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jcwat101
Research Professional
| Joined: | Tue Jul 20th, 2004 |
| Location: | Pasadena, USA |
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Posted: Thu Nov 12th, 2009 03:30 |
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If that was the talk by Dr. Coffin I'm thinking of, I think he said that it didn't show up in German prostate cancer patients. Only U.S. CFS patients have been tested so far according to what I have heard.
Joyce
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20 yrs with CFS/FM/Lyme/IBS, food sensitivities; 1,25D/25D 8/04:64/11 http://SynergyHN.com
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Bane
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Posted: Mon Nov 16th, 2009 13:06 |
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jcwat101 wrote: If that was the talk by Dr. Coffin I'm thinking of, I think he said that it didn't show up in German prostate cancer patients. Only U.S. CFS patients have been tested so far according to what I have heard.
Joyce
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2770519/
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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elizabetha
Health Professional
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Posted: Tue Nov 17th, 2009 03:06 |
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Hi all,
I am getting in on the discussion quite late but have found the discussions interesting. Nothing earth shattering to share. My story - chronic fatigue syndrome for now over 20 years, 22 actually. Just on "K"'s discussion point. I used to think that I had recovered about 50 percent. However if someone were to have dug deeper, they would have found out that I had resigned my full time job as a community health nurse, and was working casual (meaning sporadically), even part-time work (half-time) if two days were together, I would be wiped out for the next 2 days. In looking at my patterns of energy in the past. I had about 2 months of okay(not fantastic) energy activity and then I would be side-lined sometimes by a flu/cold virus, too much physical work such as gardening or sometimes, no reason at all. So the next month or so would be symptomatic. So all my plans, activities, realigned relationships, interests would have to be stopped. Basically, it was a pattern of 2 months pretty good, then one month maybe more, very rough. And yes, I was taking all the fish oils,vitamins, etc.
As I have posted elsewhere, I did get very ill after a Measles, Mumps and Rubella vaccination at the age of 31. As public health folks, we were encouraged to be revaccinated because of a severe outbreak. That was the straw on the camel's back for me and as a former athlete, it was very noticeable, week after week, I just couldn't do any of the physical activities. The downfall all within a month after the vaccination. It may have contained a bacteria with a specific genome that fit in to down the whole system, who knows. Or it could have been the untreated Rickesstia from age 21.
As I study the posts of CFS folks, it does seems that recovery is longer and that our systems are somewhat more sensitive/complex.
All for now.
regards,
Elizabeth
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Post viral cfs 23 years, Rickettsia antibodies, Hashimotos Thyroiditis. Start MP Ph 1 Feb 09 l,25 OH 41.66, 25 D 29.2 Ph 2 July Min & Az - intolerable IP, Benicar only - Aug 09 Light sensitive. Noirs. Medications: Armour Thyroid 180mg. Cipralex 3
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Dr Trevor Marshall
Foundation Staff
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Posted: Tue Nov 17th, 2009 03:21 |
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As I study the posts of CFS folks, it does seems that recovery is longer and that our systems are somewhat more sensitive/complex
Maybe the non-CFS folk just put their heads down and concentrate on healing.
Look, most people coming here with a CFS diagnosis are very, very ill. But so are the sarcies who only have a little of their lungs left. The MS folk in wheelchairs. The ALS patients.
Please don't try to draw comparisons such as this. It will not help your recovery to separate yourself from the other members 
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k
Member in Phase 3
| Joined: | Fri Aug 10th, 2007 |
| Location: | Australia |
| Posts: | 310 |
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Posted: Tue Nov 17th, 2009 21:03 |
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As I study the posts of CFS folks, it does seems that recovery is longer and that our systems are somewhat more sensitive/complex.
I completely disagree with the above statement.
I encourage you to read the posts of more non-CFS people on the MP, success stories on this site and stories on bacteriality.com.
regards
k
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CFS menorrhagia & dysmenorrhoea anxiety depression paxil 600mg calcium daily Ph1Oct07 Ph2Feb08 Ph3Sept08 25D:Jul07=50 Oct07=23 Jan08=13.2 Oct08=12.8 Sept09:10 NoIRs cover-up low lux home lite exp r/t to work
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elizabetha
Health Professional
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Posted: Wed Nov 18th, 2009 18:13 |
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| I hear where you are coming from, thank you for your input.
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Post viral cfs 23 years, Rickettsia antibodies, Hashimotos Thyroiditis. Start MP Ph 1 Feb 09 l,25 OH 41.66, 25 D 29.2 Ph 2 July Min & Az - intolerable IP, Benicar only - Aug 09 Light sensitive. Noirs. Medications: Armour Thyroid 180mg. Cipralex 3
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Dec 4th, 2009 07:50 |
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If you spend the time to listen to what Dan Peterson said during the DHHS hearings, you will find is very different from the irresponsible speech and rumors floating around the CFS patient groups, and the Internet.
Petersen directly says that XMRV is most likely not the sole cause of CFS, and he says that he cannot even be sure it is a significant factor in the disease process.
Here is the link to Dan Peterson's presentation at the DHHS. The first 30 minutes is important, as are segments 5,6,7 and 8, John Coffin from Tufts (who is a must-see)
http://www.youtube.com/watch?v=80yKflt0tcA (Part one)
Click on 'next video' to see the other parts.
The first 30 minutes is the formal presentation, and initial questions. At part 4, Whittemore gets 5 minutes. Note that her address is to the patients, not really to the committee. In segment 5 John Coffin from Tufts talks in general about retroviruses The mutation he mentions is in RnaseL (not RNA Cell as subtitled)
Coffin also talks about a prostrate cancer study in Germany where in 600 pts there was no XMRV found
Note also that the phylogeny on Coffin's last slide shows BALB/c mouse line has the Xenotropic MLV, as do many wild-type strains. This speaks to a flaw in the 'inherited' SNP hypothesis...
Coffin mentions the false positive rate of the immunological assays (the antibody assays) (Elisa) which I have labeled as essentially useless until proven otherwise, especially in the absence of PCR positivity. These faulty assays are the basis of much of the bad science being spread. The incidence found was 67% and not 97%. The 97% figure is 'reaching', not supported by the totality of the evidence.
Coffin also says the RnaseL mutation is associated with a higher incidence of prostrate cancer.
Ron Glaser at the 8:00 mark of segment 7 makes some very interesting comments about the role of viral proteins
In segment 8 at 4:30 Lenny Jason asks Coffin to list the things that can go wrong with these experiments and Coffin explains antibody polyspecificity (see Amy's presentation in Beijing at http://www.youtube.com/watch?v=SGe9UTQJdHM )
AZT comes up at 8 minutes into part 10
All that Dan has found is fully consistent with our model of a Th1-weakened innate immune system allowing an opportunistic pathogen to proliferate.
..Trevor..
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Dr Trevor Marshall
Foundation Staff
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Posted: Tue Jan 5th, 2010 23:11 |
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Just published in PLoS ONE:
"Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome" (in London)
The authors also note that the link between prostrate cancer and XMRV was also not found in Europe.
So that's that. Judy Mikovits has her $1 million personal grant from the NIH, and her share of all the money from testing samples from CFS patients. The money machine that is Modern Medicine can move one, and leave CFS patients again without hope. I wonder if any of the CFS patient groups will start talking with us now? Unlikely...
I just found that Richie Shoemaker has been gathering data specifically aimed at showing Benicar is totally ineffective - a placebo, while the other ARBs work well in CFS. He says he has now proved that. Such is Modern Medicine
---------------------------------------
STOPPRESS: I just read this critique from Suzanne Vernon (another trained virologist, apprently):
http://www.cfids.org/cfidslink/2010/010603.asp
She is incorrect in her criticism. This was a far more exhaustive and unbiased study than WPI's, and it has shown that XMRV is not causal for CFS. Those who are falling for the CFS community's mischaracterization of the results clearly need to learn a bit more about how PCR machines work, and how Polymerases work, what AZT does, and stuff like that... Life ain't easy these days. But trust me, this was a carefully done study. Very carefully done...
Last edited on Tue Jan 5th, 2010 23:22 by Dr Trevor Marshall
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Bane
Member
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Posted: Tue Jan 5th, 2010 23:48 |
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Dr Trevor Marshall wrote:
I just found that Richie Shoemaker has been gathering data specifically aimed at showing Benicar is totally ineffective - a placebo, while the other ARBs work well in CFS. He says he has now proved that. Such is Modern Medicine
This guy?
http://www.casewatch.org/fdawarning/rsch/shoemaker.shtml
http://www.delmont.com/product.htm
http://video.google.com/videoplay?docid=3380861798551306641#
Last edited on Tue Jan 5th, 2010 23:54 by Bane
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Oral Lichen Planus(mild)/Clubbed Finger (digital clubbing)Last 25D 5.6ng/ml, phase3
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Jan 6th, 2010 01:15 |
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Yes. Ritchie is regarded as one of the leading CFS researchers. He has been publishing recently, methodology is to ask his patients to measure dozens of unusual inflammatory markers (VEGF etc), and see if they correlate with the diagnosis. Which still is mold.
So I guess maybe I ought to lay off Judy Mikovits a little
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eClaire
Member in Phase 2
| Joined: | Mon Sep 25th, 2006 |
| Location: | Virginia USA |
| Posts: | 859 |
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Posted: Wed Jan 6th, 2010 01:38 |
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 On occasion, I go to CFS patient sites and get crucified for being on the MP. XMRV has been the new answer for most, with some people cautioning others to stop being so excited about it (to reserve judgment) because folk have been disappointed before by some virus or other. As for the MP, people just believe all the Vit D hype and think all of us on the MP are insane cultist. Claire
P.S. I love my olmesartan.
Last edited on Wed Jan 6th, 2010 01:39 by eClaire
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38mo on MP; CFS FMS MCS COPD hypermob. IBS/GERD osteopor.; 125D48 25D<4;
NoIRs during most daylight outings & covered up; home w/o NoIRs
Ph1.Dec06 * ModPh2.Jun07 * AbxBrk.Mar-May08 * Ph2.Oct-Nov08 * Ph1.Jan2009
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dga5000
Guests visiting Phase 1/2/3
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Posted: Wed Jan 6th, 2010 14:25 |
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Here are some of the ways the PLoS ONE and Science trials differed:
1) The blood was collected from CFS patients in different types of blood collection tubes.
2) The genomic DNA was extracted and purified using different techniques.
3) The amount of genomic DNA included in the amplification assay was different.
4) Different primer sequences were used that amplified different regions of the XMRV proviral DNA.
5) The conditions of the PCR amplification assay were different – from the numbers of cycles, to the type of polymerase used.
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CFS dx 1995; FMS 2000; Memory Loss; + Chlamydia Pnemoniae; + LMW Rnase L Protein; Alk Phos 131; MP: 14/01/05: Bolle Swisher w/ 100 lenses + NOIR 707; Betahistine Hrydrochloride 16mg (vertigo); Benicar stopped; Minocycline stopped; Added Quercetin 7/8/5; P
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Jan 6th, 2010 14:43 |
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Agreed. The UK team was fastidious and may have erred on the side of caution, the US time was not cautious at all, and had to be reigned back by NCI prior to publication.
Amy has just written a chapter for a medical textbook which explains how PCR probes which are not chosen carefully (and this was the biggest difference between the two studies) will end up amplifying RNA from the wrong organisms. The human metagenome is huge, and probe specificity will become a major problem as the size of the metagenome becomes recognized. Meanwhile, research groups are still being careless when selecting their PCR probes, both in length and depth.
However, the point of dispute is XMRV causation, and IMO the UK study would have found the virus if it had been a causal organism.
..Trevor..
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eClaire
Member in Phase 2
| Joined: | Mon Sep 25th, 2006 |
| Location: | Virginia USA |
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Posted: Wed Jan 6th, 2010 16:38 |
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Dr Trevor Marshall wrote: The UK team was fastidious and may have erred on the side of caution, the US time was not cautious at all, and had to be reigned back by NCI prior to publication.
The banter on the various sites about these differences is that they are indicative of "the fact" taht the Brits didn't do a very good job--not as good a job as the regular study.  I really wish someone would write the book "Metagenome Made Easy."
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38mo on MP; CFS FMS MCS COPD hypermob. IBS/GERD osteopor.; 125D48 25D<4;
NoIRs during most daylight outings & covered up; home w/o NoIRs
Ph1.Dec06 * ModPh2.Jun07 * AbxBrk.Mar-May08 * Ph2.Oct-Nov08 * Ph1.Jan2009
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Iona
Member in Phase 2
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| Location: | Oslo, Norway |
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Posted: Wed Jan 6th, 2010 18:18 |
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dga5000 wrote: Here are some of the ways the PLoS ONE and Science trials differed:
1) The blood was collected from CFS patients in different types of blood collection tubes.
2) The genomic DNA was extracted and purified using different techniques.
3) The amount of genomic DNA included in the amplification assay was different.
4) Different primer sequences were used that amplified different regions of the XMRV proviral DNA.
5) The conditions of the PCR amplification assay were different – from the numbers of cycles, to the type of polymerase used.
Author Contributions
Conceived and designed the experiments: SK MM. Performed the experiments: OWE SK. Analyzed the data: SK MM. Contributed reagents/materials/analysis tools: SK GW DC SW AC. Wrote the paper: SK MM. Facilitated the study by setting up the collaboration: JW. Responsible for providing samples and associated data from a well characterised and valuable cohort of subjects: Simon Wessely
This is Simon Wessely
"Your most cited paper claims that conditions such as CFS, irritable bowel syndrome and fibromyalgia are all the same illness.
If you ask people with irritable bowel syndrome whether they suffer from fatigue, they all say yes. It's just gastroenterologists don't ask that question. Likewise, if you talk to someone with CFS, you find that nearly all of them have gut problems. If you systematically interview people with these illnesses, you find that a big proportion of these so-called discrete syndromes have a large overlap with the others. You have to think that we have got the classifications wrong."
http://www.newscientist.com/article/mg20126997.000-mind-over-body.html
http://www.youtube.com/watch?v=L5foBQ1TzV0
http://en.wikipedia.org/wiki/Simon_WesselyLast edited on Wed Jan 6th, 2010 18:40 by Iona
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ME/CFS, Ulcerative Colitis| 1,25D 57,8pg/ml Jul07| Ph1 Jan08| Ph2 Feb09| Melatonin| NOIRS, covered up| 25D 8ng/ml 06.02.09|
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scooker48
Member in Phase 3
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Posted: Wed Jan 6th, 2010 18:47 |
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In my opinion, after working in libraries for more almost 38 years, all classifications systems are tortured.
Sherry
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Necrotizing granulomas biopsy 10/88; Dx 12/04 Sarcoid liver spleen. 2/2/05: VitD 25/VitD125 62. 11/7/09 D25 at 6, Liver function normal 4/08; Wear NoIRs outside. No K creme used. 5/09 Liver and kidneys normal. ACE still high at 113 on 11/7/09.
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Jan 6th, 2010 19:12 |
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Iona,
Is your post suggesting that we make a judgment concerning the citations you posted? Do you have a perspective?
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dga5000
Guests visiting Phase 1/2/3
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Posted: Wed Jan 6th, 2010 20:36 |
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Official Statement from the Whittemore Peterson Institute Regarding UK Study
The Whittemore Peterson Institute (WPI) has reviewed the paper entitled “Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome.” This study did not duplicate the rigorous scientific techniques used by WPI, the National Cancer Institute and the Cleveland Clinic, therefore it cannot be considered a replication study nor can the results claim to be anything other than a failure not just to detect XMRV, but also a failure to suggest meaningful results.
The scientific methods used by WPI are very exact and require specific techniques to ensure accuracy. Differences in techniques employed by Erlwein et al. not only explain their failure to replicate the WPI study, but also render the conclusions meaningless. These differences include, but are not limited to the following:
1) blood sample volumes and processing;
2) patient criteria/population differences;
3) number and type of tests done to assure accurate results, including white blood cell culture;
4) use of a molecular plasmid control in water versus a positive blood sample; and
5) different primer sequences and amplification protocol used to find the virus, which were not validated by a clinical control.
The WPI study was published after six months of rigorous review and three independent lab confirmations, proving that contamination had not taken place and that infectious XMRV was present in 67 percent of CFS patients diagnosed according to the Canadian and Fukuda criteria. In contrast, this latest study was published online after only three days of review. Significant and critical questions remain as to the status of patient samples used in the UK study as those samples may have been confused with fatigued psychiatric patients, since the UK has relegated “CFS” patients to psychiatric care and not traditional medical practices.
“Little is known about the prevalence of XMRV world-wide, much less the incidence of XMRV in ME/CFS or prostate cancer” emphasizes Dr. Judy Mikovits. “WPI and its NCI collaborators are actively engaged with international research teams to investigate these important questions.”
WPI does not recommend the use of anti-retroviral drugs that have yet to be proven to be effective in treating XMRV infection. However, several large pharmaceutical companies have expressed interest in developing anti-retroviral and immune modulating drugs that will effectively treat XMRV associated diseases.
WPI looks forward to the results of other scientific groups around the world, serious about replicating its scientific results, by using the same techniques as WPI and its collaborators. The fact that XMRV was detected in 67 percent of the CFS samples in the U.S. study determined a significant association between XMRV and CFS, demanding a much more serious inquiry by responsible health agencies around the world as to the cause of this debilitating disease.
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CFS dx 1995; FMS 2000; Memory Loss; + Chlamydia Pnemoniae; + LMW Rnase L Protein; Alk Phos 131; MP: 14/01/05: Bolle Swisher w/ 100 lenses + NOIR 707; Betahistine Hrydrochloride 16mg (vertigo); Benicar stopped; Minocycline stopped; Added Quercetin 7/8/5; P
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dga5000
Guests visiting Phase 1/2/3
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Posted: Wed Jan 6th, 2010 20:50 |
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All scientists enter into scientific trials with a inevitable degree of bias - hoping to get a particular result. Simon Wessely has been commited to confirming the psychiatric basis of this illness and his control over the funding sources for ME/CFS in the UK over the last 20 years has made sure almost no state monies have been spent on trying to find a physiological cause. To that end the only reason Wessely was willing to spend any of his departments funds on the study was in order to disprove it. He and his team had much to gain from not replicating the results.
Perhaps we should wait until Dr Kerr et al at St Georges (London) publish their results. Given his ground breaking studies into the genetics of ME/CFS he is at least open to the idea that a retrovirus could play some part in this terrible illness.
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CFS dx 1995; FMS 2000; Memory Loss; + Chlamydia Pnemoniae; + LMW Rnase L Protein; Alk Phos 131; MP: 14/01/05: Bolle Swisher w/ 100 lenses + NOIR 707; Betahistine Hrydrochloride 16mg (vertigo); Benicar stopped; Minocycline stopped; Added Quercetin 7/8/5; P
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Dr Trevor Marshall
Foundation Staff
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Posted: Wed Jan 6th, 2010 21:00 |
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Huge mistake by WPI. I read this as saying they have no idea how the molecular technology really works.
I would want to see a detailed analysis of primers. I want to see what WPI's primers hit in the full metagenomic database, not just on part of one XMRV genome.
If I was NCI, after I read the patient blog at http://forums.aboutmecfs.org/showthread.php?t=771 , I would withdraw all support from WPI until they clarify the selection criteria for their cohort, which, based on this blog, was clearly not just based on the Canadian and Fukuda criteria.
Crying foul over the UK cohort is a valid argument, except that we are talking about a zero appearance of XMRV, not a difference between 36% and 10%, for example. A cohort-balance complaint therefore seems a zero-sum game, to me.
WPI need to focus on the molecular methodology, but I suspect that they understand the CFS community exhibits a collective paranoia about academics who see CFS as a psychiatric dysfunction. The way to change an academic's opinion is to provide support for an alternative hypothesis, as we have done, rather than resort to name-calling.
Further, I would note that WPI's income comes from energizing the CFS patient community, and I would want to start asking questions about whether that might have clouded the objectivity of their methodology, as it clearly has clouded the form of their response.
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