Factors associated with severe oxidative stress in CFS

[fla]

Chronic fatigue syndrome: acute infection and history of physical activity affect resting levels and response to exercise of plasma oxidant/antioxidant status and heat shock proteins.

 

[Marco]

No interest here folks?

This little study appears to add another layer of understanding to PEM.

 

[Vitalic]

No interest here folks?

This little study appears to add another layer of understanding to PEM.

It's certainly relevant to me as my illness was triggered with both of those factors present (high intensity physical exertion + acute infection) the problem is we already know oxidative stress is a key component but it's most likely secondary to the pathological mechanism of the illness. I wonder how easy it is to test for abnormal HSP response though and whether that may be a viable bio-marker in a subset of patients, particularly those whose main symptoms revolve around PENE/PEM.

 

[alex3619]

Hi, this is a pay only paper, the full paper might be interesting indeed but its important to read the paper before drawing conclusions, not just the abstract. Bye, Alex

 

[Marco]

I was a heavy exerciser also but didn't have a acute infection that I'm aware of (group II?).

Immersion in cool water (which induces the production of heat shock proteins) is one of the few things that helps me avoid PEM in hot weather.

 

[Battery Muncher]

I found it interesting. Or at least I found the abstract interesting (I can't access the full paper).

I'd probably be group IV - heavy sports practice and infection.

Interesting comment on immersion in cool water, Marco, I used to do the same but kept getting ill due to it. I was forced to stop.

 

[Marco]

I don't have time to read it at the moment but the full paper is here :

http://forums.phoenixrising.me/show...ant-antioxidant-status...&p=223446#post223446

 

[Marco]

This is well worth reading in full.

One disappointment is that they tested immediately post exercise and didn't follow up over a typical PEM period of a number of days. Otherwise its a very thorough paper with some surprises :

ME/CFS patients performance on maximal exercise did not differ from sedentary controls (no differences in VOmax or lactate levels):
No differences in cytokine expression at rest compared with controls and no evidence of innate immune differences;
Protective heat shock protein expression appears to be permanently impaired;

and some confirmation of earlier findings :

high levels of oxidative stress;
no evidence for deconditioning:
switch from type I to type II muscle fibres.

Of great interest to me is that this is from France.

 

[Annesse]

So, maybe the question to ask is what do infections and high intensity physical exercise have in common? We already know that B12 is involved in the disease process. B12 is often called the energy vitamin because it helps fat and protein to metabolize in the body. It also plays a major role in the conversion of carbohydrates to glucose-your body's source of fuel. In addition, B12 enables your body to convert fatty acids into energy. It is also a promoter of normal immune function.

Intense physical exercise would deplete your body of B12. High intensity physical exercise also raises homocysteine. B12 is necessary to recycle homocysteine. So, it does impact the methylation cycle.

So, where does B12 come from? It is made by organisms in the soil. An animal that is pastured ingests B12 and we get B12 by eating proteins that come from animals that are pastured, such as eggs, meat, fish , dairy. A Tufts University study found that 40% of Americans were deficient enough in B12 to cause neurological damage. The study also found that we were consuming these proteins, but were not properly metabolizing B12. So, the problem lies in the metabolism. Is there something involved in the metabolism of B12 that would also directly impact immune function? The answer to this question could explain a great deal. It could also explain the biological findings in the disease process, such as low B12 and iron. An immune system "gone haywire" does not explain the biological findings in autoimmune disease, such as low dopamine in fibromyalgia or low acylcarnitine in the blood or muscles of people with CFS/FMS.

 

[richvank]

Hi, all.

I believe the results of this paper are consistent with the Glutathione Depletion--Methylation Cycle Block hypothesis for ME/CFS. This hypothesis proposes that the onset of ME/CFS results from genetic predisposition together with some combination of a variety of physical, chemical, biologicial and/or psychological/emotional stressors. Severe exercise is among the physical stressors, while infections are among the biological stressors.

For more information on this hypothesis, see the video and/or pdf slides on this webpage:

http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

Best regards,

Rich

 

[mellster]

So, maybe the question to ask is what do infections and high intensity physical exercise have in common? We already know that B12 is involved in the disease process. B12 is often called the energy vitamin because it helps fat and protein to metabolize in the body. It also plays a major role in the conversion of carbohydrates to glucose-your body's source of fuel. In addition, B12 enables your body to convert fatty acids into energy. It is also a promoter of normal immune function.

Intense physical exercise would deplete your body of B12. High intensity physical exercise also raises homocysteine. B12 is necessary to recycle homocysteine. So, it does impact the methylation cycle.

So, where does B12 come from? It is made by organisms in the soil. An animal that is pastured ingests B12 and we get B12 by eating proteins that come from animals that are pastured, such as eggs, meat, fish , dairy. A Tufts University study found that 40% of Americans were deficient enough in B12 to cause neurological damage. The study also found that we were consuming these proteins, but were not properly metabolizing B12. So, the problem lies in the metabolism. Is there something involved in the metabolism of B12 that would also directly impact immune function? The answer to this question could explain a great deal. It could also explain the biological findings in the disease process, such as low B12 and iron. An immune system "gone haywire" does not explain the biological findings in autoimmune disease, such as low dopamine in fibromyalgia or low acylcarnitine in the blood or muscles of people with CFS/FMS.

I think I read somewhere that high immune system activity (even if impaired or imbalanced) depletes the body of glutathione fast, so there could be the link to those biological findings.

 

[fla]

I believe the results of this paper are consistent with the Glutathione Depletion--Methylation Cycle Block hypothesis for ME/CFS. This hypothesis proposes that the onset of ME/CFS results from genetic predisposition together with some combination of a variety of physical, chemical, biologicial and/or psychological/emotional stressors.

We agree but doesn't this paper add the concept of a possible delay between the stressor and the onset? If severe exercise in your history increases the risk of M.E. later then what was damaged/broken/worn thin during the exercise years?

If a teenager does burnouts with the family car in the local parking lot, everything may look fine but if the treadwear on the tires is severe, the odds are greater of a blowout on the highway later when mom is driving the little ones to soccer practice. What is the tire tread for the human body regarding M.E.?

 

[WillowJ]

One disappointment is that they tested immediately post exercise and didn't follow up over a typical PEM period of a number of days.

that is odd because their earlier papers do that.

 

[richvank]

We agree but doesn't this paper add the concept of a possible delay between the stressor and the onset? If severe exercise in your history increases the risk of M.E. later then what was damaged/broken/worn thin during the exercise years?

If a teenager does burnouts with the family car in the local parking lot, everything may look fine but if the treadwear on the tires is severe, the odds are greater of a blowout on the highway later when mom is driving the little ones to soccer practice. What is the tire tread for the human body regarding M.E.?

Hi, fla.

The paper says "All patients were referred to our laboratory by clinicians who had identified the symptoms of and diagnosed severe infection. On the same day, subjects were first questioned about their history of sport practice ....." It isn't clear from the way the paper is worded how long before onset of CFS the exercise occurred. The way I read it is that the people in the high exercise group were getting a high level of exercise, and then developed an infection and CFS and were referred to the lab that did this study. But it really isn't very clear.

Best regards,

Rich

 

[kaffiend]

I have read some excellent reviews on the role of heat shock proteins as chaperones for glucocorticoid receptors. Without these chaperones, glucocorticoids e.g., cortisol can't be shuttled into the cytosol to control the expression of inflammatory cytokines. This has been studied in the hippocampus of animals. My laptop crashed and I haven't moved everything over from backup yet but I can post links to the papers later.

 

[Snow Leopard]

There are a lot of papers out there discussing the molecular biology of HSP and hypothetical links to various diseases (cancer and autoimmune diseases). A selection of papers on this topic:
http://mend.endojournals.org/content/22/10/2229.short
http://edrv.endojournals.org/content/18/3/306.full
http://onlinelibrary.wiley.com/doi/10.1111/j.1582-4934.2008.00273.x/full
http://www.sciencedirect.com/science/article/pii/S0304419X11000229
http://informahealthcare.com/doi/abs/10.3109/08820139809022710
http://ukpmc.ac.uk/articles/PMC3003299

Oh and this article which mentions anti-hsp as well as CFS:
http://www.bjmp.org/content/bacterial-infections-and-pathogenesis-autoimmune-conditions

 

[biophile]

After realizing the possibility that the reduced Hsp response to stressors in CFS may be further upstream than the other proposed causes of oxidative stress, I started looking for possible solutions to try. I'm currently leaning towards TEX-OE which is a Prickly Pear extract that supposedly works by stimulating heat shock factors for up to 72 hours after a single dose.

 

[Snow Leopard]

Are there any published studies which actually show the in-vivo effect of Opuntia ficus indica extract?

 

[Marco]

After realizing the possibility that the reduced Hsp response to stressors in CFS may be further upstream than the other proposed causes of oxidative stress, I started looking for possible solutions to try. I'm currently leaning towards TEX-OE which is a Prickly Pear extract that supposedly works by stimulating heat shock factors for up to 72 hours after a single dose.

A cold shower would be cheaper!

Improved antioxidative protection in winter swimmers


http://qjmed.oxfordjournals.org/content/92/4/193.full

 

[fla]

If winter swimmers can improve antioxidative protection why wouldn't severe exercise people improve theirs instead of increasing their chance of getting M.E.?

I wonder if severe brain exercise (like being a software developer) could have the same effect as severe exercise regarding oxydative stress and odds of getting M.E.?