Could Milk and Dairy cause Cancer?

Here is an heretic idea: Could the consumption of (pasteurized) cow milk and dairy cause some forms of cancer? Specifically: breast cancer?

Well, this is pure speculation – yet an epidemiologist worth his/her salary should have no problem confirming or refuting this idea.

I just leave this idea here, so I can say in 30 years: "Told you so."

IgM and IgG Seronegative Q Fever: A Hypothesis for Veterans? Medically Unexplained Chronic Multi-symptom Illnesses.

Immunoglobulin M and Immunoglobulin G Seronegative Q Fever: A Hypothesis for Veterans? Medically Unexplained Chronic Multi-symptom Illnesses.

Chagaris MJ, Smith RC, Goldstein AL.

J Spec Oper Med. 2012 Spring;12(1):37-48.

Abstract
We present Q fever as a credible hypothesis for Gulf War Veterans Illnesses (GWVIs) and as a possible etiology for prevalent symptomologies affecting currently serving servicemembers.

Q fever is caused by the bacteria Coxiella burnetii, which is endemic throughout the Middle East. Q fever may manifest in many forms of widely varying and often inconstant symptoms. Due to false-negative interpretations in current and past diagnostic testing, Q fever has not received appropriate consideration as a possible causative agent for medically unexplained veterans illnesses.

Review of current literature invites us to consider that a form of Q fever involving an incomplete immune response is a potential cause of these debilitating illnesses.

We hypothesize C. burnetii infection coincidental to exposures suppressing antibody-specific immune response results in infection mediated by immunoglobulin D (IgD). Literature indicates that successful treatment for this form of Q fever requires the concurrent administration of doxycycline and hydroxychloroquine.

Well, it is a hypothesis – without any evidence, it seems.

Usually at the acute phase of an infection you get an IgM titer increase, and after the acute phase the IgM titers level off. And an IgG titer increase follows that, usually persistent for life, even when the pathogen is long gone ("Adaptive Immune System"). So it is intruging that IgD titers might be raised and not IgM or IgG – but where is the evidence?

Because, I've seen this before and I bloody hate it: These f*cking "out of the blue" hypothesis without any evidence. Stupid quacks who write things like "Oh, CFS could be an allergy to an pathogen" without any shroud of evidence for their quack hypothesis. Is it too much to ask that they do some minimal testing for their hypothesis and supply at least some results – before publishing?

"The phenomenon of 'chronic Lyme'; an observational study."

The phenomenon of 'chronic Lyme'; an observational study.
Ljøstad U, Mygland A.

Department of Neurology, Sørlandet Hospital, Kristiansand, Norway Institute of Clinical Medicine, University of Bergen, Bergen, Norway Department of Habilitation, Sørlandet Hospital, Kristiansand, Norway

Abstract

Purposes:
To chart clinical, laboratory, and psychometric profiles in patients who attribute their complaints to chronic Lyme disease.

Methods:
We assessed the patients by clinical examination, laboratory tests, and questionnaires measuring fatigue, depression, anxiety, health-related quality of life, hypochondriasis, and illness perceptions.

Results:
We found no evidence of ongoing Borrelia burgdorferi (Bb) infection in any of the 29 included patients using current diagnostic guidelines and an extended array of tests.

Eight (28%) had other well-defined illnesses.

Twenty-one (72%) had symptoms of unknown cause, of those six met the suggested criteria for post-Lyme disease syndrome.

Fourteen (48%) had presence of anti-Bb antibodies.

The patients had more fatigue and poorer health-related quality of life as compared to normative data, but were not more depressed, anxious, or hypochondriacal.

Their beliefs about the illness were characterized by negative expectations.

Conclusion:
Our patients, who all attributed their symptoms to chronic Lyme disease, were heterogeneous.

None had evidences of persistent Bb infection, but whether current diagnostic criteria are functional in patients with longstanding complaints is controversial.

Other well-defined illnesses or sequelae from earlier Lyme disease were probable as main explanatory factor in some cases.

The patients were not more depressed, anxious, or hypochondriacal than the normal population, but they had poorer health-related quality of life, more fatigue, and negative expectations about their illness.

Unforutnatly only the abstract is available. The other "well-defined illnesses" would be interesting to collect.

And about half(!) of the patients who were seen by these doctors supposedly with "chronic Lyme" did actually not have anti-bodies against Borrelia Burgdorferi - and none had evidences of persistent infection! There are certainly some Quacks out there diagnosing people with "Chronic Lyme". And only "six met the suggested criteria for post-Lyme disease syndrome".

To Do list for Ampgligen

Show credible evidence of Ampligen’s efficacy using expanded studies that are at least six months long

Show that Ampligen is safe; ie that it does not cause autoimmune disorders or heart problems (prolonged qt intervals)

Produce studies in which patients are on more than one dose regimen

Produce studies in which at least 300 patients are on doses intended for the market

Follow the FDA’s ‘recommendation’ that rodent studies be done to examine carcinogenicity

Provide additional data on quality control issues

Fix Inspection issues at one of Ampligen’s facilities

http://phoenixrising.me/archives/8819

Is health-care a medical or a social problem?

The savage cuts to Greece's health service budget have led to a sharp rise in HIV/Aids and malaria in the beleaguered nation, said a leading aid organisation on Thursday.

The incidence of HIV/Aids among intravenous drug users in central Athens soared by 1,250% in the first 10 months of 2011 compared with the same period the previous year, according to the head of Médecins sans Frontières Greece, while malaria is becoming endemic in the south for the first time since the rule of the colonels, which ended in the 1970s.

Reveka Papadopoulos said that following health service cuts, including heavy job losses and a 40% reduction in funding for hospitals, Greek social services were "under very severe strain, if not in a state of breakdown. What we are seeing are very clear indicators of a system that cannot cope". The heavy, horizontal and "blind" budget cuts coincided last year with a 24% increase in demand for hospital services, she said, "largely because people could simply no longer afford private healthcare. The entire system is deteriorating".

It seems to me that access to health-care is the primary determinant for the quality of health-care – the biggest improvement for a health-care system is making sure all people have access.

The Darwinian "Units of Selection" are not aware of what they do

One of the most important lessons from evolution is that the Units of Selection (which are genes, by the way, not individual living beings) are not aware of what they do. There is no watchmaker (not even a blind watchmaker), no grand master plan. The units of selection don't "do it" for their benefit – it is the other way round, the units of selection that do something that is beneficial for them (in a given environment) are "rewarded".

So, does anybody need to know whether what he is doing is beneficial for him – or for someone else? Does a president need to know for whom (and how) it will be beneficial, if he invades another country in the name of his king, in the name of his religion or in the name of his nation? Does a professor for economy, a journalist or a politician need to know who benefits (beside himself) when he advocates the benefits of the invisible hand of the free market? And do patients who advocate for quack cures need to know to whom (and how) it is beneficial, if they advocate quack treatments? And does the quack need to know that only he will benefit of this quack cures?

No.

If anything, evolution teaches us that there can be a conspiracy without a conspirer. That a few are benefiting and many are harmed "can happen", without someone planing it knowingly. It would be interesting to dissect the mechanisms in each individual case – alas, I'm afraid that is beyond the scope of my feeble blog and left therefore as an exercise for the inclined reader. :-)


(That is not to say that all conspiracies have no conspirers who halfway know what they do – plenty of examples of that in history.)

iPOP (integrative personal omics profile) – tracking proteins, metabolites, metabolism, microRNAs, cytokines, antibodies, and gene transcripts in one person

Michael Snyder tracks his health status with iPOP and finds a virus causing his Type 2 Diabetes (T2DM)?

Snyder had a cold at the first blood draw, which allowed the researchers to track how a rhinovirus infection alters the human body in perhaps more detail than ever before. The initial sequencing of his genome had also showed that he had an increased risk for type 2 diabetes, but he initially paid that little heed because he did not know anyone in his family who had had the disease and he himself was not overweight. Still he and his team decided to closely monitor biomarkers associated with the diabetes, including insulin and glucose pathways. The scientist later became infected with respiratory syncytial virus, and his group saw that a sharp rise in glucose levels followed almost immediately. "We weren't expecting that," Snyder says. "I went to get a very fancy glucose metabolism test at Stanford and the woman looked at me and said, 'There's no way you have diabetes.' I said, 'I know that's true, but my genome says something funny here.' "

So much for "These people eat too much."

Topol writes in an e-mail, "this type of 'pan-ar-omic' study of individuals is now not only feasible but in select individuals with medical conditions, particularly useful clinically."

We'll have to wait until this will be used more often in research, and then it will take some considerable time, but it will reach clinical use some time, maybe in the next decade.

Read it all.

[Update] Here's another blog post about this.

Orac on AoA and Kent Heckenlively

Orac on AoA and Kent Heckenlively:

…
I know, I know, I've said before that I try to avoid that site [Age of Autism] these days, and I do. There is nothing there other than pseudoscience, logical fallacies, and conspiracy theories about big pharma, usually laced with ad hominem attacks against skeptical and science-based bloggers like myself accompanied by whining about how the critics of the antivaccine movement are so unfair in making ad hominem attacks against the bloggers at AoA. (Never mind that the attacks usually aren't ad hominem; they're about what the AoA crew writes and how lacking in reason and evidence it is, and only sometimes about the bloggers themselves. Never mind that an ad hominem can be justified if the target's behavior warrants the ad hominem.) It all becomes tiresome after a while, and it rarely manages to appall me any more as it did in the past. I must have grown a thick skin. Even when J.B. Handley launches a childish, all out broadside, it doesn't even faze me anymore.

And then I saw a post by the ever-excitable and clueless Kent Heckenlively, he who makes bizarre speculations about autism science while clearly understanding nothing about it. The post is entitled I Officially Join the Mercury Militia, and it is the most horrifying thing I've seen on AoA. In fact, it's the most horrifying story of autism quackery that I've seen since the death of Tariq Nadama at the hands of a chelationist. All I could think as I read the post is how sorry I felt for Mr. Heckenlively's autistic daughter, whom he has subjected to all manner of quackery in the pursuit of his belief that she is "mercury toxic" and that is the cause of her autism. It also shows just how far down the rabbit hole it's possible for an otherwise intelligent person to go when that person is ignorant of science and fixates on one idea after another about what causes autism. …

Ampligen ("Rintatolimod") Phase III study published

Finally!

[Update: This was not a new study, just a re-analysis http://phoenixrising.me/archives/8882]

A Double-Blind, Placebo-Controlled, Randomized, Clinical Trial of the TLR-3 Agonist Rintatolimod in Severe Cases of Chronic Fatigue Syndrome

David R. Strayer 1*, William A. Carter 1, Bruce C. Stouch 2, Staci R. Stevens 3, Lucinda Bateman 4, Paul J. Cimoch 5, Charles W. Lapp 6, Daniel L. Peterson 7, the Chronic Fatigue Syndrome AMP-516 Study Group¶, William M. Mitchell 8*

1 Hemispherx Biopharma, Inc., Philadelphia, Pennsylvania
2 BCS Consulting, Philadelphia, Pennsylvania
3 University of the Pacific, Stockton, California
4 Fatigue Consultation Clinic, Salt Lake City, Utah
5 Center for Special Immunology, Fountain Valley
6 Hunter-Hopkins Center, Charlotte, North Carolina
7 Sierra Internal Medicine Associates, Incline Village, Nevada
8 Vanderbilt University School of Medicine, Nashville, Tennessee

Abstract

Background
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a severely debilitating disease of unknown pathogenesis consisting of a variety of symptoms including severe fatigue.

The objective of the study was to examine the efficacy and safety of a TLR-3 agonist, rintatolimod (Poly I: C12U), in patients with debilitating CFS/ME.

Methods and Findings
A Phase III prospective, double-blind, randomized, placebo-controlled trial comparing twice weekly IV rintatolimod versus placebo was conducted in 234 subjects with long-standing, debilitating CFS/ME at 12 sites.

The primary endpoint was the intra-patient change from baseline at Week 40 in exercise tolerance (ET).

Secondary endpoints included concomitant drug usage, the Karnofsky Performance Score (KPS), Activities of Daily Living (ADL), and Vitality Score (SF 36).

Subjects receiving rintatolimod for 40 weeks improved intra-patient placebo-adjusted ET 21.3% (p = 0.047) from baseline in an intention-to-treat analysis.

Correction for subjects with reduced dosing compliance increased placebo-adjusted ET improvement to 28% (p = 0.022).

The improvement observed represents approximately twice the minimum considered medically significant by regulatory agencies.

The rintatolimod cohort vs. placebo also reduced dependence on drugs commonly used by patients in an attempt to alleviate the symptoms of CFS/ME (p = 0.048).

Placebo subjects crossed-over to receive rintatolimod demonstrated an intra-patient improvement in ET performance at 24 weeks of 39% (p = 0.04).

Rintatolimod at 400 mg twice weekly was generally well-tolerated.

Conclusions/Significance
Rintatolimod produced objective improvement in ET and a reduction in CFS/ME related concomitant medication usage as well as other secondary outcomes.

Orac – in passing – on the Placebo effect

Orac:

… In fact, even when publishing what could be a scientifically interesting and medically useful paper on placebo effects, its editors allowed the authors, led by Ted Kaptchuk, to spin the results in a way to imply that patients can have symptomatic relief without actual reversal of the underlying physiologic derangement that caused their symptoms in the first place and that that's OK. In this case, the disease was asthma, and the paper published showed that placebo acupuncture resulted in asthma patients feeling better but didn't reverse the airway constriction that led patients to feel short of breath in the first place. Peter Lipson quite properly described this as "folly," …

Plus some criticism of postmodernism and quack non-medicine.

Orac: the latest about Wakefield's law suit

Why Wakefield is going to loose this one – again. Must read for anybody slightly interested.

Daniel Dennett: The Hurley Model of Humor

Dan Dennett about Hurley's evolutionary model of humor:


There is a longer talk by him on the same subject, but with rather bad audio and video:

One should be careful what one wishes for

Some people (supposedly close to Dr. Mikovits) want the WPI investigated, as Maarten Maartensz reports.

Hmm.

A proper investigation of the events surrounding the WPI (unlike the suggested investigation) might be a good idea, and I would welcome a proper investigation, one that would include looking into the scientific work of Drs. Mikovits and Ruscetti. Looking into the scientific work of these fine doctors is something that can not be avoided, when investigating the WPI – and then, I am terribly afraid, such an investigation might come to conclusions that the people calling for such an investigation might not like. And that, I would enjoy.

All. Cells.

For example, it is usual to find in any viral infection that infected and uninfected cells exist in equilibrium as two discrete populations. In flow cytometric analysis, this is represented by a bimodal peak. Flow cytometric analysis of peripheral blood mononuclear cells (PBMCs) taken from CFS patients was shown in the paper as a single peak, indicating that almost every cell was infected with XMRV.

Let me translate:

In the Lombardi et al. 2009 study all cells tested by intracellular flow cytometry (IFC) showed reaction with the rat anti-MLV p30 Gag monoclonal antibody.

All cells reacted with the anti-MLV antibody.

All cells reacted.

All cells.

All. Cells.

All.

All of them.

Each and every one of these little buggers reacted with the anti-body.

All PBMCs reacted with the antibody.

B-cells.

T-cells.

NK-cells.

The whole shebang.

And not only is each type of PBMCs reacting, no, the 100% peak shift means that each cell of the PBMCs is reacting. Not a single one left that does not react.

Now, if this reaction is caused by an infectious agent, then this would mean that each and every cell would be infected.

Now if each cell would be infected, then the virus would be easy to find having the right PCR primers/probes.

No need to mess around with nested PCR, do a single round PCR and find it. Because it would be in each and every cell.

Now, Mikovits claims to have found XMRV before Christmas 2008. Ruscetti got involved shortly after that. They submitted the study in May 2009. Enough time since then to come up with the actual sequences, if it wasn't XMRV.

Yet, nothing. No sequences other than XMRV. In now over three years since Christmas 2008.

Reported average costs for clinical trials per drug: $22.4 million

And estimated median, net, corporate cost to develop a new drug: $56 million.

Our own estimate of pharmaceutical R&D is often misquoted as an average of $43 million per new drug, which commentators reject as being absurd. However, we make clear this estimate for the year 2000 does not include the cost of discovery (because it varies greatly and no one has accurate figures), nor the "cost of capital" (for reasons explained in our article which can be read here). Our estimate is the net cost to major companies after taxpayers cover about 50% of their R&D expenses. We use the median cost because the average cost gets inflated by a few costly R&D projects.
In sum, we estimate that the median, net, corporate cost to develop a new drug, based on the confidential cost data that companies reported to their policy research center at Tufts University, is $56 million in 2011, plus the unknown company costs of discovery and the artificial estimate of profits foregone, if you think it should be added. We also show that R&D costs for in-house new active ingredients are much higher, and costs for me-too variations are much lower than this single figure.
Our estimate is almost double the only solid corporate report of R&D costs, which can be found in audited tax returns from the late 1990s. Here companies reported average costs for clinical trials per drug of only $22.4 million. Not $224 million but $22.4 million
...
if the Forbes figures and business arguments are correct, then nearly all of the global pharmaceutical companies listed in their article would have gone bankrupt between 1997 and 2011.

So much for the claims that "a new drug costs over a billion dollars".

(via denialism)

NIAID on Chronic Lyme and long-term Antibiotic use

NIAID on Chronic Lyme:

The first clinical trial, which included two studies conducted at multiple research sites, provided no evidence that extended antibiotic treatment is beneficial (New Engl J Med 345: 85-92, 2001). In those studies, physicians examined long-term antibiotic therapy in patients with a well-documented history of previous Lyme disease, but who reported persistent pain, fatigue, impaired cognitive function, or unexplained numbness. Patients were treated with 30 days of an intravenous antibiotic followed by 60 days of treatment with an oral antibiotic.

These studies did reinforce the evidence that patients reporting PLDS symptoms have a severe impairment in overall physical health and quality of life. However, prolonged antibiotic therapy showed no benefit when compared with groups who received placebo.

In another study, published in 2003, researchers examined the effect of 28 days of intravenous antibiotic compared with placebo in 55 patients reporting persistent, severe fatigue at least 6 months following treatment for laboratory-diagnosed Lyme disease. Patients were assessed for improvements in self-reported fatigue and cognitive function (Neurology 60: 1923-30, 2003).

In that study, people receiving antibiotics did report a greater improvement in fatigue than those on placebo. However, no benefit to cognitive function was observed. In addition, six of the study participants had serious adverse events associated with intravenous antibiotic use, and four patients required hospitalization. Overall, the study authors concluded that additional antibiotic therapy for PLDS was not supported by the evidence.

More recently, a study supported by the National Institute of Neurological Disorders and Stroke (NINDS), also a part of the National Institutes of Health, again showed that long-term antibiotic use for Lyme disease is not an effective strategy for cognitive improvement (Neurology 70(13): 992-1003, 2008). Researchers compared clinical improvement following 10 weeks of intravenous ceftriaxone versus intravenous placebo. The patients were treated for Lyme disease and presented with objective memory impairment tests. In a complicated statistical model, the ceftriaxone group showed a slightly greater improvement at 12 weeks, but at 24 weeks, both the ceftriaxone and the placebo groups had improved similarly from baseline. In addition, adverse effects attributed to intravenous ceftriaxone occurred in 26 percent of patients. The authors concluded that because of the limited duration of the cognitive improvement and the risks involved, 10 weeks of intravenous ceftriaxone was not an effective strategy for cognitive improvement in these patients, and more durable and safer treatment strategies are still needed.

To recap:

• The people are ill 
• Long-term antibiotics do most certainly not cure
• Long-term antibiotics have dangers
• Diagnose is done through "a well-documented history of previous Lyme disease"

As far as I am concerned, there is no evidence that "Chronic Lyme" or "post-Lyme disease syndrome" (PLDS) is anything else then just another pathogen that can cause CF(S) or PVFS.

Why XMRV and "HGRV" won't go away for some patients

Once an error is communicated and stored in people’s memories, it is difficult to undo. Even when people are exposed to a correction and acknowledge that the initial claim was false, the errant information may continue to influence their attitudes. In addition, people may misremember the false claim as true over time.

"It’s Not so Rare to Have a Rare Disease"

Spittoon – It’s Not so Rare to Have a Rare Disease

When we think about diseases we often describe them as either common or rare. Common conditions — like heart disease and obesity — are complex in nature, meaning that they are influenced by both genetics and environment. Conversely, most rare diseases are strongly influenced by genetics and less so by environment. We hear a lot about common conditions because so many people have them and in contrast relatively little about rare diseases. But how rare is rare?

In the United States, a disease is defined as “rare” if it affects fewer than 200,000 individuals, or roughly one in 1500. Rare diseases are often poorly understood, with symptoms that can be difficult to diagnose, and can be life-threatening. Around 6,800 rare diseases have been identified and the large majority of them — up to 80% — are thought to have a genetic origin. Most rare diseases can’t be cured and many lack effective treatments because research on rare conditions is often hampered by a scarcity of study participants and poor funding.

If you add up all the rare diseases it turns out that about 30 million Americans suffer from a rare disease. That’s nearly 10% of the population — suddenly rare is not so rare! …

Well, they sell genetic tests, so they have toot their horn. But still: 10% have a "rare" disease. Wow.

A psychiatrist that is a pharma shill?

Just one link, there is more where this came from…

A prominent Emory University psychiatrist failed to tell the school about $500,000 he received from drug maker GlaxoSmithKline PLC while heading a government-funded research project studying Glaxo drugs, Sen. Charles Grassley alleged.

The payments to Charles Nemeroff, chairman of the Atlanta university's psychiatry department, compensated him for making presentations to doctors about Glaxo drugs, including its big-selling antidepressant Paxil, according to records Sen. Grassley obtained from Emory and Glaxo. The senator made the allegations in a letter to Emory President James W. Wagner dated Thursday.

In correspondence with Emory officials who police conflict-of-interest issues, Dr. Nemeroff repeatedly denied having a significant financial relationship with Glaxo, according to the records cited by Sen. Grassley, an Iowa Republican who has been investigating ties between academic researchers and the medical industry.

…

Statins: "Funding from the test drug company was associated with results (OR=20) and conclusions (OR=35) that favor the test drug."

In this 20 minutes lecture by Beatrice Golomb, she mentions (among others) a interesting study:


So funding from the industry can skew research results? Who would have though that!?

Study weaknesses included:

• Inadequate blinding
• Lack of concealment of allocation
• Poor follow-up
• Lack of intention-to-treat analyses

It is always the same: Blinding, blinding, blinding and proper controls – at least they got the last one right. A study that was not properly blinded may be helpful to explore association ("Could it be?") or safety at a phase I stage, but to draw definite conclusions one needs properly blinded and controlled studies.

Here's the abstract:

Factors Associated with Findings of Published Trials of Drug–Drug Comparisons: Why Some Statins Appear More Efficacious than Others
Lisa Bero, Fieke Oostvogel, Peter Bacchetti, and Kirby Lee

Abstract


Background
Published pharmaceutical industry–sponsored trials are more likely than non-industry-sponsored trials to report results and conclusions that favor drug over placebo. Little is known about potential biases in drug–drug comparisons. This study examined associations between research funding source, study design characteristics aimed at reducing bias, and other factors that potentially influence results and conclusions in randomized controlled trials (RCTs) of statin–drug comparisons.

Methods and Findings
This is a cross-sectional study of 192 published RCTs comparing a statin drug to another statin drug or non-statin drug.

Data on concealment of allocation, selection bias, blinding, sample size, disclosed funding source, financial ties of authors, results for primary outcomes, and author conclusions were extracted by two coders (weighted kappa 0.80 to 0.97). Univariate and multivariate logistic regression identified associations between independent variables and favorable results and conclusions. Of the RCTs, 50% (95/192) were funded by industry, and 37% (70/192) did not disclose any funding source.

Looking at the totality of available evidence, we found that almost all studies (98%, 189/192) used only surrogate outcome measures. Moreover, study design weaknesses common to published statin–drug comparisons included inadequate blinding, lack of concealment of allocation, poor follow-up, and lack of intention-to-treat analyses.

In multivariate analysis of the full sample, trials with adequate blinding were less likely to report results favoring the test drug, and sample size was associated with favorable conclusions when controlling for other factors.

In multivariate analysis of industry-funded RCTs, funding from the test drug company was associated with results (odds ratio = 20.16 [95% confidence interval 4.37–92.98], p < 0.001) and conclusions (odds ratio = 34.55 [95% confidence interval 7.09–168.4], p < 0.001) that favor the test drug when controlling for other factors. Studies with adequate blinding were less likely to report statistically significant results favoring the test drug.


Conclusions
RCTs of head-to-head comparisons of statins with other drugs are more likely to report results and conclusions favoring the sponsor's product compared to the comparator drug. This bias in drug–drug comparison trials should be considered when making decisions regarding drug choice.

Speculation (2)

Judy was a lad in Francis' lab. Francis' worked in Bob's lab. Francis had stories how he and Bob were finding viruses. Francis helped finding I, and there were stories how Bob suspected I in A the year before H was found (named L back then), and then "found" III after Luc had found L. In one of these stories (which Judy probably heard over and over), there was one moment were, it might have been Francis, or it might have been Bob, when he "knew" that there was a virus, he just didn't knew what virus. Some marker, something off in some lab results.

So Judy makes up something – unknown to Francis. Some markers or something off. Francis looks at it and says: "Gee, that must be a G virus." Both say: "Well, we won't find it that fast, but we can lay claim on it before someone else finds it. Let's do what Bob did. Bob got the isolate for L from Luc. We'll use the X isolate from Robert, it should be close enough. We publish in Science, and pretty soon someone will come up with a positive study." So they cobbled a study together.

In the mean time, Harvey found out what was going down. Gold rush. He'd been there before. Better get in fast. Find a study that finds some goram virus, even if it is contamination with an M virus.

Francis really believed that there must be something. Francis thought the real virus would be found quickly. He didn't think of a way out. Why, after all? There must be something there. And when the real virus was found, nobody would ask much questions whether some numbers on a piece of paper were off. And even if, nobody cared about the questions that Bob was being asked back then – nobody would care now. Success made it right back then, and success would make it right this time.

Only, success did not come. This time.

What exactly are the "Normals"?

What exactly are the "Normal Ts" in the Slide of Shame? And the "PBMCs"? And the "CD4+ T"? And "CD8+ T"?

WB670 α XMRV RT 10 sec 4/23/09

Normal T 3/11
Normal T 3/21
2905 5 AZA 4/11
PBMC 4/11
PBMC 4/10
1674 5 AZA 4/11
PBMC 4/15
HCD-57 SFFVP

997 2/18
991 3/26
CD4+ T
CD8+ T
1010 3/20?
1282 3/26
Normal T 3/21
HCD-57 SFFVP

They can't be samples from controls. If they were samples from controls, they would have a number. Because, if they turn out positive, one would like to know from whom they came. To run more tests.

Unless, Ruscetti/Mikovits don't care about the controls, because they know that the controls are not interesting.