New paper: Inability of ME patients to reproduce VO2 max indicates functional impairment

[Sean]

@alex3619 Dr. Barry Marshall (an amazing Australian doctor) proved that the bacterium Helicobacter Pylori is the cause of most peptic ulcers, by infecting himself with H. Pylori and subsequently developing peptic ulcer.

For this important "discovery", or shall we say reversal of the medical doctrine, which previously supported stress, spicy foods and stomach hyperacidity as causes of ulcers, he was awarded the Nobel Prize in Physiology.

He and Robin Warren.

 

[peggy-sue]

When on earth did the "avoid spicey foods" come in to it?

I've certainly heard it, but what is the justification?

The ancient Egyptians used cumin to calm IBS;
Ginger is good for nausea;
Garlic is antiseptic and antifungal;
And we all know about turmeric...
it goes on and on...

Do they actually mean avoid chilli, just so you can avoid the afterburn bit where you discover you should have put the toilet paper in the 'fridge?

 

[MeSci]

When on earth did the "avoid spicey foods" come in to it?

I've certainly heard it, but what is the justification?

The ancient Egyptians used cumin to calm IBS;
Ginger is good for nausea;
Garlic is antiseptic and antifungal;
And we all know about turmeric...
it goes on and on...

Do they actually mean avoid chilli, just so you can avoid the afterburn bit where you discover you should have put the toilet paper in the 'fridge?

I never know whether I should avoid chilli or not. A herbalist friend once advised avoiding chilli and black pepper for IBS-type problems, but there is stuff all over the net saying that they are GOOD for it!

Wonder if I should risk it. I have been avoiding chilli and black pepper for years but I love them.

 

[peggy-sue]

It doesn't affect M's IBS.

The only things he needs to avoid are processed foods and "chemically made" drinks (industrially produced beer, coke etc.)

Go on, be a devil, have a little hot stuff, you know you want it...

 

[MeSci]

It doesn't affect M's IBS.

The only things he needs to avoid are processed foods and "chemically made" drinks (industrially produced beer, coke etc.)

Go on, be a devil, have a little hot stuff, you know you want it...

Oooh, you wicked temptress. Are you sure your name's not Eve?

(I think I will though. )

 

[peggy-sue]

Just remember, only a teeny tiny bit - you won't be used to it and a little will seem very hot indeed.
You can have more tomorrow, your resistance will build up...
love,
Eve-y-sue.xxxxxx

 

[MeSci]

Just remember, only a teeny tiny bit - you won't be used to it and a little will seem very hot indeed.
You can have more tomorrow, your resistance will build up...
love,
Eve-y-sue.xxxxxx

Yes, Doctor.

 

[Kati]

He and Robin Warren.

My heroes.

 

[alex3619]

Chili can cause severe pain if you have a hole in your gastric lining. Spices are often high in salicylates, which means they reduce healing of gastric ulcers by blocking eicosanoid synthesis. So they can be exacerbating factors. If they can make it worse, maybe they are causal? That was, I think, the driving factors. Similarly milk can sooth an ulcer. So the advice was to drink milk. These were both simple clinical observations that led to sweeping theoretical speculation.

Hard evidence of pathophysiology is what makes the difference with CPET. There is no denying there is a problem. The question now is, for those patients with the energy crash, why is this a problem? What are the mechanisms?

I love my spicy food. Indeed, I just finished a bowl of very spicy chick pea stew, which was leftover from earlier that I had put in the fridge. Its very nice cold. Chili and other spices are also reported to be very good for suppressing candida, though I do not know for sure if that is true. What is important in my opinion for spices is to not increase your intake suddenly, and if you stop eating them for a time to reintroduce them slowly. This allows, in my view, for your enzyme systems to adapt.

 

[peggy-sue]

Thanks, Alex - that's interesting!

So it would be a good idea to find out which specific spices contain things such as salicylates.

I'm fairly fussy about spices - there are quite a few I really do not like - others I go completely overboard on.

Go on, tell me that coriander/cilantro is full of salicylates - I hate the stuff, it tastes as if somebody's squirted washing-up liquid into my food.
I can then feel justifed in asking for it to be left out when I get a bought curry.

 

[alex3619]

People either love cilantro or hate it. I can tolerate it in some dishes, but usually avoid it. Cilantro is regarded usually as moderate salicylate, but you eat it in higher quantities than, say, black pepper. Salicylate sensitivity is dose related, so a lower salicylate product eaten in large quantities may be worse than a high salicylate spice used sparingly. Coriander seed on the other hand is a high salicylate food, and most of my favourite spices are high salicylate too. However you need sprinkles or small amounts, you don't eat them by the pound.

When I was on a low salicylate diet every time I came into contact with salicylates I had a massive reaction. On a moderate salicylate diet, eaten every day, I have no such vulnerability. This is not an excuse to pig out on salicylates though. Constant dose is better. Sadly I don't seem to really learn this as every now and again I give in to impulse and crank up the spice, usually to my regret. Yet it makes for interesting food .... there is some consolation. One of the things that salicylates do to me if I eat way too much is shatter my sleep cycle.

I keep coming back to CPET and severe patients. One hypothesis I have that will not go away, it seems solid to me, is that severe patients exceed their aerobic threshold just with basic survival. I think gas analysis might show this without any exercise. After I have thought about this some more I hope to bring this to the attention of the Workwell researchers.

 

[alex3619]

I just posted the following as a first step:

https://www.facebook.com/workwellfoundation

I have been interested in CPET and ME since 2009 when I first heard about it. It seems so very obvious in hindsight, which is called a Black Swan phenomenon. I have been thinking about issues with testing severe and very severe patients. I wonder if they are mostly operating above their aerobic threshold without exercise, which is why they are bed-bound. Would it be possible to use gas analysis to show anything even without exercise? I had metabolic testing using gas analysis in about 1993 that showed my metabolism was low.

 

[beaker]

I just posted the following as a first step:

https://www.facebook.com/workwellfoundation

I have been interested in CPET and ME since 2009 when I first heard about it. It seems so very obvious in hindsight, which is called a Black Swan phenomenon. I have been thinking about issues with testing severe and very severe patients. I wonder if they are mostly operating above their aerobic threshold without exercise, which is why they are bed-bound. Would it be possible to use gas analysis to show anything even without exercise? I had metabolic testing using gas analysis in about 1993 that showed my metabolism was low.

{my emphasis }

I was over my AT when they hooked me up to the machine. Was only out of bed to go to clinic or recliner. But mostly bed doing nothing.
I wasn't the only one. In order to participate though, they made me take a few steps. They barked and yelled and screamed. I was holding on{ not suppose to } and I fell and they had to swoop a chair in under me.
They had to have something to record for the study. Next time they started w/ the chair on the treadmill. I stood up for 2 steps or so that was it. That was more than enough. It was awful. I paid too , but I wanted the drug more.

So the answer is yes, it can show that. But it's hell to do it.

 

[alex3619]

For a study they might require a few steps, if the goal is exercise testing. However I don't think this should be necessary. I think non-exercise testing would be enough, and I think portable equipment could be taken to patient's homes to test them. Now that would be useful diagnostically. However I could be making conclusions based on ignorance ... I am not an exercise scientist.

 

[Cheshire]

I’ve come across a really interesting paper by Professor George Davey Smith Professor of Clinical Epidemiology at the University of Bristol.


It has been written in response to “An integrated approach to understanding illness” Edited by... Peter White.

Although it doesn’t deal with ME/CFS, it contains lots of stimulating stuff and critiques the BPS model referring to studies of peptic ulcer and ischaemic heart disease. It also puts in perspective many factors that were once thought to be direct contributors to diseases.


http://issuu.com/maxhead/docs/bps_caution_davey_smith (it’s a scan, there are transcription errors)



I haven’t seen any post relating to it, excuse me if it’s not the case.


Here are some quotes I thought could be valuable (I could have quoted almost all the text as it is really of interest). (emphasis on words and light presentation are mine)

Some of the factors considered in the complex models are ones that would have influenced whether or not people were exposed to the transmissible agent and in this sense they are acting as distal causes. However, if the chain of causation is broken, then the disease does not occur.


For example, many psychological and social factors influence whether people smoke and thus indirectly lead to an increase in lung cancer risk. In different times and different places, though, different economic and psychological factors may influence smoking. The social class gradient of cigarette smoking has, for example, changed greatly in the UK over the last 50 years. Ultimately social and psychological factors will only influence the risk of lung cancer through influencing smoking patterns. Take away the cigarettes, and these factors will not result in lung cancer.

People versed in the history of epidemiology will know that conditions such as cholera, pellagra, beri beri, asthma, Down’s syndrome, scurvy, yellow fever, typhoid, and peptic ulcer were all at one time seen as diseases that were importantly influenced by stress or (in earlier times) ‘moral’ factors.

An important critic of the BPS model—although she never explicitly talks about it—is Susan Sontag. She published a remarkable book, Illness as metaphor, a year after Engel’s 1977 article appeared. Sontag wrote about how in plague-ridden England in the late sixteenth and seventeenth centuries, it was believed that a happy man would not get the plague.


She stated that “The fantasy that a happy state of mind would fend off disease flourished for all infectious diseases before the nature of infection was understood. Theories that diseases are caused by mental state and can be cured by willpower are always an index of how much is not understood about the physical basis of the disease. The notion that a disease can be explained only by a variety of causes is precisely the characteristic of thinking about diseases where causation is not understood.”


Diseases that are thought to be multi-determined have the widest scope for becoming metaphors for what is felt to be socially or morally wrong.

This one reminds me of something...

In his chapter in the 1948 book Progress in clinical medicine Avery Jones said “There have not been any major advances in the treatment of gastroduodenal ulcer. A better appreciation of the natural history of the disease has directed the treatment away from the ulcer towards the individual as a whole...” which was a fair summary of the BPS approach.

This one also sounds familiar

During convalescence the patient should be given a simple exposition of peptic ulcer.

A clear understanding of the need for maintaining a calm outlook on life, and of the necessity for not exceeding his natural ‘tempo’ by accepting too much work or responsibility, will be much more valuable than routine medication. The patient has got to live with his ulcer-forming tendency and it is essential to give him all the information at our disposal ... There is little doubt that healing is accelerated and more commonly completed if real rest is taken, preferably away from home, where the extra work occasioned by the illness may add to the worry of the patient. A period away from home may add perspective to domestic difficulties.

This one is just for fun, as its absurdity is just astounding!!

However such was Avery Jones’s concern not to increase stress, he added that “The diet should be served in as colourful and attractive a way as possible. A bland insipid colourless diet may cause less psychic flow of gastric juice, but it makes the patient depressed and irritable. The sustained resentment is more harmful than the increased psychic secretion.”

 

[Cheshire]

Other quotes:

About the misinterpretation of datas:

As the dismal pattern of morbidity and mortality due to peptic ulcer continued, many of the epidemiological studies—which should have identified potentially modifiable causes of the disease—continued to focus on stress as a major causal factor Interestingly, looking at these studies now, they often found that people with peptic ulcers came from large families and had more siblings than people not developing ulcers.

’ We now think that this is because the transmission of infection by H. pylori is facilitated within large sibships. Indeed, epidemiologists would tend to interpret such data as a possible indicator of the particular dynamics of infection. However, because the belief that peptic ulcer was stress-related was strong, association with family formation were taken to reflect particular psychological exposures,’ thus associations that could have served as an important clue to a modifiable—and key—cause of the disease were unfortunately taken as yet more ‘proof’ of the pre-eminent role of stress in peptic ulcer.

Commenting on a paper by Szasz and Robertson, regarding psychological factors in the aetiology of baldness, Asher wrote, ‘It is now fashionable to put forward mental causes for those illnesses where physical causes have not yet been found, such as peptic ulcer? Richard Doll relates how Mher gave him an article to read about peptic ulcer and its cause by psychological stress and asked, ‘Do you think that’s a fair account of what people think?’ Doll replied, ‘Well, it’s a bit stilted language, Richard, but yes, it’s a perfectly fair account? Asher replied, ‘Actually, it was written in 1850 about general paralysis of the insane. And I merely substituted peptic ulcer for general paralysis of the insane?

About the blindness certainty causes. One can bitterly sees the parallel with ME/CFS

In 1983, H. pylori was introduced as a candidate cause of peptic ulcer. It could be said that as we did not know about H. pylon until 1983, what does it matter that until then we had a stress model, because it did not block the development of understanding of the causes of peptic ulcer? But this may not be the case. Spiral bacteria, which clearly were H. pylori, were described in the stomach in 1889 27 and the specific hypothesis that peptic ulcers were caused by bacteria had already been advanced, with evidence, in 1875.27

These early findings were followed by repeated studies published in good journals isolating bacteria, from peptic ulcers, which would now be identified as H. pylori. Doctors in Mount Sinai Hospital advocated antibiotic treatment for peptic ulcers, which they claimed worked, in 1948.28 A patent for an antibiotic formulation for treating peptic ulcers was issued in 1961 •29
However, the stress model served to block people from building on this and moving towards an answer that would have led to a treatment that could have improved the quality of life, dramatically, for millions of people.

About psychological interventions

Various psychological treatments for peptic ulcer were advocated and large numbers of people were subjected to them.
Of course the usual claims for dramatic success were made, but properly conducted randomized controlled trials demonstrated no benefit of such time-consuming and expensive treatments.

The conclusion of one well-conducted trial was that ‘our study demonstrates a need for humility about the degree to which psycho logical interventions can effect powerful biological processes and impact on patient’s lives.’

A ‘pure’ psychosocial intervention was assessed in the recently completed Enhancing Recovery in Coronary Heart Disease Patients (ENRICHD) trial, a study considerably larger than any of those included in the preceding reviews.

Depression is perhaps the psychosocial factor with the strongest candidature for a causal relation with heart disease. Because of this, ENRICHD assessed the effect of depression reduction (through cognitive behavioural therapy—with adjunctive use of sertraline at physicians’ discretion) on the prognosis of established heart disease. The intervention was effective in reducing depression, but heart disease prognosis was the same amongst controls as in the intervention group. Indeed, lead investigators on ENRICHD acknowledged that the association between depression and heart disease may not be causal and have emphasized that the principal justification for treating depression is improved quality of life, more than reduction in mortality

However, it might be suggested that despite this, a doctor who is influenced by the BPS is the sort of doctor one would like to consult when sick. I am not so certain about this. When writing about a myocardial infarction patient whom he had seen, Engel stated, ‘In the end, whether the patient lives or dies, the biopsychosocial model further provides the physician with the conceptual tools to clearly think and plan the implications of the cardiac arrest`.

If I have a heart attack, I want to be treated by a doctor who cares about whether the patient lives or dies. I’m not really concerned about whether the doctor has the above-mentioned conceptual tools, I would rather have a doctor who keeps up to date with the best evidence on somatic treatments and gives me morphine, a thrombolytic, and aspirin, then puts me on appropriate long-term treatments.

 

[alex3619]

@Cheshire, this chapter of White's book (White was the editor) was one of the sources for my blogs I referred to in post 73.

 

[peggy-sue]

I can't work out who the authours of the quotes Cheshire put here are, but I'm a little concerned about the continued use of the expression "H. Pylon" rather than H. Pylori.

I imagine it's a typo... ?

 

[Cheshire]

@Cheshire, this chapter of White's book (White was the editor) was one of the sources for my blogs I referred to in post 73.

Sorry, didn't see it

@peggy-sue Yes, it's a PDF made out of a scan, and I yet corrected lots of mistranscriptions, but missed this one. Gone change that!

 

[MeSci]

Sorry, didn't see it

@peggy-sue Yes, it's a PDF made out of a scan, and I yet corrected lots of mistranscriptions, but missed this one. Gone change that!

also 'ben ben', which I presume should be beri beri!