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ME/CFS South Australia Inc supports the needs of sufferers of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and related illnesses. We do this by providing services and information to members.


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Medical articles

Basic information
ME/CFS: a basic overview (PDF, 57KB)
Overlap between CFS & other symptom-based syndromes (PDF, 19KB)
Multiple Chemical Sensitivity (PDF, 32KB)
MCS: Basic Overview (PDF, 18KB)
Fibromyalgia Syndrome (PDF, 34KB)

Information for ME/CFS physicians
Autonomic function in CFS (PDF, 32KB)
Cardiovascular Function & Exercise in CFS (PDF, 33KB)
ME/CFS Guidelines: Management Guidelines for General Practitioners (PDF, 460KB)
ME/CFS: Basic Facts for General Practitioners (PDF, 18KB)
Cognitive Function in CFS (PDF, 32KB)
Research Definition of CFS, known as the CDC or Fukuda (1994) [external link]

Miscellaneous articles
CFS-like states (Jan 6, 2005)
Grade Exercise Therapy for ME… or you? (Mar 2001)
Adelaide research into CFS, fibromyalgia, & brain fog (Sep 22, 2004)

Summary of CFS-like states

By John Graham
Flinders University

January 6, 2005

Right from the early US reports in the early 1980s, glandular fever-like illnesses were commonly reported and the early tests often verified recent EBV or CMV infection.

In 60 of 90 severe cases, MRI revealed white spots in subcortical white matter (Reno, Nevada).

Attempts to find strange infective agents or strange responses to them began.

In Australia, Prof Andrew Lloyd at the University of NSW documented prospectively that from cases severe enough to be included in study (EBV, RRV and Q fever, about 30% were still flat at 2 months, and 11% still flat at 1 year.

Aside from the occasional case of CMV that stayed IgM positive, there has not emerged any evidence that EBV contributes to the chronic illness.

All revert to EBV IgM negative and IgG positive (long lasting antibodies).

Other herpes family viruses may play some role in CFS, as they do in HIV (e.g. HHV6, atypical CMV variants).

Barry Marmion at IMVS and the University of Adelaide identified 20% of Q fever cases that stayed ill and fatigued despite antibiotics. He found that they had raised interleukin6 (IL6) levels, tended to have HLA haplotype HLADR11, and that bone marrow was positive for coxiella.

In the USA, a subgroup of Lyme disease sufferers also stayed ill despite antibiotics and the equivalent of resistant L forms may account for failure of antibiotic clearance of organisms (Borrelia burgdorferi).

In this group, Dr Ritchie Shoemaker has identified HLA haplotypes associated with susceptibility to borrelia toxins (haemolysins) and staph toxins (alpha and delta haemolysins.

In 1999, Cecile Jadin reported a high rate of positive rickettsial tests (Giroud Blade agglutination test) in South African cases of CFS with brain fog and often other features.

In the first 500 CFS cases that I tested in SA, about 260 were seropositive for spotted fever group rickettsial serology.

Sixteen were positive at a titre of 1/1024, 49 positive at 1/512, and 160 positive at 1/256.

This led me to discuss these findings with Dr Stephen Graves at the Australian Rickettsial Reference Laboratory in Geelong, and also Prof Peter McDonald (Flinders Medical Centre), Prof David Gordon (FMC), and Geoffrey Higgins at IMVS.

We all think that it is likely that there are some biological false positives, but the cases with titres of 1/256 and higher warrant anti-rickettsial antibiotics.

In 2002-3, 4 acute cases of rickettsial disease at had PCRs positive for SFG rickettsiae.

I have also been in e-mail dialogue with: Prof Tim Roberts and Prof Hugh Dunstan at the University of Newcastle, NSW Australia; Dr Jadin in South Africa; Dr Kenny De Meirleir and Jo Nijs at the Vrije Universiteit Brussel in Belgium; Dr Bernard Le Bleu in Montpellier in France; and Dr Ritchie Shoemaker in Pocomoke, Maryland USA.

CFS investigations

My approach 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.

4. Organisms that produce toxins. Mostly we do not measure toxins directly.

(b) Markers of inflammation

ESR, CRP, fibrinogen.

(c) Immune abnormalities

T cell subsets, autoantibodies, cytokine measurements.

(d) Organ function and biochemical parameters

E.g. LFTs, ECU, Glucose and post prandial insulin levels, calcium and magnesium levels)

(e) ECG

(f) Endocrine testing

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

E.g. If the person has an inadequate diet, low exposure to sunlight or hint of malabsorption, Vit D3 levels should be measured. (Deficient D gives impaired immune function.) I have found 66/137 cases low in D3.

(h) Newcastle Testing

This is interesting, but expensive and not supported by Medicare.

(i) Cerebral SPECT scans (TQEH) for high rate of decreased perfusion of particularly the medial temporal regions of the brain.

(j) Brain MRI on at least a 1.5 Tesla unit (in particular cases with more neurological features)

The therapeutic task in CFS is to decrease or eliminate pathogen loads, decrease environmental pollution, optimize immune function, heal any intestinal disorder, optimize nutrition, counter oxidative stress, and allow restoration of all cellular function and signalling.

All of this is in the setting of the consciousness of the person who is intimately involved in this healing task.

It necessarily involves ongoing conversations which allow each person in her or his own way to co-evolve the healing outcome.

I like to call this “a dance of understanding.”

Glutathione reduces free radical damage by reducing compounds such as hydrogen peroxide. It protects the sulphydryl (thiol) groups on the aconitase and also other thiol containing enzymes and cofactors. GSH appears to be involved in recycling vitamins E, C, coenzyme Q10 and alpha lipoic acid.

Human milk contains a ratio of whey protein to casein of 3:2,while cows milk contains a ratio of WP/casein of 1:4.

At least some data points to problems with beta casein A1 which is in virtually all Australian and New Zealand milk.

Whey proteins that I recommend contain serum albumin. alpha lactalbumin, and lactoferrin, (all rich in cystine) but do not contain lactose or casein.

Lactoferrin is a family of glycoproteins with antibacterial, antifungal and anti viral activity.

It has 40% bioavailability, and is also anti-inflammatory.

Almost 30% of the Iso Whey proteins contain branch chain amino acids (leucine, isoleucine and valine).

The Newcastle group claim that low leucine in the unexercised CFS patient denotes impaired regulation of muscle catabolism.

They find high tyrosine and high citric acid in CFS/FMS but not in healthy medical student controls.

Leucine can be lost in exercise by increased action of branch chain keto-acid dehydrogenase.

Particular supplementary products may have advantages.

Dr Robert Buist says that Pharmafood’s Iso-Whey contains approximately 32% of the 3 cystine rich proteins.

He says that the cystine in whey is more able to avoid hydrolysis in the gut, and inside the cell liberates 2 molecules of L-cysteine, and this drives the synthesis of glutathione.

At least some people with chronic fatigue also have low urinary levels of alpha ketoglutarate, or low succinate levels (further around the Krebs cycle). (Dunstan, Roberts, McGregor and Butt Newcastle, NSW)

So is the glutathione low and if so why is it?

At least some may be associated with low glycine, and perhaps some with low glutamine, and now we have evidence of the question of active mechanisms which might deplete it.

Dr Paul Cheney explains that some viruses when activated encode genes for glutathione peroxidase which will deplete selenium as selenoproteins are needed for viral replication.

These include HIV, E-B virus and presumably other herpes like viruses, as well as hepatitis B and C.

For our cells glutathione peroxidase is one of the body’s principal ways of protecting us from free radical damage.

One of the two glutathione peroxidases requires selenium for its function.

Cheney says that glutathione has antiviral activity.

Cheney says that the elevated citrate level lowers the level of 2,3 diphosphoglycerate (2,3DPG), which in turn makes it harder for haemoglobin (Hb) to give up its oxygen to tissue cells.

It is well established that 2,3 DPG is needed for haemoglobin to release O2 in low O2 tension sites.

I use alpha lipoic acid to protect aconitase and alpha ketoglutarate dehydrogenase from free radical injury, and co-enzyme Q10 to cooperate in the electron chain for generation of ATP. Both are electron donors (potent anti-oxidants). Alpha lipoic acid is likely to be the most neuroprotective substance that is readily available.

Recent evidence suggests that alpha lipoic acid also stops migration of activated T cells across the blood-brain barrier.

Cheney suggests supplements of glutathione which rises when whey protein is consumed.

I think this is well worth a try, and also use co-enzyme Q10 to protect the Krebs cycle.

Cheney also favours use of B12 and magnesium.

I like Bioceuticals “Ultra Muscleze” and probiotics.

Other researchers with interesting data include Dr Ritchie Shoemaker from Maryland, (he measures MMP9 and beta MSH) and Dr Trevor Marshall in USA (has a protocol of management) as well as Dr Peter Behan from Glasgow (good data on optimal fatty acids).

If rickettsial serology is positive, I usually try a course of anti-rickettsial antibiotics and always use probiotics.

I would be very interested to hear any comments that you may care to make.

Happy Christmas and New Year blessings to you,

John Graham

PS: In the light of Bob Gibson’s recent studies on the failure of flaxseed oil (with 50-60% alpha linolenic acid) to elevate blood levels of EPA and DHA,I now use more fish oils.

Presumably the elongases and desaturases are sufficiently involved in other conversions, to have little reserve for the actions on alphaLA.

I have recently read the first 320 pages of Osler’s Web by Hillary Johnson.

The presumption of psychiatric explanations for CFS strikes me as some of the least scientific work that I have ever seen.

In this city there are numerous (probably the majority) psychiatrists that have failed to look at the CFS literature.

I think we should insist that to acquire any plausibility let alone validity, they should have read Osler’s Web.

The imaging data including MRIs, BEAM studies,PET and SPECT is very impressive! CFS in cases with neurological symptoms is very different from depression, and more like what we see in MS or AIDS.

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