Sunday, March 31, 2013

Stephen Ralph on Psychiatry, Behçet's, ME/CFS and Misdiagnosis

Stephen Ralph DCR(D) Retired.

30th March 2013

Hello there,

In recent years I have been considering the reliability of the whole “CFS/ME” diagnostic process.

From personal experience I have encountered numerous doctors who failed to possess the detailed specialist knowledge they needed to make a diagnosis of Behçet’s disease at both GP and specialist level.

From personal experience I have learned that standard blood tests or even CT/MRI scans or indeed other diagnostic tests such as endoscopy can and do fail to detect a complex clinical disease present in a patient.

I have no doubt that there is a diagnostic black hole between the insufficient knowledge of the doctor and pathologies that are not detectable by the basic tests they choose to request which produce negative results they then choose to rely on.

The diagnoses of “CFS/ME” and now Somatic Symptom Disorder have in my view been deployed by liaison psychiatry to exploit that black hole.

Once a diagnosis has been made, that diagnosis is presumed to be accurate by subsequent doctors but in reality there is no standard of diagnosis from one doctor to another which means that the whole diagnostic system – especially for complex clinical presentations – is a total lottery.

The system to challenge a given diagnosis has not been changed in decades.

In the UK a patient has a right to ask for a 2nd opinion but there is no guarantee that the doctor who gives a 2nd opinion will have sufficient knowledge to correctly assess a complex clinical presentation where the usual round of simple tests come back negative.

And, having been given a first opinion of “CFS/ME”; the doctor who considers that patient for a 2nd opinion already has a subjective view of what could be wrong with that patient because they have been re-referred by a GP who will give a medical history that may lean towards a CFS/ME diagnosis because the GP has insufficient knowledge to write an accurate 2nd opinion referral listing all the relevant symptoms that could add up to a rare disease such as Behçet’s disease.

In my own case as an example, my GP had no appreciation that my episode of Epididymitis was relevant to a possible case of Behçet’s and so this issue was not referred to when I was sent to another out of area doctor who formed that 2nd opinion.

With regards to “CFS/ME” a GP or a psychiatrist or a general rheumatologist will give the patient a diagnosis based upon the repeated reporting of a set of “invisible” symptoms over a period of months.

At present, “invisible” symptoms are being ascribed as “medically unexplained” or as a sign of somatisation.

The doctors who make these diagnoses are not specialists in rare and complex diseases such as Behçet’s disease where there is a significant crossover of “invisible” symptoms.

In the case of Behçet’s disease the bulk of Behçet’s research is focused upon those who show all the physical signs yet the majority of those who have Behçet’s do not have to show those physical signs and indeed patients with Behçet’s may show few or no visible symptoms at an outpatient examination.

There is in fact a research black hole representing the majority of Behçet’s patients who do not have all the obvious signs of the disease which in turn misinforms those who rely upon such research to inform them about other potential cases.

In short, the diagnostic system presently in place is stacked heavily against the patient.

Having thought about this for a considerable period of time I have come to the conclusion that the pyramid built by liaison psychiatry that fuels their involvement in “CFS/ME” revolves around a simple foundation assumption that a “CFS/ME” diagnosis handed to a patient must be the correct diagnosis.

If a GP or a psychiatrist carries out tests in conjunction with an immunologist or a rheumatologist; a set of negative test results is all that GP/psychiatrist/rheumatologist needs to give a “CFS/ME” diagnosis.

If that diagnosis has been handed to a patient by doctors who have little or no knowledge of complex sero-negative clinical presentations relating to rare medical diseases then there is a significant risk that the diagnosis he or she is giving their patient is in fact the wrong diagnosis.

As people reading this will know, I was subjected to a medical misdiagnosis by a number of doctor’s including GP’s and specialists.

The number of doctors involved went into double figures over a period of 12 years in total.

Over that period, my many individual symptoms were wrongly ascribed to conditions other than Behçet’s disease but in the end when all those symptoms were put together and compared to the correct diagnostic criteria for Behçet’s disease; a doctor finally looked at the evidence and came to the conclusion that I had been misdiagnosed and that I did in fact have Behçet’s disease.

In recent months I have asked pretty well all the liaison psychiatrists in the UK if they have encountered cases of Behçet’s disease passing through their out-patient clinics and none of them has replied that they had.

Professor Sir Simon Wessely for example told me that he was no Behçet’s specialist and that he would have to phone a colleague who was. Professor Wessely did not know if he had seen cases of Behçet’s pass through his clinic wrongly diagnosed as “CFS/ME”.

I recently e.mailed Professor Wessely to ask him about the outcome of his enquiries that were aided by one of his medical students but in spite of a rapid reply to my previous sequence of e.mails; Professor Sir Simon Wessely has not replied to my query regarding his findings.

I sincerely believe that I have homed in upon the Achilles heel of liaison psychiatry and their dominance of “medically unexplained” CFS/ME or indeed their latest diagnosis of Somatic Symptom Disorder.

It is my view from the evidence that liaison psychiatry; by providing doctors with the diagnostic option of CFS/ME and SSD have been responsible for the dumbing down of the clinical diagnostic process within our NHS and indeed around the world.

It is my view from the evidence that liaison psychiatry has made the potential for medical misdiagnosis acceptable practice within the medical profession as a whole.

Instead of considering rare sero-negative auto-immune disease explanations for cases of what end up as CFS/ME, a doctor now has an easy pathway to give a benign diagnosis of CFS/ME on the grounds that their set of negative test results together with a certain set of “invisible” symptoms means that the condition they are looking at is “medically unexplained” or an example of somatised symptom disorder.

Once medically misdiagnosed, the patient is disqualified from being in receipt of medications and therapies that would have been prescribed had that patient been correctly diagnosed in the first instance.

Disqualification of access to treatment will lead to that patient suffering considerably yet the doctors concerned will not recognise the severity of that patients suffering because that suffering will be put into the wrong context by that medical misdiagnosis.

I have known a case of Behçet’s disease where a patient was wrongly diagnosed as having “CFS/ME” for more than a decade and only had that misdiagnosis overturned when they suffered ocular micro-embolisms that caused permanent blindness in one eye and partial blindness in the other eye.

Away from Behçet’s we know of patients who suffered “diagnostic overshadowing” that lead to the late diagnosis of cancer and a rare heart condition.

The symptoms of cancer and the complex heart pathology were fatal in both situations and in both examples, the symptoms of neurological cancer and the heart pathology were almost certainly wrongly ascribed to the “invisible” symptoms of “CFS/ME”.

As far as the medical profession is concerned, a medical misdiagnosis or a medically missed diagnosis are considered as being “unfortunate”.

For the patient, a medical misdiagnosis or a medically missed diagnosis have profound and serious consequences and outcomes.

None of the doctors involved in making or perpetuating a medical misdiagnosis are subsequently held to account for what they have done to those patients.

In my own case, once I had been re-diagnosed I was treated as though I had simply failed back to the bottom of the pack.

There was no process of clinical education in that no investigation took place and no doctor involved was alerted to their poor clinical opinions that lead to me being medically misdiagnosed.

In short, it is my view that the clinical diagnostic process is in fact seriously flawed.

Patient’s are at risk from the medical profession at GP and specialist level.

In particular patients are at risk from an insufficient level of expertise used to make a complex diagnosis based on negative test results and a history of “invisible” physical symptoms.

Patients who present with a history of “invisible” symptoms and a set of negative routine test results are no longer referred to a super-specialist for the objective consideration of a set of relatively rare sero-negative medical diseases.

Instead, patients are given a benign diagnosis of “CFS/ME”; a diagnosis that by virtue of its own “somatisation” description – created by liaison psychiatry - is then incredibly hard or indeed impossible to overcome.

The present system seriously needs to be challenged and changed so that the patient has a fairer chance of being correctly diagnosed in the first instance and not medically misdiagnosed by inadequately qualified members of the medical profession.

The question is – how do we go about making a powerful effective challenge that effects such a change?

If we do nothing then nothing will change.

The medical profession have proven themselves happy to maintain the status quo.

As far as liaison psychiatry is concerned, it is imperative that the present system of a flawed diagnostic process stays exactly the same as it is today.

As far as immunology or rheumatology are concerned, they surely do not want their out-patient departments packed with patients who have discovered that they have been medically misdiagnosed.

A flawed diagnostic process fuels the creation of a base of “heterogeneous” patients who are subsequently involved in Cognitive Behavioural Therapy (CBT) or Graded Exercise Therapy (GET).

Those diagnosed as having “CFS/ME” are fodder for the exclusive “closed shop” self reinforcing research carried out by liaison psychiatry and no other parts of the medical profession.

One could argue that a totally unknown number of patients who are presently medically misdiagnosed with “CFS/ME” are in fact adding credence to the views of liaison psychiatry because a misdiagnosed patient will have a set of self perpetuating and untreated disabling symptoms (fueled by an unrecognised disease process) that the patient is unable to “cast off” or rid themselves of from a course of CBT or GET.

Those patients will reliably keep on reporting “somatised” “invisible” symptoms not because they have any mental impairment but because an auto-immune disease is producing those symptoms.

Such an unknown number of medically misdiagnosed patients can be accused by liaison psychiatry of being so neurotic or so somatised that they are unable to be “cured” by CBT.

Such misdiagnosed patients will be readily available year upon year for future “peer reviewed” research studies that go to reinforcing the validity of Somatised Symptom Disorder or “CFS/ME” using medically misdiagnosed patients to helpfully legitimise those artificial mental health labels.

Such misdiagnosed patients become – in the eyes of liaison psychiatry – desperately in need of even more psychiatric interventions and their sincere professional “help”.

Such patients become so firmly shunted into the somatisation cul-de-sac that they may never have their real diagnosis established unless they suffer a loss of sight or a pulmonary embolism or another “visible” crisis event such as a brain tumour or a fatal heart condition.

However, a pyramid can be reduced to rubble if the foundations are seen and recognised to be rotten.

Once it is realised that the pyramid is built on rotten foundations then when those foundations are condemned and removed, that pyramid will be reduced to rubble.


Stephen Ralph DCR(D) Retired (diagnostic radiography)

See also…

Friday, March 29, 2013

Natural Remedies Aren't

Recently I wrote about the only "natural remedy" there is: letting "Nature" do its job. Now the point was that there are other things – herbs to name one – that are branded as "natural remedies".

The problem I have with this is that: while they might seem like "natural" (coming from "nature"), and while they may or may not remedy an disease/illness/ailment (with not actually helping being quite likely), they are not "natural remedies". The point is those "natural remedies" have not evolved to help us. Evolutions does not work like that. Plants don't have the "intention to help us, they simply don't "want" to be eaten (with some parts of plants in the form of fruits being the notable exception), and develop (through evolution) defences against being eaten in the form substances that interfere with (among others) the metabolism of the animal/bacteria/whatever trying to eat the plant. Now these substances have pharmacological "side" effects that can be beneficial in some cases.

BTW: By the same measure we should brand penicillin as a "natural remedy", which should make obvious how ludicrous the term "natural remedy" is. A more appropriate term would be "traditional remedies" (if they actually are traditional, that is), which would do away with the image of the "kindness" associated with the word "natural". It still leaves us with an medicine with unverified profile of benefits and harms, as we know that people are superstitious and will believe all kinds of BS will help – just take a look what traditional remedies were against the black plague and then again tell me what is so special about "traditional remedies".

If only

From time to time one can hear the lament from the ME/CFS community:
"If only we had the money and the attention other diseases receive!"
Well, 1 Boring Old Man tells us how it looks like in other diseases:
This represents a massive medicaide fraud [TMAP] and over $50 M of NIMH money [STAR*D, IMPACTS, CO-MED, and EMBARC] chasing a mediocre idea about how to make some mediocre drugs less mediocre that failed at every turn. It’s an outrageous waste of valuable resources that makes one wonder if anyone at the NIMH even looks at the books.

Monday, March 25, 2013

The Difference between "Grief" and "Depression"

From 1 Boring Old Man:

  • Phenomenology: This comment summarizes the phenomenologic differences; "the hallmark of grief is a blend of yearning and sadness, along with thoughts, memories and images of the deceased person, while in contrast, depressed people ‘see themselves and/or the world as fundamentally flawed, inadequate or worthless.’ In essence, the psychological pain in ‘normative grief’ emerges from loss of the ‘other’ – and self-esteem is almost invariably preserved in the early stages – while the central characteristic of depressed states is compromised self-worth. The phenomenological distinction is sharp."
  • Natural History: Depressive illnesses tend to recur. He cites ample evidence to show that grief does not recur, nor does it predispose to future depressions.
  • Staging: Another summary quote, well referenced; "Staging is another important distinction. While clinical depression may be presaged by warning signs or symptoms, and it may have a slow or abrupt onset, it generally lacks the stages integral to grief."
  • Treatment Response: "Turning to treatment specificity, Shear expressed a common argument in stating that ‘depression requires treatment and grief requires reassurance and support’. The evidence base for antidepressant medication is convincing in relation to major depression – but is limited for the management of grief and often contingent on other factors, predictably including the presence or absence of a superimposed depression." If I may quote my friend who was prescribed Elavil when he was grief stricken, and I later asked him what it did for him, he replied, "It made me constipated."
I appreciate the clarity of this article. I wouldn’t have been able to parse the differences so crisply. To me, grief and depression are just different things [I think one can often distinguish them without even taking a history, though I'm not sure that such empathic communication is kosher in the DSMs].

The pandora’s box in this article is highlighted in red above. Parker suggests that many reactive depressions would fit better with grief than Major Depressive Disorder – that instead of broadening MDD, we should be moving in the other direction and limiting the use of this diagnostic category. He says this a suggestion, "Rather than drawing bereavement within the domain of the clinical depressive disorders (as DSM-5 appears still to favour), we might better lean the other way and consider whether many currently positioned clinical depressive disorders (especially the reactive depressive conditions) might fit more comfortably within a grief paradigm."

I would see this as more than a suggestion, rather something in the range of a mandate – an imperative. The removal of the Bereavement Exclusion is more than just a another goofy change to the DSM-5, it represents a bias that pervades the whole enterprise – diagnostic expansions that don’t medicalize the DSM-5, they dehumanize it…
What I find worthy to note is that "reactive depression" is basically "grief", or put in other words it is an depressive reaction to an cause of grief (which can be a chronic disease). And that this "reactive depression" may look similar at first glance to "depression" (as in "Major Depressive Disorder"), but is something different.

If you have an chronic disease and a co-morbid "reactive depression" (possibly caused by the disease), you can learn to cope. Learning to cope with your chronic disease. And learning to cope with your grief over your chronic disease.

If on the other hand you have a chronic disease and a co-morbid "major depression", trying to cope will not help you much with the depression.

And same as with the distinction between "fatigue" and "sleepiness", the distinction between "grief" and "depression" is an important one.

(However I don't have the impression that medical science knows how to deal with depression, no do I think that medical science has a clue about it causes. I'm confident that the causes of depression are nutritional in many cases, so we'll see how that plays out.)

Sunday, March 24, 2013

Most Registered Dietitians should be shot

Robb Wolf:
One of the largest hurdles the program has faced would be funny if it did not indicate what a battle we have ahead of us: By and large, the Registered Dietitians employed by the program have refused to follow the MD prescribed low-carb diet. Even when the medical directors showed these individuals the lab changes wrought by a paleo/low-carb, the RD’s were often discharged as they were unwilling to educate the officers how to eat a low-carb, paleo type diet. Let me say this more directly: these RD’s refused to believe the data before their eyes. Not all, but most and it’s been a hell of a problem as the MD’s say one thing to the officers, the RD’s say "high carb, low fat."

Komaroff is an Idiot

I have to revise the high opinion I had of Anthony Komaroff. He jumbles all kind of definitions together and muddies the waters (when he should know better):
… What is fatigue? It's a sensation of sleepiness, muscle weakness, or a feeling that you don't have the energy to do something - either physical or mental. It's the brain that experiences fatigue; that means there are certain chemical changes in the brain that lead to fatigue - even though those chemical changes may be triggered by many different illnesses. …
Komaroff, what the heck????

No, no, no. Fatigue is not "sleepiness". Sleepiness is the urge to sleep – and you can be fatigued without being sleepy. Somnolence is "sleepiness". "Tiredeness" is maybe a combination of fatigue and "sleepiness". But one can be very well fatigued without being tired. Being chronicly "sleepy" and being chronicly "fatigued" are two different symptoms! Were you find one, it is not unusual to find the other, but they a separate sensations.

And fatigue is not the feeling of "muscle weakness". Yes, fatigue and the feeling of "muscle weakness" can go together (e.g. after doing way do much physical work) – but one can be very well fatigued without having the feeling of "muscle weakness".

Yes, one could say fatigue is the feeling that one is "lacking energy".

But for crying out loud, what is the problem with saying:
Fatigue is the feeling of EXHAUSTION.

Or you could bloody well say:
Fatigue is having the urge to rest.

And no, no, no. Fatigue (like for example the feeling of pain) is not simply "chemical changes in the brain". Both pain and fatigue are signals of the physical state of your body – if pain is the gauge of the engine temperature, then fatigue is the gauge of the petrol tank. If pain tells you "Mate, if you keep doing that, something is going end up on the fritz pretty soon", then fatigue tells you "Mate, you are running on reserve, take a rest and replenish your energy or you'll end up with power". Pain is (usually) alleviated by stopping the action that causes the pain, and fatigue is (usually) alleviated by resting. The cause is (usually) not in the brain, it is only registered in the brain.

Words fail me how someone like Komaroff, who is so seemingly methodical, can be so confused with elementary definitions of the diseases he deals with. And I find it shocking that he spreads this confusion.

PS: It is however interesting that he mentions both mental and physical fatigue, but alas, he does it not in a way that is helpful.

On Nutrition: Jumpstarting the Paleo Diet

As part of a series of posts "On Nutrition" I have recently started, I was wondering how short I could write about the Paleo Diet, so here a short "Primer" as the result:

From the following foods, eat what you like, and eat as much (or as little) as you like:
  • Eat meat, fish, animal fat
  • Eat vegetables
  • Eat fruits
  • Eat real food, not industrial "Crap In A Box"
  • Prefer traditional preparation methods (avoid novel industrial ones)
Don't overeat, but with these foods I don't have the urge to overeat like I did when I ate grains and dairy and seed oil.

Try to avoid evolutionary novel foods like the following:
  • Avoid seed oil ("vegetable oil")
  • Avoid dairy and milk (especially pasteurized milk and dairy made from it)
  • Avoid cereal grains, soy
I personally recommend to not eat any seed oil, nor dairy, nor grains. But if you can't let go of your morning toast with butter, then limiting the amount is better than consuming much from these three.

Everything else? You need to find out yourself.

Is it some food your grand-grandmother would have had access to? Then it might be OK.

Can the food be produced only industrially? Oh, oh, better stay away from the stuff.

There is more, but for a start this should be enough.

The Problem with "Skeptics"

First of all, let me open by saying that skeptics can do a a brilliant job at dissecting scientific fields. Some of the people I admire (for their informed opinion in one field) are skeptics.

However, I have seen by now quite a few skeptics (self declared and otherwise) who are very good or even brilliant in one field – and whom I would even consider based on the quality of their argument to be authorities in their field – who on the other hand are utterly daft idiots led by confirmation bias in other fields and whose word should not be trusted. A nice combination I have seen is "climate science" and "politics" – usually those who are good in "climate science" are idiots when it comes to "politics" (and vice versa).

Therefore I think the problem with skeptics is as follows: Most skeptics are firmly placed in "their camp", and only skeptical of "the other camp". If the position of "their" camp is close to reality, skeptics can really shine. If, however the position of their camp is BS, then skeptics are lost.

So I guess the label "skeptic" creates a problem. I think the solution what was once called "Materialism", which is now being rebranded as "Naturalism": An improvement of the approximate representation of reality as it exists.

Do "evolutionary novel" foods harm the health of a few/some/many/most people? Let's find out! Is the Earth's climate on the verge of collapse due to human CO2 emissions? Let's find out!

Instead, what I see with many skeptics is once they have "settled" in a field, then most skeptics tend to be quite "partisan". Their critical zeal is limited to the "other side", their own side gets a free pass time and time again. They no longer thrive for the better grasp of reality – their skepticism has vanished it seems. They limit themselves to communicating their position (or rather bawling it out into the world) – as if life were a "debate club". No matter how good your argument, the Earth is neither flat nor hollow. If you want to shout me down, that the Earth is hollow, and that the bible is right, and that the climate is collapsing, and that government is the source of all evil, and that saturated fat is evil, and that there is an "electric universe", then I will leave such a debate. You "win". But that doesn't mean you are "right", that doesn't mean that what you say is an approximate representation of reality. And it means that your "skeptical" position is quite a contradiction in terms.

The Psychological Stress Confussion

NPR interview on the topic of GWI:
DANKOSKY: So Dr. Steele, what do we know about the causes? Because there have been a number that we've heard about over the years. Maybe we can run through a few of them. One of the things that is mentioned sometimes is stress or PTSD, something that we've heard a lot about from these last few wars, Iraq and Afghanistan. How much does stress have to do with it, do you think?

STEELE: That's a really good question. I think for many years after 1991, after the war got over, a lot of folks really didn't know what to make of Gulf War Illness or Gulf War Syndrome. But at this point, now 22 years later, we actually have a lot of students that tell us a lot about what may have caused Gulf War Illness.

Most of the studies early on looked at things like stress and post-traumatic stress disorder, but we now know very definitely that Gulf War Illness, specifically in 1991 Gulf War veterans, is not a stress-induced or trauma-induced kind of disorder. The rates of things like post-traumatic stress disorder are very low in 1991 Gulf War veterans, much lower than we're seeing in current returning veterans from Iraq and Afghanistan.

However, there is a long list of potential causes that different people have looked at over the years, many things like the vaccines that veterans receive, the oil well fires that many of us remember from that time, all kinds of chemical toxicants that they were exposed to.

And just looking over the broad range of studies, at the many epidemiologic studies that have been conducted in this population, we know that several of these risk factors or toxicants have risen to the top in terms of the strength of evidence that suggests that they are connected with Gulf War Illness.

And at this point we can say that the highest risk factors relate to use of prophylactic medication given to veterans to protect them from nerve agents. That pill was called pyridostigmine bromide. In addition, there was extreme overuse of pesticides in some groups of veterans during the 1991 Gulf War. And so those are also linked to higher rates of Gulf War Illness.

And then we also know that some veterans were exposed to very low levels of nerve agents during the Gulf War, and there's also some evidence supporting an association between Gulf War Illness and the nerve agent exposures that happened during and after the war.

Overall, though, the studies consistently show no link between for example serving in combat and higher rates of Gulf War Illness.
Why is it, that if someone postulate that "stress" (or "lack of resilience" or some other "psychological fault" of the patient) is causative for a (hard to grab) disease, that there is so little scepticism? Why are people not challenged more if they spread their "psycho-stress confusion"? And we are not talking here about physical stress, no here supposed psychological stress (combined with some sort of supposed defect of the patient) should be able to cause physical disease like GWI? A disease that is unique to the gulf war veterans?

I'm sure the Theologians of the Wessely School have an explanation for why there are so many gulf war veterans have GWI – this will be an explanation however that does not create clarity, but an explanation that creates confusion instead…

Friday, March 22, 2013

The Only "Natural" Remedy

I will let you in on a secret. I will tell you the only natural remedy there is. Are you read? Here it is:

The only "natural" remedy is waiting, and letting the body do its job.

Got it?

When you are ill, simply let the body do its job.

Does your body signal thirst? Then drink water.

Does your body signal hunger? Then eat something. A nice fatty chicken soup, free of seed oil, for example, is usually considered good food when you are ill.

And if your body signals pain, then it signals that something is not good. Can you stop it? Then stop it. If your leg hurts (say because it is broken), then pain signals you to not use the leg.

Does your body send other signals you can easily understand? Follow them.

In most cases the body signals what it needs. Simple, isn't it?

What, that is not enough for you? You want to do more? You think there must be better ways? You know you can better than that? Fine, there is – depending on your disease – some more help. But none of it a "natural" remedy – so please, stop using that word. After all, you wouldn't try some "natural" strychnine, even if it were 100 % pure organic, now would you?

Trans Fatty Acids: From Neutral to Bad in 6 Years

Robb Wolf on Trans-Fatty Acids (citing Loren Cordain):
Nutritional science is not only a newly established discipline, but it is also a highly fractionated, contentious field with constantly changing viewpoints on both major and minor issues that impact public health. For example, in 1996 a task force of experts from the American Society for Clinical Nutrition (ASCN) and the American Institute of Nutrition (AIN) came out with an official position paper on trans fatty acids stating,
We cannot conclude that the intake of trans fatty acids is a risk factor for coronary heart disease” (4).
Fast forward 6 short years to 2002 and the National Academy of Sciences, Institute of Medicine’s report on trans fatty acids (5) stating,
Because there is a positive linear trend between trans fatty acid intake and total and LDL (“bad”) cholesterol concentration, and therefore increased risk of cardiovascular heart disease, the Food and Nutrition Board recommends that trans fatty acid consumption be as low as possible while consuming a nutritionally adequate diet”.

The "Whole Grains are Healthy" Myth

Fat Head:
Every time I tracked down a study purporting to prove the benefits of whole grains, the comparison was between people consuming whole grains and people consuming white flour. All we can determine from those studies is that whole grains aren’t as bad for us as white flour. To prove whole grains have real benefits, we’d have to compare people who eat whole grains to people who eat no grains.

… Well, here’s one study that actually measured changes in heart-disease risk factors after feeding subjects whole grains (WG):
A total of 316 participants … were randomly assigned to three groups: control (no dietary change), intervention 1 (60 g WG/d for 16 weeks) and intervention 2 (60 g WG/d for 8 weeks followed by 120 g WG/d for 8 weeks). Markers of CVD risk … were: BMI, percentage body fat, waist circumference; fasting plasma lipid profile, glucose and insulin; and indicators of inflammatory, coagulation, and endothelial function. …
120 grams of whole grains … that’s a lot of hearthealthywholegrain goodness. Now let’s look at the results:
Although reported WG intake was significantly increased among intervention groups, and demonstrated good participant compliance, there were no significant differences in any markers of CVD risk between groups. A period of 4 months may be insufficient to change the lifelong disease trajectory associated with CVD. The lack of impact of increasing WG consumption on CVD risk markers implies that public health messages may need to be clarified to consider the source of WG and/or other diet and lifestyle factors linked to the benefits of whole-grain consumption seen in observational studies.
Yes, I’d say the public-health messages regarding whole grains need to be clarified. Here’s my version of the clarification:
Sorry … turns out we were wrong about the whole-grain thing.

Debunking the Paleo Debunkers

Some doctors are having a go at "that fad diet" – again. And of course there are some, shall we say, "problems" when the supposedly scientific mainstream tries to debunk Paleo.

Paul Jaminet at PHD has some thoughts to offer:
Yet, in the Paleolithic, the ancestral diet was probably similar in general outline for at least 2 million years: it consisted largely of meat, marrow, and plant foods collected from open woodlands and tree-spotted grasslands. There was sufficient time for new mutations to appear and rise to fixation, and then new mutations to appear and reach fixation against this new genetic background, and so on for many cycles. It is certainly possible that humanity became adapted to this (slowly changing) Paleolithic diet, and that the genetic variety introduced in the Holocene has been insufficient to destroy our fitness for a diet like that of the Paleolithic, and insufficient to make us well adapted to new Neolithic diets.

This point – that the relevant time-scale for assessing adaptedness may be the time for the genome to reach equilibrium, not merely the time for new point mutations to appear and grow to regional prominence – is an elementary one in evolutionary biology, one that is made in our book on pages 4-6, but from the Chronicle excerpt and various reviews (including this Amazon reader review), it appears that Zuk does not acknowledge this reason why treating the Paleolithic as an environment of evolutionary adaptedness may be a “Paleoinsight,” not a “Paleofantasy.”
Tuck at Yelling Stop:
She shows 4 books on one of her first slides, two of them are The Paleo Diet and The Primal Blueprint. She's not read either of them.

Her first "rebuttal" of the paleo diet is to point out that we can't get by on meat alone since we need to eat vegetables for vitamin C.

1. Neither of those books advocates eating only meat. Both encourage you to eat organ meats and lots of vegetables.

2. She's wrong on the facts. You do not, in fact, need to eat vegetables to get vitamin C. You can, in fact, get all you need on a diet of 100% meat. This was demonstrated almost 100 years ago in a famed experiment where Arctic explorer Vilhjalmur Stefansson ate meat under medical supervision for a year …

She proceeds to attack a bunch of other claims that the paleo diet doesn't make, or she gets her facts wrong.

Falsus in uno, falsus in omnibus
Melissa from Hunt.Gather.Love takes on the atherosclerosis claims:
I've written about mummy abuse before, but today the press is having a field day with the preliminary findings of the Horus study, an examination of atherosclerosis in ancient mummies. Luckily, you don't have to listen to them, because the study is available online for anyone to read. …

But let's not forget that the atherosclerosis levels are still lower than modern levels. …

And that atherosclerosis is a complex condition that does not always lead to disease.
These straw-men arguments you see from the medical mainstream ("Paleo is a stupid and unhealthy meat-only fad-diet.") are so tiresome that I lack the energy to engage in them. I state my opinion (for what it's worth) and then leave those clowns alone, so they can reaffirm themselves by attacking straw-men in their Confirmation Bias El Dorado.

More Evidence That Seed Oil Might Be Bad For Your Health

Low serum eicosapentaenoic acid / arachidonic acid ratio in male subjects with visceral obesity

Kana Inoue, Ken Kishida, Ayumu Hirata, Tohru Funahashi and Iichiro Shimomura

Nutrition & Metabolism 2013, 10:25 doi:10.1186/1743-7075-10-25
Published: 12 March 2013

Abstract (provisional)

Visceral fat accumulation is caused by over-nutrition and physical inactivity. Excess accumulation of visceral fat associates with atherosclerosis. Polyunsaturated fatty acids have an important role in human nutrition, but imbalance of dietary long-chain polyunsaturated fatty acids, especially low eicosapentaenoic acid (EPA) / arachidonic acid (AA) ratio, is associated with increased risk of cardiovascular disease. The present study investigated the correlation between EPA, docosahexaenoic acid (DHA), AA parameters and clinical features in male subjects.

The study subjects were 134 Japanese with diabetes, hypertension and/or dyslipidemia who underwent measurement of visceral fat area (eVFA) by the bioelectrical impedance method and serum levels of EPA, DHA and AA. EPA/AA ratio correlated positively with age, and negatively with waist circumference and eVFA. Stepwise regression analysis demonstrated that age and eVFA correlated significantly and independently with serum EPA/AA ratio. Serum EPA/AA ratio, but not serum DHA/AA and (EPA+DHA)/AA ratios, was significantly lower in subjects with eVFA >=100 cm2, compared to those with eVFA <100 cm2 (p=0.049). Subjects with eVFA >=100 cm2 were significantly more likely to have the metabolic syndrome and history of cardiovascular diseases, compared to those with eVFA <100 cm2 (p<0.001, p=0.028, respectively).

Imbalance of dietary long-chain polyunsaturated fatty acids (low serum EPA/AA ratio) correlated with visceral fat accumulation in male subjects.
Or in other words:
Evidence that obese people consume disproportionate more seed oil than non-obese people.

The obese of the world have been eating seed oils like crazy the good patients they are, as ordered by the good doctors at the ADA and AHA.

What does that tell us about the advise of the ADA and AHA to consume more seed oil to avoid obesity? (Hint: It's a two letter word that starts with an capital B and ends with an capital S)

To rehash for all of you haven't internalized human essential fatty acid metabolism (shame on you):

Linoleic acid (LA) gets metabolized into arachidonic acid (AA).

Alpha-linolenic acid (ALA) gets metabolized into eicosapentaenoic acid (EPA).

Seed oil has an high content in poly-unsaturated fatty acids "PUFAs" (seed oil has an high content of ALA, and even higher content of LA), and seed oil has a low ALA/LA ratio.

Consumption of seed oil (with its low ALA/LA ratio) will lead to a low EPA/AA ratio (like no other food) and it will increase the AA level like no other food.

And this low EPA/AA ratio (that plausibly could only be caused by seed oil) correlates with obesity.

BTW: AA in turn gets metabolized into "series 2 prostaglandins" which are considered to be "more inflammatory" (red box above).

Furthermore PUFAs do negatively influence the carbohydrate metabolism and muck up the way insulin works (which will drive fat into fat cells).

And again:

No other food contains as much PUFAs as seed oil.

No other food allows you to raise your AA level like seed oil.

No other foods allows you to lower your EPA/AA ratio like seed oil.

So in my maybe not so humble opinion:
No other food besides seed oil is necessary to explain obesity.

Or put bluntly:
Obesity? Caused by increased seed oil consumption.
And look! Seed oil consumption has increased! Consumption of butter and lard have gone way down! We are doing what the ADA and AHA are telling us! Thank god!

And look! Obesity is up! Wonderful to see the marvellous advise of the ADA and AHA bearing such beautiful fruits!

 And look at this! Diabetes is going up like crazy! It brings water to my eyes to see the success of the ADA and AHA!

And look here! Heart disease is at an all time high! If that doesn't tell you that the ADA and AHA are doing a top job, I don't know what will.

So avoid seed oils, if you do not want to become obese and run the risk of getting other "diseases of civilization".

If on the other hand you do want to become obese, then follow the advise of the ADA and AHA and make sure you consume lots and lots of seed oil.

One more thing, while we are at it: If you think you are a bird or a mouse – and who am I to judge – then I guess eating nothing but seeds (and the occasional bottle of cold-pressed olive oil) is a viable and healthy diet for you and other members of your species – but please don't counsel humans on their nutrition.

Thursday, March 21, 2013

Mucus !

And here I write about a "YUCK!" topic - be warned.


I promise to make it short not with no intention to revisit it any time soon.


So here we go, you have been warned.

The Problem With "Resiliency"

1 Boring Old Man:
No matter how it’s framed, seeing the traumatized person as not resilient implies that there’s something they could’ve done. That’s what they already think and the notion of resiliency reinforces that belief, which I think is false. If they could’ve, they would’ve. The essence of the post-traumatic illness itself is an attempt to "prevent the past" – eg become more resilient going forward through hypervigilance and other maladaptive mechanisms. Traumatic symptoms are often perceived by the afflicted as a defect, something bad about themselves. It’s hard enough to help them accept that it was something that happened "to them" rather than a weakness or something they did without throwing in un-resiliency to needlessly complicate matters.
It is always the same. The doctor, when faced with problems that are hard to grab, is tempted to see it as a fault of that person (instead of an lack of knowledge) – so if that person does not get better, it is the person's fault, and the doctor is vindicated. And if the person does get better, it is as well vindication of the doctor. The doctor can't loose with "blame the patient".

(Furthermore, having experienced personally, and read many anecdotes on how our "modern" nutrition drives anxiety, I strongly suspect that nutrition might play a substantially contributing role in diseases from the psychological/psychiatric/mental/neurologic/whatever spectrum like PTSD.)

Wednesday, March 20, 2013

On Nutrition: What to try if the Paleo Diet fails

As I had some health problems that refused to clear up completely, I thought I write down some quick thoughts what one could try.

So here are a few very quick thoughts on what to do when your diet "fails" (for some amount of "fail"). And on a related note, I touch on some things (e.g. eggs and nuts) very quickly that might be a problem (cf. Robb Wolf's autoimmune protocol), despite being considered by some as staple foods for a Paleo Diet.

(This is an partial rehash of this list of foods to avoid.)

Foods that are "Paleo" (and might be OK for most) but might be a problem for some people:
  1. If you have a problem with dairy, try to avoid beef/veal* (as well as avoiding dairy). Try to avoid dairy and beef for at least at month, see if it helps – even if you don't know whether your problems were caused by dairy.

    (And yes, butter is dairy, and yes, milk-chocolate is dairy, and yes, if it contains any milk protein whatsoever you should try to avoid it and see if it helps.)
  2. In similar spirit: you might have a problem with one source of meat or fish. It might be possible that one person has health problems from chicken meat, but does fine with beef and pork. Then another person might have health problems from pork, but might do fine with other sources of meat. Same goes for fish (e.g. shell fish vs. "normal" sea fish vs. freshwater fish). You might need to experiment a bit to find out what harms you, and what doesn't (no doctor and no book will spare you from trying out things).
  3. I would suggest to avoid coconut. Coconut milk does not agree with me – I get gastrointestinal problems from coconut products. Might be something in the products I can buy here, might be coconut itself
Foods that are not (or not exactly) "Paleo" and might be a problem for some (but might be OK for others):
  1. Avoid eggs, at least for a month. Cavemen did not have regular access to eggs. I had similar problems with eggs as with dairy. Free range eggs with raw yolk might help a bit, but I'd recommend trying to remove all eggs for a month and see if it helps.
  2. Do not go on a "Very Low Carb" Diet (VLC) for a longer periods. Maybe if you feel you need to do VLC to combat diabetes then do it, and even than I would not recommend it for longer periods. Find "safe" sources of starch, maybe this list from above helps.
  3. Avoid nuts, chocolate, honey, tea, coffee, herbs, supplements, cured meat, industrial meat products (aka CIAB sausages) and similar stuff for a month – see if it helps.
  4. If you feel you need supplement your gut with probiotics, then eat  unwashed homegrown fruits and vegetables – I would not supplement with probiotics from (online) shops.
  5. Some people eat all kinds of seeds on a paleo diet (e.g. flax seed flour or other gluten-free flour). If you eat such seeds and have still health problems, I would suggesting looking into whether these are the cause.
Go ahead, try changing your diet, see if it helps you – no doctor can do that for you.

*I suspect that cow-protein in dairy elicits an (auto-)immune response in some people, and once your body reacts in that way to dairy, cow-protein in beef might cause a similar reaction. Some proteins in dairy and in beef might be similar (or even the same), as they are from the same animal – duh! And if it is auto-immune, then even gras-fed beef will not help.

Monday, March 18, 2013

Annette Woo, I Presume

It is my hope that this community can begin to heal from the negativity that was generated by a few individuals after the collapse of XMRV.
"Negativity"? After the collapse of XMRV?

What. The. Fuck.

It was a barrage of stupidity that hit the ME/CFS "community" from the moment that the WPI-Woo-Insititute and Dr. Mousovitz announced the BS results, of their possibly intentional contamination with VP62-plasmid.
 If the "community" needs to "heal" from anything, then it is all the BS that was spread for years by Mikrovitz, by the Woowhittemores and the Gerwyn-idiot-sockpuppet-army. They misdirected the scientific community and they blame others for "negativity"?

You want to tell me something about who was responsible for the "negativity" and are not capable of one honest word, of one word of apologize for the disaster that was unleashed at your Woo-Institute?

You know what Annette, I kindly ask you to go fuck yourself.

Friday, March 15, 2013

I have not read this before, therefore it hasn't happened before

Doctor to patient:

"I have not read about your symptoms being caused by nutrition, therefore it is unlikely that other people suffer from similar problems. And even if they suffer from somewhat similar symptoms it is unlikely nutrition does this in other people as well, because I have not read about it before."
Can anybody spot the problem with this approach? Take this bad joke if you need an hint.

Friday, March 8, 2013

Dairy and Somnolence

OK: I eat some dairy at 10am, drink some milk at 11am, and get drowsy some two to three hours later, at 1pm.

Thursday, March 7, 2013

Somnolence, Dairy and Beef?

I'm currently running a self-experiment where I have reintroduced dairy and beef to my nutrition. The main goal was to provoke my acne into showing its ugly head(s) (sorry for the lame pun) – with the end target of getting a proper diagnosis of Behçet's. And so far, my acne is an almost no show. Bummer.

But another "old friend" (fiend?) showed its head again: Somnolence. I am drowsy as hell in the afternoons, and have currently major problems writing this post. The somnolence has gone for good only after I dropped the beef a couple of months ago.

So it seems ironic that I used to drink my coffee with milk when I tried to fight somnolence…

[Update] Now on the next day I did not eat any more dairy (only in the evening the day before), but I am still getting tired at around 1pm. Let's see, it isn't as simple as I thought.

Saturday, March 2, 2013

Nestle Nutrition Workshop: Dairy might be bad for you – Oops

Nestle Nutr Workshop Ser Pediatr Program. 2011;67:131-45. doi: 10.1159/000325580. Epub 2011 Feb 16.

Evidence for acne-promoting effects of milk and other insulinotropic dairy products.

Melnik BC.

Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany.

Acne vulgaris, the most common skin disease of western civilization, has evolved to an epidemic affecting more than 85% of adolescents.

Acne can be regarded as an indicator disease of exaggerated insulinotropic western nutrition.

Especially milk and whey protein-based products contribute to elevations of postprandial insulin and basal insulin-like growth factor-I (IGF-I) plasma levels.

It is the evolutional principle of mammalian milk to promote growth and support anabolic conditions for the neonate during the nursing period.

Whey proteins are most potent inducers of glucose-dependent insulinotropic polypeptide secreted by enteroendocrine K cells which in concert with hydrolyzed whey protein-derived essential amino acids stimulate insulin secretion of pancreatic β-cells.

Increased insulin/IGF-I signaling activates the phosphoinositide-3 kinase/Akt pathway, thereby reducing the nuclear content of the transcription factor FoxO1, the key nutrigenomic regulator of acne target genes.

Nuclear FoxO1 deficiency has been linked to all major factors of acne pathogenesis, i.e. androgen receptor transactivation, comedogenesis, increased sebaceous lipogenesis, and follicular inflammation.

The elimination of the whey protein-based insulinotropic mechanisms of milk will be the most important future challenge for nutrition research.

Both, restriction of milk consumption or generation of less insulinotropic milk will have an enormous impact on the prevention of epidemic western diseases like obesity, diabetes mellitus, cancer, neurodegenerative diseases and acne.

"No Change In AHA Recommendations On Saturated Or Poly-unsaturated Fat"

Tuck at the blog Yelling Stop: "No Change In AHA Recommendations On Saturated Or Poly-unsaturated Fat"

AHA stays the course with their Omega-6 Seed Oil Insanity.

Friday, March 1, 2013

On Nutrition: Seed Oils, Omega-6 and First Principles

An attempt to a (sometimes polemic) precursor post on seed oils ("vegetable oils"), Omega-6 fatty acids ("n-6 fats") and Eicosanoids – with special attention to linoleic acid (18:2), which is one of the main fatty acids in seed oils.

This post will be followed by a longer post on seed oils in the hopeful near future.

I shall try to show from "first principles" alone the likely negative health implications resulting from the generally recommended increased consumption of n-6 fats – with organizations like ADA and AHA being two of worst offenders.

All points in this post should be (bloody) obvious and indisputable for anybody slightly versed in the fields of chemistry, biology, evolution and medicine.

0. Linoleic acid is essential

As the human body can not produce linoleic acid, yet various functions in the body depend on it as precursors to other molecules, linoleic acid needs to be consumed.

(I think much of the confusion over the "healthyness" of seed oils stems from this fact. Water is by the same measure essential, yet the consumption of supranatural amounts of water can kill you, and given enough persistence will in fact kill you.)

1. An increased consumption of linoleic acid increases levels of said fats in the stomach, in the blood, and finally in the tissues.

Otherwise the recommendations of the ADA and AHA would be completely nonsensical.

2. The body has no mechanism to regulate the tissue levels of linoleic acid

It is always hard to prove a negative. I am however not aware of any mechanisms by which the body would regulate the levels of specific fatty acids.

Furthermore I think it should be obvious that no such mechanism was necessary in evolutionary past, as we see in the next point:

3. No other naturally occurring food besides seed oils enables to consume such large amounts of linoleic acid

Every other naturally food in this world contains comparatively low levels of linoleic acids.

Even if someone consumes seeds (and nothing but seeds) it is difficult to reach these amounts of linoleic acid that one can consume with seed oils (and should consume, according to the ADA and AHA).

Once more: Only with seed oils is it possible to massively increase the consumption linoleic acid – no other food in the world can do that.

(Furthermore seed oils makes it possible to consume massively more n-6 than n-3 fatty acids, unlike most other foods. Usually food contains – with pork and fish being two prominent exceptions – roughly equal amounts of n-3 and n-6 fatty acids. That will be important for the eicosanoid point further down the list.)

The proof for this point (the linoleic acid content of various foods) is left as exercise to the reader – the data is available. (E.g. I can recommend the very excellent German Bundeslebensmittelschlüssel BLS, which can be searched in German for free on this commercial website. The BLS data is even available in English.)

4. Consumption of seed oils in large amounts is only possible for about a century

Before the industrial production of seeds oils, it was simply not possible to consume linoleic acid in large amounts. I think this should be self evident.

5. The recommendations of the ADA and AHA should be considered as consumption of supranatural levels of linoleic acid

As far as I know no identified deficit is addressed by the the recommendation to consume supranatural levels of linoleic acid. As far as I know no mechanism is stated by which the need would arise to consume supranatural levels of linoleic acid. Supposedly n-6 fatty acids are more healthy than saturated fat, but no mechanism has been shown so far despite decades of research.

The practice of the ADA and AHA to recommend the consumption of supranatural levels of linoleic acid reminds me of those who recommend various supplements  based on cherry-picked, slim and vague data – with arguably the volume of cherry-picked slim and vague data from the ADA and AHA being quite large.

6. There was not enough evolutionary time to adapt to the massively increased consumption of linoleic acids

Should be obvious for anybody with a little bit of experience with evolution that there was not enough evolutionary pressure and not enough time to adapt to a diet high in seed oils – if you dispute this fact, I'm afraid there is nothing I can do for you.

7. Supranatural amounts of linoleic acid in the tissue will lead to supranatural levels of series 2 prostaglandins in the tissue

So let me present my strongest evidence:
To summarize:
  • Eicosanoids are signalling molecules derived from n-3 and n-6 fatty acids, involved in processes like inflammation.
  • The left column is the n-3 cascade, the one on the right the n-6 cascade 
  • n-3 fatty acids are converted among others into PG3s (series 3 prostaglandins, a type of eicosanoids, the box to the right of EPA)
  • n-6 fatty acids converted among others into PG1s and PG2s (series 1 and series 2 prostaglandins, the boxes to the left of DGLA and AA)
  • Both the n-3 and n-6 fatty metabolism shares the same enzymes (e.g. delta6-desaturase, elongase, delta5-sesaturase, and so on) to produce their various eicosanoids.
  • While it is considered that n-3 fatty acids have a greater "affinity" to these enzymes, if you massively increase the amount of linoleic acid (on the top of the right column) – through say the ADA and AHA recommended consumption of seed oils – this will massively increase the amount of PG1 (turquoise box) and PG2 (red box, uh-huh, red isn't good, is it?)
  • PG3s (produced from n-3 fatty acids) are generally considered "less inflammatory" 
  • PG2s (produced from n-6 fatty acids) are generally considered "more inflammatory" (again, the red box) – seed oil, a bona fide candidate for a disease mechanism involved in heart disease. *
So, in one sentence:
If you eat seed oils, you increase the levels of the pro-inflammatory series 2 prostaglandins above what would be considered "natural" – no other food can do that.

If you think this is good, then you might be an idiot.

People at the ADA and AHA think that the consumption of supranatural levels of seed oil is good.

People at the ADA and AHA might be idiots.

Further studies are warranted.


* Be advised that this is not the only mechanism by which seed oils and the overconsumption of linoleic acid will cause disease – see here for a mechanism by which seed oils and the overconsumption of PUFAs could cause obesity and T2DM.


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