Is Dr. Ruscetti a Fraud?

The other thing I asked about recently (besides Dr. Mikovits) is whether the 100% peak shift was the result of falsification by Dr. Ruscetti. A nice anonymous commentator took issue:

And now you want to smear Ruscetti as well. Disgusting!

Oh dear, smearing Ruscetti? I just mused that the 100% peak shift was never the result of a process in the human body – which left for me the only option, that it looks like falsification to me.

The anonymous commentator claimed that "it has all been explained quite properly and clearly". So I guess there must be an "quite proper and clear" explanation for the 100% peak shift out there that does not involve 5AZA.

Dear anonymous commentator: Please set things straight, if you can! Please explain "quite proper and clear" the 100% peak shift, so nobody will ever dare to smear Ruscetti again! Please explain how a supposed infection with XMRV, with supposedly very low numbers of viruses, can lead to 100% of the white blood cells being infected.

I'm waiting.

Is Dr. Lombardi a Fraud?

I recently raised the question as to the possible falsification, fabrication and plagiarism in the works of the doctors Mikovits, Ruscetti and Lombardi.

There is one area that remains elusive for me so far: What role played Dr. Lombardi in this?

He has (supposedly) written the 2009 study ("Lombardi 2009") – but as we have seen already, the content from the WPI (the nested PCR) in this study is minimal.

There are some differences as who at the WPI has initiated the contact to Dr. Silverman, and who has requested the XMRV VP62 plasmid. At least it seems like it was Dr. Lombardi who had the contact to Dr. Silverman (through his prior work on RNASEL) – and not Dr. Mikovits.

But it seems like Dr. Mikovits has received the VP62 plasmid – and not Dr. Lombardi. The Addendum, with its infamous table 4, was written by Dr. Mikovits – and not Dr. Lombardi. The WPI research lab was run at that time by Dr. Mikovits – and not Dr. Lombardi.

From what I have seen, all the defenders of Judy Mikovits think that Silverman and Lombardi are the culprits. Silverman supposedly contaminated his samples, but we have already seen that Silverman was not involved in the sequences submitted by the WPI.

So what was Dr. Lombardi's role in this affair? Silent (and stupid?) bystander? Silent (and knowing) bystander? Active accomplice? Or might he have been the one contaminating the patient samples with VP62 and fooling everyone?

If there is evidence to the role of Lombardi in this affair, please point me to it!

Is Dr. Mikovits a Fraud?

As I mentioned before, table 4 from the "Addendum" looks to me like it was fabricated by Dr. Mikovits. Since Feburary I have been looking for an explanation – without luck so far. Yesterday a nice anonymous commentator has left this comment, trying to clear up some things:

It has all been explained quite properly and clearly. You just haven't been paying attention to anything that doesn't fit your preconceived notions. That twit, erv, made up the big lie and you didn't get it?

There was no falsification, fabrication or plagiarism. At worst there was a small mistake in labeling a slide and Silverman contaminated his own samples.

Have my "preconceived notions" lead my attention astray? Have I been had by "that twit"? Fallen in for "the big lie"? Oh my, better change that then.

So he(?) says that "it has all been explained quite properly and clearly". So please, tell me anonymous, were can I find this "quite proper and clear" explanation? So I can share it with the world – and hopefully change my preconceived notion that Dr. Mikovits is a fraud.

Or alternatively, please tell me were my "preconceived notions" lead my reading of table 4 astray – if you have read table 4 and can comment on it, that is.

And never mind that table 4 is not about slides and not about Silverman – if I were unkind, I would say this is an rather crude attempt to throw sand in my eyes.

(And by the way, the VP62 plasmid contamination happened at WPI, not at Silverman's lab)

Table 4: Mikovits Best Work – And Nobody Has Read It

What I find interesting is, that the best work that Dr. Judy Mikovits has published in her life – Table 4 from the Addendum – is being ignored both by her critics and her defenders. There are several statements from Dr. Mikovits that directly contradict the content of table 4 – one has just to take some time and look.

And the Addendum was written by Dr. Mikovits – not by Dr. Lombardi. And the best part: Dr. Silverman isn't even mentioned in the Addendum.

And mind you, you need to just gather statements and publications by only Dr. Mikovits. That fine reseacher can't make a factual statement without contradicting herself. To me, this looks like a web of lies – your milage may vary. And now my dear anoymice anonymouses, go and email this post to your best friends, and tell them I am smearing Mikovits again. And please don't read table 4 from the Addendum. Never ever do that – because you might end up smearing the fine Dr. Judy Mikovits.

The Psychosomatic Modell of Cancer: Bullshit or Bullshit?

The paper makes the case that sexual frustration can result in genetic mutation but fails to provide any evidence to support the claim. The paper is a perfect case study of how not to do science.

That leaves only one question: Should adherents of psychosomatic model of illness be shot before or after they graduate?

XMRV: Falsification, Fabrication and Plagiarism – and nobody clears it up

What I find interesting in the context of the works of the doctors Mikovits, Lombardi and Ruscetti is that no scientist has tried to properly take their work apart. Not Abbie Smith of erv-blog fame, not Dusty Miller – certainly not Coffin, certainly not Racaniello and most certainly not Dr. Alberts from Science. Lipkin is positively oblivious to what Mikovits has done.

Passing off VP62 plasmid as one's own isolates is plagiarism.

The 100% peak shift is the result of falsification, not a process the human body.

Table 4 from the "addendum" can realistically only be explained by fabrication.

VP62 has been talked about. But are there any consequences? Except a retraction and Mikovits getting sacked? An inquiry that would clear things up? Find a verdict? What about Ruscetti? Or even Lombardi?

The 100% peak shift has been mentioned once in the comments of erv's blog. Once. In the comment section. I am deeply impressed by Abbie Smith's courage in going up against Dr. Ruscetti, while at the same time restraining herself from indulging herself with moronic ME/CFS-patients. It would be a lot easier for her to get into a bitch fight with some deluded patients and ignore the possible fraud of Dr. Ruscetti – thank GOD she is not doing that, and thank god she has her priorities set straight.

Table 4? Nobody cares. Nobody gives a fuck. Nobody has really looked at Lombardi 2009, Mikovits 2010 and everything they published in that context. There are most certainly more other clues to their fraud in there. Table 4 is easy. Really easy. Even I get it.

"The science will sort itself out!". Yet it's the 95% ignorant scientists who make the fraudulent 1% look good. The 4% who care are too chicken to really do anything.

I don't know what I want most: An apology? An explanation? Honest words? The declaration of all acts of falsification and fabrication? Justice and punishment? Quite frankly, punishment is not high on my list, I'd rather have honest words – but if there is not some form of light being shed on this affair by the major actors, I will quite gladly settle on punishment instead. It's a pipe dream. There will be no honest words. No explanation. No shedding of light. And no punishment. Most certainly no justice.

When Shrinks Try To Define Illnesses And Treatments

How One Flawed Study Spawned a Decade of Lies

In 2001, Dr. Robert L. Spitzer, psychiatrist and professor emeritus of Columbia University, presented a paper at a meeting of the American Psychiatric Association about something called “reparative therapy” for gay men and women. By undergoing reparative therapy, the paper claimed, gay men and women could change their sexual orientation. Spitzer had interviewed 200 allegedly former-homosexual men and women that he claimed had shown varying degrees of such change; all of the participants provided Spitzer with self reports of their experience with the therapy.

Spitzer, now 79 years old, was no stranger to the controversy surrounding his chosen subject. Thirty years earlier, he had played a leading role in removing homosexuality from the list of mental disorders in the association’s diagnostic manual. Clearly, his interest in the topic was more than a passing academic curiosity – indeed, it wouldn’t be a stretch to say he seemed invested in demonstrating that homosexuality was changeable, not unlike quitting smoking or giving up ice cream.
…

Spitzer’s mission to clean the slate is commendable, but the effects of his work have been coursing through the homosexual community like acid since it made headlines a decade ago. His study was seized upon by anti-homosexual activists and therapists who held up Spitzer’s paper as proof that they could “cure” patients of their sexual orientation.

Spitzer didn’t invent reparative therapy, and he isn’t the only researcher to have conducted studies claiming that it works, but as an influential psychiatrist from a prestigious university, his words carried a lot of weight.

In his recantation of the study, he says that it contained at least two fatal flaws: the self reports from those he surveyed were not verifiable, and he didn’t include a control group of men and women who didn’t undergo the therapy for comparison. Self reports are notoriously unreliable, and though they are used in hundreds of studies every year, they are generally regarded as thin evidence at best. Lacking a control group is a fundamental no-no in social science research across the board. The conclusion is inescapable — Spitzer’s study was simply bad science.

What’s remarkable is that this classic example of bad science was approved for presentation at a conference of the leading psychiatric association, and was subsequently published in a peer-reviewed journal of the profession. …

This wasn’t just anyone claiming that the self reports were valid, it was one of the most highly regarded diagnostic assessment experts in the world.…

Is this the same APA which is defining illnesses and their cures in the DSM? And what could possibly go wrong when shrinks get to define illnesses and supposed cures?

Chris Kresser on Raw Dairy vs. Pasteurized Dairy

Chris Kresser asks in a three part series: Is Raw Milk Worth the Risk?

While this is certainly not rigorous evidence, it matches my own anecdotal experience and that of many of my patients, blog readers and radio show listeners.  I do not feel well when eat pasteurized dairy.  It gives me sinus congestion, headaches and intestinal discomfort.  Yet I thrive on raw dairy, and fermented raw dairy in particular played a substantial role in my own healing journey.

WPI back on track?

The WPI has published its new research program. From its website (highlights are mine):

[Whittemore Peterson Institute] Current Research Program
http://www.wpinstitute.org/research/research_basic.html
Friday March 25th 2012

1. Pathophysiology of chronic fatigue syndrome

This National Institutes of Health (NIH) funded study proposes to identify pathogens associated with chronic fatigue syndrome (CFS). Initially, this study relied upon microarray technology to detect viruses potentially associated with CFS. However, now, under the direction of Dr. Vincent Lombardi, this study will instead utilize unbiased next generation sequencing technology. This state-of-the-art method is not subject to the limitations of viral microarrays. Not only does this technology have the capacity to identify any viruses, it also has the ability to identify any pathogens, associated with CFS. Additionally, it will allow us to perform transcriptome analysis, which has the ability to identify differences in the immune system when compared to those who do not suffer from CFS. Therefore, all of the original specific aims of the grant will be addressed; however, transcriptome analysis may provide additional knowledge that could not be obtained using originally proposed methods. This study also proposes to investigate dysregulation in the interferon response associated with CFS.

[From the PDF]
New Strategies to Decipher the Pathophysiology of Chronic Fatigue Syndrome

The original Aims of the National Institutes of Health (NIH) RO1 grant were to identify both novel viral infections and genetic susceptibility factors in European and American cohorts of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) patients. The principal investigator (PI), Dr. Vincent Lombardi, will pursue these Aims using more advance technology in order to discover pathogens (known or unknown infectious agents) and their associated immune responses in ME/CFS.

The overall goal of this research project is to define viral and host parameters that correlate with distinct disease phenotypes in European and American cohorts of ME/CFS patients with diagnoses fulfilling the Center for Disease Control (CDC) definition and Canadian Consensus Criteria for ME/CFS. To do this, we will obtain blood samples from ME/CFS patients and healthy control subjects from specific medical practices, with the recent approval from the University of Nevada, Reno Biomedical Institutional Review Board (IRB). We will utilize next generation sequencing by synthesis (SBS) technology to detect novel virus mRNA and evaluate transcriptome differences between ME/CFS subjects and healthy control subjects. Any pathogen infection will be confirmed with a combination of quantitative PCR (QPCR) and culture methods. Additionally, we will evaluate serum chemokine and cytokine profiles using multiplex suspension antibody arrays on a Luminex platform. Finally, we will evaluate HLA and KIR genotypes and investigate possible defects in the type I interferon signaling pathway.

At the conclusion of this study, we anticipate identifying any pathogens uniquely associated with ME/CFS. We also anticipate identifying differences in the lymphocyte transcriptome as well as any differences in HLA, KIR and interferon immune parameters.

Some observations from this:

• They are still looking for "knowns and unknown" "pathogens uniquely associated with ME/CFS".
• They are switching from an microarray-assay to next generation sequencing (next generation "sequencing by synthesis – SBS").
• They are doing a transcriptome analysis
• They are still focusing for cytokine differences

Sure sounds partially promising.

The question is: Will this yield once again results that are not based in reality, unreproducible by anybody else? After all, Dr. Lombardi worked together with Dr. Mikovits on her seminal work, and he is quite firmly rooted in Woo-Land. We'll see.

2. Pathogen and biomarker discovery in Gulf War illness

This Department of Defense (DOD) sponsored project will utilize next generation sequencing technology in order to identify differentially transcribed genes associated with Gulf War illness (GWI). This information will be used to better understand the pathophysiology of GWI. Additionally, this information will be used to identify potential biomarkers for diagnostic purposes and evaluation of treatment progress.

From the PDF:
Pathogen and Biomarker Discovery in Gulf War Illness

The goal of this study is to identify potential biomarkers, including pathogens, associated with Gulf War illness (GWI), which in turn will afford physicians the necessary tools to make more accurate diagnoses. This study will be conducted under the direction of Dr. Vincent Lombardi as the principal investigator (PI).

GWI is a chronic multi-­‐symptom disorder affecting approximately one third of the veterans and civilians who served during the Persian Gulf War (Desert Storm 1990-­‐ 1991). It is a syndrome primarily described by a spectrum of symptoms, innate immune abnormalities and opportunistic infections. A wide range of acute and chronic physical symptoms are associated with GWI including fatigue, musculoskeletal pain, gastrointestinal dysfunction and cognitive problems. Unfortunately, diagnosis of GWI is difficult in that no discrete biomarkers or etiological agents have been identified. A greater understanding of the innate immune system and the associated opportunistic pathogens may provide insight into the pathophysiology of this disease.

In order to explore this issue, we will recruit subjects diagnosed with GWI who served during the Persian Gulf War, whether or not actually deployed to Iraq and surrounding areas, along with healthy control subjects, following approval of the University of Nevada, Reno Institutional Review Board (IRB). We will conduct lymphocyte transcriptome analysis of GWI subjects and compare the results to the same analysis of healthy control subjects. The transcriptome is reflective of the genes that are being actively expressed at any given time; therefore, the lymphocyte transcriptome represents a window into the innate immune system, potentially leading to an understanding of GWI pathogenesis. Transcriptome analysis also has the ability to identify any pathogens present in the immune cells, potentially identifying an etiological trigger.

We look forward to commencing this important study after obtaining IRB approval of the study protocol.


3. Cytokine dysregulation in chronic fatigue syndrome

Cytokine and chemokine dysregulation is one of the most consistently reported observations in individuals with ME/CFS; nevertheless, the mechanism of this dysregulation remains unknown. The acute onset and epidemiological patterns of ME/CFS etiopathology support the involvement of a pathogenic trigger. Consistent with this observation, is the fact that the innate immune system responds to infection by producing proinflammatory cytokines and chemokines. The microbial pattern recognition receptors, Toll-like receptors (TLRs) 3 and 4, are activated by pathogen-derived dsRNA and LPS, respectively, to produce these proinflammatory cytokines. This system is tightly regulated; however, in patients with ME/CFS, it is constitutively active. The focus of this research project is to better understand the mechanism of this dysregulation.


4. Biomarker discovery in neuro-immune and inflammatory diseases

Previously, we identified a cytokine/chemokine signature with high specificity and sensitivity in diagnosing ME/CFS patients. Our project will extend this signature to other inflammatory and neuro-immune diseases, providing physicians with necessary tools to delineate closely related neuro-immune and inflammatory diseases.

ME/CFS is a Women's Disease

Some people (mainly male doctors?) have the misogynistic perception that because ME/CFS affects more women than men, it must therefore be some form of female hysteria ("It's the vapors."). Well, I say bullshit to that. There are several autoimmune diseases that affect more women than men – a slight hint (not more, I'm afraid) that ME/CFS might share some disease mechanisms with autoimmune diseases:

Ratio of female/male incidence of autoimmune diseases:
Hashimoto's thyroiditis 10/1
Systemic lupus erythematosus (SLE) 9/1
Graves' disease 7/1
Rheumatoid arthritis 5/2
Multiple sclerosis (MS) 2/1
Myasthenia gravis 2/1

The 23andme blog this topic:

Why women are disproportionately affected by autoimmune disease is not fully known or understood, although the hypotheses are numerous. Some research suggests that estrogen may help antibody production and immune system response, but can also lead to an overly active immune system. Other research indicates that genes on the X chromosomes may play a role in these immune system mutinies, and women — who have two X chromosomes — may thus be at an increased risk over men who have only one X chromosome.

Still other research suggests that “fetal-maternal microchimerism” may be the root cause. In this strange-sounding phenomenon, a small number of the baby’s cells pass through the placenta into the mother and continue to live within the mother. The presence of these foreign fetal cells within the mother may result in an incorrect immune system response and autoimmune disease. More research, however, is needed to establish which of these hypotheses (if any) are correct.

Autoimmune diseases are serious medical concerns for women; indeed, when taken together, autoimmune diseases constitute one of the top ten causes of death among young and middle-aged women. The irony of these conditions is that the immune system, which should be a woman’s greatest ally in fighting disease, becomes her worst enemy. Why and how a body’s betrayal occurs needs to be better understood through further research.

Milk and Acne

In 2009, a systematic review of 21 observational studies and six clinical trials found clear links [between milk and acne]. Two large controlled trials found that cow’s milk increased both the number of people who got acne and its severity. Other large randomized prospective controlled trials (the gold standard of medical research) found that people who had higher sugar intake and a high glycemic load diet (more bread, rice, cereal, pasta, sugar, and flour products of all kinds) had significantly more acne. The good news is that chocolate (dark chocolate that is) didn’t seem to cause acne.
…

One scientist referred to milk as a “complex aqueous, suspended fat, liposomal, suspended protein emulsion”. What we do know is that milk is designed to grow things—namely, babies—and in the case of cow’s milk, calves. It is naturally full of what we call anabolic hormones (the same ones that body builders and A Rod use to grow big muscles, and which cause bad acne). These are mostly androgens (like testosterone) and growth hormones including insulin like growth factor 1 (IGF-1). There is no such thing as hormone-free milk.

Here’s a short list of the 60-some hormones in your average glass of milk—even the organic, raw, and bovine growth hormone free milk:

• 20α-dihydropregnenolone
• progesterone (from pregnenolone)
• 5α-pregnanedione
• 5α-pregnan-3β-ol-20-one, 20α- and 20β-dihydroprogesterone (from progesterone)
• 5α-androstene-3β17β-diol
• 5α-androstanedione
• 5α-androstan-3β-ol-17-one
• androstenedione
• testosterone
• dehydroepiandrosterone sulphate acyl ester
• insulin like growth factors 1 and 2 (IGF-1 and IGF-2)
• insulin

This is what our government suggests we drink in high doses—at least 3 glasses a day for me, a healthy adult male, according to the mypyramid.gov website.
…

The famous Nurse’s Health Study examining health habits of 47,000 nurses found that those who drank more milk as teenagers had much higher rates of severe acne than those who had little or no milk as teenagers. If you think it is the fat in milk, think again. It was actually the skim milk that had the strongest risk for acne. In other studies of over 10,000 boysand girlsfrom 9 to 15 years old, there was a direct link between the amount of milk consumed and the severity of acne.

It appears that it is not just the anabolic or sex hormones in milk that causes problem but milk’s ability to stimulate insulin production. It actually may be the lactose or milk sugar in milk that acts more like a soft drink than an egg. Drinking a glass of milk can spike insulin levels 300 percent. Not only does that cause pimples, but it also may contribute to prediabetes.

Yummy! Drink your Bovine Hormones! I wouldn't be the slightest bit surprised if milk did contribute to other diseases as well. And anabolic ("growth") hormones? Sounds like a cancer recipe to me.

Art Ayers on Milk

Art Ayers on Milk: Casein, Amyloid, Pasteurization, Homogenization

One of his comments:

Eating from the food pyramid or USDA plate will give you chronic diseases and make you a good patient.

Could not have said it better.

On "the truth"

Believe those who are seeking the truth. Doubt those who find it.
-- André Gide

"In Vitro Infidelium" on the WPI-RED-VIPdx-Connection and Conflict of Interest

"In Vitro Infidelium" on the WPI-RED-VIPdx-Connection and Conflict of Interest.

This looks like a rats-nest to me.

Do Breastfeed!

Longer duration of breastfeeding has also been shown to significantly improve a child’s immune response to infectious disease. Writing in the British Medical Journal, Kåre Mølbak and colleagues at the University of Copenhagen analyzed the incidence of diarrhea in weaned and partially breastfed children in the West African Republic of Guinea-Bissau. They determined that not only did breastfed children get sick less often than weaned children, but those who continued partial breastfeeding up until the age of three had the lowest rate of infection.

Too late for me, I guess, but might still be helpful to others.

"Now psychologists are trying to fix their field."

How awfully nice of them.

Sleep Apnea

NHLBI on: What Is Sleep Apnea?

Obviously, one big difference in the case presented above is tiredness in sleep apnea versus fatigue in ME/CFS.

What's interesting is that he thought he might have depressions.

The other interesting thing he said was: "Now that I am feeling better [with treatment] I am coming home from work with energy still."

I guess the presentation of cases is a continuum (especially considering the different types of apnea and the unknown causes of apnea) and that therefore some bona fide apnea cases may be misdiagnosed as ME/CFS.

I think sleep apnea is one of the many other conditions that need to be considered as differential diagnosis to ME/CFS. As sleep apnea more often affects men and ME/CFS more often affects women, this should be taken into consideration when trying to make a differential diagnosis.

Orac on Homeopathy and Clinical Trials

Orac on Homeopathy and Clinical Trials:

So ridiculous is homeopathy that I sometimes feel that I and my fellow skeptics are firing Howitzers at an ant when we take so much time and effort to explain why homeopathy is nonsense. On the other hand, it is homeopathy's monumental lack of scientific plausibility that makes it a perfect teaching tool to explain the difference between science-based medicine (SBM) and evidence-based medicine (EBM). Specifically, because clinical trials have unavoidable shortcomings and biases, even at a p=0.05, which would imply only approximately a 5% chance that a given trial's apparently positive results could be due to random chance alone. As John Ioannidis has taught us, in clinical trials as practiced in the real world, the chance is much higher that any given positive trial is a false positive. It also means that, the lower the prior plausibility of a remedy working, the higher the chance of false positive trials. This is exactly what we see in homeopathy, hence the panoply of homeopathy trials showing "positive" results in which the treatment group is barely different from the control and/or the results barely reach statistical significance. With something like homeopathy, which violates the laws of so many sciences, it is relatively easy to make the case that it takes a lot more than a few equivocal clinical trials to show that so much well-established science is wrong. Apparently positive clinical trials of homeopathy are measuring, in essence, the noise inherent in doing clinical trials.

Interview with Ian Lipkin

An interview with Ian Lipkin in the Disco-Mag:

… LCMV, a cause of meningitis in humans, shuts down the ability of the pituitary gland to make growth hormone. The virus doesn’t kill the cell, 
but it suppresses transcription and translation of genes, so the organism as a whole suffers but the individual cell looks OK. My contribution was showing that there were specific effects on neurotransmitters linked to the behavioral manifestations of the 
disease. This became a model for understanding how persistent viral infections affect the central nervous system. …

Haven't read it all yet. Some of the interview questions are a bit "woo", and Ian Lipkin comes off as a bit woo too – but I guess this comes with having an open mind and even Newton studied Alchemy. It is definitely interesting to see were he comes from, what he learned about different diseases and how he learned to see them.

Cytotoxic lymphocyte microRNAs as prospective biomarkers for CFS/ME

Cytotoxic lymphocyte microRNAs as prospective biomarkers for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis.
Brenu EW, Ashton KJ, van Driel M, Staines DR, Peterson D, Atkinson GM, Marshall-Gradisnik SM.

Faculty of Health Science and Medicine, Bond University, Australia.

Abstract

BACKGROUND:
Immune dysfunction associated with a disease often has a molecular basis.

A novel group of molecules known as microRNAs (miRNAs) have been associated with suppression of translational processes involved in cellular development and proliferation, protein secretion, apoptosis, immune function and inflammatory processes.

MicroRNAs may be implicated in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME), where immune function is impaired.

The objective of this study was to determine the association between miRNAs in cytotoxic cells and CFS/ME.

METHODS:
Natural Killer (NK) and CD8(+)T cells were preferentially isolated from peripheral blood mononuclear cells from all participants (CFS/ME, n=28; mean age=41.8±9.6years and controls, n=28; mean age=45.3±11.7years), via negative cell enrichment.

Following total RNA extraction and subsequent synthesis of cDNA, reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression levels of nineteen miRNAs.

RESULTS:
There was a significant reduction in the expression levels of miR-21, in both the NK and CD8(+)T cells in the CFS/ME sufferers.

Additionally, the expression of miR-17-5p, miR-10a, miR-103, miR-152, miR-146a, miR-106, miR-223 and miR-191 was significantly decreased in NK cells of CFS/ME patients in comparison to the non-fatigued controls.

LIMITATIONS:
The results from these investigations are not yet transferable into the clinical setting, further validatory studies are now required.

CONCLUSIONS:
Collectively these miRNAs have been associated with apoptosis, cell cycle, development and immune function.

Changes in miRNAs in cytotoxic cells may reduce the functional capacity of these cells and disrupt effective cytotoxic activity along with other immune functions in CFS/ME patients.

Via CO-CURE

Orac on the Placebo Effect

Orac on the placebo effect:

Placebo responses only "work" for subjective symptoms. They don't "cure" anything. At best, placebo responses are due to a change in perception of subjective symptoms that leads to their bothering the patient less. Even so, they're variable and unreliable, not something that a doctor would want to hang his hat on when he needs to relieve a patient's symptoms. At worst, placebo effects do not exist. Rather, they're due to artifacts in clinical trials, confirmation biases, and observer effects.

Lactose Intolerance was once considered "psychosomatic"

Recognition of the extent and genetic basis of lactose intolerance is relatively recent. Though its symptoms were described as early as Hippocrates (460-370 B.C.), until the 1960s the prevailing assumption in the medical community was that tolerance was the norm and intolerance either the result of milk allergy, an intestinal pathogen, or else was psychosomatic (it being recognised that some cultures did not practice dairying, and people from those cultures often reacted badly to consuming milk).

The "Psychosomatic" explanation of illness reminds me of the God of the Gaps theological perspective. The medical community must root the psychosomatic school of thought from their ranks, or they make themselves accomplices to this unscientific abuse of patients which is committed by these psycho-babble-quacks.

My Acne is caused by Milk and Dairy

I can now say, with rather high confidence, that my acne was caused by the consumption of (cow-)milk. I used to drink a lot of milk – and had a lot of acne. One and a half years ago I massively reduced my consumption of milk and milk-products, and my acne almost went away. I ceased to eat dairy and my acne went completely away. I reintroduced dairy, and my acne came back, pimples within 6 to 12 hours. It does not rise to the level to be considered proof, but for me, in my case, it is pretty clear.

Over the next months I will try Ghee ("clarified butter", which is almost free of both cow proteins and lactose, and contains almost only fatty acids) to see if this still contributes to my acne or not.

Toni Bernhard on ME/CFS

If Chronic Fatigue Syndrome is, indeed, several discrete illnesses, until they are isolated from each other and studied individually, little progress will be made in finding effective treatments or cures.
…

Because those of us with a CFS diagnosis are lumped into one group, when we read about CFS-diagnosed person being cured by a treatment, we rush out and spend hundreds, sometimes thousands of dollars on it, only to be terribly let down and possibly further harmed. Since writing How to Be Sick, I’ve lost count of the number of cures that well-intentioned people have suggested to me. But there’s no reason to believe that these cures would be effective for my particular constellation of symptoms.

If Chronic Fatigue Syndrome is several discrete illnesses, it makes sense that some people will be helped by a particular treatment, while others will not. It’s finally dawned on me that it doesn’t make sense to spend money on a treatment just because it helped or cured another person, when the two of us are unlikely to even have the same illness.

Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis

Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis
Ekua W Brenu, Mieke L van Driel, Donald R Staines, Kevin J Ashton, Sharni L Hardcastle, James Keane, Lotti Tajouri, Daniel Peterson, Sandra B Ramos and Sonya M Marshall-Gradisnik

Journal of Translational Medicine 2012, 10:88 doi:10.1186/1479-5876-10-88
Published: 9 May 2012

Abstract

Background
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is an etiologically unexplained disorder characterised by irregularities in various aspects of the immunological function.

Presently, it is unknown whether these immunological changes remain consistent over time.

This study investigates Natural Killer (NK) cell cytotoxic activity, NK cell subsets (CD56brightCD16- and CD56dimCD16+) and cytokines, over the course of a12 month period in patients with CFS/ME.


Methods
The participants in the study comprised 65 (47.2+/-11.5 years) CFS/ME participants and 21 (45.2 +/-9.3 years) non-fatigued controls.

Flow cytometry protocols were used to assess NK subsets and NK cytotoxic activity at various time points that included baseline (T1), 6 (T2) and 12 months (T3).

Cytokine secretions were measured following mitogenic stimulation of peripheral blood mononuclear cells.


Results
NK cytotoxic activity was significantly decreased in the CFS/ME patients at T1, T2 and T3 compared to the non-fatigued group.

Additionally, in comparison to the non-fatigued controls, the CFS/ME group had significantly lower numbers of CD56brightCD16- NK cells at both T1 and T2.

Interestingly, following mitogenic stimulation, cytokine secretion revealed significant increases in IL-10, IFN-gamma and TNF-alpha at T1 in the CFS/ME group.

A significant decrease was observed at T2 in the CFS/ME group for IL-10 and IL-17A while at T3, IL-2 was increased in the CFS/ME group in comparison to the non- fatigued controls.

Overall cytotoxic activity was significantly decreased at T3 compared to T1 and T2.

CD56brightCD16- NK cells were much lower at T2 compared to the T1 and T3.

IL-10 and IL-17A secretion was elevated at T2 in comparison to the T1 and T3.


Conclusion
These results confirm decreases in immune function in CFS/ME patients, suggesting an increased susceptibility to viral and other infections.

Furthermore NK cytotoxic activity may be a suitable biomarker for diagnosing CFS/ME as it was consistently decreased during the course of the 12 months study.

Now that at least looks like a proper longitudinal study with the participation of Dan Peterseon – unlike the cytokine BS from Mikovits/WPI. How close this study is to the reality of ME/CFS and how useful it will prove for research, diagnosis and treatment of ME/CFS is another question…

Dietary Villains

Forget saturated fat, forget dietary cholesterol – the two (possibly worst) dietary villains are trans fatty acids (from partially hydrogenated vegetable oils) and omega-6 fatty acids (from vegetable oils):

Hydrogenated oils have been shown to cause what is commonly termed the "double deadly effect", raising the level of LDLs and decreasing the level of HDLs in the blood, increasing the risk of blood clotting inside blood vessels.

A high consumption of omega-6 polyunsaturated fatty acids (PUFAs), which are found in most types of vegetable oil (e.g. soybean oil, corn oil – the most consumed in USA, sunflower oil, etc.) may increase the likelihood that postmenopausal women will develop breast cancer. A similar effect was observed on prostate cancer in mice.

More on the negative health effects of an over-consumption of omega-6 fatty acids (mainly from vegetable oil) can be found in the work of Bill Lands.

On Cereal Grains, Dairy and Milk

Some speculative predications:

1. Gluten is not the only agent in cereal grains that causes disease or health problems.
2. Celiac disease is not the only disease or health problem caused by the consumption of cereal grain products.
3. Lactose is not the only agent in (pasteurized cow) milk and dairy that causes disease and health problems.
4. Lactose intolerance in not the only disease or health problem caused by the consumption of dairy.
5. The diseases and health problems caused by both cereal grain and dairy do not necessarily manifest with gastrointestinal symptoms.

Digging for Dirt in Nevada

More interesting dirt from WPI/VIPdx/UNEVX:

Further email exchanges confirmed that “…XMRV testing is for both the culture and the serology tests…” and that “…ALL of the tests we run are validated and inspected by the State of Nevada,”

I asked to see the “validation data”, requested details about “the State of Nevada” and reiterated my question about why a “clinically validated” test (or tests) was withdrawn.

VIPdx replied that “The State does not “hold” this information. It is a proprietary record of the laboratory. They inspect but do not keep our records. Our validation records and test protocols are proprietary intellectual property of the laboratory.”

This is interesting too:

During the ensuing correspondence, and contrary to VIPdx’s statement to me, it emerged that “Vincent Lombardi is not the laboratory director, nor has he served in that regulatory capacity” and “they took this off their website today, it is incorrect.”

[The regulatory Laboratory Director (i.e. the person who represents the lab for regulatory purposes) was/is Sanford Barsky who, in February 2012, CFS Chronicles found to be accused of scientific fraud.
http://www.cfschronicles.com/1/post/2012/02/vote-of-no-confidence.html]

While I am pleased to see them digging up dirt on the WPI, it saddens me to at the same time that they ignore the contributions of our fine researcher and heroine at large Dr. Judy Mikovits. Just to reiterate:

January 22, 2009, Santa Barbara XMRV Seminar by Whittemore Peterson Research Director Dr. Judy Mikovits

Dr. Mikovits:
…
So you can be infected with retroviruses and be carriers and not be sick. And that’s one reason to be tested. If there is a genetic susceptibility, which we’re looking to, maybe a reason, an immune defect that was unknown as to why some people get sick and others don’t. You certainly want to know where the virus is, so if you’re a carrier you can protect your family.

Question:
Do you know how many have tested with VIP-Dx, and how many are positive?

Dr. Mikovits:
I don’t work with the company. They only take samples two days a week because it takes three days to do that, so they’ve done hundreds of samples in the last couple of months, and at least half of them are positive. Or 40 percent. And again, their doctors are looking at, the doctors who are well versed with CFS, so they’re immediately sending off. Dr. Cheney, Dr. Klimas, a doctor in Canada, Ellie Stein, maybe even Susan Levine in New York. I’m not sure, because it’s illegal for me to know those data because there’s confidentiality between the patient and the physician. But quite a number and, yes, it’s there.

…

Annette Whittemore: Earlier you said that 40% were positive [by VIP Dx]. So describe the fact that if you’re positive, you’re positive. But if you’re negative, you’re not necessarily so?

Dr. Mikovits: Yes, that’s correct. I answered that question based on the samples that came through there. Everyone who is positive is definitely positive for having the virus. But we don’t know what the people are, what the doctor is sending in, so the people might not have that disease. So it could be a clearly, distinguishing delineating marker – biomarker – or diagnostic at that point for various diseases. So a doctor might see a spectrum and say “I don’t know, maybe I’d better check.” Because the earlier you catch it, just like cancer. Early detection. Make sure the reservoir is (inaudible), make sure you don’t have that virus multiplying, and you can live a normal life. Don’t let it get (inaudible). You know the commercial out right now is “HIV doesn’t have to equal AIDS”; well XMRV doesn’t have to equal disease. If we keep it down, we keep the immune system strong.

Question: So what you’re saying is you may test negative but not be negative?

Dr. Mikovits: That’s correct. If you do it by the PCR. If you do it by VIP-Dx, at least right now, it’s running along the lines of (inaudible). We’ve got the antibody, and we’ve got three of the four tests. We’ll license it to anyone. We’re a non-profit institute, so everybody pays the same royalty, so any diagnostic company could do the gold standard. But right now, if you test negative, you’re not necessarily negative, even at VIP-Dx. Because we want to go do that serology test. Maybe we can’t find evidence of the virus. But you’ve been exposed, which would be a good thing because your levels are theoretically low, and you’ve just now made the antibodies, so you can prevent disease, as we did with Magic Johnson. But we don’t know anything about the immune response to the virus.

And this email from Dr. Judy Mikovits:

Email from Dr. Judy Mikovits on XMRV and ME
Posted by Birgitte on 14/03/2010
http://www.me-nyheter.info/?p=1191
(copy here: http://esme-eu.com/news/email-fra-dr-judy-mikovits-ang-xmrv-og-me-article304-7.html )

Dr. Judy Mikovits writes:
Regarding the ramifications of being XMRV negative. First of all the current diagnostic testing will define with essentially 100% accuracy XMRV infected patients. The negatives are more difficult as there are additional tests that can only be done in the research lab at this time and not in a clinical setting such as VIPDx. The most important test is to check your blood for an antibody to the virus. If you are positive in the serology test and have an antibody to the virus, you have evidence of infection but at the time your blood was drawn the amount of virus in your blood was below the limit that could be detected by the most sensitive test currently available clinically, which is the the one done at VIPDx. that means while you tested XMRV negative..it could be a false negative. …
…
But by definition if you have ME you must have XMRV. [????]
…
We will test everyone that tested negative to see if we can find antibodies in your blood and look for that variant that we describe..that is evidence of XMRV infection. …