Adelaide research into CFS, fibromyalgia, and brain fog

By John Graham []

September 22, 2004

In CFS, fibromyalgia, and brain fog, my approach now involves a look for:

(a) Pathogens

1. Coagulase positive and negative staphylococci in the nose, (Direct swab and culture)

2. Altered gut flora, (Newcastle NSW)

3. Intracellular pathogens, especially the herpes family of viruses, mycoplasmas and rickettsiae.

Here the difficulty is that serology is indirect, and PCR and culture are most useful if we have samples of tissue harbouring the organisms.

For rickettsiae, I have 240 positives in 464 tested.

4. Organisms that produce toxins. Mostly we do not measure toxins directly, but the work of Ritchie Shoemaker supports this in Lyme disease, and nasal staph carriage (these make alpha and delta haemolysins!).

(b) Markers of inflammation

ESR, CRP, fibrinogen.

(c) Immune abnormalities

T cell subsets, autoantibodies, (ANA) cytokine measurements.

(d) Tests of organ function

For example, LFTs, ECU, Glucose and post-prandial insulin levels, calcium and magnesium levels, Hyper insulinaemia reaching >100 is very common and may be related to down regulation of the PPARgamma receptor.

(e) ECG

(f) Endocrine testing

(g) Homocysteine (high in about 10% of caucasians)

(h) Special tests as needed after clinical histories lead me to think of them

If the person has an inadequate diet, low exposure to sunlight or hint of malabsorption, Vit D3 levels should be measured. (I have 50 low D patients in 115 tested!)

If on Plaquenil or related drugs, 1,25 dihydroxy D should be measured, but Marshall says more about this!
My patients with low D3 do seem to have high 1,25 dihydroxy D levels.

Statins and beta blockers are common drugs, which can contribute to fatigue or decreased exercise tolerance. Statin fatigue or leg heaviness can be improved by lessening the statin dose and adding co-enzyme Q10, which statins deplete.

Overseas findings

I will highlight the most striking findings overseas.

Dr Kenny De Meirleir [,390] has found a high ratio of 37kDa RNAse-Lto 83kDa RNAse L this is present in >90% of his CFs patients but only 1% in controls and depressives.

In the absence of acute infection or chronic inflammation, a high RNase L ratio could distinguish CFS patients from healthy volunteers and patients with depression.

Additional large studies and follow-up studies are required to confirm the stability of this high ratio of RNase L isoforms in a CFS group.

FMS patients have a high rate of carriage of coagulase negative staphs which produce toxins with adverse effects on muscle. (Newcastle, NSW)

This is why I use nasal bactroban or similar.

There is data showing a very high rate of FMS in people with endometriosis.

I agree with Dr Paul Cheney [] who supports corrective methods for the Krebs cycle, and the Newcastle group who are stong advocates of probiotics.

The Marshall plan [ marshall/] is remarkably similar to my recent plan. Angiotensin inhibitors would vasodilate the brain areas shown on the SPECT scans (R Casse, R Kwiatek et al), but are also PPAR agonists and down regulate inflammatory cytokines!

I use telmisartan instead of olmesartan, and quercitone as my preferred form of quercetin.

If you would like more details or references, please let me know,

John Graham

PS: I emphasize that CFS is not sarcoidosis and I have only 2 proven cases of sarcoidosis in more than 1,000 patients.

In Australia, sarcoidosis is usually less severe than in USA.
This group should not receive vit D.

The other D data of Marshall is not validated by Medline literature.

People should be careful about claiming too much about TH1 and TH2 settings of T cells.



Reprinted from

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