Monday, December 31, 2012

Judy Mikovits: Unemployed and Bankrupt

And here I was thinking that Karma does not exist… – silly me.

So if we are lucky Dr. Mikovits will no longer be able to take advantage of a vulnerable patient population – one can dream.

Pity however that Lombardi and Ruscetti don't have the same luck as Saint Judy.

Komaroff and his Ampligen Vote

Anthony Komaroff voted against the FDA approval of Ampligen. Now there is some huffing and puffing in the ME/CFS blogosphere about this (which I will not dignify with a link): Some are writing that he is removed from the ME/CFS patient population (and that could as well be from Mars, not from Earth). Some paint him as a sort of underhanded malicious villain (and presumably bought by someone).

Personally, I think this is utterly stupid.

There is an article posted on "Medscape Medical News" (via) that sheds some little light on Komaroffs decision:
Anthony Komaroff, MD, Simcox/Clifford/Higby Professor of Medicine at Harvard Medical School, Boston, Massachusetts, voted no on both efficacy and safety. "As a physician who has cared for many of these patients for nearly a quarter of a century, nothing would please me more than solid evidence of an effective therapy, but I think there are enough questions about the conduct of the studies that it does not meet the standard of adequate evidence."
Even if I don't know the details behind his decision, I think his explanation is reasonable. It is reasonable to vote agains a drug, if one thinks that there are questions about the conduct of the drug studies. And my impression is that Anthony Komaroff never says or does anything without having the facts to back him up. If he says the FDA should not approve Ampligen, we should better listen.

And just because there is no currently approved drug for ME/CFS, that does not mean we should accept badly done drug studies.

What if Ampligen does not work as we hope? What if its efficiency or safety are actually worse than what the patient anecdotes suggest? In that case an approval could do us some serious harm. Directly, by harming patients who receive the drug and by costing money needed for proper research. And indirectly because "we" lobbied for an ineffective and/or dangerous drug. This would play right into the hands of the psychobabblers.

And what is really awful, that we see like in 2010 with the XMRV-fraud the same stupid behavior by "patient advocates" and "patient activists", who treat critics like villains. Case in point in 2010 was John Coffin who (rightfully) criticized Mikovits, who said nothing but the truth (and that in a very polite and unassuming manner), and who in turn was portrayed by "patient advocates" and "patient activists" as if he were the baby-eating-anti-christ himself.

And now it seems that Komaroff is the target of this misguided anger.

So, let me tell all those stupid "patient advocates" and stupid "patient activists" out there:
It is you, who are malicious. By ignoring valid criticism. By ignoring the valid reasons behind the criticism. By ascribing malicious motives to critics, motives that only exist in your head.

With friend like these "patient advocates" and these "patient activists", we don't need enemies.

Sunday, December 30, 2012

The Great Chronic Lyme Mirage

I found some interesting comments by Phillip J. Baker (who seems to be associated with the American Lyme Disease Foundation) underneath an otherwise not recommendable article & discussion (or rather an article & discussion which can only be recommendable as a negative example for the display of confirmation biases and cognitive dissonances).

Especially this comment by Phillip J. Baker struck a chord with me:
Believe what you will, Phyllis, but you are wrong. Ceftiofur and ceftriaxone are chemically different in structure. Embers et al. have provided no assurances in their work that they have similar PK and PD properties, let alone the same MIC. It is incumbent upon them to provide such data, as well as to show that therapeutic regimen used was adequate to clear the huge inoculum that was used to produce a disseminated infection. Obviously, their experimental design did not mimic the Klempner study, which is what Mario was initially funded to do. Why he chose to use ceftiofur is for him to explain, not me. As I said before, ceftiofur has not been approved by the FDA for use in humans and there are no published data showing that it is effective for treating borreliosis in animals, let alone humans. There is one report showing that it is not effective for treating borreliosis in ponies.

Phillip J. Baker
on February 24, 2012 at 1:52 pm
He goes on to notice in another comment:
I must say that I find it strange that the term ceftriaxone is used throughout the Embers et al. paper, and it is only in the first paragraph on page 9 that it is first mentioned that ceftiofur was actually used. I find that very strange indeed.
So to claim that Lyme is still active despite anti-biotics, Embers et al. have to pull these two tricks:
  1. Use a "huge inoculum" to intruduce an amount of pathogens not encountered in the wild, causing an "massive disseminated infection" not encountered in the wild.
  2. Use an antibiotic that (most likely) is not effective in clearing the pathogen (let alone in this massive disseminated infection) – and hide that as good as you can.
What Phillip J. Baker describes are the tactics of quacks.

No wonder anybody with at least a couple of working brain cells left*, who looks into the matter comes to the conclusion that "Chronic Lyme" is a BS quack diagnosis.

And just for the record: I do think that these patients have an organic disease, which severely affects their lives – however there is no evidence** that this disease is Lyme. There are many many diseases that can cripple your live, and possibly some of which are yet of unknown.

* As to so called "Lyme Literate Medical Doctors" ("LLMD"):
They do not seem to have any working brain cells left. My (purely anecdotal and not evidence based) advise is to stay away from medical doctors who have no working brain cells. LLMD? Just say no. Choose a doctor instead with working brain cells, this is usually better for your health.

** As to any non-standard tests used to detect "Chronic Lyme": I can offer you an even more reliable Lyme test! I will match any price, just give me a call!

Saturday, December 29, 2012

WTF? Beef and Somnolence?

The things you learn with an elimination diet, and then re-challenging with that food. My somnolence seems to have been caused by beef. Hmm.

I need more data to confirm or refute that. Hmpf.

Thursday, December 27, 2012

Google Trends: Paleo vs. Weight Watchers

"Fad diet" my ass.

Ok, I cherry picked. Here's what it looks like with correct search terms:

Still, it's a nice upwards trend for Paleo, without the seasonal BS for Weight Watchers.

Needed Nutritional Intervention Studies

I was thinking that we need some nutritional studies with regards to pathogenic effects of evolutionary novel foods, and whether a evolutionary "correct" diet (aka "the" Paleolithic Diet or "Paleo" for short) can alleviate health problems.

Patients should receive nutritional intervention in the form of counseling and be assigned to one of two groups:
  • The control group should receive counseling based on the consensus view on optimal nutrition. As the "gold standard" with regards to nutrition seem to be the advise from the U.S. Department of Agriculture(!) (USDA), from the American Heart Association (AHA) and from the American Diabetes Association (ADA), the control group should receive counseling based on their advise.
  • The treatment group ("Paleo") should receive counseling based on the avoidance of foods containing evolutionary novel ingredients (more or less an "Elimination Diet" based on evolutionary plausibilty):
    1. Avoidance of cereal grains and soy
    2. Avoidance of dairy
    3. Avoidance of seed oils
    Pre-intervention levels of those four ingredients should be recorded. Calorie-countring should not be recommended, macro-nutritient ratios should not be prescribed, the diet should neither be low-carb, nor low-fat, nor low-meat – so the health effects of these four evolutionary novel food ingredients can be investigated. However, some minimum recommendations of what foods to primarily eat should be made.
Diseases should include the "Diseases of Affluence", but not be limited to them:
  • Obesity (doh!)
  • Type 2 Diabetes
  • Asthma
  • Hypertension
  • Gout
  • Acne*, Dermatitis, Psoriasis, etc.
  • Allergies (Hay Fever and the like)
  • Cardiovascular Diseases
  • Depression
  • Anxiety
  • Other neurological/psychological/mental/etc. health problems (e.g. Bipolar Disorder)
  • Multiple Sclerosis (MS), cf. Terry Wahls
  • ME/CFS
A pilot study for each disease should include at least 10 patients from that chosen disease.

The dietary advise should be followed for 3 months, possibly with an extension to 6 and 12 months.

Objective markers for each disease (e.g. weight for obesity) should be recorded as the primary disease makers by the investigators before the study, at 1 month, and after that at each 3-month-point. Surrogate markers should be recorded in addition, but not for the primary measurement of outcomes.

Patients should have a simple food and symptom diary. If possible, the patient should be encouraged to record disease makers, both objective (e.g. daily activity level with an odometer, daily weight) and subjective (e.g. perceived fatigue).

After a patient stops a diet (either at the end of study, or patient drops out), she/he should be (if possible) followed for another month with regards the aforementioned disease markers and symptoms.

If positive health effects from an Paleo Diet are found for one disease, follow-up studies could be further refined with an focus on individual components (e.g. only dairy, or dairy from pasteurized* milk).

There is a lot do and many pitfalls to avoid before such studies would get off the ground…

* As I traced my acne back to dairy from pasteurized milk (and to a lesser extent to eggs), studies finding an positive effect of avoidance of dairy could further look into the difference between raw-milk dairy and pasteurized-milk dairy.

Sunday, December 23, 2012

Carl Zimmer on The Evolution of Cavities

Carl Zimmer on The Evolution of Cavities:
… The Streptococcus mutans the scientists found in people’s mouths shared 1490 genes in common–a core genome, as it’s known. These shared genes varied from mouth to mouth, Stanhope found, with minor mutations sprinkled among them. It’s possible to tally up these mutations and use them to reconstruct some of the history of their ancestors. Stanhope and his colleagues found that Streptococcus mutans underwent a population explosion. And that explosion started ten thousand years ago.

It may well be no coincidence that this was also when our ancestors began to farm. Those early farmers shifted to diets dominated by corn and other grains–which turned the human mouth into an endless banquet of carbohydrates.

Stanhope and his colleagues were also able to pinpoint some of the genes that were important forStreptococcus mutans’s adaptation to civilization. Fourteen genes, for example, show signs of having experienced strong natural selection. Some of those evolved genes are essential for breaking down sugar. Others help the bacteria survive in the acidic conditions that arise in the mouth when we eat starches.

So Streptococcus likes our farming. Hmm.

Friday, December 21, 2012

Another Nail In The Coffin for the "Calories In = Calories Out" Theory

Dr. Briffa:

In this study, sedentary overweight and obese adults were randomised to one of three exercise groups for a period of 8 months.
  1. aerobic exercise (treadmill, cross trainer machine, stationary bicycle) for a total of 12 miles a week at 65-80 per cent maximal intensity.
  2. resistance training on 3 days per week designed to burn the same number of calories as the aerobic exercise of group 1.
  3. both aerobic exercise and resistance training combined (group 1 exercise plus group 2 exercise)
The results revealed that both groups 1 and 3 lost weight and fat, and group 3 lost no more weight and fat than group 3 (despite doing twice as much exercise). Group 2 did not lose weight. All this led the authors to conclude that aerobic exercise is superior for weight loss. But what I (and perhaps other people) really want to know is just how effective the aerobic exercise was in terms of weight loss.

It turns out that individuals in group 1 lost a total of 1.66 kg (about 3.5 lbs) of fat. Remember, though, this is over an 8-month period, so the pounds were not exactly dropping off. Now, let’s factor in the amount of exercise the amount of exercise required to achieve this weight loss result…

Individuals exercised for a total of about 2 hours a week which means that the total amount of exercise over the study period came to about 70 hours. For each hour of exercise individuals lost about 1 ounce (or about 30 grams) in weight.

Monday, December 17, 2012

Post-Mono can look like CFS

CFIDS in 2009: Post-Mono CFS in Teen Girls

Ben Z. Katz, M.D., of Northwestern University has just published results from a study of teens who were followed for two years after the onset of acute infection with Epstein-Barr virus (mononucleosis). The article is published in the July 2009 issue of Pediatrics. Criteria for CFS were met by 13 percent of adolescents at 6 months after acute infection. Seven percent remained ill at 12 months, and 4 percent met CFS criteria at 24 months. With time, most adolescents recovered. Only 2 adolescents with CFS at 24 months seemed to have recovered or had an explanation for CFS at 12 months, but then were reclassified as having CFS at 24 months.

All 13 adolescents who had CFS 24 months after onset of mononucleosis were girls. Compared with those who did not have CFS at 24 months, they reported greater fatigue severity at 12 months. Corticosteroid treatment during the acute phase of mononucleosis was not associated with an increased risk for the development of CFS.

This study was funded by NIH and its principal investigator is Renee Taylor, PhD, at University of Illinois-Chicago. Dr. Katz and Dr. Taylor are also collaborating with Association-funded researcher Gordon Broderick, PhD, who is studying the same patient group to understand differences between those who recovered from mono and those who remained ill at various time points. Read more about the Association's study at

An article about the study was circulated by Reuters and can be read at

Medscape News also reported on the publication at You can also find continuing education courses about CFS on Medscape to share with your healthcare professional, including the one sponsored by the CFIDS Association of America that has attracted more than 243,000 page views since it went live in October 2008. The CFS course is located at

Journal citation: “Chronic fatigue syndrome after infectious mononucleosis in adolescents.” Katz BZ, Shiraishi Y, Mears CJ, Binns HJ, Taylor R. Department of Pediatrics, Division of Infectious Diseases, Northwestern University Feinberg School of Medicine and Children's Memorial Hospital, Chicago, Illinois 60614, USA. Pediatrics. 2009 Jul;124(1):189-93.

CFS Facts – ME/CFS Misdiagnosis on a grand scale?

I found a interesting blog on ME/CFS, a blog which I haven't stumbled up before: "CFS Facts"

[Update] I have seen the blog before, but I discarded it for the amount of BS, mainly the lickspittle Mikovits-friendly content… [/Update]

This is from their latest blog-post:
Misdiagnosis on a grand scale?

Our editorial in the most recent Breakthrough magazine (Autumn 2012) seems to have stuck a chord, so the text is now available on our website

The key point – that many people referred from primary care with a diagnosis of ME/CFS are found to have another, treatable condition when assessed at a specialist clinic – might not surprise patients themselves, since many have already questioned their own diagnosis and/or have had difficulties with the "patient-GP encounter" (for the patient view see and for the GP view ). Yet, the accumulating evidence of misdiagnosis on such a scale should be astonishing to healthcare professionals, and ought to greatly concern the NHS as an institution. Something is far wrong, and it needs to be fixed.

* * *
I've said the same thing. Some doctors will never diagnose CFS, no matter what; they'll call it depression even when there are symptoms reported that aren't seen in depression. Other doctors will diagnose CFS in any patient who's tired, regardless of the reason.

Dr. Bell has noted that fully half of people initially diagnosed with hypochondria are eventually diagnosed with something very real that matches the symptoms they complained of all along.

Trust the patient!

The Transition from Abiotic Chemistry to Cellular Life

Slowly step by step science is finding out how life got started. This paper about the metabolism of early organisms caught my eye, especially that bit.
The earliest form of carbon fixation identified by scientists achieved a special kind of built-in robustness -- not seen in modern cells -- by layering multiple carbon-fixing mechanisms. This redundancy allowed early life to compensate for a lack of refined control over its internal chemistry, and formed a template for the later splits that created the earliest major branches in the tree of life.
So I take it, basically these early organisms had two metabolic pathways – let's call them "1" and "2". Pathway 1 took precursor molecule A and converted it (with the help of energy) into something useful for the organism – and pathway 2 did that the same with precursor molecule B. Now, as the "refined control" was missing in that early stage of life, the organism had to take what was available. Precursor molecule A is available? Use pathway 1! Precursor molecule B is available? Use pathway 2!

Sunday, December 16, 2012

Primates with Phytoestrogens: Aggressive and Anxious

“With all of the concern today about phytoestrogen intake by humans through soy products, it is very useful to find out more about the exposure to such compounds in living primates and, by analogy, human ancestors,” said study co-author Katharine Milton, professor in UC Berkeley’s Department of Environmental Science, Policy and Management and an expert on the dietary ecology of primates. …

Effects of phytoestrogen consumption in other studies have included more aggression, less body contact, more isolation, higher anxiety and impaired reproduction.
Seriously, avoid soy.

ME/CFS – The Good, The Bad and The To Be Determined

If you follow the usual blogs about ME/CFS, you will come up repeatedly with the same "players" in the field of ME/CFS. So I thought it is a good idea to compile a list with my opinions on several of those people, as a reference.

Whenever there is reason for a differential appraisal (both "good" things and "bad" things to mention) I will try to do so (Sarah Myhill being a nice case in point).

As always, this is
a) my personal opinion – YMMV
b) work in progress, so I will revise and amend it over time.

Therefore take it with some grains of salt.

And if you feel there is an error somewhere (or that some important information is missing), feel free to write a short comment!

(And BTW, the sorting within each list is alphabetical, by first name)

And, oh, TBD stands for "To Be Determined". These are basically points where I need to know more, before I can make a call (one way or the other).

"The Solid"
- because I think the following people are trustworthy (and helpful) most of the time:
NameWhat's GoodWhat's Not So GoodTBD
Alan Light
Kathleen Light
University of Utah
1. Solid research with exercise challenges and gene expression. [1] [2]

2. Alan Light has a genuine passion to research pain and fatigue.
Christopher Snell
University of the Pacific
1. Solid research with exercise challenges [1]--
David Bell
Retired Pediatrician
1. 12 and 25 year follow-up studies in the Lyndonville cohort [1](In hindsight)
Should have been more critical of XMRV
Julia Newton
Newcastle University
1. Proper differential diagnosis for ME/CFS patients [1]

2. Research into POTS

"The OKish"
- because I haven't seen those people commit any major blunders.
NameWhat's GoodWhat's Not So GoodWhat's TBD
Anthony KomaroffOnly makes claims he can back up with facts.

Makes it clear when he is talking about speculation.
His research into the brain's involvement in ME/CFS may be very excellent. But what is its practical (diagnostic? therapeutic?) application 
Daniel PetersonHis involvment in Simmaron Research is a definitive plus for all ME/CFS patientsHis initial involvement in XMRV was not so good
(though he was anything but the driving force)
His involvement in Ampligen
Lucinda BatemanContributes to good research with her ME/CFS patient cohortCould have more critical distance to the psychosomatic school [1]Does a "by the book" symptomatic treatment addressing all individual symptoms.
Nancy KlimasContributes to good research with her ME/CFS patient cohortHer work involving NK-cells (natural killer cells)

"The (may or may not be) OKish"
- because I think I have reason to be cautious
NameWhat's GoodWhat's Not So GoodWhat's TBD
John Chia
Jose MontoyaHis focus on Herpes-Viruses.His focus on Herpes-Viruses.His focus on Herpes-Viruses.
Martin Lerner
Robert SuhadolnikHis research into "2-5A synthetase/RNase L" pathways seems to have lead nowhere with regards to ME/CFS.

"Those who have the appearance of quacks"
- and I do not trust a word from them without checking it thrice:
NameWhat's GoodWhat's BadWhat's TBD
Jacob TeitelbaumAddressing sleep problemsSeems to lack basic medical understanding  in some areas [1]-
Jamie Deckoff-JonesNothing I'm aware of1. IMHO she is an example of 100% pure and unadulterated woo.

2. Disciple of Mikovits
Judy MikovitsNothing.1. Was the lead in what looks like intentional contamination to fabricate/falsify study results in Lombard 2009

2. She loves to tell stories – that have little or no relation to reality – to impress CFS-patients
Kenny MeirleirNothing I'm aware of1. Was involved in the XMRV disaster [1]

2. Peddles (highly dubious) urine tests [1]

3. Claims that close to 80% of his patients reported “complete clinical recovery” after Ampligen treatment [1]
Martin Pall-1. Toxins, Nitrostress and somesuch woo are supposedly everything one needs to know

2. Proponent of all kind of woo like "electromagnetic field (EMF) hypersensitivity (EHS)"
Doubtful that any of his research will stand up to scrutiny (But then again: Whenever there is any doubt, there is no doubt.)
Michael MaesSome of his therapeutical interventions weakly resemble an "Paleo Diet"1. Most of his research is "all over the place".

2. Has written a paper together with Gerwyn/V99.
Doubtful that any of his research will stand up to scrutiny (But then again: Whenever there is any doubt, there is no doubt.)
Paul CheneyNothing I'm aware ofEverything he says seems suspect to me.-
Sarah Myhill1. "Caveman Diet" / "Stone Age Diet" (properly known as "Paleo Diet")

2. Stopping the usage of counterproductive medication
95% of her "CFS Book" (see PDF) scores high on the QDC (with the noted execptions left and right).1. Vitamin B12. Maybe.

2. Her research (with collaborators) into mitochondrial problems may or may not be based in reality – hard to tell
Simon Wessely
(and his fanclub)
Nothing I'm aware of1. Peddler of idealistic BS [1]

2. One of the main proponent of the psycho-pathologization of ME/CFS patients, tries to establish psychological treatment as the sole treatment for all ME/CFS patients

3. Libels the entire ME/CFS patient community

Saturday, December 15, 2012

The Social Function of Psychology

Dan Dennett - The Evolution of Confusion

In his talk "The Evolution of Confusion", Dan Dennett asks an import question: What is the function of of theology? And his answer is basically: To explain the unexplainable, mainly to the priests, to get rid of nagging questions.

Now, one can ask the same about psychology, what is its function? Well, nominally it is the "Science of the Psyche", the study of the human mind, how it works, why it is the way it is, and if it doesn't work as it could*, then to ask what are the pathological changes and its causes, and to investigate what could be done to alleviate those problems. And as such, it is a legitimate field of science, and a legitimate field of medicine. Especially evolutionary psychology is producing some very interesting scientific results IMHO (cf. "The Robot's Rebellion", Keith E. Stanovich).

However, there are some problems with the science in psychology: Considerable stuff in psychology is still pre-scientific claims, idealistic BS, unscrutinized common sense (because "everybody knows that!"), unrefuted faulty science, confirmation biases of the researchers and many ad-hoc just-so stories with unverifiable and unfalsifiable narratives.

And that leads me to one of the main problems with psychology, one of the social functions of psychology (and a scientifically, medically and humanistically quite undesirable function at that): Psychology produces narratives, for general practitioners and for the public. Narratives, that seemingly explain medical and social problems that seem to be otherwise unexplainable:

" … because, you see, that person is mentally not well … "

And such a verdict, spoken with scientific authority, ends any discussion of other factors. It shuts down any questions whether the perceived mental illness might actually be something else, whether it really is all "just in the mind" of the person. And if it is an illness that objectively manifests itself with mental symptoms, it stops most inquiry into non-psychological factors. If there are other factors, factors that should be considered as the actual cause, the psychological narrative is very effective in closing down these avenues of inquiry.

How convenient, for those confronted with the seemingly "mental ill", if they can come up with a simple answer – and not have to tackle more complex problems that reality throws at them. The patient is the problem, case closed, next patient please. And the psychologist delivers a seemingly scientific rationale why a doctor should not devote his resources to an seemingly "unhelpable" case.** And if the patient lacks insight (and possibly rightfully so) into his mental illness, this becomes a self-fulfilling prophecy.***

Now I wrote above "psychology seemingly explains" because in my view in many areas it simply plays into "common knowledge" and does not actually explain anything in a social, medical, biologic and evolutionary context. And I write "problems that seem to be otherwise unexplainable", because if one takes time and a critical approach, I am convinced one will find in many cases other explanations, more plausible explanations (albeit more complex explanations, in most cases), for many things that are seemingly explained by psychology.


* Defining how the psyche should work, or what "normal" behaviour is, that is already very difficult – In whose interest should we define how the psyche should work: The individual's interests? The society's interest? The interests of psychologists? Or some self selected upholders of moral standards? And if we define disease as pathologic ill function in the environment of evolutionary selection (because a fish out of water is not diseased), that raises the question in the face of changes in our social environment: What is normal function in a substantially changed environment anyway?

** During our evolutionary past, this might have been an advantage for the group. Help those that need little help, and can be easily and fast helped ("acute" conditions that pass) – abandon those that you can't help ("chronic" conditions). Such a behavior today would rightfully branded as "social darwinism" – our evolutionary past has left its mark on our behavior, I'm afraid.

*** And anyway, if certain social conditions don't make you angry and mad, there is something wrong with you. Plenty of examples to go around, so feel free to pick one that makes you angry and mad.

Tuesday, December 11, 2012

More SNAFU – Coconut Milk gives me The Runs

So I tried out coconut milk (over some time now), and every time I ate it, I got "The Runs" (aka diarrhea).

Don't know what causes this (and don't particularly care at the moment), but according to the information I have, per 100 gram coconut (except coconut oil) there are several grams of "Pentosans" and "Hexosans", which are pentose/hexose-sugar-polymers (aka carbohydrates) and AFAIK can be classified as "fibers". And in addition coconuts contains a couple of of hundred milligrams of "poly uronic acids" per 100 gram.

Both pentosans/hexosans and poly uronic acids, so I would speculate, have the potential to interfere with the normal state of gastro-internal affairs – but nothing concrete is known, I'm afraid.

So more SNAFU, and one more food that I know does not agree with me… Oh well.

A pity, as it makes cooking more varied. But then again I never was a big fan of coconuts…

Eggs – The Other Cause Of Acne?

While I am pretty certain that my acne was caused by dairy (from pasteurized milk), I had some small acne flares from time to time despite not eating any dairy – now I think I narrowed the other cause of acne down to eggs.

And it would make sense, as both milk and eggs contain immunoglobulins. And both pasteurized milk and eggs are heat treated.

One small observation (which I need to confirm yet) is that the acne from eggs is slightly different:
  • Eggs seem to cause mainly pustules ("pimples") with round white purulent material, and mainly at what seems to be follicles (e.g. at the arms)
  • Dairy from pasteurized milk on the other hand seems to cause mainly inflamed papules/nodules at what seems to be (sweat? sebaceous?) glands (e.g. around the nose)
But same as with acne from milk, it is a "winner takes it all" situtation, with two to three spots and the rest of the skin looking fine.

Situation Normal, All Fucked Up – I guess.

Sunday, December 9, 2012

The need for a Electronic Lab Notebook

Some of the problems in medical research could have been avoided had we had a proper electronic trail for any inquiry into possible misconduct.

From the top of my head, there are a few things a electronic paper trail should include (possibly more):

  • Material received, put to storage, removed from storage, transferred, shipped, etc.
  • Experiments performed, for what project/study, with what materials, in what lab, with which equipment, by whom and with what results (e.g. Western Blots, EM images, Antibody titers, Gene Sequences and so on)
  • Results received from third parties
  • Patient/Control samples should be coded ("blinded") by default
  • The person who does patient/control sample coding
  • The time of code-breaking for each sample
  • Any corrections to the record (with before/after record)
Of course everything must be recorded with a time-stamp. And all materials (reagents, patient samples, and so on) must have a machine readable label.

The entire electronic paper trail should be kept at the lab and updates be send regularly (Weekly? Or better daily?) to a central storage (e.g. NIH).

Access to the study-relevant electronic paper trail at the central storage (including records from third parties) should be made available at the time of submission for peer-review to the editors/reviewers.

Parts (at least) of the electronic paper trail relevant to the published paper should be made available as supporting online material.

In case of a formal inquiry the entire electronic record of the lab (and third parties) for the time under inquest should be available to the inquiry board.

John Maddox and "Self-"Correcting Science

There is one nice angle about John Maddox and his "courage to stand up science": In the mid- to end-eighties he launched an "investigation" into the Gallo/Montagnier/HIV disaster. When Gallo told Maddox things that shed serious doubt on Gallo's version of events, Maddox choose not to publish his findings.

While John Maddox choose not to pursue any leads he had, Abraham Karpas continued to turn up unpleasant facts about Gallo's research. And he would write them to Nature (I guess to "correct science"), where Maddox resided. And what courage did Maddox have? Karpas described it as "writing for Nature's wastebasket".  His research into Gallo's research ended up being published in the New Scientist and Scientific American, but not in Nature.
(John Crewdson, "Science Fictions", page 340)

So much for Maddox's "courage to stand up for science".

And so much for science being "self-correcting". It seems to me that personal biases and the mechanisms of the academic institutions strongly obstruct any corrections.

This whole "self-correcting science" meme seems like something told to little children, so they stop asking annoying questions.

(In Crewdson's book at the beginning of chapter 17 there is a nice side story involving Margot O'Toole turning up troubling "inconstancies" in the work of David Baltimore, after being a postdoc on one of his studies. His answer? Not to worry, these problems don't matter and the scientific process was "self-correcting" anyway – so she should let the matter rest.)

Saturday, December 8, 2012

Gallo a Quack?

Well, who knew that? It seems like Gallo was quite a quack. In 1990 he claimed to have a cure for Kaposi's Sarcoma, when all he had was some experiments with mice (Crewdson, page 354-355).

Any other scientist doing such a thing would qualify as quack, so should we make an excuse for him?

Friday, December 7, 2012

The dog ate my shipment of LAV

"We never got any LAV."

"Oh, on second thought, we had LAV, but we couldn't get it to grow."

"We had 48 isolates of HTLV-3B, long before we heard of LAV, or got any samples."

"And when we handled LAV, it was never in the same lab as our HTLV-3B."

"Oh, HTLV-3B might be similar to LAV, but that's because the patient was in France!"

"The contamination happened at Pasteur's lab, not ours! So Pasteur must have contaminated their LAV with the stuff we send them."

"What we send Pasteur, and when? I think it might have been that we send them our HTLV-3B long after we received LAV, actually."

"Our 48 isolates? That might have been 48 frozen blood samples, not isolates – isn't that the same?"

"Oh, come to think of it, LAV might have contaminated our HTLV-3B pool. But it doesn't make a difference, we discovered HTLV-3B first. And HTLV-3B is something different than LAV."

Any similarities to how Ruscetti/Mikovits played their XMRV saga ("The contamination happened at Silverman's lab, not ours!") are purely coincidental.

(By the way, this was my 500th published post…)

John Maddox and having the courage to stand up for science

More from John Crewdson's "Science Fictions" book, chapter 12:

John Maddox could have singlehandedly sunk most of Robert Gallo's claims regarding his work in 1982/1983, had Maddox published in Nature the interview he had with Gallo on September 19, 1986.

But John Maddox choose not to publish the interview, later stating that:
I think that it literally is impossible to tell who's right and who's wrong.
That is John Maddox, standing up for science.

And from the "can't make this shit up" department:

The tapes of the Maddox/Gallo interview, that were kindly provided to John Crewdson, contained "a gap of several minutes during which the conversation is obliterated by music".


The Augean Stables of NCI Frederick

In response to the latest John Maddox prize for scientific BS, I have picked up John Crewdson's book "Science Fictions" again, as John Maddox has some involvement of the lost years of HIV. And boy, I can't help to notice that NCI Frederick resembled – to my eyes – already back than in the Nineteen-Eighties an Augean Cesspool.

(Some of it is burried in the copious notes at the end of the book – which I have inexcusably ignored – e.g. page 579 about the sacking of George Todaro after he refused to "fall in line" with regards to the BS the HHS put up to defend Gallo against the legitimate claims by the Institute Pasteur.)

Tuesday, December 4, 2012

Some more speculation on ME/CFS

  • Efforts to finger the family of Enteroviruses as the causative agent in a large sub-group seem to have gone nowhere (e.g. Chia, or the British in the Eighties)
  • Efforts to finger the family of Herpesviruses as the causative agent in a large sub-group seem to have gone nowhere (e.g. Montoya)
  • Efforts to finger Retroviruses as the causative agent in a large sub-group turned out to be a large fraud
  • Cytokine studies seem to have gone nowhere to identify large sub-groups
  • Lot's of things can be misdiagnosed as ME/CFS (e.g. Newton et. al 2010)
  • Many pathogens can cause Post-Viral-Fatigue, that may or may not be the same thing as ME/CFS (among others Hickie et. al 2006)
At the moment I would say:
  • The ME/CFS patients are not suffering all from the same disease
  • ME/CFS is an umbrella term for many different diseases. 
  • Localized outbreaks (localized both in time and in space) are most likely caused by one distinct causative agent.
  • The agent in one outbreak is most likely different from the agent in another outbreak.
  • There is not one single causative agent that is shared by a majority of people with ME/CFS.
  • The ME/CFS patient population is heterogenous. 
Therefore I would say:
Any research that works under the assumption of a homogenous ME/CFS patient population will fail.
Symptoms alone are probably not specific enough to delineate sub-groups*, objective measurable data (e.g. exercise challenge ala Snell, gene expression ala Light, RNA deep sequencing ala Lipkin, orthostatic measurements, and so on) is needed to delineate sub-group.

The question that remains: How do patients divided up into sub-groups? Are there a few disease entities that make up a majority of ME/CFS cases? (Of which I am no so sure any more) Or are there many many sub-groups, with a highly fractioned "landscape" with many many diseases hiding under the label ME/CFS?

I think certain properties (non-refreshing sleep, VO2max exercise intolerance) can be shared by different disease entities. And even the neurological symptoms may be a (common) result of different pathological processes.

* Possibly with the exception of the POTS/Ad2A sub-group, which has the potential to be a single disease entity in its own right.

Monday, December 3, 2012

A list of well-meaning people

"A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it."
Thomas Kuhn on paradigm shifts, using a quote from Max Planck
In that spirit: may these well-meaning people – who are unfortunately unable to see the light – continue to live a long life, during which they shall be rightfully ignored by patients, by society and by the scientific community alike, until they die of old age.
  • Professor Michael Sharpe, University of Oxford
  • Professor Peter White, Queen Mary University of London
  • Dr Esther Crawley, Reader in Child Health, University of Bristol
  • Professor Stephen Holgate CBE, MRC Clinical Professor of
    Immunopharmacology, University of Southampton
  • Professor Rona Moss-Morris, Head of Health Psychology, King's College London
  • Dr Charlotte Feinmann, Reader, UCL
  • Professor Hugo Critchley, Chair in Psychiatry, Brighton and Sussex
    Medical School
  • Dr Brian Angus, Reader in Infectious Diseases, Nuffield Department of
    Medicine, University of Oxford
  • Dr Steven Reid, Clinical Director for Psychological Medicine, Central
    and North West London NHS Foundation Trust
  • Professor Patrick Doherty, Professor of Rehabilitation, York St John University
  • Professor Paul Little, Professor of Primary Care Research, University
    of Southampton
  • Dr Maurice Murphy, HIV Consultant, Barts Health NHS Trust
  • Professor Tim Peto, Consultant in Infectious Diseases and General
  • Medicine, Nuffield Department of Medicine, University of Oxford
  • Professor Sir Mansel Aylward, Chair, Public Health Wales, Cardiff University
  • Dr Alastair Miller, Consultant Physician, Royal Liverpool University Hospital
  • Professor Diane Cox, Professor of Occupational Therapy, University of Cumbria
  • Professor Jonathan Sterne, Professor of Medical Statistics and
    Epidemiology, University of Bristol
  • Dr Margaret May, Reader in Medical Statistics, University of Bristol
  • Professor George Davey-Smith, Professor of Clinical Epidemiology,
    University of Bristol
  • Dr Jade Thai, Senior Research Fellow, University of Bristol
  • Dr Gabrielle Murphy, Clinical Lead Physician, Fatigue Service, Royal
    Free London NHS Foundation Trust
  • Dr Hazel O'Dowd, Consultant Clinical Psychologist and CFS/ME Team
    Leader, Frenchay Hospital Bristol
  • Dr Brian Marien, Director, Positive Health
  • Professor Willie Hamilton, Professor of Primary Care Diagnostics,
    University of Exeter
  • Dr Selwyn Richards, Consultant Rheumatologist, Poole Hospital NHS Trust
  • Professor Alison Wearden, Professor of Health Psychology, University
    of Manchester
  • Professor Trudie Chalder, Department of Psychological Medicine, King's
    College London.
And last, but not least, I wish the same to Professor Simon Wessely.

And please, don't harass these fine scientists or their respected institutions, don't write to them, don't talk to them, don't listen to them, do not give them a platform to spread their insidious ideas and do not set foot in their institutions – refraining from these activities will be the best for all involved.

Like a Snowflake in the Summer Sun

Darwinian paradigm is the bedrock on which all biological sciences are now based, and no psychological explanation can hope to survive if it is incompatible with it.
-- Stevens and Price (2000)
Something the Wessely school will never be able to explain: What evolutionary advantage would it offer if an important system – as the perception of fatigue undoubtedly is – what advantage would it offer if such an system breaks (and not to mention why it should break at the level of the psyche, as doubtlessly no psyche as we have in the humans is involved in the sensing of fatigue in other animals).

Sunday, December 2, 2012

Understanding Simon Wessely and his Paternalistic Counter-Enlightenment

Attention conservation notice: I will try to outline my impressions of what Simon Wessely's position on ME/CFS is – in order to understand the reason why his (and his peer's) practice is so insidious.

(Apologies for the amount of Wessely related content lately, but it seems that if there is nothing else ME/CFS-related to write about, one can always find a ME/CFS-quack to take apart.)

First to illustrate his position, some quotes from Simon Wessely's and Sharpe's work "Chronic Fatigue and Neurasthenia: A Review" (courtesy of a comment by ErnRoberts on the "noodlemaz" blog):
Our hypothesis is that fatigue syndromes are universal, but that culture is important in understanding the transition from symptoms to disability.

Where there is considerable concern around concepts such as immune dysfunction, viral persistence, and environmental toxicity (irrespective of the true prevalence of all of these factors), there may be a greater likelihood of symptom persistence and severe disability. …
Poor outcome in CFS is predicted by longer illness duration, more severe symptoms, older age, depression, and lack of social support, and also by a strong belief in physical causes.

Severely disabled patients attending specialist clinics have a particularly poor prognosis
… a reduction in the belief that activity is damaging is associated with recovery during rehabilitative therapy, suggesting that it may be a critical psychological target for effective rehabilitation …

“Patients’ beliefs about their illness and associated coping behaviour will be influenced by the information received from others.

A striking social aspect of CFS is the high level of activity of patient support and advocacy organizations, mainly over the Internet.

Studies from the United Kingdom have reported that patients who are members of a support group have a poorer outcome, despite similar illness duration and disability, and a poorer response to rehabilitation.

It is unknown whether this reflects self-selection into such groups or the effect of the group on patients’ beliefs, coping, and willingness to engage in rehabilitation.

Other factors include the experience of repeated questioning of the legitimacy of one’s illness by doctors and others, which probably serves to drive some patients to join advocacy organizations.

Perhaps unsurprisingly, in fibromyalgia, the acquisition of a disability pension is also associated with a worse prognosis. … 
Whatever the biological aspects of CFS, cognitive-behavioural models assume that the symptoms and disability are perpetuated, at least in part, by psychological, behavioural, and social factors.

Biological factors are assumed [Hear, hear! A true scientist who tries to falsify his theories!] to be either only partially responsible for the illness or largely reversible.
So I take it that Wessely believes that people with ME/CFS have a "false" believe that they have a bodily disease, and a "false" perception of "normal" bodily sensations. Furthermore he believes it is this "false" believe that is the only thing wrong* (which can be shown to be wrong).

Now, it seems his believe is that this "false illness perception" is what actually cause patients to stay ill – the worse the "perception", the worse the prognosis of getting better.** (Here Simon Wessely seems to have the made classic correlation/causation error, and putting the cart before the horse – why he can't do simple 2-day exercise challenges, à la Dr. Snell, which would falsify his theory, that can remain anybody's guess.)

Alas, it is not mainly this wrong premise about "false illness believes" that is primarily insidious, but the paternalistic practice that follows from this.
There is some controversy about whether giving patients a diagnosis of CFS is helpful or harmful.

There are those who feel that a diagnosis enables patients to both conceptualize their illness and communicate about it with others.

Others are concerned about the potentially harmful effect of a diagnosis, arguing that it medicalizes and pathologizes symptoms in a way that can exacerbate social and occupational disability.
The Management [sic] Plan

This should be explained [sic] to the patients as following from the formulation, focusing on illness perpetuating factors and consisting of elements aiming to

(a) relieve symptoms such as depression, pain, and sleep disturbance with agents such as antidepressants,

(b) assist the patients efforts at coping by stabilizing activity and retraining the body to function effectively (graded exercise, CBT), and

(c) assist the patients in managing the social and financial aspects of their illness and where possible remaining in or returning to employment (problem solving)
Patients seen in specialist settings in Western cultures with the label of CFS or its equivalents are often resistant to psychological labels and/or explanations.***
Simon Wessely does not seem to believe that an patient of his is accessible to rational dialogue, he even deems it harmful. Someone with a humanistic and enlightened perspective would talk to a patient, try to explain the disease model and get what I would call "rational buy-in" – instead, it seems Simon Wessely believes that ME/CFS patients need to be sucker-punched into a (disguised) mental illness diagnosis and a therapy they are not meant to understand (and could not give their informed consent to, obviously).

I feel that Simon Wessely believes it is wrong, wrong, wrong to tell the patient the truth – that must be the reason why there is such a disconnect between what says to the unwashed masses when he speaks to the public (and therefore to "his" patients) and what he tells to his peers.

The "Management [sic] Plan" seems to be one big fat lie, as the targets that are stated towards the patient ("relieve symptoms … with antidepressants", "assist … at coping" and "assist in managing the social and financial aspects of their illness") differ substantially from the "false illness believes" that are the root cause according to Simon Wessely.

And obviously selling a therapy to which people can not give informed consent – by the very rationale of the therapy – is usually something that does not jibe well with the medical authorities (or at least I assume so in any modern post-feudal nation). One more reason why Simon Wessely does good (at least good in his interest) to keep his intentions muddy and unclear to outsiders, and his practices effectively hidden from scrutiny.

Simon Wessely, an truly idealistic paragon of the Counter-Enlightenment – quick, someone make him a Baron or something for his fight against the unwashed masses!


* As to his claim that
“The bulk of evidence indicates that there are no proven pathologic or biochemical abnormalities of muscle or muscle metabolism, either at rest or with exercise, other than those associated with deconditioning”.
I refer you to the following lectures: Christopher Snell 2012, Alan Light 2011 and Alan Light 2007, all of which show pathological changes in a majority of tested ME/CFS patients during an exercise challenge – changes that can not be explained by false illness believes, deconditioning or sedentary behavior. But apparently a properly designed exercise challenge is rocket surgery and beyond the reach of even our very talented Simon Wessely.

** Especially the statements that "severely disabled patients attending specialist clinics have a particularly poor prognosis" and that "the acquisition of a disability pension is also associated with a worse prognosis" are truly awful statements, laying blame on specialists taking patients seriously and the approval of the disability pension. Anybody who has tried (in any country) to apply for such a pension knows that one is put under quite some scrutiny, and one has to be quite diseased to be approved (the very few fraudulent cases non-withstanding) – that those that passed such scrutiny have worse prognosis is apparently an unexpected surprise for Simon Wessely and prove in his cart-before-the-horse-world that the approval does the harm.

*** Could it just be, that patients might have good reason to reject the psycho-pathologization by Simon Wessely and his peers? And maybe even have rational cause to be angry at being psycho-pathologized in the face of a bodily disease (cf. Snell and Light)? I would even go so far and argue that if the practice of Simon Wessely does not make you angry, that you might be a bit lacking in your thinking department. What a perverted world, where those who praise Simon Wessely are seen as mature and intelligent.

Saturday, December 1, 2012

Dude, where is my vocabulary?

Just a short observation:

One thing I have noticed how utterly inadequate my vocabulary is, when I try to describe my daily problems to any of the doctors I have seen so far.

Now I may lack training the fine art of being a patient, but what I notice is that my doctors did not display much expertise in inquiring about these kinds of symptoms. Yeah, I have "unrefreshing sleep". Yeah, when I finally get up in the morning my muscles "ache" and feel "stiff". Yeah I feel "fatigued" even before I do something. Yeah, I have "a bit" of "short breath" when I actually do physical activity.

I tried once to convey to a doctor the impact these problems have on my life. Doctors don't like alarmism, I had to learn. Only people with visible disease signs are allowed to state that they are severely impacted by disease, it seemed to me.

Since then, I try to be dry and factual, but lacking a nuanced vocabulary, I get the feeling my doctors don't receive the message I have to transmit. And that they don't ask questions to get the nuances that are missing – e.g. "How strong is the shortness of breath?" or "How unrefreshing is your sleep?" – and don't offer anything in the way of nuanced vocabulary is a bad sign.

I guess one could talk about pain for hours – dull pain, diffuse pain, focal pain, burning pain, just a little pain, feeling like being crushed – but for symptoms related to fatigue? No such luck.

This is a problem that needs to be addressed.

Getting insulin sensitive when you don't want it

Peter over at Hyperlipid has a go at why consumption of seed oil (with a high linoleic acid content, aka omega 6 PUFA) is a stupid idea – excellently written, as always.

Protons: Physiological insulin resistance:
… Under full starvation a rat lives off of its fat. If linoleic acid is what is being released from the adipocytes under fasting conditions it provides significantly less FADH2 relative to NADH in to the electron transport chain of all fat burning cells than the mix of fatty acids from the adipocytes of lard fed rats. ie there is less physiological insulin resistance. This failure means you fail to keep glucose levels normal during starvation. Let's rub that in: Failure to develop physiological insulin resistance during starvation results in hypoglycaemia and hunger.

Exactly the same will happen in any soy oil fed USA citizen. The end result will still be the failure to develop the essential physiological insulin resistance which is needed to keep blood glucose normal during fasting.

When the average soy oil fattened American is asleep they HAVE to, finally, stop snacking on carbohydrate crap, which is the only way they can maintain a decent blood glucose level. At this time blood glucose falls, simply because their muscles stay insulin sensitive and glucose falls in to them. The brain will not accept hypoglycaemia. Some time, in the middle of the night, there has to be a Refrigerator Raid.

And, OMG, they eat calories! And calories count! Did I ever mention gluttony? Or, perhaps, is the Refrigerator Raid simple physiology?

The 22h daily fasted rats have a locked refrigerator. However hungry they feel due to hypoglycaemia, they are not getting any extra food. But why is there extra weight loss under starvation? Insulin was tricky to measure from a rat in the 1970s, but I know that the safflower loaded then starved rats had the lowest insulin as they are both insulin sensitive and hypoglycaemic. Low insulin = more lipolysis = more ketones and more weight loss. Logical.

Now let's go a step further. Blood glucose is low. It's low because the F:N ratio of linoleic acid is low and that's what is being released from adipocytes. This is metabolism. Individual cell by individual cell, it's a metabolic phenomenon. Picked up by the brain as hypoglycaemia. …

Protons: Physiological insulin resistance addendum:
… The whole point of a ketogenic diet (epilepsy excepted) is to induce starvation-appropriate physiological insulin resistance. What is the point of setting up a ketogenic diet which does not have the ability to convert from running on glucose to running on fat? …


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