Thursday, January 31, 2013

ME/CFS? Don't spend money on tests.

I just recently read about a ME/CFS patient being robbed 2500 (!) British Pounds by one of our resident ME/CFS quacks. The patient went to Belgium for a short visit, and got one blood drawing for 2500 GBPs.

Oh my, oh my, oh my.

This is not how a proper differential diagnosis is done. A differential diagnosis rather follows a "rinse and repeat" pattern:
  1. First, the doctor needs to get an overview of symptoms.
  2. The she/he needs to consider the symptoms and think about what it might be, or might not be.
  3. The doctor should then have list of a few diseases that could be it.
  4. On that basis it may make sense to order one or the other test – it makes most definitely no sense to order tests for thousands of Dollars/Euros/Pounds
  5. Taking into account the test-results and the symptoms, the doctor gets a preliminary diagnosis, based on which treatment can be chosen.
  6. If there are signs that the diagnosis is not the correct one, some (or all) of the steps above need to be repeated.
A diagnosis based on a short consult and expensive tests is not worth the paper on which it is printed! Every symptom could be important.

I for an example did not put enough value into my skin symptoms. Turns out the aphthous ulcers I had (together with other skin symptoms) are a key sign for Behçet's – and there is no blood test (or otherwise) for Behçet's. The only thing a doctor can do is carefully make note of all the symptoms, and knowing to look up the diagnosis of Behçet's.

Blood tests alone are a waste of money, especially if a doctor orders lots of them.

If you have ME/CFS, don't spend large amounts of money on tests – you need the money, I'm certain.

If your doctor wants to extract $$$$$ from you for diagnosis, tests or treatments: Change your doctor. Even if he claims that the tests or the treatments are a bargain. Especially if he wants thousands of bucks from you for tests and claims it is a bargain. And especially if he does the tests in an lab that is closely associated with her/him.

My advise: If a doctor sees you as a walking ATM, then change this doctor, because she/he is bad for you and your health.

There are some tests that might be called for, e.g. tests for hypothyroidism, BUT THE WORTHWHILE TESTS ARE PAID FOR BY THE INSURANCE. There are some test that might be "interesting" (like the NK-cell function test), but they do nothing to help you get "more legit" as a patient, or to choose a better therapy.

And just because someone is "Anti-CBT" or "Anti-GET", that does not mean he knows what he does.

Wednesday, January 30, 2013

Sugar and Seed Oil

A speculative prediction, from the "So I can tell you 'Told Ya!'" department: Sugar is pathogenic only in the presence of Seed Oils ("Vegetable Oils").

Monday, January 28, 2013

Rituximab for Behçet's

While I think that (pasterized) milk, dairy and eggs are causing Behçet's, it is interesting to see that Rituximab seems to be helping Behçet's patients.
Rituximab in intractable ocular lesions of Behcet's disease; randomized single-blind control study (pilot study).

Davatchi F, Shams H, Rezaipoor M, Sadeghi-Abdollahi B, Shahram F, Nadji A, Chams-Davatchi C, Akhlaghi M, Faezi T, Naderi N.

Behcet's Unit, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

Ocular lesions, the main morbidity of Behcet's disease (BD), are the most difficult to treat. The aim of this study was to evaluate the efficacy of rituximab.

Inclusion criteria were retinal vasculitis and edema, resistant to cytotoxic drugs. Twenty patients were randomized to a rituximab group (RG) or cytotoxic combination therapy group (CCTG). Rituximab was given in two 1000-mg courses (15-day interval). Subjects received methotrexate (15 mg/weekly) with prednisolone (0.5 mg/kg per day). The CCTG received pulse cyclophosphamide (1000 mg/monthly), azathioprine (2-3 mg/kg per day) and prednisolone (0.5 mg/kg per day). The primary endpoint was the overall state of patients' eyes and the Total Adjusted Disease Activity Index (TADAI). Secondary endpoints were: visual acuity (VA), posterior uveitis (PU), and retinal vasculitis (RV). The baseline data were compared at 6 months by paired sample t-test and analysis of variance.

TADAI improved significantly in the RG (t = 3.340, P = 0.009), but not in the CCTG (t = 2.241, P = 0.052). For secondary endpoints (RG/CCTG), the mean VA improved in two patients versus three (2/3), remained unchanged in 1/1, and worsened in 7/6 patients. The mean PU improved significantly in the RG (t = 3.943, P = 0.001), not in the CCTG (t = 2.371, P = 0.028). RV improved, but not statistically (t = 2.027, P = 0.057 vs. t = 1.045, P = 0.31). Edema of retina, disc and macula improved significantly in both, but much better for the RG (t = 2.781, P = 0.012 vs. t = 2.707, P = 0.014).

Rituximab was efficient in severe ocular manifestations of BD, TADAI improved significantly after 6 months with rituximab, but not with CCT.
And one more study:
Treatment of retinal vasculitis in Behçet's disease with rituximab.

Sadreddini S, Noshad H, Molaeefard M, Noshad R.

Tabriz University of Medical Sciences, Golgasht St., Tabriz, Iran.


Behçet's disease (BD) is more common in eastern than western countries. Physicians have frequently encountered problems in its treatment, especially eye involvement. Recurrent oral and genital aphthous ulcerations are the hallmarks of Behçet's disease but other organs can be involved and ocular disease is one of the most disabling manifestations. Up to now, there are some problems in treatment of the retinal vasculitis due to Behçet's disease. We reported one patient, with visual loss due to retinal vasculitis that was resistant to prednisolone and azathioprine. Our patient was treated successfully with rituximab and his remission was sustained for 24 months of follow-up. Rituximab is a chimeric monoclonal antibody that acts against the specific B cell antigen, CD20. The recent success of rituximab in autoimmune diseases, which is considered to be T cell-mediated, indicates that B cells must have a much broader role in the pathogenesis of autoimmune diseases than generally appreciated.
Behçet's is a rare disease, so very few studies are being done.

However, if you have disease that might be helped by Rituximab, my (slightly educated) guess is to try consume no milk, no dairy and no eggs for at least 4 weeks to see if it helps – it's worth a shot.

Sunday, January 27, 2013

Type 1 Diabetes – Dairy and Gluten to blame?

Environmental agents and type 1 diabetes

The most investigated dietary component associated with type 1 diabetes is cow-milk protein. Exposure to cow milk in early life (e.g. because of lack of breast feeding) has been linked with type 1 diabetes in humans and diabetes-prone BB rats. However, there is inconsistency in the studies, perhaps due to the variable composition of milk, with genetic variation in cow proteins. The findings are also consistent with the existence of a subset of milk-sensitive diabetes-prone individuals. Immune tolerance to insulin might also be compromised by early exposure to cow milk, which contains much less insulin than does human milk.

Wheat gluten is a potent diabetogen in BioBreeding (BB) rats and NOD mice, animal models of type 1 diabetes. Between 5% and 10% of type 1 diabetic patients have gluten-sensitive enteropathy (coeliac disease) and many more have antibodies to transglutaminase, a circulating marker of coeliac disease. Wheat may therefore be involved in the pathogenesis of type 1 diabetes, possibly inducing subclinical gut inflammation.
Or how about this:
An abrupt change in the incidence of type 1 diabetes after the migration of Polynesians to New Zealand was suggested most likely to result from the early introduction of dairy products into the infant diet, accompanied by an earlier weaning in New Zealand (Elliott 1992). A positive correlation has been reported between per capita consumption of unfermented milk proteins in populations worldwide (Scott 1990) or fluid cow milk consumption in children aged 0 to 14 years and incidence of type 1 diabetes (Dahl-Jørgensen et al 1991, Fava et al 1994). In addition, countries with the lowest prevalence of breast feeding at 3 months of age had the highest incidence of the disease (Scott 1990).

A putative role for cow's milk in the pathogenesis of Behçet's

Humoral and cell mediated immune response to cow's milk proteins in Behçet's disease.
Ann Rheum Dis. 2002 May;61(5):459-62.

Triolo G, Accardo-Palumbo A, Dieli F, Ciccia F, Ferrante A, Giardina E, Licata G.

Dipartimento Biomedico di Medicina Interna e Specialistica (Section of Rheumatology and Clinical Immunology), Policlinico Universitario, Palermo, Italy

To investigate the humoral and cellular immune response against cow's milk proteins in Behçet's disease and to distinguish any behaviour during active or inactive disease.

Peripheral blood mononuclear cells from 16 patients and from eight normal controls were cultured in the presence of phytohaemagglutinin (PHA), beta-casein, beta-lactoglobulin, or chicken egg albumin. Interferon gamma (IFNgamma) and interleukin 4 (IL4) were measured in the culture supernatants by enzyme linked immunosorbent assay (ELISA). Serum samples from 46 patients with Behçet's disease and from 37 healthy subjects were also studied for antibody detection. Antibodies to beta-casein, beta-lactoglobulin, and chicken egg albumin were determined by ELISA.

High IFNgamma but not IL4 levels were found in the supernatants of lymphocytes from patients with active disease cultured in the presence of cow's milk proteins. Levels were comparable with those obtained in cultures stimulated with PHA. A significantly higher level of anti-beta-casein and anti-beta-lactoglobulin IgG and IgA antibodies was found in patients with active Behçet's disease. No relation was found between their occurrence and the age of the patients, the duration of disease, or the presence of gastrointestinal abnormalities. Antibodies to chicken albumin were detected at low levels and with a prevalence similar to that of healthy subjects.

The results indicate that an active immune response occurs in Behçet's disease. This response involves an increased frequency of antibodies to cow's milk protein and a strong Th1 polarisation after exposure to these antigens. The occurrence of these abnormalities supports a putative role for cow's milk proteins immune response in the pathogenesis of Behçet's disease.
This research is motherfucking 10 years old.

You gotta be kidding me.

Let me repeat:
This research is motherfucking 10 years old.




Words fail me.

PS: And may I suggest that you stop eating eggs, in case you have Crohn's disease? Figure 1 in the PDF strongly hints at that…

On Nutrition: Food To Avoid

(Just a very quickly written heretic list.)

This deserves a longer post, with reasons for every point – alas, it is not meant to be at the moment. The list is heavily influenced by the Paleo Diet (avoid evolutionary novel foods) and my personal experience (avoid foods that lead to acne flares, gastrointestinal problems, excessive hunger and other ill health).

So here we go.

Food that most likely will not kill you immediately, but quite likely in the long run
  1. Trans-Fatty Acids
    (AKA "partially hydrogenated seed oil", AKA margarine, AKA shortening)
    Stay away from it. Seriously, this shit is dangerous in the long run.
  2. Seed Oil
    (AKA vegetable oil, especially sunflower oil)
    Small amounts every now and then will not kill you. But the high Omega-6 content will kill you in the long run, if you consume much seed oils. Some seed oils are at the "less dangerous" end of the scale – especially olive oil. Nevertheless, eat in small amounts, if at all.
  3. Dairy
    (AKA cow milk, AKA milk products, especially from pasteurized milk)
    My advise: Stay away from milk and milk products (e.g. desert, milk-chocolate) – it will be better for your health.
  4. Cereal Grains and other seeds
    (AKA wheat, soy, corn)
    It will be better to avoid grains and other seeds, trust me. Bread causes me to get very very hungry after a couple of hours, for some hours.
  5. Eggs
    Eat in moderation, if at all. If you have health problems that don't quite go away on a paleo diet, stop the consumption of eggs and see if it helps.
  6. Industrially Produced Meat Products
    Especially sausages. Seriously, they put all kind of crap in there. If you have a local butcher (that you think you can trust) then buy sausages there.
  7. Honey
    It is not natural to consume honey every day. Cavemen did had little access to honey.
  8. Legumes
    (AKA Beans, AKA Pulse, AKA Peas, AKA Lentil)
    Might be OK if traditionally prepared. I avoid it, as it causes gastrointestinal problems for me.
  9. Supplements
    Avoid, unless you have a medical condition where you know that you need them.
  10. FODMAPs
    Causes gastrointestinal/IBS problems for some people – haven't check it myself.
  11. (Coconut Milk)
    Causes gastrointestinal problems for me, so I don't eat it.
And of course, many of these foodstuffs hide in "Crap In A Box" foods – better not to eat crap, I reckon.

And don't consume additional vitamins (unless you have known vitamin deficiency, or have other health problems you know where vitamins are beneficial).

Foods in health limbo (if I knew!)
  1. Rice
    Honestly, if I knew. I try to eat it in moderation – once a week, at most.
  2. Potatoes
    (AKA "White Potatoes")
    From the family of nightshades.
    If you have health problems that don't go away with a nutritional intervention, stop the consumption of nightshades (including tomatoes) and see if it helps.
  3. Other Nightshades
    If I knew. 
  4. Nut, Seeds
    I avoid them at the moment.
  5. Shellfish
    I avoid shellfish at the moment.
  6. Raw Milk and Dairy made out of it
    I avoid it at the moment. But it is better than milk products from pasteurized milk. I avoid all dairy at the moment, regardless of raw or not.
  7. Cured Meat
    If I knew. I try to eat it in moderation
  8. Beef
    I avoid beef at the moment, as dairy causes definitely for me inflammatory and/or auto-immune problems – so I am suspicious of all cow products (except clarified butter) and cautiously removed beef from my diet. My fears regarding beef might be unwarranted though, and I will try to reintroduce beef in the future.
  9. Tea
    Seriously, if you drink lots of tea, this might be problem. Cavemen did not drink lots of tea. I avoid it.
  10. Coffee
    I need my coffee. Might be better to limit the consumption or even avoid coffee.
  11. Sugar
    Eat in moderation, at most. It might be better to avoid sugar – but I think the bad reputation that sugar receives lately is only partially based in reality.
Foods that should be OK

(Unless you know that they cause health problems for you, e.g. if you have an known allergy)
  1. Fish
  2. Meat
    Freshly prepared, regardless of origin (beef, pork, chicken, turkey, lamb, and so on)
  3. Animal Fat, Saturated Fat
    (I'm a heretic after all)
  4. Tubers, Roots, Carrots and such
  5. Most Vegetables
    (AKA Greens)
  6. Most Fruits
  7. Salt
And ignore macro nutrient ratios, and ignore all talk about low-carb (LC) or very-low-carb (VLC) for now.

Turned out to be quite a long heretic list, after all. Has to be enough for now.


    Someone whose blog I read linked to the following rant:
    A farewell to bioinformatics

    I’m leaving bioinformatics to go work at a software company with more technically ept people and for a lot more money. This seems like an opportune time to set forth my accumulated wisdom and thoughts on bioinformatics.

    My attitude towards the subject after all my work in it can probably be best summarized thus: “Fuck you, bioinformatics. Eat shit and die.”

    Bioinformatics is an attempt to make molecular biology relevant to reality. All the molecular biologists, devoid of skills beyond those of a laboratory technician, cried out for the mathematicians and programmers to magically extract science from their mountain of shitty results.

    And so the programmers descended and built giant databases where huge numbers of shitty results could be searched quickly. They wrote algorithms to organize shitty results into trees and make pretty graphs of them, and the molecular biologists carefully avoided telling the programmers the actual quality of the results. When it became obvious to everyone involved that a class of results was worthless, such as microarray data, there was a rush of handwaving about “not really quantitative, but we can draw qualitative conclusions” followed by a hasty switch to a new technique that had not yet been proved worthless.
    I know next to nothing about bioinformatics. I know nothing about the author. But it resonates with me because of what I have seen with researchers trying to "extract science" from cytokine studies in ME/CFS.

    Yes, it is plausible that cytokines are involved in ME/CFS. But considering that we know next to nothing about the possibly many disease that constitute ME/CFS, and considering that any disease is probably not a simple "this or that cytokine is too high or too low" case, I will keep on saying: Cytokine studies should be attempted, but we any "results" need to be rechecked in another cohort, and the results may turn out to be underwhelming or worthless.

    Saturday, January 26, 2013

    How common is HSV-1?

    HSV-1, famous for causing cold-sores, seems to be very common:
    A 2006 study found evidence of HSV-1 infection in 57.7 percent of American adults, ages 14 to 49. Bryan Cullen, a virologist at Duke University, told me he's seen studies showing that closer to 70 percent of adults are infected — although only something like 1/3rd of those will ever get cold sores.

    HSV-2, the main cause of genital herpes, on the other hand seems to be much less common, as HSV-2 is sexually transmitted – while HSV-1 is transmitted through normal contact between family members. Less than a fifth of the population seem to have HSV-2, with a sinking number of people are being infected it seems.

    Wednesday, January 23, 2013

    Aphthous Ulcers linked to Presence of Antibodies against Cow Milk

    Humoral immunity to cow’s milk proteins and gliadin within the etiology of recurrent aphthous ulcers?

    Objectives: The goal of this study was to determine the incidence of serum antibodies to gliadin and to cow’s milk proteins (CMP) using ELISA test, within patients who have recurrent aphthous ulcers (RAU).

    Subjects and Methods: Fifty patients with recurrent aphthous ulcers and fifty healthy people were included in this research.

    Levels of serum IgA and IgG antibodies to gliadin and IgA, IgG and IgE to CMP were determined using ELISA.

    Results: The levels of serum antigliadin IgA and IgG antibodies were not significantly higher in patients with RAU in comparison with the controls (P = 0.937 and P = 0.1854 respectively).

    The levels of serum anti-CMP IgA, IgG and IgE antibodies were significantly higher in patients with RAU in comparison with the controls (P < 0.005, P < 0.002 and P < 0.001 respectively).

    In general, the increased humoral (IgA or IgG) immunoreactivity to CMP was found in 32 of 50 patients, while 17 of them showed the increased levels of both IgA and IgG immunoreactivity to CMP.

    At the same time, 16 out of 50 patients had IgA, IgG and IgE immunoreactivity to CMP.

    Conclusion: These results indicate the strong association between high levels of serum anti-CMP IgA, IgG and IgE antibodies and clinical manifestations of recurrent aphthous ulcers.

    When will acne be linked to (pasteurized) cow milk?

    Behçet's Disease can look like CFS

    Info Video by the American Behçet's Disease Association

    It all sounds so familiar. Crippling chronic fatigue, friends saying "you are faking", doctors don't now what's wrong. So people are relieved and almost happy when they finally – after years in most cases – get a proper diagnose that explains their symptoms.

    Tuesday, January 22, 2013

    The Great Chronic Lyme Mirage – Advocates Gone Wild

    Bullying Borrelia: When the Culture of Science is Under Attack
    (Full Text PDF)

    Paul G. Auwaerter, MD, and (by invitation) Michael T. Melia, MD

    Although Lyme disease responds to short courses of antibiotics, tick-borne Borrelia burgdorferi has been advanced by some as a frequent explanation for medically unexplained symptoms such as continual fatigue, musculoskeletal pains, and subjective neurocognitive dysfunction.

    Often called “chronic Lyme disease” by adherents of this philosophy, it is loosely defined, and practitioners liberally prescribe nostrums, including prolonged antimicrobial therapies, in a belief that this eradicates suspected infection.

    Perhaps due to the lack of supportive data, proponents of this theory have developed their own meetings, literature, activist groups, and substantial internet activities to advance their views.

    Forces motivating this movement are explored, as are tactics used to advance non-scientific ideas that have included legal action and garnering legislative endorsement.

    While neither logical nor evidence-based, “chronic Lyme disease” harnesses corrosive energies that taint modern medicine and society.

    We know it all too well from ME/CFS: A minority of quack-doctors are proposing valid sounding theories with regards disease mechanisms – which goes hand in hand with cures they claim to have – and some patients and relatives are more than happy to advocate in their name. And when one calls out their lack of evidence, and the likelihood that the supposed cure does in many (if not most) cases harm, one is branded as an enemy. To hell with those malicious patient advocates and malicious patient activists, and to hell with these "LLMD" quack doctors.

    And yes, people who supposedly have "Chronic Lyme" are ill with an (in all likelihood) organic disease. But no, it is not "Chronic Lyme" and in most cases it isn't even Post Lyme.

    Monday, January 21, 2013

    "Vanishingly Small"

    Michael Sharpe: The first thing is it’s a big problem, it’s a big problem in primary care and primary care chooses who they send to secondary care and it is across medical specialities about a quarter to a third of the patients seen fall into this category, so it’s a big problem. The second question is, do these people all go on to have [sic] disease that to have the symptoms explained if you just wait. And again the evidence is and our studies in neurology suggest even after a year very, very few people once they’ve been assessed by a neurologist turn out [sic] to have a disease. So it isn’t that if you wait the disease will always become clear, it usually doesn’t.

    Norman Swan: And if you go and see a better neurologist?

    Michael Sharpe: And if you go and see a better neurologist, people of course do end up doing this, they go and see multiple doctors in the hope that one of them will find a symptom [sic], but once you’ve seen a competent specialist doctor the chance of a second [specialist] finding something becomes vanishingly small.
    Hear hear!
    In the United States, a disease is defined as “rare” if it affects fewer than 200,000 individuals, or roughly one in 1500. Rare diseases are often poorly understood, with symptoms that can be difficult to diagnose, and can be life-threatening. Around 6,800 rare diseases have been identified and the large majority of them — up to 80% — are thought to have a genetic origin. Most rare diseases can’t be cured and many lack effective treatments because research on rare conditions is often hampered by a scarcity of study participants and poor funding.

    If you add up all the rare diseases it turns out that about 30 million Americans suffer from a rare disease. That’s nearly 10% of the populationsuddenly rare is not so rare!
    I would say no doctor knows all of these 6,800 identified rare disease – the chances that any doctor misses a disease in a patient are very high if it is something the doctor does not deal with everyday. Given a patient with a random rare disease, every doctor will fail to make proper diagnosis, even if he is specialized in neurology. The only chance the patient has is to find the doctor who knows the disease.

    And then there are the not so rare diseases (mediums diseases? well done diseases?), where I seriously doubt that most specialists know all diseases. Some doctors don't even know Behçet’s, for crying out loud!

    To dismiss the utter importance of a proper differential diagnosis for supposedly "medically unexplained" symptoms is not acceptable behaviour for any doctor.

    Plus, on average it takes 2 years for a patient with a chronic disease to receive a diagnosis (without any guarantee whatsoever that it is the correct diagnosis). The long tail is made up of people who have a disease that could be identified with current medical knowledge, however the medical profession is unable to deliver them a diagnosis in an acceptable time-frame. So equalling "Patient has no diagnosis after 1 year" with "Patient has no disease" is a highly unethical shell game by the good doctor – these fucking clueless butchers malicious psychoquacks very fine disciples of the Wessely school always try to move the pea when you are not looking carefully.

    Leaving behind what is currently known, there are people who have diseases that are – gasp! – currently unknown to medical science. Who here would stand up and claim that every disease and every disease mechanism has been identified, that medical science knows it all, has all tests needed to identify diseases in a patient, and that there is nothing new to learn for medical science any more? If you are standing now, you are an idiot.

    I will not dignify the rest of the bullshit that Michael Sharpe bloviates, except to remark that Sharpe is throwing lots of sand in everybody's eyes – including his own in his confirmation bias frenzy – to intentionally blur many medical concepts, psychological concepts and appealing to what he presents as some sort of "common sense" to push the psycho-woo of the Wessely School. If Sharpe were really interested in the reality of diseases with their peripheral fatigue and peripheral pain (and not his make-believe confirmation-bias psychological-woo "It's the brain who makes the symptom"), he would heed to look at the scientific work of people like Alan Light or Christopher Snell. Sharpe works very hard so patients with demonstrable physical disease should receive treatment by psychologist, and by psychologists alone – that this may be in his financial interest, but not in the medical interest of his patients, that he is unable to realize. Alas, as Thomas Kuhn and Max Planck have remarked before, we have to wait until they have died of old age and a new generation not entangled in idealistic BS has replaced these jokers.

    To finish, I would say the chances that Michael Sharpe is a competent doctor, who acts in the interest of his patients, these chances are vanishingly small. However the chances that he is a psychoquack look more like on the order of being 1.0 (p<0.0000001).

    My personal advise: Stay away from psychoquacks. First of all they feel harassed if you demand attention for your medical problems – medical problems are not their department, after all. And secondly it it might be bad for your health.

    Sunday, January 20, 2013

    Differential between Behçet's and ME/CFS is needed

    Some of the symptoms of Behçet’s:
    • Unpredictability: impossible to predict onset or clearing-up of symptoms, onset of symptoms sudden, difficulties in keeping to arrangements, appointments, working, affairs, managing household, family, social activities, hobbies
    • Arthritis: reduced mobility or complete immobility, pain.
    • Oral ulcers: pain,diet restricted to soft or liquid food, inability to eat at all, inability to talk, dribbling, dehydration, malnutrition.
    • Genital ulcers: immobility, sex-life affected, embarrassment, suspicion, urinary retention, pain.
    • Visual level: fear of onset of blindness, handicapping according to level of impairment and ability to adapt, pain.
    • Skin: disfiguring and embarrassing skin lesions, easy bruising, poor slow healing, pain.
    • Gastro-intestinal: wind, diarrhoea (with blood and mucus) or constipation, severe abdominal pain. Mimics inflammatory bowel diseases, irritable bowel syndrome. Stomach ulcers, ulcers in gullet. Risk of perforated ulcer. Dehydration, malnutrition
    • Thrombophlebitis: immobility, pain.
    • Thrombosis: immobility, pain. Risk of embolism.
    • Ears: hearing loss, tinnitus, vertigo
    • Chest: wheezing, breathlessness, haemorrhages, haemoptysis, pleurisy, pain.
    • Cardio-vascular: breathlessness, haemorrhages, dysrhythmias, pericarditis, valve problems, pain. Risk of ruptured aneurysms.
    • Neurological: paralysis, strokes (CVAs), transient ischemic attacks (TIAs), memory & concentration impairment, seizures, migraine-type or meningitis-type headaches, double vision, incontinence, impotence, strange sensations, motor impairment ranging from mild clumsiness to vegetative states, personality changes, psychoses.
    • Fatigue: profound persistent exhaustion affecting all activity.
    • Feverishness: effects like having ‘flu, night sweats, bizarre sense of feeling cold or warm.
    (Remember no patient has all symptoms! See below for the diagnostic criteria for Behçet’s.)

    I marked those who I think are the most prominent overlap with ME/CFS. One can see that there is some kind of overlap (not including some of the neurological and gastro-intestinal symptoms that doubtlessly some of the ME/CFS patients have as well)

    If some of primary symptoms of Behçet’s (oral ulcers, eye inflammation) are not pronounced (or in rare cases even oral ulcers can be absent), then it is easy to misdiagnose Behçet’s as ME/CFS.

    Again, this shows how utterly important a proper differential diagnosis is in cases of suspected ME/CFS. There are many known diseases out there that can look to the untrained eye like another case of ME/CFS.

    Of course there are newer and older diagnostic criteria. These are the newer (and probably better) 2006 ICBD criteria:
    Add points for every symptom:
    • Oral aphthosis ("mouth ulcers"): 1 point
    • Skin lesions (e.g. acne): 1 point
    • Vascular lesions: 1 point
    • Positive pathergy test: 1 point
    • Genital aphthosis ("genital ulcers"): 2 points
    • Eye lesions: 2 point
    3 points or more? It is most likely Behçet's.
    And what are the older diagnostic guidelines for Behçet's?
    1. International Study Group strict research level guidelines for diagnosis

    Must have:
    • mouth ulcers (any shape,size or number at least 3 times in any 12 months)
    Along with 2 out of the next 4 ‘hallmark’ symptoms:
    • genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men)
    • skin lesions (papulo-pustules, folliculitis, erythema nodosum, acne in post-adolescents not on corticosteroids)
    • eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous)
    • pathergy reaction (papule >2 mm diameter, 24-48 hrs or more after needle-prick)
    2. Practical clinical guidelines for patients not included in research cohorts

    Must have:
    • mouth ulcers
    Along with 1 out of the 4 ‘hallmark’ symptoms above

    Along with 2 of the following symptoms:
    • arthritis/arthralgia
    • nervous system symptoms
    • stomach and/or bowel inflammation
    • deep vein thrombosis
    • superficial thrombophlebitis
    • cardiovascular problems
    • inflammatory problems in chest and lungs
    • problems with hearing and/or balance
    • extreme exhaustion
    • changes of personality, psychoses
    • any other member of the family with a diagnosis of Behçet’s disease
    3. 'Suspected' or 'possible' diagnosis

    Usually given when someone does not have mouth ulcers or has mouth ulcers but does not have 1 of the 4 'hallmark' symptoms but has other symptoms and signs of inflammation and other causes for these have been ruled out.
    Care must be taken for a differential between ME/CFS and Behçet's. As with all diagnostic criteria:
    • someone who meets some set of diagnostic criteria for a disease, does not necessarily have the disease – and could have another disease instead
    • and someone who barely meets the criteria may actually have the disease (see "suspected diagnosis" above)
    regardless of whether it is Behçet's, ME/CFS or any other disease.

    Saturday, January 19, 2013

    HHS Publishes ME/CFS Primer

    The National Guideline Clearinghouse (NGC) of the HHS has published the ME/CFS primer of the IACFSME!


    Psychiatric conditions in Behçet’s

    Psychiatric conditions in Behçet’s

    Psychiatric conditions occur only very rarely in Behçet’s syndrome, when parts of the brain which look after emotion and thought are affected by the meningoencephalitis noted above. Occasionally patients may present with hallucinations, and abnormal thoughts such as paranoia, and difficulty thinking and remembering. This is most uncommon and normally settles down well with the correct treatment.

    Separate to this is the syndrome of fatigue, anxiety and depression which can also cause thinking and memory problems, but which is not related to a problem within the brain. This, in contrast, is very much more common, not just in Behçet’s syndrome but in most chronic and difficult conditions. This is not surprising, but some Doctors, even GPs, fail to recognise this and I have found that this is frustrating to patients. It has been shown that patients with Behçet’s syndrome show higher ratings on depression and anxiety scores, and that these scores vary with the severity of the underlying illness. So-called fibromyalgia symptoms (aches and pains with tiredness) also correlate with how the Behçet’s is behaving, but it is also true that the symptoms of anxiety and depression can make the Behçet’s feel worse when it is not actually in relapse. So it is a very complicated problem. Fatigue management and a positive outlook to the disease are best. Avoidance of overtiredness and planning of the day, to allow rest before and after an activity, work well, and most find that fatigue improves and memory becomes more efficient. It’s easy for Doctors to prescribe and hard for the patients to do!

    Could it be Behçet’s?

    Interesting question: Do I have Behçet’s?

    With my old diet I had all these following symptoms, (almost) enough to meet the diagnostic criteria for Behçet’s:
    • Minor aphthous ulceration [every couple of months in the mouth]
    • Pseudofolliculitis [maybe a very very slight, but my follicles were always red]
    • Papulopustular lesions [sometimes some]
    • Acneiform nodules [not sure, I thought it was acne]
    • Extreme exhaustion [Wouldn't call it "extreme", but yes I am quite fatigued]
    • Nervous system symptoms [do muscle twitches and migraines count?]
    (I am not sure if I might have had a very slight iritis, an inflammation of the iris. My eyecolor changed from green-brown – with brown "patches" – to a more uniform green with slight brown. And the blood veins in the white of my eye got less visible.)

    These are the symptoms I had on my old diet, some of which I still have. And some of the symptoms return when I leave the path of the Paleo Diet and venture into my old diet (mainly when I eat pasteurized milk products or when I eat eggs).

    And every symptom counts. I really paid not much attention to the aphthous ulcers in my mouth. They came and went again, I could live with them and they were the least of my problems – and why concern myself or even a doctor with such a small thing?

    I fear I need go again on my old diet to provoke these symptoms. But not at the moment.

    At the moment I am too tired to write more – but is interesting the things one finds.

    Stephen Ralph on Behçet’s, ME/CFS and Misdiagnosis by Psychologists (2)

    See part 1 here.
    Permission to Repost

    Hello there,

    In the background during my absence from campaigning, I have been plugging away at trying to get individuals of influence aware of the associations between the invisible symptom set of ME and the invisible symptom set of Behçet’s syndrome.

    I was recently told by one doctor dealing with “CFS” that he could only find 11 research papers on Behçet’s syndrome and that one of those was in German.

    This doctor then proceeded to give me all the classic stereotypical presentations of Behçet’s syndrome including patients having clusters of mouth ulcers, genital ulcers, eye involvement in the form of uveitis.

    And together with this I discussed the fact that the HLA B51 blood test that can show positive for a case of Behçet’s is more often than not negative for a patient who has Behçet’s.

    I then pointed out the following which will become crucially important in the coming months.

    If you take a look at this link.... you will see the various levels of symptom certainty needed to make a diagnosis of Behçet's Syndrome.

    The certainty level exists for the purposes of clinical research which means that anyone who participates in clinical research will have the top level of certainty diagnosis and many of the easily visible and detectable signs of Behçet’s disease.

    However, you will also see on that web page that it is still viable to have Behçet’s disease without all the obvious classic signs.

    Even if you do not have those classic signs, you can still be diagnosed as having Behçet’s syndrome.

    The fact is that nobody appears to have carried out any research into the other end of the scale…. The end of the scale where patients who can have Behçet’s have hardly any or indeed no visible signs that would be observable by a specialist at an out-patient appointment.

    Stephen Ralph on Behçet’s, ME/CFS and Misdiagnosis by Psychologists (1)

    See part 2 here.
    Permission to Repost

    Dear Reader,

    As some of you reading this will know, I was dragged into the world of Myalgic Encephalomyelitis and Chronic Fatigue Syndrome way back in 1996/1997. At around this time I jointly set up MEActionUK and the companion website

    At that time I had been a practicing diagnostic Radiographer at a busy district general hospital in Dorset.

    During the three years of my training and subsequently over the period of practice I extensively covered human anatomy, physiology, pathology, patient care and hospital practice as well as radiographic photography, equipment and radiation physics.

    Some of our lectures mirrored those of medical students.

    We were familiar with “Gray’s Anatomy” for the sort of detail we needed to cover.

    Although optional, I attended an autopsy during my training to enable me to appreciate the internal anatomy that we had been studying for many months.

    I also observed open heart valve replacement surgery – the anaesthetist let me stand where he usually stood so I could see what was where and how the surgery proceeded.

    Our education and my subsequent career was comprehensive until I was forced to retire due to ill health.

    Over the 10 years of my education and career in diagnostic radiography, it was drummed into me that there was an overriding importance within my profession to provide the best quality radiography possible to enable the doctor to form the correct diagnosis with thanks to the information presented to the radiologist (a doctor specialising in reading x-ray’s and performing x-ray examinations) or indeed any generic doctor or even medical students examining our work in a busy A&E.

    If our work wasn’t to the highest of standards then we understood that there was a sliding scale of risk that a radiologist or non-specialist doctor could draw the wrong conclusions – missing a pathology from poor radiographic technique and then forming the wrong diagnostic opinions about what they were looking at.

    Friday, January 18, 2013

    Exercise and Intermittent Fasting Are Good For The Brain

    In a recent NIH video-cast called "CC Grand Rounds" (first half of the video) Mark Mattson shared some insights he gained from basic research. Mainly that exercise is good for the brain, sedentary behavior is bad for the brain. And secondly, intermittent fasting has similar beneficial qualities for the brain. Both are "stressors" that seem to have beneficial advantages – something the Paleo Diet community has been harping about for ages (because that's what life has been in evolutionary times: you needed to move to get food, and sometimes you ended up without food for a day or two).

    Does this have implications for ME/CFS patients? Well, if there is a level of low intensity exercise you can manage as patient – say going once or twice a day downstairs, rest, and then up again – then you should do it.

    Obviously don't do exercise if you are crashed/relapsed. And if you crash/relapse after exercise, you are doing too much. Or the activity level of the exercise is too high.

    If going once a day to the bathroom is about the exercise that you can do as an ME/CFS patient: than don't do more, but try to do it.

    And if your exercise consists of (slightly) wiggling your arms and feet for 10 seconds while lying in bed, then rest half an hour, and then do 10 more second, then well, do that – but try to do at least that.

    Find a low intensity level of exercise which you can maintain without crash/relapse!

    And if you do something as an ME/CFS patient, do pace yourself (e.g. rest often enough).

    And should you try intermittent fasting? I surely will give it a try. One thing I found helpful was that with a Paleo Diet (and no cereal grains), my hunger became much more manageable. One remark Mark Mattson made is that intermittent fasting may be hard to start, but after two or three weeks people get used to it. I'll see.

    Faecal Transplant – Appearantly A Very Good Clostridium Difficile Treatment

    Ed Yong:
    Last week, I wrote about scientists who developed a stool substitute and used it to cure gut infections in two women. This sham poo contained 33 gut bacteria, which were meant to displace the harmful ones that were causing diarrhoea in the patients.

    … [Now] the first results from a [larger] faecal transplant trial [to treat Clostridium difficile] have been published in the New England Journal of Medicine, and they are a resounding vindication for the technique.

    The infusions of faeces cured 94 percent of patients who received it (15 out of 16), all of whom had already suffered at least one relapse of C.difficile. By comparison, the standard antibiotic—vancomycin—only cured 27 percent of patients (7 out of 26). The difference was so great that the Dutch team behind the study had to stop the trial early. Everyone eventually received the faecal transplants.

    The technique had no negative side effects except for the rare bout of constipation, and diarrhoea for a few hours after the infusions. That’s nothing compared to the gastrointestinal agony of a bout with C.difficile.

    I’ve written about the trial for Nature News, so head over there for the details. For now, I’ll highlight a couple of points from the trial.
    This ties in nicely with what David Healy said: drugs that "really" work show their effects in small trials.

    Faecal Transplant is still in its infancy, but I'm sure there are a few more diseases were a faecal transplant might at least prove helpful.

    [Update] From the Nature News article:
    “Those of us who’ve been doing this procedure for some time didn’t need any more convincing, but the large medical community needs to go through these steps,” says Alexander Khoruts, a gastroenterologist at the University of Minnesota in Minneapolis, who was not involved in the trial. “It’s an unusual situation where we have more than 50 years of worldwide experience and more than 500 published cases, and only this far along does a randomized trial appear.”

    There is something definitely wrong in the land of evidence based medicine. Clearly there is no alternative to the scientific method (I shudder to think of those "alternative/integrative/traditional/holositic/whatever" quacks who believe in things that don't even pass the hurdle of evidence-based-medicine) – but there seem to be so many places where medicine is stuck, for decades it seems. While I'm sure that evidence-based-medicine beats the alternative quacks, one can at the same time not trust evidence-based-medicine to now what works, or what doesn't.

    Thursday, January 17, 2013

    Fuck That.

    David Healy - Time to abandon evidence based medicine?
    And all that is not even including the carnage done by quacks

    Fuck that.

    We have all these amazing medical, technological and scientific advances, which should put us in a position to fight diseases in a way that would make all the Pasteurs and all the Enders' and all the Salks and all the Sabins of past times green with envy. Where is the evolution in medicine? Why does it seem to me that we are stuck in a dead end?

    The medical profession does well with clearly defined illness – say HIV/AIDS – that, if left untreated, lead to clearly measurable, visible adverse outcomes. But things like depression? MS? T2DM? In all likelihood, the treatment may lead to worse outcomes than if the illness is left untreated.

    And this hits me at the moment. My doctor is willing to try out medication for my ME/CFS and therefore I'm currently looking into what agonist drugs are available to stimulate the alfa 2A receptor which is shown to be involved in at least subgroup of patients. Besides
    • the almost total lack of scientific interest in ME/CFS by the medical commuity that leads to a situation where every person with ME/CFS is going from one "personal drug trial" to the next because guiding trial data is non-existent,
    • besides not having any certainty whatsoever what actually the pathology is in my case (besides some personal indication that the alfa 2A receptor might be involved for me as well),
    • besides not knowing if a stimulation with an Ad2A agonist is actually the right thing to do, if it is the Ad2A in my case,
    • and besides not knowing what the actual (vs. claimed) spectrum of adverse reactions of these drugs is,
    besides that I am totally at loss whether the supposed alfa 2a agonists actually do what the pharmaceutical industry claims they do.

    Should I give Guanfacine a try? Or rather Tizanidine? Maybe Xylazine? What about Lofexidine?  Is Brimonidine only for occular hypertension?

    I know, let's play guinea pig! And if one doesn't work, or makes me awful, then we try the next! Oh boy, what fun.

    I feel like I might go to a pharmacists, and at gun point take any random medication and try that – and not be worse off…

    But it sure is nice to see a psychologist like David Healy sharing his good insight into the problems of his profession and giving his best to address them properly.

    Informed Consent? Psychologists Don't Need No Stinking Informed Consent

    The function of ‘functional’: a mixed methods investigation


    Objective The term ‘functional’ has a distinguished history, embodying a number of physiological concepts, but has increasingly come to mean ‘hysterical’. The DSM-V working group proposes to use ‘functional’ as the official diagnostic term for medically unexplained neurological symptoms (currently known as ‘conversion disorder’). This study aimed to explore the current neurological meanings of the term and to understand its resilience.

    Design Mixed methods were used, first interviewing the neurologists in a large UK region and then surveying all neurologists in the UK on their use of the term.

    Results The interviews revealed four dominant uses‘not organic’, a physical disability, a brain disorder and a psychiatric problemas well as considerable ambiguity. Although there was much dissatisfaction with the term, the ambiguity was also seen as useful when engaging with patients. The survey confirmed these findings, with a majority adhering to a strict interpretation of ‘functional’ to mean only ‘not organic’, but a minority employing it to mean different things in different contexts – and endorsing the view that ‘functional’ would one day be a neurological construct again.

    Conclusions ‘Functional’ embodies real divisions in neurologists' conceptualisation of unexplained symptoms and, perhaps, between those of patients and neurologists: its diversity of meanings allows it to be a common term while meaning different things to different people, or at different times, and thus conceal some of the conflict in a particularly contentious area. This flexibility may help explain the term's longevity.
    Honestly, who doesn't love it when psychologists mislead patients, and lie to them?

    HIIILARIOUUUUS, I tell you.

    "First do no harm?" Hippocrates, shmoppocrates.
    Trust us!

    Give up your anti-psychological attitude!

    We mean you no harm!

    Now do as I say and calmly take your pills for your *cough* functional *cough* disorder.
    If the psychologist does not understand what is wrong with the patient, the first order is to blame the patient and the second order is to lie to him. And then put the patient on anti-depressents, or even better anti-psychotics, for good measure – that'll teach those unruly patients, foolishly seeking help for their medical problems at a psychologist.
    Informed consent, to god-damned hell with informed consent!

    We don't use informed consent. In fact, we don't need informed consent.

    We treat patients without any stinking informed consent, you god-damned cabrón and chinga tu madre!

    Wednesday, January 16, 2013

    Physical activity is not a adequate treatment for depression

    BMJ: Facilitated physical activity as a treatment for depressed adults: randomised controlled trial

    The addition of a facilitated physical activity intervention to usual care did not improve depression outcome or reduce use of antidepressants compared with usual care alone.
    Who would have thought? You can't simply "walk off" your depression. Now what does that tell us about GET, which seems to be equally common sense to psycho-quacks?

    Tuesday, January 15, 2013

    Wolfgang Lutz on Anxiety

    (Adapted from a comment of mine at the blog Ad Libitum)

    A consistent theme I notice (which for me started with my personal experience) when I read in blogs/forums about personal nutrition experience is that people with anxiety problems, who go Paleo/Atkins/Lutz/VLC/whatever diet, is that they get rid of their anxiety problems after a change in nutrition.

    People talk a lot about nutrition in the context of obesity and diabetes and cardiovascular disease and what not – the elephant in the room is to which mental/psychological problems/diseases does nutrition contribute, and by how much?

    E.g. Wolfgang Lutz mentioned in the german edition of his book that he got rid of anxiety. However it is only one short paragraph and it is hidden in the back of the book. As this passage is only in the german edition of Wolfgang Lutz's book, I think it is important to translate the passage into english.

    It is a bit difficult to translate, as he uses an older idiom for his psychological ailments, which tends to be a bit ornate and flowery. In addition there were (due to the pre-scientific nature of psychology) a few changes in meaning of words, both in german and in english, and I am not really intimate with the history of each term  – how do you translate "seelisch" in the context of that short passage? As emotional, psychological, mental? What were the "Komplexe" that plagued him? I have a vague idea what he meant, but unfortunately he choose not to elaborate on that topic and did not deliver a more precise description (I guess the social stigma of not being able to handle your psychological problems…).

    So take my translation with some grains of salt.
    … I was [before my change in nutrition] in a constant state of emotional agitation and imbalance, which might have not been visible by others though. Somehow I was always plagued by complexes, anxious about something, expected bad news, and had the feeling to be constantly driven/pushed.

    [After the change in nutrition] … Generally, my mood was much more balanced, and I could enjoy my life more than before; the feeling of inner arousal was gone. Only now I could recognize that palpitations in dangerous situations were gone – such as in traffic – and that I no longer broke out in sweat so easily. Making decisions was now much easier for me, which especially benefited the time I spent on radiology and giving dictations. Suddenly I had time for my hobbies, which I had to abandon because I had no energy left to spare for them.

    Wolfgang Lutz – "Leben ohne Brot" ("Life without bread"), page 247
    He makes good observation about obesity ("male" obesity pattern vs. "female" obesity pattern), he fails to record his (and his patients!) improvement on the "psychological front" in more detail however. Getting rid of anxiety and increasing energy was – at least for me – by far me more important than getting rid of a few (or even many) pounds. Was this "mental energy" he couldn't spare for his hobbies, or was this full blown fatigue (or even CFS?) that dragged him down? We'll never know.

    Here is the passage in the german original, for all you kraut-speaking schweinhunde :-)
    … Schließlich befand ich mich [vor der Kostumstellung], gemessen an heutigen Maßstäben, in einem ständigen seelischen Erregungszustand und Ungleichgewicht, was allerdings nach außen vielleicht nicht so sehr in Erscheinung trat. Ich war immer irgendwie geplagt von Komplexen, hatte vor irgendetwas Angst, erwartete eine unangenehme Nachricht, und hatte das Gefühl ständig angetrieben zu sein.

    [Nach der Kostumstellung] … Überhaupt war meine Stimmung viel ausgeglichener, und ich konnte mein Leben nun mehr als früher genießen; das Gefühl der inneren Erregung war verschwunden. Jetzt erst merkte ich, dass ich in gefährlichen Situation, z.B. im Straßenverkehr, kein Herzklopfen mehr bekam und dass ich nicht mehr so leicht schwitzte. Ich konnte mich viel schneller entschließen als vorher, was sich besonders in einer Verkürzung der Durchleuchtungs- und Diktatzeiten äußerte. Plötzlich hatte ich wieder Zeit für meine alten Hobbies, die ich vorher eines nach dem anderen aufgegeben hatte, weil ich hierfür keine Energien mehr erübrigen konnte.

    Wolfgang Lutz – "Leben ohne Brot", Seite 247

    Insanity at the USDA

    Fat Head: USDA Report: We Eat Less Fat, But Fat Is Killing Us
    A new report from the USDA says Americans are eating less fat than we did 30 years ago. Here’s the opening from an online article about the report:
    On average, Americans are eating 10g less fat per day today than they were in the late 1970s, according to new research. In a report comparing food consumption patterns in 1977-78 versus 2005-2008, Biing-Hwan Lin and Joanne Guthrie from USDA’s Economic Research Service found that on average, Americans consumed 75.2g of fat in 2005-08 compared with 85.6g in 1977-78.

    Meanwhile, the percentage of total calories derived from fat also declined substantially from 39.7% to 33.4% between 1977 and 2008, said the authors.
    Hallelujah! Now that USDA itself is admitting we’re eating less fat, surely they’ll finally also admit that the rise we’ve seen in obesity and metabolic syndrome in the past 30 years can’t be blamed on fat. I can just hear the press conference where they announce they’re allowing whole milk back in schools …
    However, with more Americans eating out than ever before, a growing proportion of the fat that they do consume is the unhealthy, saturated, variety, said the authors, noting that almost a third (31.6%) of calories were from foods consumed outside the home in 2005-8 compared with just 17.7% in the late 1970s.

    “Food consumed away from home is higher in saturated fat than foods consumed at home [in the 2005-8 data set]. The higher percent of calories from saturated fat in fast-foods was especially noteworthy at 13.5%, compared with 11.9% in restaurant foods, 12.3% in school foods, and 10.7% in foods consumed at home.”

    Similarly, foods consumed away from home in 2005-8 contained significantly more sodium (1,820mg of sodium per 1,000 calories), than foods consumed at home (1,369mg sodium per 1,000 calories); with foods from restaurants and fast-food outlets particularly sodium-dense at 2,151mg and 1,864mg of sodium per 1,000 calories, respectively.
    Head. Bang. On. Desk.

    Faced with their own evidence that fat didn’t commit the crime, the USDA researchers nonetheless rounded up the usual suspects: Saturated Fat and his evil sidekick Sodium.
    Go read it all.

    Monday, January 14, 2013

    Take the Meds – We have nothing else

    It feels wrong, somehow, and that feeling of wrongness-but-I-can't-explain it is what prompts a national dialogue, but what Dr. Anderson really did that causes the consternation isn't prescribing the Adderall but saying out loud that it isn't for ADHD-- breaking the unspoken rules of the system by telling the press what none of use dare say even to our patients: that we're not medicating a diagnosis, we're using a diagnosis to justify the medication we have to use anyway because we have nothing else to do but give out medications.

    Where is the Evolution in Medicine?

    The sequencing of the human genotype promised a lot, but it delivers only slowly and in small doses. Maybe gene expression studies will change that, but I won't hold my breath. I heard the gut microbiome is the latest rage and it will solve all our problems (it may be important, but not that important).

    Meanwhile medicine seems to be wholly incapable to tackle massive problems like obesity, diabetes and cardiovascular disease. In diseases like MS progress seems glacial, despite the resources dedicated to its research.

    What I am relatively hopeful however is that an better understanding of the evolutionary context of our nutrition (aka "The Paleo Diet" and somesuch) will be a game changer in medicine – and surely bring us a much needed improvement for our health.

    So it brings me pleasure that I found a new blog from that area, Ad Libitum, of which I post just this one snippet:
    You know, the first time I read Good Calories, Bad Calories, it struck me that there was a missing chapter right after the dementia chapter. There should have been one on psychiatric illness. It is no coincidence that our epidemic of metabolic derangement has coincided with a huge explosion of anxiety and depression, especially of the atypical kind. My bet is that whatever is making us fat is making us miserable too. Processed carbs? Hyperinsulinaemia? I don’t know. Whatever it is, it’s killing us in multiple ways.

    Post-Mono can look like CFS - An Follow-Up

    A follow-up to this:
    Chronic fatigue syndrome following infections in adolescents

    Katz BZ, Jason LA.


    To review the recent epidemiology, pathophysiology, and treatment of postinfectious chronic fatigue syndrome (CFS) in adolescents.

    Thirteen percent of adolescents (mainly women) met the criteria for CFS 6 months following infectious mononucleosis; the figure was 7% at 12 months and 4% at 24 months.

    Peak work capacity, activity level, orthostatic intolerance, salivary cortisol, and natural killer cell number and function were similar between adolescents with CFS following infectious mononucleosis and recovered controls.

    Autonomic system, oxygen consumption, peak oxygen pulse, psychological and cytokine network differences were documented between those who recovered and those who did not.

    The prognosis of CFS is better in adolescents than in adults.

    Activity level, exercise tolerance, and orthostatic testing could not distinguish patients with CFS from adolescents who have recovered from infectious mononucleosis (controls), while certain cytokine network analyses, life stress factors, and autonomic symptoms could.
    Via Adrienne Dellwo
    … Looking at post-mono adolescents, researchers found it was mainly the girls who continued to have symptoms long term.

    Many of those who fit the ME/CFS diagnostic criteria early on no longer did at follow up.

    Here's at look at how the length of time post-infection effected the diagnostic rate:

    6 months: 13%
    12 months: 7%
    24 months: 4%

    Researchers say the following factors distinguished those with ME/CFS from kids who'd fully recovered:
    - Certain cytokine network test results
    - Oxygen consumption, at rest and during exercise
    - Life stress factors (such as those caused by long-term illness)
    - Symptoms of autonomic nervous system dysfunction

    They did not find significant differences in activity level, exercise tolerance or orthostatic testing.

    Speculation on Type 2 Diabetes

    I just wanted to post here one more piece of speculation, that it is seed oils that cause or primarily contribute to Type 2 Diabetes (and possibly Obesity) – so in two or three decades I can say: "Told you."

    Sunday, January 13, 2013

    The "Gold Standard" in ME/CFS Care

    Currently, when the question comes to what ME/CFS* patients should receive as treatment, it is recommend that "Cognitive Behavioral Therapy" (CBT) and "Graded Exercise Therapy" (GET) be used – this was supposedly established in the "PACE trial".

    Now, which data was collected in the "PACE trial" with regards to recovery rates and positive outcomes, when CBT and GET are used to treat ME/CFS?
    The requested data relating to recovery rates and positive outcomes do not exist. That is to say that such analyses have not been done and there is no intention to do so. The reason for this is that the analysis strategy has changed from the original protocol.”
    Come again?

    There is no data on recovery rates and positive outcomes with CBT and GET as therapy?

    So this is the gold standard in ME/CFS care?

    This is the best that these psychology-quacks can come up with?

    As the Americans say: You gotta be shittin me.


    * ME/CFS is an syndrome, most possibly a group of several disease, with demonstrable primary physical pathologies not due to deconditioning nor caused by mental/psychological problems.

    Saturday, January 12, 2013

    Byron Hyde is a Lying Cunt

    Byron Hyde is spreading lies about Vincent Lombardi (and about Robert Suhadolnik).

    Byron Hyde said that Suhadolnik barely knew Lombardi (and that Suhadolnik had a low opinion of Lombardi), when in fact they wrote a paper together.

    What a lying cunt.

    Dr. Lustig Schools A Dietitian

    Fat Head: Dr. Lustig Schools A Dietitian
    A reader sent me a link to an interview with Dr. Robert Lustig, telling me that a registered dietitian called into the show to explain how it’s all about low-fat diets and calories in/calories out, which prompted Lustig to slap her down.

    I listened to the entire interview, but if you only have time to enjoy hearing a dietitian put in her place, skip ahead to about 47 minutes in.  You can listen to the interview here.

    Friday, January 11, 2013

    Getting ill while being ill…

    It is interesting that one can get ill while being ill. But why not? Got ME/CFS? Throw in some cold to get fun and interesting pain!

    And the pain I feel is different from relapse-pain – I wasn't aware that there are so many muscles in my neck – and they all seem to hurt! Lovely.

    The things you learn…

    Tuesday, January 8, 2013

    The Great Chronic Lyme Mirage – Herx Edition

    Halperin / ALDF:
    … Early work indicated that patients with acute, active early Lyme disease, as indicated by the presence of an erythema migrans (EM) skin lesion (when large numbers of spirochaetes are presumably present), sometimes exhibited a Jarisch–Herxheimer-like reaction within 24 h after initiation of treatment (Weber et al., 1988; Maloy et al., 1998).

    This led to the notion that any worsening of symptoms during treatment constituted ‘Herxing’, regardless of the duration of symptoms or treatment at the time of the worsening.

    The logical in-consistency of postulating that treatment-resistant disease was due to a small number of undetectable bacteria, while at the same time concluding that symptoms arising or worsening during antibiotic therapy were due to the release of large amounts of pharmacologically active bacterial products, was either discounted or never considered.

    However, this then completed the very tidy but circular conceptual model.

    If patients improved, even transiently, after treatment, this validated the diagnosis and justified further treatment; the possibility of a placebo effect or natural fluctuation in symptom severity was either never considered or completely rejected.

    If patients worsened, this was considered to be due to a Jarisch–Herxheimer reaction, similarly validating the diagnosis.

    If there were no response to therapy, this validated the assumption that this infection is highly resistant to standard antimicrobial therapy. …
    The more I see of these "LLMD" quacks, the more I am sure that "Chronic Lyme" is a quack diagnosis.

    The people who are misdiagnosed with "Chronic Lyme" have a disease, no question – and in most if not all cases it is an organic disease – but I am rather sure that it is not a active/persistent/latent ("chronic") lyme infection.

    At the same time I believe that a very very small number of people who are misdiagnosed with "Chronic Lyme" might have "Post Lyme", where the bug is gone but the organic damage stays, same as there are Postviral Fatigue Syndromes and other postviral CFS-like diseases.

    However, I am certain that no "LLMD" quack would be able to differentiate Post Lyme from Post Mono. These LLMDs see a patient and can only diagnose "Chronic Lyme", it seems …

    As Tom Waits once sang:
    LLMD always try so hard to look like real doctors
    They couldn't catch a cold,
    baby don't waste what's left of your health
    So unless you have an acute infection and take short term antibiotics for it (for a couple of weeks) stay the hell away from antibiotics if they are given long-term, especially when they give you a long time supposed "Herx" reaction – because a "long-time Herx reaction" is not Herxheimer (due to Lyme "die off"), but the side-effects of antibiotics that are destroying your health.

    David Gorski on Nutritional Science

    Long read, some problems in science (and Gorski surely sees only a selection of those), and much food for thought (ha!).

    This figure caught my eye:
    All results for salt, pork, olive and bacon are on one side of Relative Risk = 1, however with some results coming close to it? Come on, WTF! This smells like publication bias! And then there is milk and onion and beef and sugar and carrot. Just look at them! And don't get me started on tea…

    Looks like some of the results are more a mirror of prevailing biases, than a result of inquiry into reality.

    Nutritional Causes for "Somatoform Disorders"?

    This came in via
    … Finally, even though the investigated groups did not differ in their health habits, a tendency to always live and eat healthy had a specific and adverse effect on physical impairment in somatoform patients. This result is rather counterintuitive, but may be explained with an increased selective attention to bodily processes in general and somatosensory amplification [30,52]. Therefore, the respectable attempt to improve one's health may contribute to a vicious cycle of symptom perpetuation. …
    Hmm, a person eats "healthy" – cereal grains instead of meat, seed oils instead of saturated fat, and lot's of dairy to top it off – and their "somatoform" impairment gets worse?

    Truly a paradox.

    If you accept that "healthy" food is healthy, that is.

    If you have reason to believe that "healthy" food is actually bad for health and can cause disease – because most of the "healthy" food is evolutionary novel – this paradox goes away. And one can suspect that "somatoform disorders" are actually bodily diseases caused or at least perpetuated by unwise nutritional choices…

    Of course these psycho*s will ignore any of this and continue to believe in their psychosomatic/somatoform woo.

    Friday, January 4, 2013

    Byron Hyde on Vincent Lombardi

    Interesting gossip about Vincent Lombardi (and later on interesting gossip about Steven Straus).

    But forget the rest Byron Hyde, I don't think Byron Hyde is a name one needs to remember.

    [Update] Byron Hyde is a lying cunt. Vincent Lombardi published a paper with Suhadolnik in 1999. So forget Byron Hyde, he tells BULLSHIT. [/Update]

    (As always, the MassCFIDS does an excellent job, but unfortunately does Dr. Hyde not add much to our knowledge about ME/CFS – unlike Dr. Bell or Dr. Komaroff)

    Thursday, January 3, 2013

    Eat Modern Foods, Get Modern Diseases

    Dietary patterns and odds of Type 2 diabetes in Beirut, Lebanon: a case--control study

    In Lebanon, Type 2 diabetes (T2D) has a major public health impact through high disease prevalence, significant downstream pathophysiologic effects, and enormous financial liabilities. Diet is an important environmental factor in the development and prevention of T2D. Dietary patterns may exert greater effects on health than individual foods, nutrients, or food groups. The objective of this study is to examine the association between dietary patterns and the odds of T2D among Lebanese adults.

    Fifty-eight recently diagnosed cases of T2D and 116 population-based age, sex, and place of residence matched control participants were interviewed. Data collection included a standard socio-demographic and lifestyle questionnaire. Dietary intake was evaluated by a semi-quantitative 97-item food frequency questionnaire. Anthropometric measurements including weight, height, waist circumference, and percent body fat were also obtained. Dietary patterns were identified by factor analysis. Multivariate logistic regression analysis was used to evaluate the associations of extracted patterns with T2D. Pearson correlations between these patterns and obesity markers, energy, and nutrient intakes were also examined.

    Four dietary patterns were identified: Refined Grains & Desserts, Traditional Lebanese, Fast Food and Meat & Alcohol. While scores of the "Refined Grains & Desserts" had the highest correlations with energy (r = 0.74) and carbohydrates (r = 0.22), those of the "Fast Food" had the highest correlation with fat intake (r = 0.34). After adjustment for socio-demographic and lifestyle characteristics, scores of the Refined Grains & Desserts and Fast Food patterns were associated with higher odds of T2D (OR: 3.85, CI: 1.13-11.23 and OR: 2.80, CI: 1.14-5.59; respectively) and scores of the Traditional Lebanese pattern were inversely associated with the odds of T2D (OR: 0.46, CI: 0.22-0.97)

    The findings of this study demonstrate direct associations of the Refined Grains & Desserts and Fast Food patterns with T2D and an inverse association between the Traditional Lebanese pattern and the disease among Lebanese adults. These results may guide the development of nutrition interventions for the prevention and management of T2D among Lebanese adults.
    Plain and simple: Eat modern foods, get modern diseases.


    5-AZA A. Melvin Ramsay Acne Advocacy Alan Light Alternative medicine is an untested danger Ampligen Andrew Wakefield Anecdote Anthony Komaroff Antibiotics Antibodies Anxiety Aphthous Ulcers Apnea Asthma Autism Autoimmune Disease Behçet’s Ben Katz Bertrand Russell Biology Blood sugar Bruce Carruthers Caffeine Calcium Cancer Capitalism Cardiology Carmen Scheibenbogen CBT/GET CDC Celiac Disease Cereal Grains CFIDS Chagas Charité Charles Lapp Christopher Snell Chronix Clinician Coconut Milk Cognition Common Sense and Confirmation Bias Conversion Disorder Coxiella Burnetii Coxsackie Criteria Crohn's Cushing's Syndrome Cytokine Daniel Peterson Darwinism David Bell Depression Diabetes Diagnostic Differential Disease Diseases of Affluence DNA DNA Sequencing Dog DSM5 EBV EEG Eggs Elaine DeFreitas Elimination Diet Enterovirus Epstein-Barr ERV Etiology Evolution Exercise Challenge Faecal Transplant Fame and Fraud and Medical Science Fatigue Fatty Acids Fibromyalgia Francis Ruscetti Fructose Gene Expression Genetics Giardia Gordon Broderick Gulf War Illness Gut Microbiome Harvey Alter Health Care System Hemispherx Hemolytic Uremic Syndrome Herpesviridae High Blood Pressure Historic Outbreaks HIV HPV Hyperlipid Ian Hickie Ian Lipkin Immune System Infection Intermittent Fasting It's the environment stupid Jacob Teitelbaum Jamie Deckoff-Jones Jo Nijs John Chia John Coffin John Maddox José Montoya Judy Mikovits Karl Popper Kathleen Light Kenny De Meirleir Lactose Lamb Laszlo Mechtler LCMV Lecture Leonard Jason Leukemia Life Liver Loren Cordain Low Carb Low-Dose Naltrexone (LDN) Luc Montagnier Lucinda Bateman Ludicrous Notions Lumpers and Splitters Lyme Mady Hornig Mark Hasslett Martin Lerner Mary Schweitzer MCS ME/CFS Medical Industry Medicine is not based on anecdotes Michael Maes Migraine Milk and Dairy Mitochondria MMR Money and Fame and Fraud MRI Multiple Chemical Sensitivity Multiple Sclerosis Mutton My Symptoms n-1 Nancy Klimas Narcolepsy Neurodermitis Neuroscience NK-Cell Nocebo NSAID Nutrition Obesity On Nutrition Pain Paleo Parathyroid Pathogen Paul Cheney PCR Pharmaceutical Industry Picornavirus Placebo Polio Post Exertional Malaise POTS/OI/NMH PTSD PUFA Q Fever Quote Rare Disease Research Retrovirus Rheumatoid Arthritis Rituximab RNA Robert Gallo Robert Lustig Robert Silverman Robert Suhadolnik Rosario Trifiletti Sarah Myhill Sarcasm Science Sequencing Seth Roberts Shrinks vs. Medicine Shyh-Ching Lo Simon Wessely Sinusitis Sjögren's Somnolence Sonya Marshall-Gradisnik Speculation Stanislaw Burzynski Statins Stefan Duschek Study Sucrose Sugar Supplements Symptoms T1DM T2DM There is no such thing as Chronic Lyme There is no such thing as HGRV Thyroid Tinitus To Do Toni Bernhard Tourette's Treatment Tuberculosis Vaccine Video Vincent Lombardi Vincent Racaniello Virus Vitamin B Vitamin D VP62 When Evidence Based Medicine Isn't Whooping Cough Wolfgang Lutz WPI XMRV You fail science forever