tag:blogger.com,1999:blog-66223182571330158782024-03-12T22:01:06.979-04:00ParakochA Journey Through DiseaseTony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.comBlogger659125tag:blogger.com,1999:blog-6622318257133015878.post-20193510340448114832014-08-31T05:41:00.000-04:002014-08-31T05:48:20.534-04:00Cushing's Syndrome cause by Cereal Grains (and/or Sugar)?The dog of my mother has Cushing's – probably, we need to do more tests. Anyhow, the dog has a lot of problems, which may or may not be connected to Cushing's:<br />
<br />
<ul>
<li>(Probably) Cushing's, thin legs, bigger stomach</li>
<li>Muscle problems: weakness, (temporary) limbing</li>
<li>Fatigued</li>
<li>Liver problems (I swear, he hasn't been drinking)</li>
<li>Cataract</li>
<li>Hearing problems</li>
<li>Probably a few other small things</li>
</ul>
<div>
Now, the only things wrong in his nutrition were Cereal Grains and Sugar. No dairy that I know of. His nutrition contained probably some seed oil, but I don't know what. Possibly some chicken egg through noodles.</div>
<div>
<br /></div>
<div>
As his condition worsned, and the dog started limping, and dragging one hind-leg, we had to do something. The doctor first suspected arthitis, and the dog got anti-inflamatory medication and anti-pain medication. I changed the dogs diet at the same time and removed cereal grains and sugar for his diet. The result was that he improved somewhat.</div>
<div>
<br /></div>
<div>
Next he got anti-biotics and again anti-pain medicaiton. The dog improved again somewhat. I started giving the dog more carbs (rice and potatoes). The combination of anti-biotics and carbs seems to have done some help.</div>
<div>
<br /></div>
<div>
Now he is off the anti-biotics, and got less carbs, and the dog is more fatigued again.</div>
<div>
<br /></div>
<div>
Now, it is difficult to say whether the dog improved due to the medication, or due to the change in nutrition. But I'll be damned if cereal grains and sugar are not bad for dogs.</div>
<div>
<br /></div>
<div>
We'll keep looking. </div>
<div>
<br /></div>
<div>
Let's see, this week the dog get another test, and then maybe some medication for Cushing's. It is really sad to see the dog like that, but at least it improved noticeably over the last weeks.</div>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-3175066068195213422014-04-11T05:40:00.001-04:002014-04-11T05:40:54.659-04:00"Pathways to Prevention for ME/CFS"I posted a comment on the CFIDS website regarding <a href="http://solvecfs.org/pathways-to-prevention-for-mecfs/">"Pathways to Prevention for ME/CFS"</a>:<br />
<blockquote>
Prevention? Prevention needs some sense of the cause(s), if I am not mistaken.<br />
<br />
Yes, there are tentative, speculative causes. But all the so far presented "definitive" causes of ME/CFS share one thing in my eyes: complete lack of credibility. There is no trustworthy research pointing to an cause.<br />
<br />
And would prevention look like? <br />
<br />
For pathogens, it would be the prevention of the spreading of that pathogen. Problem is, there is no identified pathogen. Horning/Lipkin draw a blank. So against which pathogen do you want to prevent? Problem is, there are no known ones.<br />
<br />
Sure, the psych*-doctors know that it is the patient who is to blame. Excuse my sarcasm, but to them it is the patient who is doing something wrong, in his/her wicked ways, as patients are – the patients simply "need" guidance by professional psych*-doctors. So their "prevention" would be some form of "education". Maybe teaching "resilience to fatigue"? Problem is, they think the disease exists in the minds of their patients, but their disease model exists only in the doctor's heads, not in reality.<br />
<br />
Or do you want to somehow target groups at risk, and do something? Problem is, there are no identified risk groups. (Again pardon my sarcasm) Sure, the psych*-doctors will tell you it is crazy women who are at risk, but that is not reality – everybody is "at risk".<br />
<br />
Did I miss some school of thought here? Oh, maybe the mainstream nutritional disciples will scare us of cholesterol, or saturated fat, or whatever they think is the current bogey man. Problem is, these things aren't the cause either.<br />
<br />
So you need some preformed notions about ME/CFS to even consider "prevention". And the problem is that none of those preformed notions about ME/CFS are in any way backed up by robust studies.<br />
<br />
It is noble to think about preventing ME/CFS, but unless we know more about the cause(s), any talk about "prevention" is pure fantasy, a waste of resources, and potentially quite harmful to the patient.<br />
<br />
Try to find out affected pathways, try to find out cause(s) – and demand loud and clear that any prevention is based on clearly identified pathways and causes. I am afraid that any result of such a conference will be: "Doctors need to teach crazy women how to avoid tormenting their doctors with their problems." They might formulate it with more psych*-medical jargon, so it doesn't sound so offensive.<br />
<br />
The CFIDS needs to be highly critical of this – otherwise this could have catastrophic effects on the people with ME/CFS.</blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-10660495428186785682014-03-20T04:56:00.001-04:002014-03-21T18:52:53.300-04:00Lipkin And Horning Draw A BlankFrom the tweets from the 2014 "Stanford ME/CFS Symposium" I can see that Lipkin focuses on the "microbiome" (aka all the "good" and "bad" bacteria that live in your gut).<br />
<br />
While he does not say it explicitly, he found no prevalent infections nor any prevalent immune system problems in people with ME/CFS. Granted, he found some leads with regards to IL-17 and eotoxins – but I am cautious and don't expect that anything will come from this.<br />
<br />
And while I think that there is possibly a connection to the gut (and to nutrition!) in many diseases, I however think the reason that Lipkin looks in the gut is because he has exhausted the paths of inquiry that involve the body "proper".<br />
<br />
Furthermore Lipkin appears to think that ME/CFS is one "monolithic" disease, so the only place where this one disease must hide (in his view) is in the microbiome in the gut.<br />
<br />
I think he is wrong on two accounts:<br />
<br />
1. I think there is good evidence that ME/CFS is <b><u><i>not</i></u></b> one monolithic disease, but instead a set of symptoms that can be caused by several diseases.<br />
<br />
2. Lipkin is – as so many in medical research and the medical profession – unaware of the pathogenic potential of some the foods we eat (with dairy, cereal grains and seed oils/PUFA/TFA in my mind being probably the prime suspects).<br />
<br />
For me, this is the disenchantment of Lipkin, as I had some hope that he might be able find at least one prevalent disease in people with ME/CFS.<br />
<br />
(And BTW some of the things he said on "Autism and GI complains", on "Kawasaki syndrome and candida in the troposphere" and on "Chronic Lyme" are borderline woo. I do not think that Lipkin is a good ally. However if he investigates these things properly, and then clearly announces if he draws a blank, then I am OK with his lines of inquiry. The problem starts when he does <i>not</i> clearly say when he draws a blank…)<br />
<br />
Personally I don't expect that Lipkin/Horning will find anything useful in the gut/microbiome – but it is good that they continue their inquiry, if only that they might spread more awareness of the disease or might find something by a lucky coincidence. One never knows…<br />
<br />
<b>[Postscript]</b> One other thing is noteworthy: Lipkin found no evidence whatsoever that ME/CFS is caused by HHV-6 / HHV-6B. He found 3 or 4 patients – out of 586(!) – with HHV-6 or HHV-6B. This more or less invalidates the entire argument by the HHV proponents that ME/CFS is caused by an ongoing HHV infection. I think especially the attention given to Montoya (and others) in that regards is not warranted.<br />
<br />
<b>[Postscript 2]</b> One more thing: As Lipkin didn't explicitly say it, let me put it in clear words:<br />
<br />
<div style="text-align: center;">
<span style="font-size: x-large;"><u><b>Lipkin found <i>no</i> evidence for an ongoing infection in people with ME/CFS.</b></u></span></div>
<br />
Clear enough for you?<br />
<br />
If ME/CFS is caused* by pathogens (viruses or possibly bacteria), then they are long gone after the initial acute infection**. A case of "hit and run", if you want – the pathogen is gone, the damage stays.<br />
<br />
No need to treat a pathogen that is gone, as that will usually do more harm than good. Or as they say at NASA:<br />
<br />
<div style="text-align: center;">
<span style="font-size: large;">Things are never so bad that they can't be made worse.</span></div>
<br />
<u>So the first order of business: Don't make things worse.</u> Anti-viral
and anti-bacterial and anti-whatnot medications have a high potential to
make things worse – best to use them only if you are <u>really really
sure</u>.<br />
<br />
So, if there is no pathogen, what can you do? The best one could do is to identify the damage, and try to treat it (e.g. orthostatic intolerance with medication targeting the blood preasure – speak with your doctor!). If there is anything that alleviates symptoms, then doing it might be a good ides. Change nutrition, try a Paleo Diet, try an Eleminaion Diet. But please, stop claiming that phantom ME/CFS viruses, and phantom ME/CFS bacteria, and phantom ME/CFS fungi supposedly hide in the gut of people with ME/CFS, or in their tissues, or god knows where – you are hurting yourself and hurting other people.<br />
<br />
PLEASE. STOP. IT.<br />
<br />
Please?<br />
<br />
-- <br />
* There seems however to be evidence to indicate that <u>acute</u> infections can cause ME/CFS in some cases.<br />
<br />
** Unless you are one of those rare 1 in a 100 ME/CFS cases were it is <u>clearly</u> established that there is an ongoing infection – and no, "Chronic Lyme" is <u>not</u> a ongoing infection, and <u>neither</u> is "Candida", <u>nor</u> "Chlamydophila pneumoniae" or any other somesuch woo terms being peddled by people who don't know better. These are makebelieve terms that only fool people (including those who doctors who use these terms).<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-8165474094863015742014-01-28T13:41:00.002-05:002014-01-28T13:41:23.501-05:00The second acne cause: House dust and/or house dust mites?As I have written before, I have been having problems with acne. And while I traced down milk and dairy (and more specific pasteurized dairy) as the primary cause, my acne still didn't go away fully. <a href="http://parakoch.blogspot.com/2013/11/loose-ends-and-chasing-ghosts.html">I had some suspects</a>, but I found one more I had overlooked so far: House dust and/or house dust mites…<br />
<br />
Not sure yet, I will see if this is indeed the cause.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-71472921990628234342014-01-14T14:03:00.000-05:002014-01-14T14:03:27.733-05:00Unfinished Blog-Post: A Post-Mortem for Lombardi et al. 2009 - The Response to CommentsA long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
<a name='more'></a><br />
<br />
Response to Comments on “Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome”<br />
Judy A. Mikovits1,* and Francis W. Ruscetti2<br />
<br />
1 Whittemore Peterson Institute, Reno, NV 89557, USA.<br />
2 Laboratory of Experimental Immunology, National Cancer Institute–Frederick, Frederick, MD 21701, USA.<br />
*To whom correspondence should be addressed. E-mail: judym@wpinstitute.org<br />
<br />
Received for publication 10 November 2009.<br />
Accepted for publication 19 April 2010.<br />
Science 14 May 2010: <br />
Vol. 328 no. 5980 p. 825 <br />
DOI: 10.1126/science.1184548<br />
<br />
We reported the detection of the human gammaretrovirus XMRV in 67% of 101 patients with chronic fatigue syndrome (CFS) and in 3.7% of 218 healthy controls, but we did not claim that XMRV causes CFS. Here, we explain why the criticisms of Sudlow et al., Lloyd et al., and van der Meer et al. regarding the selection of patients and controls in our study are unwarranted.<br />
<br />
Our study (1) documented the presence of a recently discovered human retrovirus, XMRV, in a high proportion of patients with chronic fatigue syndrome (CFS) in comparison with healthy controls. Sudlow et al. (2), Lloyd et al. (3), and van der Meer et al. (4) raise concerns about the cases and controls described in our study and thus the validity of our results. First, we wish to emphasize that our study was not intended to be a detailed clinical description of CFS or an epidemiological study that would relate particular symptoms, demographics, duration, pattern of onset, and the like to the presence or viral load of XMRV. The study was not, nor was it designed to be, a case-control study as Sudlow et al. (2) imply, for it was the first demonstration of the replication and production of infectious XMRV in human blood cells. The fact that a number of the patients tested were from regions of CFS outbreaks does not invalidate the clinical diagnosis. We hope that our report will stimulate the performance of many case-control studies that use appropriate virus detection. We certainly recognize that such studies will be required to determine what role XMRV plays in the pathogenesis of CFS.<br />
<br />
Samples included in our study (1) were from CFS patients who fulfilled both the Fukuda criteria and the Canadian Consensus Criteria (CCC), regardless of severity. We regret that a sentence in the original supporting online material in (1) implied that immunological abnormalities were part of the CFS diagnosis; indeed, while many such patients do exhibit such abnormalities (5, 6), they were not required for diagnosis. All patients that met Centers for Disease Control and Prevention and CCC criteria were accepted; none were excluded. Patient samples were obtained from 2006 to 2009 and stored in the Whittemore Peterson Institute (WPI) repository. We did not state in Lisbon (7) or elsewhere that the samples analyzed in (1) were only from patients from documented outbreaks of CFS, nor did we state that the 101 patients described in (1) exhibited all the immunological abnormalities described in our Lisbon conference presentation. In fact, only 25 samples in (1) came from patients identified during the 1984 to 1988 CFS outbreak in Incline Village, Nevada. The remaining 76 samples included patients with sporadic cases from 12 U.S. states and Canada, including California, New York, North Carolina, Wisconsin, Michigan, Oregon, New Mexico, New Jersey, North Dakota, Texas, and Florida. Patients in the study were 67% female, reflecting the reported gender incidence of CFS, with an age distribution of 19 to 75 years of age (mean of 55). The healthy control population, which was similar in age and gender to the patients, was composed of healthy people who visited doctors’ offices in the western United States between 2006 and 2008. The great majority, although not all, of the patients analyzed were matched in geographic location with controls. As this was not an epidemiological case-control study, we did not attempt to discern where the patients believed they contracted CFS; at the time of sample collection, some were undoubtedly living in an area different from the location where they first became ill.<br />
<br />
The information we provide here and in the accompanying Supporting Online Material (8) should lay to rest any concerns about “bias” or “confounding.” Again, the primary aim of the work described in (1) was not to characterize this clinical condition or to prove a cause for CFS but to demonstrate the existence of an infectious gammaretrovirus in patients who had been diagnosed with CFS. We achieved our goal using four different experimental strategies. The original description of HTLV-1 and HIV-1 involved only one or two patients (9–12), whereas we detected XMRV in 75 individuals.<br />
<br />
We did not state that our study (1) proves the cause of CFS. A large number of infectious and noninfectious agents have been implicated in CFS, and it is that fact that makes the puzzle of CFS all the more difficult to solve. At no time have we wished to raise false hopes among a group of patients who, in general, have not been treated well by the medical research community. We are aware that many different pathogens have previously been reported to be associated with CFS but have not been proven to be causal.<br />
<br />
We further note that no cytokine profiles were presented in (1), nor did we state that abnormal cytokine levels, altered natural killer cell activity, or particular RNase L profiles were a requirement for inclusion in the study. Unpublished comments made during a medical conference (7) exploring hypothetical connections with immune system defects, viral reactivation, and malignancies should not be used to judge the merits of the science in the published paper. Regarding the concern raised by Sudlow et al. (2) about potential “expectation bias,” we point out that the National Cancer Institute (NCI) and the Cleveland Clinic, whose scientists independently performed experiments and coauthored (1), were certainly not “established” as laboratories for the purpose of studying CFS. All samples were blinded, as mandated by the NCI and WPI institutional review board approvals. All experimental procedures were done by the same personnel, in the same physical laboratory space, under identical protocols. <b><span class="Apple-style-span" style="color: red;">Investigators at NCI received 100 samples from individuals without knowing their health status; furthermore, the samples were sent to NCI directly without passing through the WPI laboratory space.</span></b> <b><span class="Apple-style-span" style="color: blue;">Laboratory workers at the NCI and the WPI who performed the polymerase chain reaction (PCR) and immunological studies used coded, blinded samples that did not reveal the CFS status of the individuals. The WPI has examined all 218 control and 101 patient samples by both PCR and serological methods for the presence of XMRV nucleic acid and antibodies.</span></b> <span class="Apple-style-span" style="color: blue;">In addition, NCI used plasma from all 100 samples they received in infection experiments with LNCaP cells.</span> It was not feasible to examine all 101 patient and 218 control samples with all four XMRV detection methods described in (1), due to time and resource constraints.<br />
<br />
Of the technologies used to identify and isolate XMRV in patients with CFS, <span class="Apple-style-span" style="color: blue;">PCR from DNA or cDNA from unstimulated peripheral blood mononuclear cells is the least sensitive method</span>. <span class="Apple-style-span" style="color: #999999;">We contend that the three recently published negative PCR studies (13–15) do not qualify as being studies that fail to replicate our study, as neither the same PCR methodologies were used nor did these studies draw on the additional cell culture and immunological methods that we employed to observe XMRV nucleic acids and proteins. Although we offer to send samples in which we have detected XMRV, the groups that published these results neither requested nor analyzed any samples we had found positive for XMRV in our laboratories.</span><br />
<br />
<span class="Apple-style-span" style="color: #999999;">Sudlow et al. erroneously state that we did not consider alternative explanations for the findings, namely that patients with poor general health may be more susceptible to viral and other infections. On the contrary, we raised as a question for future study: “Is XMRV infection a causal factor in the pathogenesis of CFS or a passenger virus in the immunosuppressed CFS patient population?” (1). We recognize that the presence of XMRV could be due to enhanced susceptibility to retroviral infection after development of CFS. A causal role of XMRV in CFS is an intriguing possibility, given the known immunosuppressive, neurotropic, and serious consequences of infection with other known retroviruses.</span><br />
<br />
Supporting Online Material<br />
<br />
<span class="Apple-style-span" style="color: #999999;">The following information pertains to the patient samples studied in Lombardi et al. (S1).</span><br />
<span class="Apple-style-span" style="color: #999999;">Samples banked in the WPI repository from 2006 to 2009 were selected for our study from patients who fulfilled both the 1994 CDC Fukuda Criteria for CFS (S2) as well as the 2003 Canadian Consensus Criteria (CCC) (S3) for ME/CFS and who signed informed consent. While there are differences between the two criteria, the most important is that the CCC requires post-exertional malaise for the diagnosis and the Fukuda criteria have post-exertional malaise as one of the eight symptoms, at least four of which are required for diagnosis. Post-exertional malaise is felt by many clinicians to be the sine qua non of CFS.</span><br />
<br />
<span class="Apple-style-span" style="color: #999999;">The samples banked in the WPI repository had persistent and relapsing fatigue for at least six months. All known medical conditions causing severe fatigue were excluded, and patients included had at least four of the following eight symptoms: tender cervical or axillary lymph nodes, persistent sore throat, impaired cognition and/or short term memory, muscle pain, multi‐joint pain, headache, unrefreshing sleep and post exertional malaise.</span><br />
<br />
<b><u>One hundred and eighteen control samples</u> </b>were <b><u>provided by a local medical practice [in Nevada]</u></b> drawn between 2004 and 2007, under University of Nevada, Reno IRB approval, with a female to male ratio of approximately 2 to 1. Subjects donated blood during a routine health visits and were certified by the physician to be healthy at the time of their visit. <b><u>An additional one hundred samples of purified genomic DNA and plasma and were purchased from a local company supplied for paternity/forensic testing.</u></b> <b>Samples purchased were specified to be taken from the twelve states represented by the <u>majority of the sporadic samples in our study</u>.</b><br />
<br />
[What happened to "<a href="http://parakoch.blogspot.com/2012/02/sample-selection-in-lombardi-2009.html">320 control samples from same geographic locations</a>"?]<br />
<br />
All control samples were de‐identified prior to being supplied to us as required by the NIH and UNR IRB protocols for these studies. CFS patient PBMC were collected from heparinized blood and aliquoted into four samples for analysis of RNA, DNA, and protein. PBMC aliquots were frozen in plasma and DMSO for later culture. Samples were prepared within 6 hours of blood draw and frozen immediately in ‐800C or liquid nitrogen depending upon the sample type. Samples were taken from patients on at least two different time points within three months of each. Additional supporting supplementary laboratory testing was not a factor in sample selection.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-25809688400309918102014-01-14T14:02:00.001-05:002014-01-14T14:02:53.319-05:00Unfinished Blog-Post: A Post-Mortem for Lombardi et al. 2009 - The AddendumA long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
<a name='more'></a><br />
<br />
Reposted is here the study "Mikovits et al. 2010", the so called "Addendum" to "Lombardi et al. 2009". This is work in progress.<br />
<br />
Please note:<br />
<ul><li>All emphasis, color and comments mine</li>
<li>Comments are in square brackets</li>
<li>Colors denote possible origin of research results<br />
(<span class="Apple-style-span" style="color: blue;">WPI/Mikovits</span>, <span class="Apple-style-span" style="color: red;">NCI/Ruscetti</span> and <span class="Apple-style-span" style="color: #38761d;">CC/Silverman</span>)</li>
<li><span class="Apple-style-span" style="color: magenta;">IFC possibly done at NCI/Ruscetti (not ruled out: UniN, Reno)</span></li>
</ul><br />
Some remarks:<br />
<ul><li>The study and the "Addendum" were most likely written by different persons. "PBMCs" in the study versus "PMCs" in part of the Addendum</li>
<li><span class="Apple-style-span" style="color: #38761d;">Silverman</span> is not mentioned as co-author of the Addendum</li>
<li>Mikovits is author of the Addendum (PI for the study) </li>
<li>Lombardi is co-author (was author for the study)</li>
<li>Ruscetti is PI (was co-author for the study)</li>
<li>The other groups from NCI are not mentioned as co-authors of the Addendum</li>
<li>The quote:<br />
<blockquote>In our October 2009 publication, we established XMRV infection in the blood products of our patient population by <b><u>five different methods</u></b>. Of these methods, <span class="Apple-style-span" style="color: #38761d;">single-round PCR on DNA from peripheral blood mononuclear cells (PBMCs), the least sensitive method, <b><u>required us to use samples from a subset of chronically ill patients we had observed to have persistent viremia</u></b>.</span></blockquote>asdf</li>
<li>asdf <blockquote>"<b><u>performing the multiple methods on the same 57 blood samples</u></b>"</blockquote>yet only 35 samples were tested by all methods.</li>
</ul><br />
<br />
Virulence 1:5, 386-390; September/October 2010; © 2010 Landes Bioscience<br />
<b><u>Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome</u></b><br />
<span class="Apple-style-span" style="color: blue;">Judy A. Mikovits,1,* Vincent C. Lombardi,1 Max A. Pfost,1 Kathryn S. Hagen 1</span> and <span class="Apple-style-span" style="color: red;">Francis W. Ruscetti 2 </span><br />
<br />
<span class="Apple-style-span" style="color: blue;">1 Whittemore Peterson Institute; Reno, NV USA; </span><br />
<span class="Apple-style-span" style="color: red;">2 Laboratory of Experimental Immunology; Cancer and Inflammation Program; National Cancer Institute-Frederick; Frederick, MD USA</span><br />
<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Addendum to: Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, et al. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syn- drome. Science 2009; 326:585–9; PMID: 19815723; DOI: 10.1126/science.1179052.</div><div><br />
</div><br />
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In October 2009, we reported the first direct isolation of infectious xenotropic murine leukemia virus-related virus (XMRV). <b><u>In that study</u>, we used a combination of biological amplification and molecular enhancement techniques to <u>detect XMRV in more than 75% of 101 patients with chronic fatigue syndrome (CFS)</u>.</b><br />
<br />
[This is a misrepresentation of Lombardi et al. 2009, after all it reported a 67% detection rate.]<br />
<br />
<span class="Apple-style-span" style="color: #999999;">Since our report, controversy arose after the publication of several studies that failed to detect XMRV infection in their CFS patient populations. In this addenda, we further detail the multiple detection methods we used in order to observe XMRV infection in our CFS cohort. </span><br />
<br />
<span class="Apple-style-span" style="color: blue;">Our results indicate that PCR from DNA of unstimulated peripheral blood mononuclear cells is the least sensitive method for detection of XMRV in subjects’ blood.</span> We advocate the use of more than one type of assay in order to determine the frequency of XMRV infection in patient cohorts in future studies of the relevance of XMRV to human disease.<br />
<br />
<span class="Apple-style-span" style="color: #999999;">Patient selection poses a challenge to any study of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In our October 2009 paper, samples banked from 2006 to 2008 were selected for our study from severely disabled patients who fulfilled the 1994 CDC Fukuda Criteria for chronic fatigue syndrome1 as well as the 2003 Canadian Consensus Criteria (CCC) for ME/CFS.2 The CCC requires</span><br />
<span class="Apple-style-span" style="color: #999999;">post-exertional malaise, which many clinicians feel is the sine qua non of ME/ CFS. Furthermore the CCC further requires that patients exhibit post exertional fatigue, unrefreshing sleep, pain and neurological/cognitive manifestations, rather than these being optional symptoms.3 Many clinicians interested in CFS are switching to the Canadian criteria because they feel it is more descriptive of the clinical entity being defined. The Fukuda criteria have the advantage of a longer period of usage and existence of many publications that have added modifications. Suffice it to say that the clinician author of the Science paper elected to use both criteria, thus bypassing the argument of which criteria were better. Moreover, the emphasis in the Science paper was directed toward the virology, not the clinical description of ME/CFS.</span><br />
<br />
In our October 2009 publication, we established XMRV infection in the blood products of our patient population by <b><u>five different methods</u></b>. Of these methods, <span class="Apple-style-span" style="color: #38761d;">single-round PCR on DNA from peripheral blood mononuclear cells (PBMCs), the least sensitive method, <b><u>required us to use samples from a subset of chronically ill patients we had observed to have persistent viremia</u></b>. </span><br />
<br />
<span class="Apple-style-span">[How was this "</span><span class="Apple-style-span" style="color: #38761d;"><b><i>observation</i></b></span><span class="Apple-style-span">" of "</span><span class="Apple-style-span" style="color: #38761d;"><b><i>persistent viremia</i></b></span><span class="Apple-style-span">" take place? qRT-PCR? Gut feeling? CFS illness score? Tea leaf reading?</span> Or did they test their "least sensitive" method to produce consistent results? And what were these?]<br />
<br />
<br />
<span class="Apple-style-span" style="color: #38761d;">In Figure 1A of our Science paper, we showed that DNA of 7 of 11 patients exhibited the expected gag and env PCR amplification products from single-round PCR with XMRV primers. We included this figure to demonstrate that samples exhibited gag products upon nested PCR, though PCR with nested env primers did not result in detectable products from these samples (Table 1).</span><br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span class="Apple-style-span" style="color: #38761d;">Table 1. XMRV detection using cDNA from 22 unstimulated PBMCs gag gene</span></div><div><br />
</div><br />
<br />
Samples that are negative for XMRV by one of our PCR assays are sometimes positive by other assays. For example, in Figure 1A of the Science paper, patient 1118 was negative by single round PCR on DNA from unstimulated PBMCs, but positive in other assays (Science Figs. 2A and D, 4A and S5). Of the 34 patients whose PBMCs were negative for XMRV by DNA or cDNA PCR, 17 were positive for infectious virus when co-cultured with the LNCaP indicator cell line, as XMRV gag and env PCR products were detected in the cell line following their infection with XMRV from the patient PBMCs (Table 2). Both gag and env products obtained from either single-round or nested PCR were sequenced and shown to be 99% identical to XMRV VP62.<br />
<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Table 2. Co-Culture with LNCaP of PBMCs from 12 patients PCR negative for <i>env</i></div><div><br />
</div><br />
<br />
<span class="Apple-style-span" style="color: #999999;">Subsequent to our October 2009 publication, two papers from the United Kingdom 4,5 and a paper from the Netherlands 6 have appeared in which the authors report the lack of detection of XMRV PCR products from DNA of unstimulated PBMCs, using patient populations selected by only the Fukuda criteria or the Oxford criteria rather than both Fukuda and CCC criteria. We regret that these authors did not request <u>positive control samples of our patients who exhibit XMRV PCR products even when assayed by the least sensitive detection method, namely PCR of DNA from unstimulated PBMCs</u>. Given that </span><span class="Apple-style-span" style="color: blue;">only 7% of our 101 patients’ PBMCs exhibit products upon DNA PCR (Table 3 and 4),</span><span class="Apple-style-span" style="color: #999999;"> and that a number of patients were included in the UK studies who do not fulfill the CCC criteria, very few, if any, of the samples would be expected to be positive by DNA PCR. We also note that both studies followed different methods than ours for blood collection, DNA quantities and isolation and PCR, possible sources of the disparate results.</span> The XMRV detection results of the 101 patients are listed in Table 4.<br />
<br />
<span class="Apple-style-span" style="color: #999999;">The negative reports of PCR tests for XMRV has raised questions whether our findings could be due to <u>contamination of our PCR experiments by mouse genomic XMRV-gag specific PCR products</u> and <u>no env specific PCR products following single round DNA PCR of DNA of unstimulated PBMCs</u>. </span><br />
<br />
<span class="Apple-style-span" style="color: #999999;"><b>In contrast, when cDNA was prepared from PBMCs, 67% of the nested PCR, which inevitably raises questions of contamination, is not essential to detect XMRV in <u>highly viremic ME/ CFS patients</u>.</b> </span><br />
<span class="Apple-style-span" style="color: #999999;">[This sentence makes no fucking sense. None whatsoever.]</span><br />
<span class="Apple-style-span" style="color: #999999;">[And again, how were these "<i>highly viremic ME/ CFS patients</i>" determined? qRT-PCR? Gut feeling? CFS illness score? Tea leaves? Or did they test their "least sensitive" method to produce consistent results? And what were these?]</span><br />
<br />
<br />
The remaining 90 samples described in the paper exhibited very few DNA, which contain gag and env sequences highly similar to XMRV. Positive PCR results for XMRV were obtained independently in multiple laboratories led by co-authors of the Science paper. In the summer of 2006, prior to work on XMRV at the Reno Whittemore-Peterson Institute (WPI), 30 mL of heparinized peripheral blood were obtained from patients resid- ing in the US, Canada and Europe coming to be treated at the well-known Sierra Internal Medicine practice, located in Incline Village, NV. Once collected, 48 of these blood samples were shipped directly to NCI where cDNA was prepared for planned microarray experiments. After the WPI observed an XMRV PCR product from a patient sample in 2009, the NCI began testing these stored samples by PCR. cDNA from 42 of the 48 samples sent to the NCI lab in February 2007 tested posi- tive for XMRV gag by nested PCR. Neither the WPI nor NCI labs where PCR was per- formed had ever worked with mouse tissues or had been exposed to XMRV from other sources. The env sequences amplified from LNCaP cells infected by patient PBMCs exhibit less similarity to mouse genomic DNA than to XMRV VP62, further indi- cating the presence of XMRV infection rather than mouse genomic DNA contami- nation. After we developed a sensitive cell culture assay for detection of XMRV, we assayed our cell lines and patient material with a highly sensitive assay (developed and kindly provided by Bill Switzer, CDC) to detect the presence of mouse tissue con- tamination by the identification of murine mitochrondial cytochrome oxidase by real time PCR. All of the cell lines and 101 patient materials tested negative for mouse contamination.<br />
<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Table 3. Summary of multiple viral assays from a group of 57 patients</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Table 4. XMRV detection results of 101 patients </div><div><br />
</div><br />
<br />
In our experience from <b><u>performing the multiple methods on the same 57 blood samples [Only 35 samples were tested by all methods!]</u></b>, the most sensitive blood-based assays for detection of XMRV in decreasing order (Table 3) are:<br />
(1) <span class="Apple-style-span" style="color: blue;">performing nested PCR for gag sequences</span> from <span class="Apple-style-span" style="color: magenta;">LNCaP cells that have been co-cultured with subject’s plasma or activated PBMCs</span>,<br />
(2) <span class="Apple-style-span" style="color: #a64d79;">the presence of antibodies to XMRV Env in subject’s plasma</span>,<br />
(3) <span class="Apple-style-span" style="color: blue;">presence of gag products by nested PCR</span> on stimulated PBMCs or detection of viral proteins expressed by activated PBMCs with appropriate antisera,<br />
(4) <span class="Apple-style-span" style="color: blue;">nested RT-PCR</span> of plasma nucleic acid or PCR from cDNA from unactivated PBMCs and<br />
(5) PCR of DNA from unactivated PBMC prepared from subject’s blood.<br />
<br />
Despite association with both prostate cancer and CFS, many questions remain regarding the prevalence of XMRV in the human population, the incidence of XMRV in disease, and the extent of genetic variation between XMRV isolates. <b><u>The genetic variation between XMRV isolates currently identified is only 0.03%</u></b>, <b><u>despite the fact that the viral sequences were obtained from isolates from two vastly different diseases in patients from geographically distinct areas</u></b>. This variation is smaller than the variation observed between HTLV-1 isolates.7 <b><u>As in the case with HTLV, the lack of diversity implies that XMRV recently descended from a common ancestor.</u></b> 8<br />
<br />
[That'll be VP62, which recently descended from 22Rv1.]<br />
<br />
<br />
The high degree of similarity to xenotropic murine leukemia virus suggests that a cross-species transmission event was likely involved in the evolution of XMRV.9<br />
<br />
[Not cross-species transmission, but rather cross-tissue transmission while xeno-grafting 22Rv1.]<br />
<br />
<br />
<span class="Apple-style-span" style="color: #999999;">Further examination of XMRV from human subjects may reveal more extensive sequence variation, which also may confound its detection unless PCR primers are designed with this possibility in mind.</span><br />
<br />
<span class="Apple-style-span" style="color: #999999;">We have not claimed in our October 2009 publication or in other venues that XMRV is the cause of CFS, only that its detection in the majority of our ME/CFS patient cohort allows us to form a testable hypothesis as to an infectious basis for this devastating disease. Future work should establish what role XMRV may play in development of prostate cancer, ME/CFS and other diseases.</span><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-25461383276655680562014-01-14T14:01:00.002-05:002014-01-14T14:01:51.441-05:00Unfinished Blog-Posts: Comparison between the results of Lombardi 2009 and the "Addendum"A long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
<a name='more'></a><br />
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Comparison between the results of <a href="http://parakoch.blogspot.com/2012/02/numerical-results-of-lombardi-2009.html">Lombardi 2009</a> and <a href="http://parakoch.blogspot.com/2012/01/does-table-number-4-lie.html">table 4 from the "Addendum</a>"<br />
<br />
<table border="1"><tbody>
<tr> <td rowspan="2">.</td> <td>Lomb.</td> <td>Adden.</td> <td>Lomb.</td> <td>Adden.</td> <td>Lomb.</td> <td>Adden.</td> </tr>
<tr> <td colspan="2"><div style="text-align: center;">Positive</div></td> <td colspan="2"><div style="text-align: center;">Negative</div></td> <td colspan="2"><div style="text-align: center;">Tested</div></td> </tr>
<tr> <td><span class="Apple-style-span" style="color: blue;">"Non-Nested" PCR (NA)</span><br />
<span style="color: blue;">(cDNA nested PCR)</span></td> <td><span class="Apple-style-span" style="color: blue;">NA</span></td> <td><span class="Apple-style-span" style="color: blue;">min 17</span><br />
<span class="Apple-style-span" style="color: blue;">max 25</span></td> <td><span style="color: blue;">NA</span></td> <td><span class="Apple-style-span" style="color: blue;">min 66</span><br />
<span class="Apple-style-span" style="color: blue;">max 74</span></td> <td><span style="color: blue;">NA</span></td> <td><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="color: black;"></span></span><br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span class="Apple-style-span" style="color: blue;"><span style="color: blue;">min 93</span></span></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span class="Apple-style-span" style="color: blue;"><span style="color: blue;">max 101</span></span></div></td> </tr>
<tr> <td><span style="color: blue;">"Nested PCR"</span><br />
<span style="color: blue;">(cDNA nested PCR)</span></td> <td><span style="color: blue;">68</span></td> <td><span style="color: blue;">min 73</span><br />
<span style="color: blue;">max 81</span></td> <td><span style="color: blue;">33</span></td> <td><span style="color: blue;">min 28</span><br />
<span style="color: blue;">max 36</span></td> <td><span style="color: blue;">101</span></td> <td><span style="color: blue;">min 93</span><br />
<span style="color: blue;">max 101</span></td> </tr>
<tr> <td>"Western Blot (WB)"<br />
(LNCaP co-culture with PMCs)</td><td>19</td> <td>min 34<br />
max </td> <td>11</td> <td><br />
</td> <td>30</td> <td>min 45<br />
max 53</td> </tr>
<tr> <td><br />
("Infectious agent in plasma")</td> <td>10</td> <td></td> <td>2</td> <td><br />
</td> <td>12</td> <td>min 46<br />
max 54</td></tr>
<tr> <td>"Antibodies in Plasma"<br />
<br />
</td> <td>9</td> <td>min 35<br />
max 43</td> <td>9</td> <td>min 11<br />
max 19</td> <td>18</td> <td>min 46<br />
max 54</td></tr>
<tr> <td>"Western Blot (WB)"<br />
(LNCaP co-culture with PMCs)</td><td>19</td> <td>min 34<br />
max </td> <td>11</td> <td><br />
</td> <td>30</td> <td>min 45<br />
max 53</td> </tr>
<tr> <td><br />
(LNCaP culture with plasma)</td> <td><br />
</td> <td>min 48<br />
max 56</td> <td><br />
</td> <td>min 3<br />
max 11</td> <td><br />
</td><td>min 51<br />
max 59</td></tr>
</tbody></table><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-88447386090522727462014-01-14T14:01:00.001-05:002014-01-14T14:01:16.194-05:00Unfinished Blog-Post: "February 1983: Gallo proposes that AIDS is probably caused by a retrovirus, presumably a variant of HTLV-1 or II"A long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
<a name='more'></a><br />
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Transcribed by OCR, some errors corrected manually – may still contain errors.<br />
<blockquote>
<b><u>The chronology of AIDS research</u></b><br />
Nature 326, 435 - 436 (08 April 1987); doi:10.1038/326435a0<br />
(e.g., <a href="http://books.google.de/books?id=U6KTCeHgwcsC&lpg=PA156&ots=Y9Zpx5RMeu&dq=%22September%201983.%20At%20the%20Cold%20Spring%20Harbor%20meeting%20on%20human%20T-cell%20leukaemia-lymphoma%20viruses%3A%20Montagnier%20and%20co-workers%20%22&pg=PA155#v=onepage&q&f=false">available here</a>)<br />
<br />
This statement from Gallo and Montagnier constitutes part of the agreement between the US and French AIDS research groups.<br />
…<br />
<br />
<b>February 1983.</b><br />
<br />
At the Cold Spring Harbor Workshop on AIDS, Gallo proposes that AIDS is probably caused by a retrovirus, presumably a variant of HTLV-1 or II. <br />
<br />
<b>May 1983.</b><br />
<br />
Barro-Sinoussi, Chermann, Momagnier and co-workers (1983). publish:<br />
<br />
(1) the isolation and identification of a non-transforming retrovirus (later called lymphadenopathy-associated vino (LAV)). different from HTLV-I and HTLV-II, in cultures of T lymphocytes derived from a patient with lymph-adenepathy syndrome;<br />
<br />
(2) the continuous passage of the virus by its transient growth in cultures of T lymphocytes of normal blood donors;<br />
<br />
(3) the identification of a major protein associated with this virus, p25, not immunologically cross-reactive with the p24 of HTLV-I; and<br />
<br />
(4) the detection by immunoprecipita-tion of antibodies against this protein in two patients. Essex and co-workers (1983) detect antibodies cress-reactive with HTLV-I membrane protein in 25-30% of AIDS patients.<br />
<br />
Gelman and co-workers (Gallo's group) (1983) find evidence for presence of the viral genume of HTLV-I or an HTLV-I variant in 2 of 33 AIDS patients.<br />
<br />
<br />
<b>September 1983.</b><br />
<br />
At the Cold Spring Harbor meeting on human T-cell leukaemia-lymphoma viruses:<br />
Montagnier and co-workers (1984) report:<br />
<br />
(1) the identification of LAV-like viruses from 5 patients with lymphadenopathy and 3 patients with AIDS (homosexual, haemophiliac, Haitian);<br />
<br />
(2) the selective affinity of LAV for CD4(T4) helper lymphocytes:<br />
<br />
(3) the presence of antibodies (enzyme-linked immunosorbent assay, ELISA) against the main LAV antigens in patients with lymphadenopathy-associated syndrome (LAS) (63%) and AIDS (20%);<br />
<br />
(4) that LAV is morphologically similar to equine infectious anaemia virus (EIAV) and different from HTLVs; and<br />
<br />
(5) the antigenic cross-reactivity between core proteins of EIAV and LAV (virus isolates from LAS patients are called LAV, and from AIDS patients are called IDAV).<br />
<br />
Gallo and co-workers (1984) report the presence of HTLV-I antibodies in 10% of AIDS patients and isolates of HTLV-I or HTLV-II or variants of it in fewer than 10% of such cases.<br />
<br />
<b>March-April 1984.</b><br />
<br />
Montagnier et al. (1984) by using more sera of horses infected with EIAV confirm cross-reactivity of the core proteins of LAV with that of EIAV and identify a second viral protein, p18.<br />
<br />
Vilmer, Chermann, Montagnier and co-workers (1984) confirm previous isolation of an LAV-like virus from one haemophiliac and isolate another one from his asymptomatic brother.<br />
<br />
<b>May 1984.</b><br />
<br />
Gallo's group (1984) reports:<br />
<br />
(1) mass and continuous production in a clone of a permanent cell line (H9) of HTLV-III from two AIDS patients and four additional isolates (SN, BK, CS, WI) also infectious for another clone (114) derived from the same parental cell line (Popovic, Sarngadharan, Gallo and co-workers).<br />
<br />
(2) 48 virus isolations, that is, 18 of 21 patients with pre-AIDS, 3 of 4 clinically normal mothers of juveniles with AIDS, 26 of 72 juveniles and adults with AIDS, 1 of 22 healthy male homosexuals, and 0 of 115 heterosexual subjects (Gallo, Salahuddin, Popovic and colleagues). The use of anti-p24 hyperimmune sera proves that the 48 isolates belong to the same kind of virus;<br />
<br />
(3) The introduction of the Western blot technique for clinical detection of antibodies in 88% of 48 patients with AIDS, 79% of 14 homosexuals with pre-AIDS and less than 1% of hundreds of heterosexuals. A gp41 is identified as a major viral antigen (Sarngadharan, Popovic, Gallo and co-workers). Later, it is demonstrated by Veronese, Sarngadharan and Gallo to be the HTLV-III viral transmembrane component of the envelope.<br />
<br />
(4) Partial characterization of the immunologically reactive proteins by the Western blot technique. (Schupbach, Sarngad-haran, Popovic, Gallo and co-workers).<br />
<br />
<b>June 1984.</b><br />
<br />
Safai, Gallo, Pupovic and Sarngailharan report 34 of 34 (100%) of AIDS patients positive for HTLV-III antibodies, 16 of 19 (84%) of LAS patients and 0 of 14 (0%) of controls (1984).<br />
<br />
Brun-Vezinet, Barre-Sinoussi, Montagnier, Chermann arid co-workers (1984) publish detection of antibodies against LAI/ proteins by ELISA in 74,5% of the patients presenting with iymphadenopathy syndrome, 37,5% of patients with frank AIDS, 18% of healthy homosexuals, 1% of blood donors.<br />
<br />
<b>July 1984.</b><br />
<br />
Kalyanarainan, Iviontagnier, Francis and co-workers (1984) report the detection of anti-p25 (LAV) antibodies in 51 of 125 (41%) of AIDS patients, 81 of 113 (72%) of LAS patients, and 0 of 70 of healthy individuals;<br />
<br />
Montagnier and co-workers (1984) report the growth of LAV in continuous B-cell lines, most of them transformed by Epstein-Barr virus.<br />
<br />
Kiatzmann, Gluckman., Chermann, Montagnier and co-workers (1984)42 publish:<br />
<br />
(1) the selective isolation of LAU. from CD4+ (T4 4) lymphocytes of a healthy carrier of the virus;<br />
<br />
(2) the inhibition of CD4 cell growth at the same time of in vitro virus production;<br />
<br />
(3) the simultaneous disappearance of the CD4 antigen at the surface of the infected CD4 lymphocytes.<br />
<br />
<b>August 1984.</b><br />
<br />
A third group, Levy et al., (1984) isolate virus antigenically and structurally related to LAV from San Francisco AIDS patients.<br />
<br />
<b>September 1984.</b><br />
<br />
Cheinsong-Popov, Weiss and collaborators publish identical prevalence of antibodies against antigens of HTLV-III grown in H9 line and of LAV-1 grown in CEM line in UK patients with AIDS or at risk of AIDS (1984).<br />
<br />
Goedert, Gallo and co-workers (1984) report that in a cohort of homosexual men at risk of AIDS, 53% were antibody-positive for HTLV-III. In HTLV-III antibody positive subjects, AIDS developed at 6.9% per year.<br />
<br />
<b>October 1984.</b><br />
<br />
Brun-Vezinet, Montagnier, Dot. Quinn and co-workers (1984) publish the presence of antibody against LAV in 35 of 37 Zairean patients with AIDS.<br />
<br />
Zagury, Gallo and co-workers (1984) isolate HTLV-III from cells cultured from semen of two patients with AIDS.<br />
<br />
<b>November 1984.</b><br />
<br />
Hahn, Gallo and co-workers (1984) report the molecular cloning of HTLV-III virus.<br />
<br />
Kitchen, Allan, Essex and co-workers (1984) (1985) identify the viral external glycoprotein gp120, a finding confirmed by Montagnier and co-workers (1985).<br />
<br />
<b>December 1984.</b><br />
<br />
Alizon, Barre-Sinoussi, Wain-Hobson, Montagnier and co-workers (1984) report the molecular cloning of LAV-1.<br />
<br />
Wong-Stool, Shaw, Gallo and co-workers (1984) discover genomic heterogeneity of HTLV-III.<br />
<br />
Dagleish, Weiss and co-workers (1984) and independently Klatzmann, Gluckman, Montagnier and co-workers (1984) show the CD4 molecule is involved in the receptor to the virus.<br />
<br />
Popovic, Read-Connole and Gallo (1984) publish a series of CD4-positive human neoplastic cell lines susceptible to and permissive for HTLV-III, including HUT78, Molt3 and CEM cell lines. <br />
<br />
<b>January 1985.</b><br />
<br />
The nucleotide sequence of the AIDS virus genome is established independently at the Pasteur Institute (1985), at the NCI/NIH (1985), at Genentech, Inc. (1985) and at Chiron (1985), revealing the similarity of the various isolates.<br />
<br />
Sodroski, Wong-Staal, Gallo, HeseMae and co-workers (1985) demonstrate transactivation of transcription in HTLV-III infected cells.<br />
<br />
Shaw, Gallo and co-workers (1985) discover the presence of virus in the brain. <br />
<br />
<b>March 1985.</b><br />
<br />
Redfield, Gallo and co-workers (1985) describe heterosexual transmission of HTLV-III. </blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-70999878723603979712014-01-14T13:59:00.003-05:002014-01-14T13:59:48.783-05:00Unfinished Blog-Post: A Post-Mortem for Lombardi et al. 2009 - Unanswered QuestionsA long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
<a name='more'></a><br />
<br />
<b><u>1. When and how were the samples gathered and processed by the phlebotomists?</u></b><br />
Full paper trail about gathering of samples (for each sample, patient and controls, with original sample number and reported sample number):<br />
<b><u><br />
</u></b><br />
<b>Background:</b><br />
VIPdx lab required the samples to be received within 24 hours after blood draw – this seemed to be important and the question is if the study followed this protocol.<br />
<br />
Furthermore, 100 of the control samples were bought from a company specializing in supplying control samples for studies. Any differences between these samples and the other samples would be interesting.<br />
<br />
<br />
<b><u>2. When and how were the samples received, processed and stored at the lab?</u></b><br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Full paper trail about the gathering of the samples (for each sample, patient and controls, with original sample number and reported sample number)</div><div><br />
</div><br />
<b>Background:</b><br />
VIPdx lab required the samples to be received within 24 hours after blood draw, supposedly to be immediately processed at the lab – this seemed to be important and the question is what processing was done at the lab after receiving the samples.<br />
<br />
<br />
<br />
<b><u>3. When were the samples tested, in what lab, with what method and with what result?</u></b><br />
Full paper trail of <i>all</i> tests performed (for each sample, patient and controls, with original sample number and reported sample number)<br />
<br />
<b>Background:</b><br />
The study itself did not answer how the samples that Silverman received were selected. In the Addendum it was mentioned for the first time that. It would be interesting to find out how the testing regime was.<br />
<br />
Furthermore there are many conflicting results reported by Mikovits as to how many samples were positive, so this would be needed to reconcile the reports with the actual testing. The handling of the control samples would be interesting as well.<br />
<br />
<br />
With this, one would need to compile the following table for each sample:<br />
<br />
<ul><li>When was the sample drawn and how was it handled (materials used, etc.)?</li>
<li>When was the sample received by the lab(s)</li>
<li>How was the sample processed and stored by the lab</li>
<li>What test(s) were performed, when, at which lab and with what results?</li>
</ul><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-75239858595761278252014-01-14T13:59:00.001-05:002014-03-25T08:44:14.940-04:00Unfinished Blog-Post: To Pull A GalloA long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
<br />
BTW: It is this post I most regred not finishing – it is mainly missing one table in the middle, listing some parallels between the story of "Fictional Gallo" and those who brought us the XMRV fraud. However the so inclined readers might be able to find parallels by themselves.<br />
<br />
<a name='more'></a><br />
<br />
<b><u>The Grand Tragedy of Robert Gallo and The Rotten Farce of Judy Mikovits</u></b><br />
A fictional story of rotten apples<br />
<blockquote class="tr_bq">
Progress, far from consisting in change, depends on retentiveness. When change is absolute there remains no being to improve and no direction is set for possible improvement: <i>and when experience is not retained, as among savages, infancy is perpetual</i>. <i>Those who cannot remember the past are condemned to repeat it.</i><br />
-- <b>George Santayana</b>, <a href="http://en.wikiquote.org/wiki/George_Santayana">The Life of Reason (1905-1906)</a></blockquote>
As a prelude: my excuses if I focus on aspects you already know and don't explain things you are in need of elucidation – I tried to write one text, not to broad, not too deep, including all facts and speculations that are needed to retrace my conclusions.<br />
<br />
The <b>XMRV virus</b> was claimed by a few researchers to be the 3rd discovered human retrovirus ("HGRV"), after the discovery of <b>HTLV</b> and <b>HIV</b> in the late seventies and early eighties.<br />
<br />
To understand the history of HIV research and of XMRV research, one has to look not only at the common (or separating) aspects of the virology, immunology or pathology of these three viruses, but one has to look at connections outside of the scientific inquest to gain insight.<br />
<br />
One such aspect connecting HTLV, HIV and XMRV research lies in the persons doing the research:<br />
<br />
<b>Judy Mikovits</b> was central in the claims that XMRV is connected to CFS. She worked in the eighties in Francis Ruscetti's lab, and she choose Ruscetti to do some work for her XMRV studies.<br />
<br />
<b>Francis Ruscetti</b>'s lab was where Judy Mikovits worked in the eighties. Ruscetti in turn was involved in the discovery of HTLV. He helped to bolster Mikovits' claim that XMRV was found in the blood of CFS patients.<br />
<br />
And it was <b>Robert Gallo</b>'s lab where Francis Ruscetti worked, when he researched HTLV – the Robert Gallo who rose fame due to his involvement in the discovery of HIV.<br />
<br />
I shall try to outline that it was the success of Robert Gallo's behavior coupled with the ignorance or outright condonation of Robert Gallo's work that gave rise to a culture of laying claims to viruses with possibly falsified and fabricated evidence, in order to claim priority in case an actual (even if different) virus was found.<br />
<br />
Before I continue about the circumstances and relationships surrounding the history of HIV research (and thereafter the history of XMRV research), I will make a very short excursion into the history of HIV itself. There exists a group of viruses, now called HIV, which infect humans and cause – if left untreated – the spectrum of diseases called AIDS. That much is now firmly established fact.<br />
<br />
As a passing remark: If there is any doubt about HIV causing AIDS, I think it was Robert Gallo's behavior and the protection he received that made HIV denial possible. By "muddying the waters", in order to weaken the claims made by the French group around Luc Montagnier, Robert Gallo prepared (in my opinion) the ground for HIV denial to arise – he most certainly is the darling of the HIV-denial movement. And in my view, the "<i>XMRV/HGRV cult</i>" we see today is not coincidently similar to <i>HIV denialism</i>, but it is the same reaction by laymen to the same type of "water muddying" of those who should know better.<br />
<br />
HIV (the <i>Human</i> Immunodeficiency Virus) came into existence when the <i>Simian</i> Immunodeficiency Virus (SIV) jumped from its simian host to a human host. This in fact happened several times, giving us different strains of HIV.<br />
<blockquote class="tr_bq">
<a href="http://scienceblogs.com/erv/2012/01/always_make_sure_your_illegal.php">HIV-1 is related to a virus we can find in African primates, SIV.</a> SIV crossed over from chimpanzees to the human population to make 'HIV' sometime in the late 1800s, early 1900s. This event happened at least three times, giving us the three groups of HIV-1, Groups M, N, and O, however it most likely has occurred numerous times over the course of human evolution, it just never lead to a pandemic like what we have with HIV-1 today. You can go get blood samples from African hunters right now and find viruses not found in any other human.</blockquote>
For some considerable time only relative few people were being infected with HIV, before HIV infections reached a critical mass of people and "took of" in the very early eighties.<br />
<br />
So here ends my short excursion of the history of HIV and I switch over to the history of HIV research. When people started to realize that they had a <a href="http://en.wikipedia.org/wiki/Pandemic">pandemic</a> at their hands (and could no longer shrug it of as "<a href="http://parakoch.blogspot.com/2012/02/oh-irony-2.html">epidemic hysteria</a>" or "Gay Plague", <a href="http://parakoch.blogspot.com/2012/02/as-long-as-patient-will-suffer-cruel.html">in some form of cruel homophobic stupidity</a>), researchers started to look for the pathogen that caused this disease.<br />
<blockquote>
<i>… it really seems as though old Hegel, in the guise of the World Spirit, were directing history from the grave and, with the greatest conscientiousness, causing everything to be re-enacted twice over, once as grand tragedy and the second time as rotten farce, </i>Caussidière for Danton, L. Blanc for Robespierre, Barthélemy for Saint-Just, Flocon for Carnot, and the moon-calf together with the first available dozen debt-encumbered lieutenants for the little corporal and his band of marshals. Thus the 18th Brumaire would already be upon us.<br />
-- <b>Friedrich Engels</b>, <a href="http://www.marxists.org/archive/marx/works/1851/letters/51_12_03.htm#cite">Letter to Karl Marx In London (1851)</a></blockquote>
Since I've heard of XMRV and learned of all the inconsistencies in the claims by various researchers to have found evidence of this virus (or one of its more or less closely related viruses) in the blood of CFS patients, I was struggling to understand the behavior of the involved scientists, namely Judy Mikovits, Vincent Lombardi, Francis Ruscetti, Harvey Alter and Shyh-Ching Lo. I could find no <i>scientific</i> explanation, no reason, no rationale in the (sorry to invoke Godwin) <a href="http://www.youtube.com/watch?v=pR5q0ajW8Ko">reality defying bunker-like insistence</a> that <b><u><i>IT MUST BE XMRV</i></u></b>. Especially the behavior of Judy Mikovits seemed erratic and surreal to me. Well, as I found out, I could not find a <i>scientific</i> rationale because the rationale is <i>not</i> of scientific nature.<br />
<blockquote class="tr_bq">
Of the writings dealing with the same subject at approximately the same time as mine, only two deserve notice: Victor Hugo’s Napoleon le Petit and Proudhon’s Coup d’Etat. Victor Hugo confines himself to bitter and witty invective against the responsible producer of the coup d’etat. <i>The event itself appears in his work <b>like a bolt from the blue</b>. He sees in it only the violent act of a single individual.</i> He does not notice that he makes this individual great instead of little by ascribing to him a personal power of initiative unparalleled in world history. Proudhon, for his part, seeks to represent the coup d’etat as the result of an antecedent historical development. Inadvertently, however, his historical construction of the coup d’etat becomes a historical apologia for its hero. Thus he falls into the error of our so-called objective historians. I, on the contrary, demonstrate how the class struggle in France <i>created circumstances and relationships that made it possible for a grotesque mediocrity to play a hero’s part</i>.<br />
-- <b>Karl Marx</b>, <a href="http://www.marxists.org/archive/marx/works/1852/18th-brumaire/preface.htm">The Eighteenth Brumaire of Louis Bonaparte. Karl Marx – Preface to the Second Edition (1869)</a></blockquote>
To understand Judy Mikovits' behavior in the last years – to see that her behavior was <i>not</i> like a "<i>bolt from the blue</i>" – we have to first understand Robert Gallo's role in the discovery of HIV in the early eighties. Then, I am firmly convinced, when the circumstances and relationships that were fostered by Robert Gallo and the US government to take credit for the discovery of HIV are understood, then a connection between Gallo's behavior and Mikovits' behavior will become discernable. I will <i>not</i> focus on the circumstances and relationships that govern the research of CFS – as much as it would be needed, I will only note that it were these circumstances that allowed the mediocre (at best) Judy Mikovits to play a hero's part.<br />
<br />
So to start with the currently accepted view of Robert Gallo, this is what <a href="http://en.wikipedia.org/w/index.php?title=Luc_Montagnier&oldid=476525063">Wikipedia has to say on Luc Montagnier</a> – and in turn about Robert Gallo. I will consider this the "official" narrative of Robert Gallo's work:<br />
<blockquote class="tr_bq">
The question of whether the true discoverers of the virus were French or American was <i>more than a matter of prestige</i>. A US government patent for the AIDS test, filed by the United States Department of Health and Human Services and based on what was claimed to be Gallo's identification of the virus, was at stake. In 1987, both governments attempted to end the dispute by arranging to <i>split the prestige of discovery and the proceeds from the patent 50-50</i>, naming Montagnier and Gallo co-discoverers. The two scientists continued to dispute each other's claims until 1987. It was not until President François Mitterrand of France and President Ronald Reagan of the USA met that the major issues were ironed out. The scientific protagonists finally agreed to share credit for the discovery of HIV, and in 1986, both the French and the US names (LAV and HTLV-III) were dropped in favor of the new term human immunodeficiency virus (virus de l'immunodéficience humaine, abbreviated HIV or VIH) (Coffin, 1986). <i>They concluded that the origin of the HIV-1 Lai/IIIB isolate discovered by Robert Gallo was the same as that discovered by Montagnier</i> (but not known by Montagnier to cause AIDS). The compromise allowed Montagnier and Gallo to end their feud and collaborate with each other again for a chronology that appeared in Nature that year.<br />
<br />
The Chicago Tribune published an investigative report by reporter John Crewdson in 1990 which questioned whether Gallo's laboratory had taken the virus from Montagnier, which led to National Institutes of Health (NIH) and Congressional investigations that ultimately cleared Gallo's group from any wrongdoing. In 1994, when further investigations revealed that there was no evidence that Gallo had invented the AIDS test and that the Pasteur Institute had applied for a patent for its own test months before Gallo, the NIH agreed to <i>award a greater share of the patent royalties to the Pasteur Institute</i>.</blockquote>
So, we can conclude from this – without spinning any conspiracy theories – that besides the personal prestige and ego of Robert Gallo, and besides the prestige of US research at large, some money was involved and the matter of how to distribute this money hinged around the question who had a claim to be the discoverer of HIV, and who not – and the answer to this question was important enough that it involved the heads of state, both of the US and of France.<br />
<br />
Furthermore, we can conclude, <a href="http://parakoch.blogspot.com/2012/02/hiv-and-american-isolate.html">without any remaining doubt or controversy</a>, that the virus that Robert Gallo isolated was in fact sent to him from Luc Montagnier – that it was Montagnier and <i>not</i> Gallo who isolated the virus first. And I will note in passing that over the years the <i>Official Narrative</i> moved away from Gallo's point of view towards Montagnier's.<br />
<br />
And one more remark: This narrative is, in my not so humble opinion, heavily dominated by the view from the US. After reading some articles on Wikipedia on that topic one can not help oneself but to feel sorry for the injustice Robert Gallo has befallen by not receiving the Nobel prize – as even the article about Luc Montagnier is interwoven with the story of Robert Gallo, who is mentioned 28 times in Montagnier's article (while <a href="http://en.wikipedia.org/w/index.php?title=Robert_Gallo&oldid=473720230">Gallo's article</a> mentions Montagnier only 15 times).<br />
<br />
From 1991 to 1995 John Dingell investigated Robert Gallo and the role of the NIH. <a href="http://en.wikipedia.org/w/index.php?title=John_Dingell&direction=next&oldid=475545179">This is what Wikipedia has to say on the Dingell report</a>:<br />
<blockquote class="tr_bq">
In 1991–1995 Dingell's staff investigated claims that Robert Gallo had used samples supplied to him by Luc Montagnier to fraudulently claim to have discovered the AIDS virus. <i>The report concluded that Gallo had engaged in fraud and that the NIH covered up his misappropriation of work by the French team at the Institut Pasteur.</i> The report contended: <br />
<blockquote>
<i>The real inventors of the HIV blood test were the (Pasteur) scientists. Even more important, the CDC data, together with the extensive data already accumulated by the (Pasteur) scientists, showed that the (Pasteur) virus-discovered long before the putative LTCB virus-was the cause of AIDS.</i></blockquote>
<i>The report was never formally published as a subcommittee report because of the 1995 change in control of the House from Democrats to Republicans.</i> Other accusations against Gallo were dropped, and while Montagnier's group is considered to be the first to isolate the virus, Gallo's has been recognized as first to prove that this virus was the cause of AIDS. </blockquote>
It seems that Robert Gallo got off the hook here, because the Republicans who won the House majority didn't have the interest to investigate this any further – not exactly a clean bill for Robert Gallo I'd say.<br />
<blockquote class="tr_bq">
There was no doubt as to who made the fundamental discoveries. <br />
-- <b><a href="http://www.nytimes.com/2008/10/07/health/07nobel.html?hp">Maria Masucci</a></b>, Member of the Nobel Assembly in 2008</blockquote>
And so the Nobel Assembly spoke.<br />
<blockquote class="tr_bq">
The truth may be puzzling. <i>It may take some work to grapple with. It may be counterintuitive. It may contradict deeply held prejudices. It may not be consonant with what we desperately want to be true. But our preferences do not determine what's true.</i> We have a method, and that method helps us to reach not absolute truth, only asymptotic approaches to the truth — never there, just closer and closer, always finding vast new oceans of undiscovered possibilities. Cleverly designed experiments are the key.<br />
-- <b>Carl Sagan</b>, <a href="http://www.csicop.org/si/show/wonder_and_skepticism/">Wonder and Skepticisim</a></blockquote>
From here I will largely diverge from the "official narrative" and draw from the 1990 article "<i>Lab rat: What AIDS researcher Dr. Robert Gallo did in pursuit of the Nobel Prize, and what he didn't do in pursuit of a cure for AIDS</i>" of <a href="http://en.wikipedia.org/wiki/Seth_Roberts">Seth Roberts</a> (which can be found <a href="http://sethroberts.net/spy/index.html">here</a> and <a href="http://books.google.co.uk/books?id=Tu_Vp4DEqiQC&lpg=PA76&dq=gallo%20machiavelli&pg=PA70#v=onepage&q&f=false">here</a>). His account draws from his own research and from <a href="http://en.wikipedia.org/wiki/John_M._Crewdson">John Crewdson</a>'s 1990 work for the Chicago Tribune (who reported not to be able to find any evidence for the 48 patient samples of Gallo's "HTLV-III" paper). John Crewdson later published the 2002 book "<a href="http://www.sciencefictions.net/"><i>Science Fictions</i></a>" and he has an <a href="http://www.sciencefictions.net/documents.html">extensive cache of documents</a> on his website. Further material can be found in the book from Michael Koch or the Dingell Report (1991-1995). Much material is unfortunately gathered on HIV-denial sites like virusmyth.com – reader discretion is advised.<br />
<br />
I have neither the time, the knowledge nor the energy to go deeply into the work of these people – and can neither verify nor refute the veracity of their accounts – so I will focus on the article "Lab Rat" and call Seth Roberts' portrait of Robert Gallo the "<i>Fictional Gallo</i>". Whether or not this <i>Fictional Gallo</i> overlaps with the real Robert Gallo (or how much) shall not be of interest for the moment: I'll use the idealistic construct of this <i>Fictional Gallo</i> only for arguments sake, in order to have a reference to compare with the behavior of Mikovits and Ruscetti.<br />
<br />
So first go and read <a href="http://sethroberts.net/spy/index.html">Seth Roberts' article "<i>Lab Rat</i>" now</a>!<br />
<br />
I wait so long here.<br />
<br />
It's a few pages, so take your time.<br />
<br />
Ok, you read it?<br />
<br />
Good, so I will continue.<br />
<br />
<br />
<table border="1"><tbody>
<tr> <td><div style="text-align: center;">
Actions by</div>
<div style="text-align: center;">
Fictional Gallo</div>
</td> <td><div style="text-align: center;">
Actions by</div>
<div style="text-align: center;">
Mikovits and Ruscetti</div>
</td> </tr>
<tr> <td>.</td> <td>.</td> </tr>
</tbody></table>
<br />
It seems, Mikovits and Ruscetti knew of the <i>Fictional Gallo</i>.<br />
<blockquote class="tr_bq">
The theory is usually the correct one, that introduces the fewest assumptions and postulates the fewest entities, while retaining sufficient explanatory power.<br />
-- <b>Occam's Razor</b> (<a href="http://parakoch.blogspot.com/2012/02/occams-razor.html">Parakoch edition</a>) </blockquote>
Now, we could assume the following:<br />
<ol>
<li><i>Fictional Gallo</i> is fictional. It is all an coincidence, the actions of <span class="Apple-style-span" style="-webkit-border-horizontal-spacing: 2px; -webkit-border-vertical-spacing: 2px;">Mikovits and Ruscetti</span> were fully independent of Gallo, and just look superficial similar.</li>
<li><i>Fictional Gallo</i> is fictional. <span class="Apple-style-span" style="-webkit-border-horizontal-spacing: 2px; -webkit-border-vertical-spacing: 2px;">Mikovits and Ruscetti arrived coincidentally at a similar modus of operation as the Fictional Gallo</span>. </li>
<li><i>Fictional Gallo</i> is fictional. However <span class="Apple-style-span" style="-webkit-border-horizontal-spacing: 2px; -webkit-border-vertical-spacing: 2px;">Mikovits and Ruscetti took this Fictional Gallo as a blue print for their actions nonetheless</span>. </li>
<li><i>Fictional Gallo</i> is more or less identical to the real Gallo. That's where Mikovits and Ruscetti have learned their trade.</li>
</ol>
To #1: We would have to make assumptions about the individual motives of each and everyone involved. These individual reasons might exists, and one could come up with something for all of them – it might become a long text. It was this lack of explanations that brought me to think in the direction of this blog-post in the first place.<br />
<br />
#2: Or, we could assume that everybody involved came (without knowing <i>Fictional Gallo)</i> independently to the same conclusion, to act like <i>Fictional Gallo. W</i>e could assume that <i>Fiction Gallo</i> was fictional with regards to the Robert Gallo, but not with regards to practices of the business – maybe the dishonest scientists took their own actions, and projected them on <i>Fictional Gallo</i>?<br />
<i><br />
</i><br />
<i><span class="Apple-style-span" style="font-style: normal;">#3: We might assume that it could be possible, that Judy Mikovits</span><span class="Apple-style-span" style="font-style: normal;"> </span><span class="Apple-style-span" style="font-style: normal;"><i>assumed</i></span><span class="Apple-style-span" style="font-style: normal;"> – erroneously – that the</span><span class="Apple-style-span" style="font-style: normal;"> </span><span class="Apple-style-span" style="font-style: normal;"><i>Fictional Gallo</i></span><span class="Apple-style-span" style="font-style: normal;"> </span><span class="Apple-style-span" style="font-style: normal;">was an accurate portrayal of the real Robert Gallo. And she might have assumed (again, erroneously) that the scientific community, which condoned or ignored the behavior of</span><span class="Apple-style-span" style="font-style: normal;"> </span><span class="Apple-style-span" style="font-style: normal;"><i>Fictional Gallo</i></span><span class="Apple-style-span" style="font-style: normal;"> would condone her behavior too. And it could be possible that Francis Ruscetti or Harvey Alter harbored – independently – similar, erroneous, thoughts, when they joined the Gold Rush to find the hypothetical pathogen that causes CFS.</span></i><br />
<br />
#4: Or, alternatively: We could assume that the <i>Fictional Gallo</i> was not fictional but instead a more or less accurate portrayal of the actual Robert Gallo. And that this was common knowledge among those who either knew the real Robert Gallo, or worked with people who knew him. Occam's Razor would say that #4 makes fewer assumptions while it would explain what we have seen – it is, as if Judy Mikovits took article "Lab Rat" out of Spy Magazine, plucked this <i>Fictional Gallo</i> out of the article, breathed life into this him – to make him material reality, to validate the reports from John Crewdson and Seth Roberts.<br />
<br />
And as a another passing note: It appears to me that Occam's Razor, properly applied, would make minced meat from the <i>Official Gallo Narrative</i>.<br />
<br />
The rotten farce that hit the WPI was most certainly <u>not</u> a <i>bolt out of the blue</i> – it was fostered in the context of what I termed here the "<i>Fictional Gallo</i>". Whatever the people at the WPI and NCI did, it does not explain the behavior of the others involved – unlike the account of the <i>Fictional Gallo</i>, who quite evidently seems to have laid the ground for what we have seen here.<br />
<br />
<br />
Another thing that could be used to test accuracy the <i>Fictional Gallo</i> hypothesis is the following: Surely someone else has tried to "Pull a Gallo" before Mikovits and Ruscetti. The countless pathogens fingered in MS come to my mind – not all will be a case of confirmation bias and unintended bad science. The people who came out of Gallo's lab are certainly prime candidates. E.g. the work of Francis Ruscetti has certainly <i>not</i> received the attention it deserves. Alas, his research is for other busy-bodies to explore – this task is not mine. Most certainly not all scientists in that area are active spreaders of rumor viruses, but surely Judy Mikovits isn't the only one. But it might be necessary to <a href="http://en.wikipedia.org/wiki/Augeas">reroute the Potomac River to wash out the filth from the stables in Bethesda</a>.<br />
<br />
This vulture culture may very well have existed independently of Robert Gallo – but the events surrounding the discovery of HIV were certainly an catalyzing moment. Not only made it cleat that there were <i>no</i> negative consequences whatsoever to be feared, but there were was prestige, influence and money <i>actually to be gained</i> by exhibiting such a behavior. Oh, what a shallow mind, who enjoys being praised as an extraordinary scientist, when in reality he is nothing more than a scientific con artist, and vain at that. At least Robert Gallo has some money and prestige as comfort.<br />
<br />
<br />
My view is that Robert Gallo has a claim to be the discoverer of HIV <a href="http://en.wikipedia.org/wiki/If_and_only_if">if and only if (iff)</a> Luc Montagnier has not. It is my opinion, had Gallo worked in France and Montagnier in the US, then Gallo would have been nothing but a footnote in the discovery of HIV.<br />
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It is my impression that criticism of Robert Gallo is something that is not done in the US. Criticism of Robert Gallo seems to be akin to HIV denialism, in the eyes of some. I fully expect that some will equal this blog-post with HIV denialism. The tragedy is that <i>exactly</i> this sacrosanct position of Gallo, which made the HIV denialism possible in the first place.<br />
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As far as I know Robert Gallo never denied AIDS (although he he showed some homophobic inclinations), <b><u>but Gallo was the first to deny HIV</u></b>. While it was Montagnier who discovered HIV (under the name LAV), it was Gallo who against reality for a long time very rigoursly insisted that it was "his" HTLV – first Gallo claimed to have found HTLV-I, then he took Montagniers' LAV and called it HTLV-III, thereby even insisting that it was a different genus than it actually was. It was Gallo's denial of HIV/LAV that did cost the fight against HIV/AIDS at least a year – you do the math on how many people could have been potentially saved had the spread of HIV been curtailed a year earlier. (And that is not counting the damage HIV denial does, which is directly fueled in no small part by Gallo's actions.)<br />
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Now, why CFS? The estimated prevalence of CFS (<a href="http://parakoch.blogspot.com/2012/02/cfs-me-and-pvfs-share-more-similarities.html">or ME or PVFS</a>) is about 0.5% of the population. If one uses relaxed criteria (like the empirical), the prevalence rises to 2-3%. Up to 10% of the population are reported to suffer from chronic fatigue (CF, without the S). And <i>that</i> my friends, is a huge market for tests, 20 to 30 Million people in the US alone. And someone who has no understanding of CFS could assume that if <i>one</i> virus causes CFS, then many more of those 10% with CF might be affected of this <i>one</i> virus as well. I think it was a wager by Mikovits/Lombardi/Ruscetti (albeit a <i>not</i> very <a href="http://en.wikipedia.org/wiki/Scientific_wager">scientific</a> wager at that, in my not so humble opinion), that with enough publicity this <i>one</i> virus would be found, and their patent might cover tests for this <i>one</i> virus. And who knows, maybe they could count on having <a href="http://en.wikipedia.org/wiki/Regulatory_capture">captured the government</a> in any upcoming patent dispute? Back then it was Ronald Reagan who took sides for Robert Gallo – who might be the next president to side with scientific hacks? Having captured part of the patient community is surely helpful in letting them write letters to Washington.<br />
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Only, <a href="http://parakoch.blogspot.com/2012/02/different-pathogens-can-cause-cfs-like.html">it looks like different pathogens can cause CF(S)</a>. Tough luck for patients, and tough luck for wagering scientific con artists (though any bullshitting CFS quacks can continue their businesses selling supplements, herbs and psychobabble – for now). It might pay off for patients, in case Lipkin finds <i>something</i>. This wager might not pay off for the <strike>con artists</strike> scientists involved, even if Lipkin finds something (we'll have to see how this will unfold). But do they have anything <i>to actually fear</i>? Is there any actual form of investigation and punishment that might have to fear? What will dissuade prospective scientific con artists from reading Seth Roberts' article "Lab Rat" and deciding to do what <i>Fictional Gallo</i> did?<br />
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(And then <a href="http://parakoch.blogspot.com/2012/02/hopefully-that-will-be-case.html">there are voices that say that maybe Ruscetti's people might be more involved in the Lipkin study</a> than might be good for that study)<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-88388527308328286922014-01-14T13:58:00.000-05:002014-01-14T13:58:31.310-05:00Unfinished Blog-Post: Team GalloA long time ago I started some blog-posts, but never found the time nor energy to finish them. Now I have long lost interest in the matter and will publish them all "as is" – maybe someone will find these raw thoughts helpful.<br />
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The record of <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%28alter%5BAuthor%5D%29%20AND%20gallo%5BAuthor%5D">Harvey J. Alter</a> with Gallo is rather shortish, but I would need more information about the relative importance of the studies: <br />
<blockquote>
1: Saxinger C, Alter HJ, Eichberg JW, Fauci AS, Robey WG, Gallo RC. Stages in the progression of HIV infection in chimpanzees. AIDS Res Hum Retroviruses. 1987;3(4):375-85. PubMed PMID: 3482160.<br />
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2: Alter HJ, Eichberg JW, Masur H, Saxinger WC, Gallo R, Macher AM, Lane HC, Fauci AS. Transmission of HTLV-III infection from human plasma to chimpanzees: an animal model for AIDS. Science. 1984 Nov 2;226(4674):549-52. PubMed PMID: 6093251.</blockquote>
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And Fauci – <a href="http://www.cfscentral.com/2011/10/rituximab-genentech-tony-fauci-and.html">hmmm</a>. There seem to be some people both in the HIV/AIDS and in the ME/CFS community who harbor some grudge against Fauci.<br />
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So let's see about <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%28fauci%5BAuthor%5D%29%20AND%20gallo%5BAuthor%5D">Anthony S. Fauci</a> and Gallo: <br />
<blockquote>
1: Fauci AS, Gallo RC, Koenig S, Salk J, Purcell RH. NIH conference. Development and evaluation of a vaccine for human immunodeficiency virus (HIV) infection. Ann Intern Med. 1989 Mar 1;110(5):373-85. Review. PubMed PMID: 2464961.<br />
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2: Saxinger C, Alter HJ, Eichberg JW, Fauci AS, Robey WG, Gallo RC. Stages in the progression of HIV infection in chimpanzees. AIDS Res Hum Retroviruses. 1987;3(4):375-85. PubMed PMID: 3482160.<br />
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3: Volkman DJ, Popovic M, Gallo RC, Fauci AS. Human T cell leukemia/lymphoma virus-infected antigen-specific T cell clones: indiscriminant helper function and lymphokine production. J Immunol. 1985 Jun;134(6):4237-43. PubMed PMID: 2580910.<br />
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4: Alter HJ, Eichberg JW, Masur H, Saxinger WC, Gallo R, Macher AM, Lane HC, Fauci AS. Transmission of HTLV-III infection from human plasma to chimpanzees: an animal model for AIDS. Science. 1984 Nov 2;226(4674):549-52. PubMed PMID: 6093251.<br />
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5: Popovic M, Flomenberg N, Volkman DJ, Mann D, Fauci AS, Dupont B, Gallo RC. Alteration of T-cell functions by infection with HTLV-I or HTLV-II. Science. 1984 Oct 26;226(4673):459-62. PubMed PMID: 6093248.</blockquote>
Not too long, the shared Gallo/Fauci record. But what is more likely: That he was critical of Gallo's contribution to HIV/AIDS research or that he supported Team Gallo (if only by inaction)? Whatever Fauci did or didn't do, it did not harm his rise to the top of the NIAID.<br />
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John Coffin is interesting, as he <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=gallo%5BAuthor%5D%20AND%20Coffin%5BAuthor%5D">never authored together with Gallo</a>. <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Montagnier%5BAuthor%5D%20AND%20Coffin%5BAuthor%5D">He seems to have taken more to the side of Team Science together with Montagnier instead</a>:<br />
<blockquote>
1: <b>Coffin J</b>, Haase A, Levy JA, <b>Montagnier L</b>, Oroszlan S, Teich N, Temin H, Toyoshima K, Varmus H, Vogt P, et al. <br />
<b>Human immunodeficiency viruses.</b><br />
Science. 1986 May 9;232(4751):697. PubMed PMID: 3008335.<br />
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2: <b>Coffin J</b>, Haase A, Levy JA, <b>Montagnier L</b>, Oroszlan S, Teich N, Temin H, Toyoshima K, Varmus H, Vogt P, et al. <br />
<b>What to call the AIDS virus?</b><br />
Nature. 1986 May 1-7;321(6065):10. PubMed PMID: 3010128.</blockquote>
Still, I guess that John Coffin just thinks in scientific terms and is oblivious to the "politics" of his research field. It would be interesting to read these two papers to get a perspective on John Coffin, what exactly his position with regards to Team Gallo was – this would be interesting when reviewing how Team Gallo reacted when Coffin got involved in XMRV. What was Coffin's verdict on Gallo's contributions?<br />
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Not surprising is the record for <a href="http://www.ncbi.nlm.nih.gov/pubmed?term=%28gallo%5BAuthor%5D%29%20AND%20ruscetti%5BAuthor%5D">Francis W. Ruscetti</a>, as he has worked with Gallo for a long time: <br />
<blockquote>
1: Ruscetti FW, Morgan DA, Gallo RC. Functional and morphologic characterization of human T cells continuously grown in vitro. J. Immunol. 1977. 119: 131-138. J Immunol. 2007 Aug 1;179(3):1415-22. PubMed PMID: 17641005.<br />
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2: Ferrero D, Pregno P, Tarella C, Ruscetti FW, Pileri A, Gallo E. Trophoblast cell line conditioned medium for in vitro culture and antigenic characterization of acute myeloid leukemia clonogenic cells. Cancer Res. 1987 Dec 1;47(23):6413-7. PubMed PMID: 3499973.<br />
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3: Ruscetti FW, Robert-Guroff M, Ceccherini-Nelli L, Minowada J, Popovic M, Gallo RC. Persistent in vitro infection by human T-cell leukemia-lymphoma virus (HTLV) of normal human T-lymphocytes from blood relatives of patients with HTLV-associated mature T-cell neoplasms. Int J Cancer. 1983 Feb 15;31(2):171-80. PubMed PMID: 6600720.<br />
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4: Ferrero D, Tarella C, Gallo E, Ruscetti FW, Breitman TR. Terminal differentiation of the human promyelocytic leukemia cell line, HL-60, in the absence of cell proliferation. Cancer Res. 1982 Nov;42(11):4421-6. PubMed PMID: 6957259.<br />
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5: Gootenberg JE, Ruscetti FW, Gallo RC. A biochemical variant of human T cell growth factor produced by a cutaneous T cell lymphoma cell line. J Immunol. 1982 Oct;129(4):1499-505. PubMed PMID: 6980938.<br />
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6: Gallo RC, Mann D, Broder S, Ruscetti FW, Maeda M, Kalyanaraman VS, Robert-Guroff M, Reitz MS Jr. Human T-cell leukemia-lymphoma virus (HTLV) is in T but not B lymphocytes from a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci U S A. 1982 Sep;79(18):5680-3. PubMed PMID: 6982476; PubMed Central PMCID: PMC346968.<br />
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7: Tarella C, Ruscetti FW, Poiesz BJ, Woods A, Gallo RC. Factors that affect human hemopoiesis are produced by T-cell growth factor dependent and independent cultured T-cell leukemia-lymphoma cells. Blood. 1982 Jun;59(6):1330-6. PubMed PMID: 6979356.<br />
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8: Tarella C, Ferrero D, Gallo E, Pagliardi GL, Ruscetti FW. Induction of differentiation of HL-60 cells by dimethyl sulfoxide: evidence for a stochastic model not linked to the cell division cycle. Cancer Res. 1982 Feb;42(2):445-9. PubMed PMID: 6948604.<br />
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9: Nelli LC, Dalla-Favera R, Markham PD, Ruscetti FW, Wong-Staal F, Gallo RC, Reitz MS. Restricted expression of integrated primate type-C virus (gibbon ape leukemia virus-simian sarcoma virus) proviral DNA in nonproductively infected human B lymphoblasts. Virology. 1982 Feb;117(1):195-206. PubMed PMID: 6278736.<br />
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10: Ruscetti FW, Chou JY, Gallo RC. Human trophoblasts: cellular source of colony-stimulating activity in placental tissue. Blood. 1982 Jan;59(1):86-90. PubMed PMID: 6274452.<br />
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11: Robert-Guroff M, Ruscetti FW, Posner LE, Poiesz BJ, Gallo RC. Detection of the human T cell lymphoma virus p19 in cells of some patients with cutaneous T cell lymphoma and leukemia using a monoclonal antibody. J Exp Med. 1981 Dec 1;154(6):1957-64. PubMed PMID: 6274993; PubMed Central PMCID: PMC2186543.<br />
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12: Poiesz BJ, Ruscetti FW, Reitz MS, Kalyanaraman VS, Gallo RC. Isolation of a new type C retrovirus (HTLV) in primary uncultured cells of a patient with Sézary T-cell leukaemia. Nature. 1981 Nov 19;294(5838):268-71. PubMed PMID: 6272125.<br />
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13: Gootenberg JE, Ruscetti FW, Mier JW, Gazdar A, Gallo RC. Human cutaneous T cell lymphoma and leukemia cell lines produce and respond to T cell growth factor. J Exp Med. 1981 Nov 1;154(5):1403-18. PubMed PMID: 6975346; PubMed Central PMCID: PMC2186515.<br />
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14: Salahuddin SZ, Markham PD, Ruscetti FW, Gallo RC. Long-term suspension cultures of human cord blood myeloid cells. Blood. 1981 Nov;58(5):931-8. PubMed PMID: 6271310.<br />
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15: Posner LE, Robert-Guroff M, Kalyanaraman VS, Poiesz BJ, Ruscetti FW, Fossieck B, Bunn PA Jr, Minna JD, Gallo RC. Natural antibodies to the human T cell lymphoma virus in patients with cutaneous T cell lymphomas. J Exp Med. 1981 Aug 1;154(2):333-46. PubMed PMID: 6973601; PubMed Central PMCID: PMC2186420.<br />
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16: Ruscetti FW, Collins SJ, Woods AM, Gallo RC. Clonal analysis of the response of human myeloid leukemic cell lines to colony-stimulating activity. Blood. 1981 Aug;58(2):285-92. PubMed PMID: 6972788.<br />
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17: Rho HM, Poiesz B, Ruscetti FW, Gallo RC. Characterization of the reverse transcriptase from a new retrovirus (HTLV) produced by a human cutaneous T-cell lymphoma cell line. Virology. 1981 Jul 15;112(1):355-60. PubMed PMID: 6166122.<br />
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18: Markham PD, Ruscetti FW, Kalyanaraman VS, Ceccherini-Nelli L, Miller NR, Reitz MS, Salahuddin SZ, Gallo RC. Restricted expression of retrovirus nucleic acids and proteins in primate type C virus (gibbon ape leukemia virus-simian sarcoma virus)-initiated human B-lymphoblast cultures. Cancer Res. 1981 Jul;41(7):2738-44. PubMed PMID: 6265066.<br />
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19: Kalyanaraman VS, Sarngadharan MG, Poiesz B, Ruscetti FW, Gallo RC. Immunological properties of a type C retrovirus isolated from cultured human T-lymphoma cells and comparison to other mammalian retroviruses. J Virol. 1981 Jun;38(3):906-15. PubMed PMID: 6264163; PubMed Central PMCID: PMC171228.<br />
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20: Ruscetti FW, Gallo RC. Human T-lymphocyte growth factor: regulation of growth and function of T lymphocytes. Blood. 1981 Mar;57(3):379-94. Review. PubMed PMID: 7006707.<br />
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<br />
21: Reitz MS Jr, Poiesz BJ, Ruscetti FW, Gallo RC. Characterization and distribution of nucleic acid sequences of a novel type C retrovirus isolated from neoplastic human T lymphocytes. Proc Natl Acad Sci U S A. 1981 Mar;78(3):1887-91. PubMed PMID: 6262827; PubMed Central PMCID: PMC319240.<br />
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22: Gallo RC, Poiesz BJ, Ruscetti FW. Regulation of human T-cell proliferation: T-cell growth factor and isolation of a new class of type-C retroviruses from human T-cells. Haematol Blood Transfus. 1981;26:502-14. PubMed PMID: 6274766.<br />
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23: Poiesz BJ, Ruscetti FW, Gazdar AF, Bunn PA, Minna JD, Gallo RC. Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma. Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9. PubMed PMID: 6261256; PubMed Central PMCID: PMC350514.<br />
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24: Poiesz BJ, Ruscetti FW, Mier JW, Woods AM, Gallo RC. T-cell lines established from human T-lymphocytic neoplasias by direct response to T-cell growth factor. Proc Natl Acad Sci U S A. 1980 Nov;77(11):6815-9. PubMed PMID: 6256763; PubMed Central PMCID: PMC350380.<br />
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25: Ruscetti FW, Mier JW, Gallo RC. Human T-cell growth factor: parameters for production. J Supramol Struct. 1980;13(2):229-41. PubMed PMID: 6972470.<br />
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26: Gallagher R, Collins S, Trujillo J, McCredie K, Ahearn M, Tsai S, Metzgar R, Aulakh G, Ting R, Ruscetti F, Gallo R. Characterization of the continuous, differentiating myeloid cell line (HL-60) from a patient with acute promyelocytic leukemia. Blood. 1979 Sep;54(3):713-33. PubMed PMID: 288488.<br />
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27: Collins SJ, Ruscetti FW, Gallagher RE, Gallo RC. Normal functional characteristics of cultured human promyelocytic leukemia cells (HL-60) after induction of differentiation by dimethylsulfoxide. J Exp Med. 1979 Apr 1;149(4):969-74. PubMed PMID: 219131; PubMed Central PMCID: PMC2184853.<br />
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28: Markham PD, Ruscetti F, Salahuddin SZ, Gallagher RE, Gallo RC. Enhanced induction of growth of B lymphoblasts from fresh human blood by primate type-C retroviruses (gibbon ape leukemia virus and simian sarcoma virus). Int J Cancer. 1979 Feb;23(2):148-56. PubMed PMID: 216638.<br />
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29: Collins SJ, Ruscetti FW, Gallagher RE, Gallo RC. Terminal differentiation of human promyelocytic leukemia cells induced by dimethyl sulfoxide and other polar compounds. Proc Natl Acad Sci U S A. 1978 May;75(5):2458-62. PubMed PMID: 276884; PubMed Central PMCID: PMC392573.<br />
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30: Gallo RC, Gallagher RE, Wong-Staal F, Aoki T, Markham PD, Schetters H, Ruscetti F, Valerio M, Walling MJ, O'Keeffe RT, Saxinger WC, Smith RG, Gillespie DH, Reitz MS Jr. Isolation and tissue distribution of type-C virus and viral components from a gibbon ape (Hylobates lar) with lymphocytic leukemia. Virology. 1978 Feb;84(2):359-73. PubMed PMID: 74897.<br />
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31: Ruscetti FW, Morgan DA, Gallo RC. Functional and morphologic characterization of human T cells continuously grown in vitro. J Immunol. 1977 Jul;119(1):131-8. PubMed PMID: 141483.<br />
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32: Morgan DA, Ruscetti FW, Gallo R. Selective in vitro growth of T lymphocytes from normal human bone marrows. Science. 1976 Sep 10;193(4257):1007-8. PubMed PMID: 181845.</blockquote>
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<a href="http://www.ncbi.nlm.nih.gov/pubmed?term=Mikovits%5BAuthor%5D%20AND%20Ruscetti%5BAuthor%5D">Mikovits connection to Ruscetti would make her part of Team Gallo</a>:<br />
<blockquote>
1: Silverman RH, Das Gupta J, Lombardi VC, Ruscetti FW, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Mikovits JA. Partial retraction. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science. 2011 Oct 14;334(6053):176. PubMed PMID: 21998366.<br />
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<br />
2: Simmons G, Glynn SA, Komaroff AL, Mikovits JA, Tobler LH, Hackett J Jr, Tang N, Switzer WM, Heneine W, Hewlett IK, Zhao J, Lo SC, Alter HJ, Linnen JM, Gao K, Coffin JM, Kearney MF, Ruscetti FW, Pfost MA, Bethel J, Kleinman S, Holmberg JA, Busch MP; Blood XMRV Scientific Research Working Group (SRWG). Failure to confirm XMRV/MLVs in the blood of patients with chronic fatigue syndrome: a multi-laboratory study. Science. 2011 Nov 11;334(6057):814-7. Epub 2011 Sep 22. PubMed PMID: 21940862.<br />
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3: Silverman RH, Das Gupta J, Lombardi VC, Ruscetti FW, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Mikovits JA. Partial Retraction. Science. 2011 Sep 22. [Epub ahead of print] PubMed PMID: 21940859.<br />
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4: Mikovits JA, Lombardi VC, Pfost MA, Hagen KS, Ruscetti FW. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Virulence. 2010 Sep-Oct;1(5):386-90. PubMed PMID: 21178474; PubMed Central PMCID: PMC3073172.<br />
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5: Mikovits JA, Huang Y, Pfost MA, Lombardi VC, Bertolette DC, Hagen KS, Ruscetti FW. Distribution of xenotropic murine leukemia virus-related virus (XMRV) infection in chronic fatigue syndrome and prostate cancer. AIDS Rev. 2010 Jul-Sep;12(3):149-52. Review. PubMed PMID: 20842203.<br />
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6: Lombardi VC, Ruscetti FW, Das Gupta J, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science. 2009 Oct 23;326(5952):585-9. Epub 2009 Oct 8. Retraction in: Alberts B. Science. 2011 Dec 23;334(6063):1636. Partial retraction in: Silverman RH, Das Gupta J, Lombardi VC, Ruscetti FW, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Mikovits JA. Science. 2011 Oct 14;334(6053):176. PubMed PMID: 19815723.<br />
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7: Taub DD, Mikovits JA, Nilsson G, Schaffer EM, Key ML, Petrow-Sadowski C, Ruscetti FW. Alterations in mast cell function and survival following in vitro infection with human immunodeficiency viruses-1 through CXCR4. Cell Immunol. 2004 Aug;230(2):65-80. PubMed PMID: 15598422.<br />
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8: Puri A, Rawat SS, Lin HM, Finnegan CM, Mikovits J, Ruscetti FW, Blumenthal R. An inhibitor of glycosphingolipid metabolism blocks HIV-1 infection of primary T-cells. AIDS. 2004 Apr 9;18(6):849-58. PubMed PMID: 15060432.<br />
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9: Muegge K, Young H, Ruscetti F, Mikovits J. Epigenetic control during lymphoid development and immune responses: aberrant regulation, viruses, and cancer. Ann N Y Acad Sci. 2003 Mar;983:55-70. Review. PubMed PMID: 12724212.<br />
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10: Mikovits J, Ruscetti F, Zhu W, Bagni R, Dorjsuren D, Shoemaker R. Potential cellular signatures of viral infections in human hematopoietic cells. Dis Markers. 2001;17(3):173-8. PubMed PMID: 11790884.<br />
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11: Fang JY, Mikovits JA, Bagni R, Petrow-Sadowski CL, Ruscetti FW. Infection of lymphoid cells by integration-defective human immunodeficiency virus type 1 increases de novo methylation. J Virol. 2001 Oct;75(20):9753-61. PubMed PMID: 11559808; PubMed Central PMCID: PMC114547.<br />
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12: Ruff MR, Melendez-Guerrero LM, Yang QE, Ho WZ, Mikovits JW, Pert CB, Ruscetti FA. Peptide T inhibits HIV-1 infection mediated by the chemokine receptor-5 (CCR5). Antiviral Res. 2001 Oct;52(1):63-75. PubMed PMID: 11530189.<br />
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13: Li BQ, Wetzel MA, Mikovits JA, Henderson EE, Rogers TJ, Gong W, Le Y, Ruscetti FW, Wang JM. The synthetic peptide WKYMVm attenuates the function of the chemokine receptors CCR5 and CXCR4 through activation of formyl peptide receptor-like 1. Blood. 2001 May 15;97(10):2941-7. PubMed PMID: 11342415.<br />
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14: Li BQ, Fu T, Dongyan Y, Mikovits JA, Ruscetti FW, Wang JM. Flavonoid baicalin inhibits HIV-1 infection at the level of viral entry. Biochem Biophys Res Commun. 2000 Sep 24;276(2):534-8. PubMed PMID: 11027509.<br />
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15: Mikovits JA, Young HA, Vertino P, Issa JP, Pitha PM, Turcoski-Corrales S, Taub DD, Petrow CL, Baylin SB, Ruscetti FW. Infection with human immunodeficiency virus type 1 upregulates DNA methyltransferase, resulting in de novo methylation of the gamma interferon (IFN-gamma) promoter and subsequent downregulation of IFN-gamma production. Mol Cell Biol. 1998 Sep;18(9):5166-77. PubMed PMID: 9710601; PubMed Central PMCID: PMC109102.<br />
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16: Mikovits JA, Taub DD, Turcovski-Corrales SM, Ruscetti FW. Similar levels of human immunodeficiency virus type 1 replication in human TH1 and TH2 clones. J Virol. 1998 Jun;72(6):5231-8. PubMed PMID: 9573296; PubMed Central PMCID: PMC110106.<br />
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17: Derse D, Mikovits J, Ruscetti F. X-I and X-II open reading frames of HTLV-I are not required for virus replication or for immortalization of primary T-cells in vitro. Virology. 1997 Oct 13;237(1):123-8. PubMed PMID: 9344914.<br />
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18: Turley JM, Fu T, Ruscetti FW, Mikovits JA, Bertolette DC 3rd, Birchenall-Roberts MC. Vitamin E succinate induces Fas-mediated apoptosis in estrogen receptor-negative human breast cancer cells. Cancer Res. 1997 Mar 1;57(5):881-90. PubMed PMID: 9041190.<br />
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19: Mikovits JA, Hoffman PM, Rethwilm A, Ruscetti FW. In vitro infection of primary and retrovirus-infected human leukocytes by human foamy virus. J Virol. 1996 May;70(5):2774-80. PubMed PMID: 8627751; PubMed Central PMCID: PMC190134.<br />
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20: Derse D, Mikovits J, Waters D, Brining S, Ruscetti F. Examining the molecular genetics of HTLV-I with an infectious molecular clone of the virus and permissive cell culture systems. J Acquir Immune Defic Syndr Hum Retrovirol. 1996 May 1;12(1):1-5. Review. PubMed PMID: 8624755.<br />
<br />
<br />
21: Ouaaz F, Ruscetti FW, Dugas B, Mikovits J, Agut H, Debré P, Mossalayi MD. Role of IgE immune complexes in the regulation of HIV-1 replication and increased cell death of infected U1 monocytes: involvement of CD23/Fc epsilon RII-mediated nitric oxide and cyclic AMP pathways. Mol Med. 1996 Jan;2(1):38-49. PubMed PMID: 8900533; PubMed Central PMCID: PMC2230037.<br />
<br />
<br />
22: Fong SE, Pallansch LA, Mikovits JA, Lackman-Smith CS, Ruscetti FW, Gonda MA. cis-acting regulatory elements in the bovine immunodeficiency virus long terminal repeat. Virology. 1995 Jun 1;209(2):604-14. PubMed PMID: 7778292.<br />
<br />
<br />
23: Derse D, Mikovits J, Polianova M, Felber BK, Ruscetti F. Virions released from cells transfected with a molecular clone of human T-cell leukemia virus type I give rise to primary and secondary infections of T cells. J Virol. 1995 Mar;69(3):1907-12. PubMed PMID: 7853532; PubMed Central PMCID: PMC188805.<br />
<br />
<br />
24: Mikovits JA, Meyers AM, Ortaldo JR, Minty A, Caput D, Ferrara P, Ruscetti FW. IL-4 and IL-13 have overlapping but distinct effects on HIV production in monocytes. J Leukoc Biol. 1994 Sep;56(3):340-6. PubMed PMID: 7916030.<br />
<br />
<br />
25: Li CC, Ruscetti FW, Rice NR, Chen E, Yang NS, Mikovits J, Longo DL. Differential expression of Rel family members in human T-cell leukemia virus type I-infected cells: transcriptional activation of c-rel by Tax protein. J Virol. 1993 Jul;67(7):4205-13. PubMed PMID: 8510222; PubMed Central PMCID: PMC237790.<br />
<br />
<br />
26: Hoffman PM, Dhib-Jalbut S, Mikovits JA, Robbins DS, Wolf AL, Bergey GK, Lohrey NC, Weislow OS, Ruscetti FW. Human T-cell leukemia virus type I infection of monocytes and microglial cells in primary human cultures. Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11784-8. PubMed PMID: 1465399; PubMed Central PMCID: PMC50641.<br />
<br />
<br />
27: West M, Mikovits J, Princler G, Liu YL, Ruscetti FW, Kung HF, Raziuddin. Characterization and purification of a novel transcriptional repressor from HeLa cell nuclear extracts recognizing the negative regulatory element region of human immunodeficiency virus-1 long terminal repeat. J Biol Chem. 1992 Dec 15;267(35):24948-52. PubMed PMID: 1459999.<br />
<br />
<br />
28: Mikovits JA, Lohrey NC, Schulof R, Courtless J, Ruscetti FW. Activation of infectious virus from latent human immunodeficiency virus infection of monocytes in vivo. J Clin Invest. 1992 Oct;90(4):1486-91. PubMed PMID: 1401081; PubMed Central PMCID: PMC443195.<br />
<br />
<br />
29: Raziuddin, Mikovits JA, Calvert I, Ghosh S, Kung HF, Ruscetti FW. Negative regulation of human immunodeficiency virus type 1 expression in monocytes: role of the 65-kDa plus 50-kDa NF-kappa B dimer. Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9426-30. PubMed PMID: 1946356; PubMed Central PMCID: PMC52730.<br />
<br />
<br />
30: Mikovits JA, Raziuddin, Gonda M, Ruta M, Lohrey NC, Kung HF, Ruscetti FW. Negative regulation of human immune deficiency virus replication in monocytes. Distinctions between restricted and latent expression in THP-1 cells. J Exp Med. 1990 May 1;171(5):1705-20. PubMed PMID: 2332735; PubMed Central PMCID: PMC2187891.<br />
<br />
<br />
31: Twardzik DR, Mikovits JA, Ranchalis JE, Purchio AF, Ellingsworth L, Ruscetti FW. Gamma-interferon-induced activation of latent transforming growth factor-beta by human monocytes. Ann N Y Acad Sci. 1990;593:276-84. PubMed PMID: 2115757.<br />
<br />
<br />
32: Ruscetti FW, Mikovits JA. Differential regulation of the two IL-2-binding proteins. Physiological consequences. Year Immunol. 1989;5:38-45. Review. PubMed PMID: 2652929.<br />
<br />
<br />
33: Ruscetti FW, Mikovits JA, Kalyanaraman VS, Overton R, Stevenson H, Stromberg K, Herberman RB, Farrar WL, Ortaldo JR. Analysis of effector mechanisms against HTLV-I- and HTLV-III/LAV-infected lymphoid cells. J Immunol. 1986 May 15;136(10):3619-24. PubMed PMID: 2422259.</blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-20496303520167114072013-12-03T10:55:00.001-05:002013-12-03T10:55:28.442-05:00Do I Have A Bad Day? Or Am I Getting Ill While Being Ill?I feel like I got ill, I feel like some virus or some bacteria hit me – in addition to my "unnormal" disease. I feel like someone had run me over with a steamroller. Though, I don't know, it could be just an exceptionally bad day with my unnormal disease – a disease which no doctor wants to have a part of (and those doctors that do want a part of, those I don't trust). <br />
<br />
That's the annoying thing, I never know how good or bad I will feel, how much I will be able to do any given day. And I will never know when I feels worse, if that is "normal" business of my unnormal disease, if the unnormal disease is simply acting up – or if I got the flu or something in addition to my unnormal disease. Or if it was caused by something I ate yesterday, or if I did too much yesterday, or if I stayed a bit too long outside in the cold, or whatever.<br />
<br />
This sucks.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-31579340043263879802013-11-26T10:08:00.001-05:002013-12-24T17:03:31.902-05:00Spam for fraudulent HIV "cure"Just wanted to mention, I got this spam from "Gina" for a fraudulent HIV "cure" – whatever you do, keep in mind that these quacks want to take your money.<br />
<blockquote>
My name is Gina, i am from Cape Town in South Africa, I was once a prostitute in my area. I got effected with HIV due to the nature of my job, In May 06 2013 i was tested positive to HIV, this is a true life experience. I never taught there's some one who could ever get my HIV-AIDS cured with his healing spell, i have tried almost everything but I couldn't find any solution to my disease. I always spend a lot to buy a HIV drugs from hospital and taking some several medications but no relieve, until one day i was just browsing on the internet when i came across of abuyespelltemple@xx I quickly contacted him, and he asked me some few questions and i did all things he asked me to do, i did not pay him for his service until I was finally cured, only to see that at the very day which he said i will be healed, all the strength that has left me before rush back and i became very strong and healthy. I went to hospital for the final test to the virus and the result shows i am HIV</blockquote>
If see such a spam comment, do not contact them! It is best to delete their spam.<br />
<br />
[Update] Well, two spam comments on the same day, probably from some sockpuppet, on how this quack supposedly helped people with spells and holy water:<br />
<blockquote>
Am from UK I give thank to a great doctor who help me out of my illness I was very sick I thank god who use this man to help, it started when i travel to Florida for visit there I meet a lady not knowing to me that she HIV positive I really like the lady because she was beautiful I always see her every moment I close my eye I went to tell her how I feel for her but I don’t know if she know that she HIV I went to bed with her I contacted the virus too when I get home for month my doctor come to check on me and he discover that I have HIV he was shock and tell me I was so confused and so surprised to hear that I was taking HIV drug to cure it for good a 2year I decided to look for cure them I meet this post on internet I contacted him for help… well DR. OKORUNDO proving to be a great man and he heal me.. According to him he said is the power of his gods well I thank god am back again if you need cure for your HIV….you can still contact him or his email or number I promise he is 100% he</blockquote>
And this one:<br />
<blockquote class="tr_bq">
I want to say hello to the world at large, I am very grateful for the good deeds DR. OKORUNDO did for me, I was a HIV patient, everything went bad for me, I couldn’t do things with my friends anymore, I loosed my job, I loosed everything, I was even waiting for death itself, I went searching on the internet I saw many testimonies on how different spell casters helped people in curing their deadly diseases, I collected one spell caster’s email, which dr.okorndo I emailed him and he answered me, I told him all problems, he ask me not to worry, that I will be free from the deadly disease, which I did, he casted the spell, and told me that he will send a holy water to me through courier services, I was surprised, because he did not mention it to me before, I paid for the courier delivery service, I got a holy water, he asked me to drink it which I did and he asked me to go for a medical check-up in a hospital, I went to the hospital I went for a HIV test, I was tested HIV negative, I was</blockquote>
If you contact him, I will guarantee you will loose your money and you will loose what what remains of your health. <div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-22407143718344828282013-11-23T16:26:00.001-05:002013-11-26T10:10:31.527-05:00Loose Ends And Chasing GhostsI might have made some progress, but some loose ends make me feel like I am chasing ghosts.<br />
<br />
The good news is, I think I am making progress. In summer this year my health was tiny bit better then half a year before. Now it is again a tiny bit better than in summer. Alas, I do less, so maybe that is the reason why I feel better… And whenever I try to do something I still get worse. But my tolerance for doing stuff is slowly improving (I think, I have no real measure). I did some light work on Friday, and today (Saturday) I felt the work from yesterday, but could still do some more – after that I felt awful.<br />
<br />
One "trick" I found is that when I feel awful after doing some (light) work, I can feel better when I drink water – more water than I would normally drink (e.g. two glasses when I would drink only one). However when I drink too much, I feel sick… Fear not, I found another "trick": After drinking too much water, I need to take some sugar (a teaspoon or two, or a fruit) to feel better again. (and oh, I forgot to mention: I feel immediately better – within a couple of minutes – after I take a dump. I wish I knew if this is some blood pressure thing, or if this is some liver thing, or what.)<br />
<br />
Another thing I noticed: When I take a bit of sugar, my nose "cleans up". Usually it feels a bit congested, but after taking a bit of sugar (which has to contain fructose – glucose alone does <i>not</i> do the trick!) my nose clears up and I can better breathe (BTW, funny thing, sometimes an orgasm clears up my nose as well…). However if I take to much sugar my nose "dries up" a bit. Something is wrong here, and I don't know what.<br />
<br />
The improvement is so slow though, that it is painful (not literally painful, but every day seems like the last). And, whenever I do a bit more (maybe an hour or two a day), I get worse again.<br />
<br />
And while I gained about one kilogram over the past month (or two), I am still eleven kilogram under my March weight. I have been carelessly eating stuff when I am not hungry, and that's the revenge for this. <br />
<br />
What seems to unchanged is that my sleep is not a slightest bit restorative – on the contrary, I feel much better before sleep, than compared after a "good night's sleep". Shucks. In the morning my muscles hurt and they are stiff. My brain feels only half awake in the morning. I need to take a strong coffee, take a hot shower and about 2 to 3 hours to feel halfway like a human being.<br />
<br />
Unfortunately there are still some loose ends. A couple of months ago I made an experiment of only eating fish, no more pork. During that time I developed some slight acne again. Which got slightly worse after I stopped fish and ate pork again. I even got some <a href="http://parakoch.blogspot.com/2013/10/return-of-aphthous-ulcer.html">aphthous ulcers</a>.<br />
<br />
Now it took some time before the acne wound down again, during which time I removed olives, mustard, bananas and sausages from my nutrition.<br />
<br />
Yesterday I ate a banana (not completely ripe), fish (smoked mackerel) and olives and got one slight ulcer.<br />
<br />
So what did cause my acne/ulcers outbreak over the past months?<br />
<ul>
<li>Some weird fish protein / pork protein thingy</li>
<li>Olives</li>
<li>Mustard</li>
<li>Sausages (or rather the casing of sausages)</li>
<li>Bananas (possibly unripe?)</li>
<li>Smoked meat/fish</li>
<li>Food contaminations</li>
<li>Toothpaste (certain brand)</li>
<li>Something completely else</li>
<li>All of the above</li>
<li>Some of the above </li>
<li>None of the above</li>
<li>No external cause</li>
</ul>
Back to chasing ghosts…<br />
<br />
And lest I forget: I have been occasionally eating some bread, and I do have the impression that I feel worse afterwards. The effect isn't too strong (and I could not swear that it is caused by bread), but I feel kind of "dehydrated" and "dry" for half a day to maybe one day.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-82634983062616312852013-11-15T12:32:00.002-05:002013-11-15T12:35:38.563-05:00The War On Cancer<a href="http://eatingacademy.com/nutrition/war-cancer">Peter Attia</a>:<br />
<blockquote>… I don’t need to say much about cancer that you don’t already know. You probably know that about one in three Americans will develop cancer in their lifetime, and you probably know that about half of them will succumb to the disease. <b>What you may not know, however, is that we have made virtually no progress in extending survival for patients with metastatic solid organ tumors since the “War on Cancer” was declared over 40 years ago. In other words, when a solid organ tumor (e.g., breast, colon, pancreatic) spreads to distant sites, the likelihood of surviving today is about what it was 40 years ago with rare exceptions.</b> We may extend survival by a few months, but not long-term (i.e., overall) survival.<br />
<br />
We screen better today for sure, but subtracting lead-time bias, it’s not clear this extends overall survival. We’ve had success in treating and even curing hematologic cancers (e.g., some forms of leukemia and lymphoma). Certainly testicular cancer patients (especially seminomatous) are better off today and those with GI stromal tumors (GIST), too. Surgical control of cancer is much better today and some local treatments (e.g., specific radiation), too. But for the most part, when a patient has metastatic cancer today, the likelihood of living 10 more years is virtually unchanged from 40 years ago.<br />
<br />
…</blockquote><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-19654007527501578232013-11-12T06:12:00.001-05:002013-11-12T06:12:46.442-05:00Nutrition Research: "Dissonant With Scientific Principles"<blockquote>
But by not training mentees in the basics of science and skepticism, the nutrition field has fostered the use of measures that are so profoundly dissonant with scientific principles that they will never yield a definitive conclusion. As such, we now have multiple generations of nutrition researchers who dominate federal nutrition research and the peer review of that work, but lack the critical thinking skills necessary to critique or conduct sound scientific research.</blockquote>
<a href="http://climateaudit.org/2013/11/11/a-scathing-indictment-of-federally-funded-nutrition-research/">Steve McIntyre has some of the details.</a> <div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-42483612887082614942013-11-05T04:07:00.001-05:002013-11-05T08:44:18.632-05:00The ME/CFS Zoo HypothesisA constant question regarding ME/CFS (and fibromyalgia) goes something like this:<br />
<ul>Is it <i>one</i> disease, or is it a "spectrum", or is it <i>multiple</i> (distinct) diseases that look the same?</ul>
I that regard: I find the <a href="https://en.wikipedia.org/wiki/Blind_men_and_an_elephant">"Blind men and an elephant" parable</a> helpful – and would like to expand it.<br />
<br />
First of all, let me recount from the Wikipedia page a slightly modified summary of the parable:<br />
<blockquote class="tr_bq">
In various versions of the tale, a group of blind men touch an elephant to learn what it is like. Each blind men feels a different part, but only one part, such as the trunk, or an foot, or the tusk.<br />
<blockquote class="tr_bq">
A Jain version of the story says that six blind men were asked to determine what an elephant looked like by feeling different parts of the elephant's body. The blind man who feels a leg says the elephant is like a pillar; the one who feels the tail says the elephant is like a rope; the one who feels the trunk says the elephant is like a tree branch; the one who feels the ear says the elephant is like a hand fan; the one who feels the belly says the elephant is like a wall; and the one who feels the tusk says the elephant is like a solid pipe.</blockquote>
Afterwards the blind men talk to each other and learn that they are in complete disagreement. Some of the stories differ in how violent the conflict becomes, and how (or if) the conflict among the men and their perspectives is resolved.<br />
<br />
In some versions, they stop talking, start listening and collaborate to "see" the full elephant. When a sighted man walks by and sees the entire elephant all at once, they also learn they are blind. While one's subjective experience is true, it may not be the totality of truth.</blockquote>
My impression is that many in the ME/CFS "community" think that most of the studies are equally "true" – I think that is the first mistake. To stay in the parable: Some of the blind men have never touched an elephant (or any other animal, for that matter) and simply make things up. Here you have blind men who describe not an elephant, but maybe an park bench, or an found umbrella, or maybe an object that exists only in their fantasy (and even describing that they suck). Yes Virginia, I'm talking about Lombardi, Mikovits and Ruscetti. There are others. Like those blind men trying to describe the color of the elephant. Somehow, now I have to think of the names Meirleir, Maes and Gerwyn. <br />
<br />
And even if you sieve out all the blind men describing inanimate objects (or worse, make-believe objects), you get some who grabbed some random animal in the zoo and tried to described it. Now if they can describe two (or more) of those animals, <i>and</i> the differences between them, <i>and</i> if they do <i>not</i> try to make you believe that they describe the whole animal, I think they are much more trustworthy than those who want to make you believe they describe <i>only</i> an elephant, and that they know the <i>entire</i> elephant.<br />
<br />
If you have someone who says "<i>Here I found two animals with distinctly different tusk, one has leather like skin, the others is furry</i>", well then we are on to something. Currently I have seen few people who would fit that bill: Alan Light (et al.), and maybe Julia Newton (come to my mind).<br />
<br />
But one thing should be clear, all those harping about how we need better criteria to "sieve out all non-elephants" (to stay within the parable) should know that:<br />
a) Your are an "blind men" yourself<br />
b) You might be an "non-elephant" yourself<br />
c) The studies you trust might describe non-elephants<br />
d) The studies you trust might describe non-elephant animals that are different from you<br />
<br />
Yes, better (and more stringent) criteria might be helpful, but what we need are ways to look at "a collection of zoo animals" (parable again), and learn to differentiate them properly, both in a research setting, and in a clinical setting.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-73760166055099896582013-10-25T13:12:00.001-04:002013-10-25T13:12:55.062-04:00"There is a categorical lack of clinical evidence to support the use of statin therapy in primary prevention."<a href="http://stan-heretic.blogspot.com/2013/09/statins-review-paper.html">Via Stan the Heretic</a>: <br />
<blockquote class="tr_bq">
There is a categorical lack of clinical evidence to support the use of statin therapy in primary prevention. Not only is there a dearth of evidence for primary cardiovascular protection, there is ample evidence to show that statins actually augment cardiovascular risk in women, patients with Diabetes Mellitus and in the young. Furthermore statins are associated with triple the risk of coronary artery and aortic artery calcification.</blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-17534495728210980192013-10-25T12:07:00.001-04:002013-10-28T16:56:56.442-04:00Don't Trust The Authorities<a href="http://blogs.discovermagazine.com/crux/2013/10/02/the-shocking-truth-of-the-notorious-milgram-obedience-experiments/">Milgram a fraud?</a> <br />
<blockquote class="tr_bq">
… In the fifty years since publication of Milgram’s first journal article the obedience research continues to be cited as evidence of an enduring psychological truth: inside all of us is a Nazi concentration camp guard waiting to be called into service. Yet my archival research and examination of primary sources and that of other scholars contradicts this claim.<br />
<br />
Milgram himself was privately aware of the methodological weakness of his research and struggled with many of the issues about the validity of experiments and their generalisability beyond the lab. Privately Milgram reflected that his work was more art than science, and described himself as a “hopeful poet.” …</blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-25355333122238510382013-10-23T15:41:00.002-04:002013-10-23T15:41:41.456-04:00Positive Psychology? Smelling Bull. <a href="http://narrative.ly/pieces-of-mind/nick-brown-smelled-bull/%20">Nick Brown Smelled Bull</a> (<a href="http://climateaudit.org/2013/10/21/nick-brown-smelled-bs/">via</a>)<br />
<br /><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-26636263364472953192013-10-16T02:48:00.000-04:002013-10-16T02:48:07.987-04:00Return Of The Aphthous UlcerSo today I woke up with an aphthous ulcer in my lip – bummer. Now I try to backtrack what I did yesterday what might have been different:<br />
<ul>
<li>I used a different brand of toothpaste yesterday morning (I have not used that brand for some time now).</li>
<li>I had a long test, which was a bit stressful (but not overly stressful).</li>
<li>I increased my sugar intake yesterday afternoon: six cubes of sugar and a banana (both of which I had avoided the weeks before).</li>
<li>The banana was quite ripe. It was OK, but not quite ripe (the peel was only yellow, not getting black yet). </li>
<li>In the evening I ate a liverwurst (the brand of liverwurst was fine the last time, and they declared everything to be pork).</li>
</ul>
Out flies my theory about as dairy being the <u>sole</u> cause of aphthous ulcers… I still have much much more seldom aphthous ulcers than I used to have, so what ever it was, I have reduced it.<br />
<br />
So was it the toothpaste, the stress, the sugar, the banana or the liverwurst? Damn, if I knew… At the moment I tend to go with the toothpaste theory, closely followed by the banana. The liverwurst might have been a problem, but I think the stress and the sugar are unrelated (but I am not sure).<br />
<br />
Damn, damn, damn.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-55875868028423731622013-10-15T15:46:00.001-04:002013-10-15T15:46:07.272-04:00Migraine JokeHow many people do you need to investigate migraine?<br />
<blockquote>
<a href="http://www.nature.com/ng/journal/v45/n8/full/ng.2676.html">Genome-wide meta-analysis identifies new susceptibility loci for migraine</a><br />
Verneri Anttila<br />
Bendik S Winsvold<br />
Padhraig Gormley<br />
Tobias Kurth<br />
Francesco Bettella<br />
George McMahon<br />
Mikko Kallela<br />
Rainer Malik<br />
Boukje de Vries<br />
Gisela Terwindt<br />
Sarah E Medland<br />
Unda Todt<br />
Wendy L McArdle<br />
Lydia Quaye<br />
Markku Koiranen<br />
M Arfan Ikram<br />
Terho Lehtimäki<br />
Anine H Stam<br />
Lannie Ligthart<br />
Juho Wedenoja<br />
Ian Dunham<br />
Benjamin M Neale<br />
Priit Palta<br />
Eija Hamalainen<br />
Markus Schürks<br />
Lynda M Rose<br />
Julie E Buring<br />
Paul M Ridker<br />
Stacy Steinberg<br />
Hreinn Stefansson<br />
Finnbogi Jakobsson<br />
Debbie A Lawlor<br />
David M Evans<br />
Susan M Ring<br />
Markus Färkkilä<br />
Ville Artto<br />
Mari A Kaunisto<br />
Tobias Freilinger<br />
Jean Schoenen<br />
Rune R Frants<br />
Nadine Pelzer<br />
Claudia M Weller<br />
Ronald Zielman<br />
Andrew C Heath<br />
Pamela A F Madden<br />
Grant W Montgomery<br />
Nicholas G Martin<br />
Guntram Borck<br />
Hartmut Göbel<br />
Axel Heinze<br />
Katja Heinze-Kuhn<br />
Frances M K Williams<br />
Anna-Liisa Hartikainen<br />
Anneli Pouta<br />
Joyce van den Ende<br />
Andre G Uitterlinden<br />
Albert Hofman<br />
Najaf Amin<br />
Jouke-Jan Hottenga<br />
Jacqueline M Vink<br />
Kauko Heikkilä<br />
Michael Alexander<br />
Bertram Muller-Myhsok<br />
Stefan Schreiber<br />
Thomas Meitinger<br />
Heinz Erich Wichmann<br />
Arpo Aromaa<br />
Johan G Eriksson<br />
Bryan J Traynor<br />
Daniah Trabzuni<br />
North American Brain Expression Consortium UK Brain Expression Consortium Elizabeth Rossin<br />
Kasper Lage<br />
Suzanne B R Jacobs<br />
J Raphael Gibbs<br />
Ewan Birney<br />
Jaakko Kaprio<br />
Brenda W Penninx<br />
Dorret I Boomsma<br />
Cornelia van Duijn<br />
Olli Raitakari<br />
Marjo-Riitta Jarvelin<br />
John-Anker Zwart<br />
Lynn Cherkas<br />
David P Strachan<br />
Christian Kubisch<br />
Michel D Ferrari<br />
Arn M J M van den Maagdenberg<br />
Martin Dichgans<br />
Maija Wessman<br />
George Davey Smith<br />
Kari Stefansson<br />
Mark J Daly<br />
Dale R Nyholt<br />
Daniel I Chasman<br />
Aarno Palotie<br />
for the International Headache Genetics Consortium</blockquote>
I am now migraine free, after having figured out my nutrition. I was able to stop using Ibuprofen – something that was before unthinkable for me.<br />
<br />
Will they ever find out? They did "brain tissue expression quantitative trait locus analysis" after all. Should count for something, shouldn't it?<br />
<br />
Idiots.<br />
<br />
And Nature, that bloody tabloid.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-13768293345657388202013-10-15T14:20:00.004-04:002013-10-15T14:20:47.226-04:00"Something I've been eating is doing bad things to my body."<a href="http://chronicfatigue.about.com/b/2013/09/18/one-week-in-my-elimination-diet.htm">Adrienne Dellwo</a>:<br />
<blockquote>I'm really not loving this diet. I've been cranky, I've had headaches, and I've caught myself grinding my teeth multiple times. I have cravings that rapid-cycle from one thing to the next. The food I'm eating rarely makes me feel full and satisfied.<br />
<br />
But there is a silver lining - my inflammation is way down. I've lost several pounds. I can wear my wedding ring without my finger going numb, and my hair isn't falling out in clumps. My pain is down, especially in my hands, where I've had nerve compression. My hip, which still aches, isn't locking up on me, and I can go down stairs without that painful catch in my knee. I've even ridden my bike a little.<br />
<br />
What that tells me is: something I've been eating is doing bad things to my body. …</blockquote><div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-48027859466839967802013-09-27T16:44:00.000-04:002013-09-27T16:47:29.205-04:00Does Dairy Cause Cystic Acne?<a href="http://weheartthis.com/2009/05/29/my-fight-against-cystic-acne/#comment-19877">Cystic acne caused by dairy?</a><br />
<blockquote class="tr_bq">
… having suffered with cystic acne all my life, I recently discovered that milk is the cause. It makes sense since I was allergic to milk as a child but didn’t think about the effects it would have in my adulthood. I’ve [quit] drinking or eating anything with dairy and haven’t had a new cyst for 4 months. Prior to the non-dairy diet, I would get a cyst every 2 weeks. Anyway, if you’ve been a long time sufferer, maybe avoiding milk will help you too.</blockquote>
<a href="http://weheartthis.com/2009/05/29/my-fight-against-cystic-acne/#comment-98298">One more:</a><br />
<blockquote>
… a few years ago I decided I’m gonna stop drinking milk, and I WAS drinking only lactose free milk for a while but I read something about milk contributing to hair loss and cysts, so just stopped drinking milk and switched to almond milk (kroger family stores has the best one, closest in consistency and flavor to real milk than any other alternative)… guess what? NO MORE THIGH CYSTS! …</blockquote>
<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0tag:blogger.com,1999:blog-6622318257133015878.post-87947759135635596682013-09-16T04:25:00.002-04:002013-09-16T04:25:49.946-04:00A Cause of Chronic Immune System ActivationYou want to know a secret? An overlooked cause of chronic immune system activation?<br />
<br />
It's right there on your plate: Nutrition.<br />
<br />
Forget about "gut flora disbalance" or somesuch BS. Forget about makebelieve "latent viruses" supposedly hiding somewhere in the tissue (hiding like commies during McCarthy's withhunt). If you want to know what has the potential to activate the immune system, you should look on your plate.<br />
<br />
For decades I had acne (and other inflammation of the skin) and it only receded when I reduced dairy. When I increased dairy again, the acne came back. Over the past year I had to learn that acne can be caused by other (ruminant) animal products like veal, lamb or sheep.<br />
<br />
Got milk? Maybe that's the reason you got an activated immune system.<br />
<br />
Connecting gut problems with nutrition should be easy, one thinks. So if one has known gut problems, why not think about nutritional causes? And from my experience, I can say that skin tissue (and oral mucosa) can be affected by nutrition – and the skin is probably (considering the path nutrients take through the bloodstream) the furthest away from the gut*. So it is only a small leap to consider that <i>every</i> tissue between the gut and the skin can be affected negatively by nutrition. Right?<br />
<br />
There is only one way to find out: Do an elimination diet. (Almost) no doctor will help you that, no "multi-center microbiology deep-sequencing study" will help you with that, and certainly no virus-hunter (real or imaginary) will help you with that.<br />
<br />
<br />
<br />
--<br />
* Unless of course you consider that mathematically the
gut wall and the skin are part of the same surface. And that
evolutionary the different epithelial tissues might be very closely related anyway.<div class="blogger-post-footer">
<i><b><br/>From the blog-feed for <a href="http://parakoch.blogspot.com/">http://parakoch.blogspot.com/</a>.</b></i> Go see ME/CFS Pathophysiology Lectures: <a href="http://parakoch.blogspot.com/2012/10/christopher-snell-2012-lecture-clinical.html">Christopher Snell 2012</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2011-lecture-gene-expression.html">Alan Light 2011</a>, <a href="http://parakoch.blogspot.com/2011/06/alan-light-2007-lecture-physiology-of.html">Alan Light 2007</a></div>Tony Machhttp://www.blogger.com/profile/14823430729798784689noreply@blogger.com0