice are infinitesimal. On the other hand, the odds of similar events having happened many times is very high I would think, since there have been so many chances. In the last few years it has been found that many cell lines produce viruses like XMRV which are capable of infecting human cells in tissue culture. Lipkin said in a press conference that 85% of Montoya’s samples contained retroviral sequences and in the XMRV study, 6% of patients and controls were positive for an antibody to SFFV, a very nasty murine retrovirus, but everybody is choosing to ignore those clues because that well is poisoned. Nobody wants to be the next Judy Mikovits. Lo and Alter both dropped it like a hot potato, returning to other research, never mind the question of how all these labs, Mikovits, Ruscetti, Silverman and Lo/Alter had managed to consistently contaminate the patient samples at a higher rate than the controls.

Take a look at this paper: Are human endogenous retroviruses triggers of autoimmune diseases? Unveiling associations of three diseases and viral loci by Bjørn et al. “We speculate the possibility that recombinants or mixed viral particles are formed and that the resulting viruses stimulate the innate immune system, thereby initiating the autoimmune response.” They looked at multiple sclerosis, type 1 diabetes mellitus, and rheumatoid arthritis. It is one of several recent papers heading in this direction.

I hypothesized way back when that ME/CFS is related to MS. There are case reports of MS improving when patients take antiretrovirals, Multiple sclerosis patient walks after taking HIV drugs, and new cases of MS are rare or nonexistent in patients taking AIDS drugs, HIV and lower risk of multiple sclerosis: beginning to unravel a mystery using a record-linked database study.

Our very own Gerwyn Morris published an excellent paper on the subject of ME and MS being related diseases. Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. I’d like to take this opportunity to acknowledge Gerwyn’s extraordinary achievement. If you search “Morris Gerwyn” on PubMed, his name appears as an author on 23 papers since 2013, usually as first author.

Lots of evidence has been published about the MS retrovirus, MSRV. Viral particles have clearly been detected, but it is less clear if these particles are ever infectious. There are several new papers reporting findings similar to this one, Two endogenous retroviral loci appear to contribute to Multiple Sclerosis.

Which brings us back to where this blog began. Are retroviruses at the bottom of ME/CFS? Might antiretrovirals be effective for ME/CFS and other diseases? Despite the thorough trashing of retroviruses in our disease and the intense ongoing fear mongering about how dangerous antiretroviral drugs are, apparently people are still trying it in Europe. The experience five years ago, when maybe a hundred people tried various regimens in a completely uncontrolled fashion, was some subjective improvement in about half, and no complete recoveries, except for one notable exception.

The exception was a teenager who had only been sick for eight months. His mother wrote in the comments on this blog. He recovered fully, took the drugs for 6 months, stopped and as far as I know, didn’t relapse. I still find it upsetting that the prescribing physician was too cowardly to come forward and write a case report. How many teenagers could have been treated acutely since then? There were no injuries that I ever heard of. I was in touch with many of the doctors who were prescribing and there was lots of sharing, doctors and patients together, the only time I’ve ever seen that happen. One doctor I knew prescribed for 50 patients and concluded that it was better than placebo, but not worth the risk of prescribing it.

However encouraging the Naviaux paper may be with respect to advancing the case that ME/CFS is, in fact, a real and dreadful disease, it is discouraging with respect to finding treatment. A viable drug target seems unlikely. We are left with global strategies, hoping for synergy between therapies that don’t stand alone, same as now. But just as I was feeling dour about dauer…

The NIH compilation of responses to their request for proposals was published here. Read bottom of page 3 to top of page 4. I’m not going to mention any names for Google, because I don’t want to increase the risk of regulatory repercussions against a doctor brave enough to report successes with antiretrovirals. Also please read pages 9-12.

Then I heard from a patient in Europe who is having success with antiretrovirals after 20+ years of illness. In his own words:

I have been ill with ME since my mid-teens in 1994. Onset was in two stages. Firstly a gradual onset, whereby I was feeling increasingly more tested after the combined measleas/rubella vaccine, followed a few weeks later by the polio booster. And then secondly once that prodrome had got its hold, the downward cascade was always inevitable, and just waiting for me around the corner. 1994-2014 were harsh and brutal years. I hovered around 55% on the Bell scale and it was torture enough.

From September 2014 to July 2015 I took tenofovir 245mg. Improvement was an upward curve, albeit with some turbulence. Sometimes taking half- week, or full-week, or month-long breaks when I felt my body needed a rest from it so as to hold its own for a while. From August 2015 to September 2016 I added raltegravir to tenofovir and initially at full dose daily which sent me to sleep almost in the first few days. During this period I toggled around until I found the right balance for me. I got it right in the end around about June/July 2016 and the past two/three months have been great. My current regimen is tenofovir 245mg Tuesday through Friday, and on Tuesday and Thursday I also take raltegravir 400mg x 2. My original baseline was about 55% on the Bell scale for the twenty or so years when I was sick. I am now 95-100% and can go to the gym once weekly thanks to the antiretrovirals where I can build up quite a healthy sweat and recuperate normally. My VO2 max continues to increase substantially and my CD3-4-8 counts are x2.5 to 3 fold what they were before I started the antiretrovirals. Life is very good. I also take celebrex and multivitamin/antioxidant supplements and I am monitored closely.

This year I feel more confident about the winter than I did in 2014 on just tenofovir and than in 2015 when I was grappling with adding raltegravir. They were bad winters even though the arv’s did help me through better I guess. Winter 2016 can throw at me what it wants however. Now that I have hit the perfect treatment regimen with the antiretrovirals I am sure it will be a better winter. It was worth sticking it out and learning. I thank Dr Judy Mikovits and my physician over in Germany, along with the continued support of a rare and dedicated French doctor over there in Paris. Finally I thank two doctors over there in the UK for listening. I salute them all as men and women of true honour.
Several people wrote to ask what happened with antiretrovirals for my daughter and me. Ali and I plateaued without recovering fully. After the initial improvement, there was really no way to know what was happening. We both had a very mild flare of symptoms for the first six weeks and then a noticeable increase in energy and resilience. We started with AZT and Isentress, then switched the AZT to Viread a year later. Ali stayed on the two drugs for three years, not wanting to rock the boat, as she was doing relatively well. I stopped the Isentress after about a year and half and took Viread alone after that. We both improved during the three years we took antiretrovirals, but we were doing lots of other things documented on this blog. Since there was always the possibility that we might do better without them, eventually we decided we should find out. As it turned out, we didn’t decline when we stopped. I had some trouble coming off Viread, because my always labile blood pressure went crazy when I stopped, twice. Go figure. In the end, I weaned without any sort of noticeable decline. When we started, we were all so hopeful. Judy believed we’d be able to monitor viral load in a year, but it wasn’t to be. Our combined copays were breaking the bank and after three years, with no way to monitor and able to stop, it just didn’t make sense to continue. I would consider antiretroviral drugs again if either of us crashed completely.

My experience treating six very informed patients was similar to what other doctors have reported, 50% improved subjectively. Two had adverse reactions to Viread, including one who had responded initially; both resolved quickly when the drugs were stopped. Two patients continued long term, one on two drugs and one who opted for Viread monotherapy. I didn’t see anything dramatic enough to make me very encouraged though. I had successes with other things that were similar in scale with less risk to the patient and the doctor. However, it’s possible that tinkering with lower doses and less than every day regimens would make the drugs we have more useful for ME/CFS, even if they were designed for a virus we don’t have. Although we do not want to encourage resistance to the drugs, it’s possible that a small dose of a reverse transcriptase inhibitor would work for us. I heard from a doctor in Europe who reported complete recovery in 2011 after nine months on micro dose AZT (20-30mg/day). I don’t know how it turned out long term, but will write to him and ask.

Dr. Michael Snyderman is still doing remarkably well, still able to work in his hematology oncology practice at 75, controlling his cancer like a chronic disease, specifically like AIDS. He has been taking HAART for over 6 years, having twice passed his median survival, meaning there was less than a 25% chance that he’d still be alive by now. I will share his data here in the near future. He is still hoping to collaborate with Roswell Park Cancer Center in his hometown of Buffalo, NY to help patients who have cancer and who have a poor prognosis. The same viruses that infect cancers infect the immune system. If cancer patients benefit as he expects they will, initiatives can be made with the neuroinflammatory disorders including ME/CFS. There is now a reliable virus detection methodology, ViroCap invented by the Wylies at Washington University and the Wylies are interested in collaborating with this research.

These are leads, the only leads we have. If drugs developed for a completely different retrovirus have some activity against a disease, think what could happen with some attention to the process that is actually occurring. The technology, next generation sequencing, already exists to begin to answer our questions, but the various software platforms that analyze the data are still in their infancy. The metabolomics studies are happening because there is a new toy. There are going to be lots of new toys in the near future. It already didn’t happen by random doctors prescribing off label. Since it wasn’t a slam dunk, it needs to be formally and properly studied.

It is possible that the metabolites that Naviaux et al have identified as a potential diagnostic panel might be useful for monitoring success with antiretrovirals. Dr. Naviaux has answered questions here, stating that he thinks the use of antibiotics and antivirals aren’t indicated and I mostly agree with him, planning to share my thoughts on treatment in a future blog.

I continued to go slowly uphill after I last blogged about ME/CFS almost two years ago, but nothing like a full recovery. I was able to work a little and I was able to ride on the back of a tandem, close to a thousand miles in two years according to Strava, half of it on dirt. Still lots of symptoms, but a life, where once there wasn’t one, plus a way to get endorphins. My recovery was slow after exercise; I felt drained the next day, but nothing like full blown PEM. I was still maintaining the fantasy that someday I would recover fully. But a year ago, while hiking, I twisted my ankle and broke my distal fibula. It was a minor fracture that should have healed without problems in 6 weeks. Instead I got RSD/CRPS (reflex sympathetic dystrophy/complex regional pain syndrome), a very challenging and painful condition. It takes most of my energy just to cope and I’ve been out of commission since it started, able to attend only to my own treatment (HBOT).

After 5 years of managing patients, I had to retire completely. I only worked with a very small number of patients, scattered all over the country, who saw me in person once a year in Hawaii or Arizona, but I got to know them very well, because most of the contact was electronic, day to day, moment to moment even, and that works well for ME/CFS patients. It was enough to learn quite a bit about the spectrum of disease, what works and what doesn’t, especially given that almost everyone I saw had been around the block and came with voluminous records, having failed treatment with the best. I’d like to share my impressions while still fresh, so intend to keep blogging, if I don’t get too beat up over this one ;-).

http://www.x-rx.net/blog
I don't understand what she is saying....I know of a person who did very well on anti-retrovirals as well (and had to quit them unfortunately) and there are probably dozens who didn't do well. You can find people who did great on antivirals and many others who didn't. There's was the doctor who used staphyloccocus vaccine. I know of two people who recovered while on Valcyte. Several people have recovered on Ampligen. Ditto with Rituximab.

These things happen...

If she's trying to convince people that retroviruses and anti - retroviruses are it - I'm just not getting it. I think, like these other treatments, that they might be it for some patients but her sample size is darn small and the outcomes are not very encouraging. If I had money I wouldn't put them into anti-retrovirals. They have been looked for quite a bit.

I think that if Lipkin thought there was something to those findings he would have looked into them. If he thought they were important he would have studied the heck out of them before publishing anything.

Saying that metabolomics is just the new toy is more of Deckoff Jones' unfortunate propensity to be dismissive. Metabolomics has been around for a long time. Davis gloamed onto it because it was the first test which really showed something in Whitney.

By the way those papers that Gerwyn Morris is co-author on are probably entirely written by Michael Maes . Maes asked me to be a co-author and I was for one paper but I didn't have a thing to do with it and I didn't feel comfortable continuing. Why Michael Maes is having patients for co-authors I have no idea but it gives me the willies. Gerwyn Morris was an XMRV fanatic long after it had been disproven. I bumped up against him many times on Phoenix Rising. He was one of the strangest characters....
 

Remy

Administrator
Saying that metabolomics is just the new toy is more of Deckoff Jones' unfortunate propensity to be dismissive.
I don't want to put words in someone else's mouth but from my view she isn't being dismissive but being real.

These deficits are widespread and are unlikely to be fixed by any single drug. They are common to a wide range of related illnesses. That means that they aren't the cause.

And unweaving the disease back to a real root cause is still but a dream. I don't see the metabolomics as the cause, they are a result of the illness. I don't see how we fix those deficiencies without finding the root.

And how do we find something we don't really know yet? That's what she is saying with the paragraph about how they recombine and reconfigure. Maybe that's why all the previous pathogen testing has failed thus far?

I have no idea what kind of pathogen we should be looking for but I think we should still be looking regardless.

It seems obvious to me that we are in a hibernation or dauer state. I wrote about that in a post 3 years ago without spending a dime. It's nice to see it in black and white but is it truly all that helpful for getting us better ? I hope so, but fear not.

The question in my mind still is WHY? Sounds like JDJ would like to know why too.
 

Strike me lucky

Well-Known Member
I don't want to put words in someone else's mouth but from my view she isn't being dismissive but being real.

These deficits are widespread and are unlikely to be fixed by any single drug. They are common to a wide range of related illnesses. That means that they aren't the cause.

And unweaving the disease back to a real root cause is still but a dream. I don't see the metabolomics as the cause, they are a result of the illness. I don't see how we fix those deficiencies without finding the root.

And how do we find something we don't really know yet? That's what she is saying with the paragraph about how they recombine and reconfigure. Maybe that's why all the previous pathogen testing has failed thus far?

I have no idea what kind of pathogen we should be looking for but I think we should still be looking regardless.

It seems obvious to me that we are in a hibernation or dauer state. I wrote about that in a post 3 years ago without spending a dime. It's nice to see it in black and white but is it truly all that helpful for getting us better ? I hope so, but fear not.

The question in my mind still is WHY? Sounds like JDJ would like to know why too.

I agree. They really just showing all the bits that are broken. They have had decades to find the cause im not sure they will find anything the way they are looking.

Medicine cant even diagnose chronic active infections and i heard lipkins testing infections in cfs isnt sensitive enough, why else would he not find any infections in cfs when many others have. Theres still the question of why dr montoyas cfs patients 85% had a retrovirus vs 6% of controls. Lipkin noted this but just talked it down as a nothing?? Originally enteroviruses were a suspect but besides dr chia, no one is going near it.

They need to really greatly improve pathogen testing and needs to be done by someone who isnt a government mouth piece.

Theres a few treatments that have helped people, avs abx arvs ampligen etc etc. I think they are better off trialling treatments in cfsers and studying their physiology and noting the ones that improve and try to understand why. I think this way might be more effective working backwards from treatments that help and following them to the abnormalities.

Rituximab has been talked up so much but it seems to be falling over and they dont really know why it helps some but doesnt seem to be very many outside of norway that are improving. One rumor i heard was that the norway pts respond due to a genetic autoimmune issue only particular to Norwegians.

The metabolomics work is of help but the net needs to be widened with alot more researchers studying different aspects of this illness. Also i think treating cfs doctors need to be given more scope with trialling off label treatments as long as the drug has a good safety profile, serendipity might be the only way to find treatments.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I don't want to put words in someone else's mouth but from my view she isn't being dismissive but being real.

These deficits are widespread and are unlikely to be fixed by any single drug. They are common to a wide range of related illnesses. That means that they aren't the cause.

And unweaving the disease back to a real root cause is still but a dream. I don't see the metabolomics as the cause, they are a result of the illness. I don't see how we fix those deficiencies without finding the root.

And how do we find something we don't really know yet? That's what she is saying with the paragraph about how they recombine and reconfigure. Maybe that's why all the previous pathogen testing has failed thus far?

I have no idea what kind of pathogen we should be looking for but I think we should still be looking regardless.

It seems obvious to me that we are in a hibernation or dauer state. I wrote about that in a post 3 years ago without spending a dime. It's nice to see it in black and white but is it truly all that helpful for getting us better ? I hope so, but fear not.

The question in my mind still is WHY? Sounds like JDJ would like to know why too.
S
I don't want to put words in someone else's mouth but from my view she isn't being dismissive but being real.

These deficits are widespread and are unlikely to be fixed by any single drug. They are common to a wide range of related illnesses. That means that they aren't the cause.

And unweaving the disease back to a real root cause is still but a dream. I don't see the metabolomics as the cause, they are a result of the illness. I don't see how we fix those deficiencies without finding the root.

And how do we find something we don't really know yet? That's what she is saying with the paragraph about how they recombine and reconfigure. Maybe that's why all the previous pathogen testing has failed thus far?

I have no idea what kind of pathogen we should be looking for but I think we should still be looking regardless.

It seems obvious to me that we are in a hibernation or dauer state. I wrote about that in a post 3 years ago without spending a dime. It's nice to see it in black and white but is it truly all that helpful for getting us better ? I hope so, but fear not.

The question in my mind still is WHY? Sounds like JDJ would like to know why too.
Say that metabolomics is simply a new toy seems kind of dismissive to me...:) but that's kind of how Deckoff_Jones writes - no big deal really.

I actually think you and she are right that metabolomics is looking at downstream effects. Davis's and Naviaux's idea with metabolomics and the other omics is that they will, though, more quickly than anything, point to the root of the illness....THis is because they are scanning vast areas of our biology. Being able to understand what they find and fine-tuning it so that we can get to cause is the big question for them I think.

Pathogens, pathogens, pathogens - I still think herpesviruses and perhaps other pathogens are involved but either don't show up in the blood or show up in such minimal amounts that they're mostly not thought to be important. Unfortunately they may be in the tissues or the central nervous system. Pridgen, the WPI and Chia all think they've found evidence of pathogens in gut tissues....in a way its not encouraging when everyone finds evidence of different pathogens (lol)

I think the latest pathogen tests - which are just looking for pieces of DNA associated with pathogens - should show up recombinations (???)

I do think that when they get to the source of ME/CFS and FM that they are going to show similarities to a number of other diseases; similar basic pathways are going to be disturbed and then there are going to be branches leading off of them which lead to a more fatiguing illness (ME/CFS) an FM type illness (pain).
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I agree. They really just showing all the bits that are broken. They have had decades to find the cause im not sure they will find anything the way they are looking.

Medicine cant even diagnose chronic active infections and i heard lipkins testing infections in cfs isnt sensitive enough, why else would he not find any infections in cfs when many others have. Theres still the question of why dr montoyas cfs patients 85% had a retrovirus vs 6% of controls. Lipkin noted this but just talked it down as a nothing?? Originally enteroviruses were a suspect but besides dr chia, no one is going near it.

They need to really greatly improve pathogen testing and needs to be done by someone who isnt a government mouth piece.

Theres a few treatments that have helped people, avs abx arvs ampligen etc etc. I think they are better off trialling treatments in cfsers and studying their physiology and noting the ones that improve and try to understand why. I think this way might be more effective working backwards from treatments that help and following them to the abnormalities.

Rituximab has been talked up so much but it seems to be falling over and they dont really know why it helps some but doesnt seem to be very many outside of norway that are improving. One rumor i heard was that the norway pts respond due to a genetic autoimmune issue only particular to Norwegians.

The metabolomics work is of help but the net needs to be widened with alot more researchers studying different aspects of this illness. Also i think treating cfs doctors need to be given more scope with trialling off label treatments as long as the drug has a good safety profile, serendipity might be the only way to find treatments.
Lipkin screwed up on the herpesvirus testing - no way it was going to show up the way he did it.

With clues being found for both Rituximab and Ampligen regarding which types of patients they work in - that's a big step forward.

I hope that's not true for Rituximab! Dr. Peterson is giving it a try, by the way.

One way the metabolomics and other omics research may help is that they can identify pathways that have been disturbed and then they can match those pathways to drugs that we might not even have considered that can effect. Ron Davis is just waiting for the evidence to show up; he has samples of every FDA approved drug there is; he can test these in the lab with ME/CFS patients samples....Drug repurposing is on the top of his list.
 
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Tammy7

Well-Known Member
Pathogens, pathogens, pathogens - I still think herpesviruses and perhaps other pathogens are involved but either don't show up in the blood or show up in such minimal amounts that they're mostly not thought to be important.
I concur! Darn it ................I wish you would read that book I sent you! One chapter.
 

Strike me lucky

Well-Known Member
Pathogens, pathogens, pathogens - I still think herpesviruses and perhaps other pathogens are involved but either don't show up in the blood or show up in such minimal amounts that they're mostly not thought to be important. Unfortunately they may be in the tissues or the central nervous system. Pridgen, the WPI and Chia all think they've found evidence of pathogens in gut tissues....in a way its not encouraging when everyone finds evidence of different pathogens (lol)
I think finding pathogens and different pathogens amongst cfsers is a sign theres immune suppression going on?? One reason why i dont discount retroviral involvement as it fits well but lyme also fits into an immune suppression type of occurance??

Treating them , the different pathogens individually might be needed as well as correcting whats suppressing the immune system??
 

Strike me lucky

Well-Known Member
Aren't the pathogens suppressing the immune system? Look what HIV does to a person's immune system.
Yes but which one? Hiv example is why i think something not yet known is suppressing the immune system and causing these other pathogens to keep infecting. The common pathogens found in many cfsers even herpes viruses are usually well controlled by the immune system, its only those with immune defiencies, hiv etc that have issues with them.
 

Tammy7

Well-Known Member
The common pathogens found in many cfsers even herpes viruses are usually well controlled by the immune system,
I can only speak for myself.............I have EBV which is a herpetic virus and my immune system didn't take care of it. I do get what you are saying though...........perhaps other things are coming into play. Those "OTHER" things can be things like poor diet, heavy metals, other co-infections we aren't aware of, poor liver function, etc.............and yes I'm going to say it.............Vaccinations...... when all combined together prevent our immune systems from functioning properly to ward off a virus. I think though that you are thinking of something more sinister that hasn't been discovered yet?
 

Remy

Administrator
I think this guy is on the right track potentially too...we shouldn't rule out bacterial causes just yet, I don't think.

http://coolinginflammation.blogspot.com/2009/07/chronic-disease-cryptic-infections.html

Chronic Disease, Cryptic Infections, Hibernation
Suppression of Inflammation and Surviving Cytokine Storms

There are numerous unanswered questions in modern medicine. What is aging, for example? Why do people become more inflamed as they age? What’s with all of the chronic, degenerative diseases? Why is lipid metabolism (LDL, HDL, triglycerides) linked to degenerative diseases, along with immune system function and inflammation? I am only going to start the answers here.

I might as well continue to be cryptic and give you the string of words/concepts I am trying to connect to answer the other questions:
Hydrogen sulfide (H2S), endorphins, hibernation, nuclear receptors (PPARs), antibiotics, chronic inflammatory diseases (fibromyalgia, arthritis, chronic fatigue, Lyme, Morgellon’s, Alzheimer’s, prostatitis, pancreatitis, cancers, etc.), autoimmunity, leaky gut/kidney/brain barrier, autism and H1N1.

First a word of advice: Beware of assuming that molecules are specific, i.e. with unique interactions, and that a small molecule will bind to one and only one protein target. [There are lots of bizarre exceptions to the assumption: Aldolase acts as a structural protein for Toxoplasma motility. Fluorescein is added to make protein fluorescent, but the fluorescein is also transported into cells on its own, i.e. fluorescein and rhodamine labeling can give different results. Heparin binds to most extracellular proteins and it is mostly a hydrophobic interaction -- heparin is not just for clotting anymore.]

Observations from the literature:
  • Maternal autoimmunity is linked to autism.
  • Autism is linked to leaky gut and chronic inflammation.
  • Gut/kidney/brain barriers are based on integrity of extracellular matrix (heparan sulfate) that is compromised by inflammation.
  • Chronic diseases require inflammation and circulating inflammatory cytokines (TNF, IL-1, IL-6) are elevated..
  • NSAIDs induce leaky gut and release of bacteria toward liver.
  • Phagocytosis of bacteria leads to transport of some bacteria, e.g. Chlamydia pneumoniae to other sites of inflammation, e.g. gut to joints.
  • Opiods can induce hibernation in rodents.
  • Sulfides can induce hibernation in rodents.
  • H1N1 my cause lethal pneumonia by lung cytokine storm.
  • Inflammatory cytokines and inflammation result from activation of NFkB.
  • Hibernation involves PPARs (another nuclear receptor transcription factor).
  • Omega-3 fatty acids reduce inflammation via COX-2 prostaglandins, but also by binding to PPARs.
  • For most of the diseases under consideration, suppression of inflammation will eliminate symptoms.
  • Antibiotics can impact all of these diseases in unpredictable ways. In some cases complete remission can be achieved and in other cases antibiotics can produce lethal cytokine storms.
  • Bacterial cell wall components, e.g. lipopolysaccharide, lipid A, are intensely pyrogenic, i.e. inflammatory.

Cryptic Bacteria in our Tissues

The role of bacteria in numerous diseases, including cancers, has been proposed since the early isolation of bacteria from human tissues. Many of these bacteria are difficult to culture and have variable forms viewed by microscope. Because these bacteria are difficult for microbiologists to handle with conventional approaches, their existence and significance has always been questioned. Use of antibiotics to treat chronic, inflammatory conditions has seemed inconsistent with the unproven existence of a bacterial cause. Thus, there is surprise when the inappropriate use of antibiotics leads to a cure.

Cryptic Bacteria Suppress Local Inflammation and Promote Chronic Inflammation

I think that the fundamental problem is the assumption that human tissue is sterile, i.e. free from microorganisms, such as bacteria, unless there is overt infection. Part of the sterile assumption derives from the intense inflammatory response to bacteria. In order for bacteria to survive in tissue, the bacteria must suppress inflammation and the tissue must tolerate the slow leaching of inflammatory bacterial materials.

Chronic Disease Hypothesis

Based on the cryptic bacterial infection hypothesis, many, if not all chronic diseases are initiated by inflammatory events that release bacteria into the blood stream carried in phagocytic cells. The cells migrate and take up residence at a region of inflammation. The bacteria produce molecules that produce tissue hibernation and quell local inflammation in response to the bacteria. The bacteria are, however, a source of ongoing irritation to the tissue and a chronic inflammatory disease results.

Eradication of Cryptic Bacteria

Antibiotics would be a typical choice for killing infecting bacteria. In the case of cryptic, chronic infections, however, application of therapeutic antibiotics may be problematic. The established infections may have produced privileged locations isolated from the vascular system and protected by a bacterial community, e.g. a biofilm. Alternatively, the death of the bacteria and release of pyrogenic factors my produce life-threatening inflammation, that requires careful support.

Hibernation in Rodents Provides Treatment Clues

The compromise of tissue inflammation in response to cryptic bacteria is similar to the physiology of rodent hibernation. In both cases, systemic inflammation is suppressed. At the cellular level, this means that other signaling pathways silence the inflammatory NFkB expression pattern. One of the major nuclear receptors that is activated in hibernation is PPAR. PPAR is activated by opiods and H2S, which also induce hibernation in rodents. There are numerous analogs, inhibitors and H2S donors that could be used to disrupt hibernation (free local suppression of inflammation) or reduce symptoms by suppressing systemic inflammation.

Inflammation Compromises Tissue/Blood Barriers

Inflammation causes a disruption of the integrity of the endothelial extracellular matrix at sites of local inflammation. NFkB activation shuts down the expression of genes involved in heparan sulfate proteoglycan (HSPG) synthesis makes the tissue/blood barrier leaky. Locally this facilitates the recruitment of lymphocytes and neutrophils for defense, but systemically it leads to leaky gut/kidney/brain barriers that permit bacteria to cross.

Convergence of Therapies to Attack Cryptic Infections

The central approaches to attack cryptic infections are a combination of antibiotics and suppression of cytokine storms. These approaches are used in Marshall’s Protocol [http://bacteriality.com/ ], which also exploits a vitamin D receptor antagonist, Olmesartan, that also inhibits NFkB and inflammation.

EDIT BY ME to add this note by the author: "Marshal's use of benicar may be just to suppress inflammation through its effects on NFkB, the inflammation transcription factor. This effect makes sense and the action on the vitamin D receptor and the rationale for vitamin D avoidance is to me unsupported. Marshal is not a medical doctor, nor is his spokesperson Amy Proal."

A similar protocol has been developed by Dr. Michael Powell to inhibit hibernation and attack cryptic infections:
http://www.faqs.org/patents/app/20090163448

These approaches are similar to the lengthy use of antibiotics for the treatment of chronic Lyme disease.

It is very interesting to note that some of the most effective treatments for a long list of degenerative chronic diseases, autoimmune diseases and cancers, use essentially the same protocol that should attack cryptic bacteria and provide support for ensuing inflammation.
About Me

I grew up in San Diego and did my PhD in Molecular, Cellular and Developmental Biology (U. Colo. Boulder). I subsequently held postdoctoral research positions at the Swedish Forest Products Research Laboratories, Stockholm, U. Missouri -Colombia and Kansas State U. I was an assistant professor in the Cell and Developmental Biology Department at Harvard University, and an associate professor and Director of the Genetic Engineering Program at Cedar Crest College in Allentown, PA. I joined the faculty at the College of Idaho in 1991 and in 1997-98 I spent a six-month sabbatical at the National University of Singapore. Most recently I have focused on the role of heparin in inflammation and disease.
 
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weyland

Well-Known Member
This is just the wildest statement; it's exact opposite of what Ron Davis thinks they're doing. He thinks most everyone else is not looking for the answer but he is.
Where is there any evidence that these new findings are causal? Something is causing and maintaining this state, that makes it downstream for sure.
 

weyland

Well-Known Member
in a way its not encouraging when everyone finds evidence of different pathogens (lol)
I think it is encouraging because the disease is so heterogeneous. It would be more bizarre if the same single pathogen was found in all patients that had such different symptoms.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I concur! Darn it ................I wish you would read that book I sent you! One chapter.
I did. It was impressive. Unfortunately I am in Oregon and the book is in Las Vegas :sorry:
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I think this guy is on the right track potentially too...we shouldn't rule out bacterial causes just yet, I don't think.

About Me

I grew up in San Diego and did my PhD in Molecular, Cellular and Developmental Biology (U. Colo. Boulder). I subsequently held postdoctoral research positions at the Swedish Forest Products Research Laboratories, Stockholm, U. Missouri -Colombia and Kansas State U. I was an assistant professor in the Cell and Developmental Biology Department at Harvard University, and an associate professor and Director of the Genetic Engineering Program at Cedar Crest College in Allentown, PA. I joined the faculty at the College of Idaho in 1991 and in 1997-98 I spent a six-month sabbatical at the National University of Singapore. Most recently I have focused on the role of heparin in inflammation and disease.
Wow! That's impressive. Do you have a link to this guy?

Simmaron is also looking at insect borne diseases - they haven't been assessed yet either I don't think. I wouldn't be surprised if they don't show up in some people.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
Where is there any evidence that these new findings are causal? Something is causing and maintaining this state, that makes it downstream for sure.
I now agree :eggonface: but I think it is probably the quickest way to get at cause...Davis and Lipkin are still doing pathogen studies - so they are still looking at that angle. Unless they are herpesviruses at very low levels I don't know if they are going to show up in the blood though.
 

Tammy7

Well-Known Member
I think it is encouraging because the disease is so heterogeneous. It would be more bizarre if the same single pathogen was found in all patients that had such different symptoms.
Perhaps different strains of the same pathogen was what was causing the variable symptoms.
 
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