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SOMA IINLLTH ASSOCIATION OF AUSTRALIA LIMITED

UNDER-INVESTIGATION OF SYMPTOMS IN CHRONIC FATIGITE SYNDROMB (CFS) AND

MULTTPLE CTmMTCAL SENSrrnVrrY SYNDROMB (MCSS).

Statement by Dr C M Reading: B.Sc., Dip.Ag.Sci.,MBB.S.,F.R.A.N.Z.C.P.,A.C.N.E.M.

Since 1980I have treated over two,thousand patients for CHRONIC FATIGUE SYNDROME and well over

a hundred for MULTIPLE CHEMICAL SENSITIVITY. All these patients, when thoroughly investigated,

showed food and chemical sensitivitiet / intolerances on the CYTOTOXIC TEST, especially to cow's milk,gluten-containing grains, legumes and beans, all of which can cause severe malabsorption state for vitamins,

minerals, amino acids, etc. These patients tend to have severe nutrient deficiencies due to malabsorption,

and are usually low in Vits. BL, 82rB6, C, A, Folic Acid and, less often, B 1"2. They often have anaemia due to

the above deficiencies but may hav,e sideropaenia - low iron without anaemia. Many have low serum zinc,

and hair analysis shows low calciurn, magnesium, manganese, molybdenum, iron, chromium, zinc, selenium

and cobalt, raised copper and aluminum, and unsatisfactory lead, mercury and nickel levels.

(The Cytotoxic Test is accepted by the LANCET, Letter, January 24,1987.)

The glare/photophobia so often observed in CFS patients indicates low iron, low Retinol A and low Zinc -hence white dots in nails often, despite a normal haemoglobin/fiIm, and thus not anaemia. Many patients

also have raised IgE and a host of inhalant allergies to pollens (grass, weeds, trees - pollinosis), moulds, mites,

etc., as well as food allergies, and are sensitive to fumes, chemicals, perfumes, petrol, etc.

Most CFS patients have missed coeliac disease (nine out of ten in a row, diagnosed as CFS by a leading

Sydney hospital - POW) and missed because most psychiatrists do not routinely have measurements done ofEndomysiat IgA, Gluten IgA and ltgG or alpha-gliadin IgA and IgG, reticulin antibodies and IgM to see ifthese are raised, nor do they look for low C3, C4 and raised immune complexes as seen in coeliac disease, IgMcan be raised-to-low also in coeliac disease.

An extremely high percentage of CFS/MCSS patients are MISSED COELIACS and about 5To TTeMISSED

SLB -which is not usually even considered. AII CFS patients should be tested for ANF and, if positive, then

do dsDNA; and, if not raised (diagnosing SLE), then ENA screen, C3, C4 complements, immune complexes,

anti-lymphocyte antibodies, immunoglobulins (IgA, IgM, IgG) and if any of the above are abnormal (despite a

negative ENA screen) then a skin biopsy on unexposed skin with immunofluorescent technique toconfirm/diagnose SLE.

Many patients with CFS show white dots in their nails which is" associated with low 86, zinc and pyroluriawith kryptopyrroles in the urine, and if these levels are high there is high risk for acute intermittentporyphyria, especially if reacting to drugs , chemicals, fumes, perfumes and chlorpyrifos/pesticides and

herbicides which can cause a flare-up of porphyria, as also can barbiturates, sulphnamides, neuroleptics, etc.

Most CFS/MCSS patients have severe autoimmune disease (as seen with SLE, coeliac disease, and show

gastritis, thyroidiotis, ,cholangitis, vasculitis, autoimmune neuritis,etc.) and need a gluten-free diet or a diet

design to reverse SLE. Thbse patients, in my experience, have severe cow's milk alpha-casein, +/-

alpha-lactalbumin, */- beta-lactalbumin, sensitivity/intolerance when antibodies to these peptides of cow's

milk are measured - as well over a thousand patients since 1980. (cont.)

Under-investigation of symptoms in CFS and MCSS: (cont')

When intolerant/hypersensitive to cow's milk albumin-globulin, then these cross-react with egg and beef

albumin and globulin, and also need to be avoided. In addition, because of the suppressed/compromised

immune system and often low cortisol DHEA, MCSS patients (often being coeliacs) are at risk for opportunist

pathogenes such as candida albicans, mycoplasma, rickettsia, helicobacter pylori, chlamydia pneumoniae and

campylobacter jejuni aggravating/aomplicating their treatment. These pathogens need to be identified

and killed off.

High levels of aluminium, copper and , Iess often, lead and mercury are seen in CFS/MCSS patients and show

especially on hair analysis. They also have low serum cortisol +/- low serum DHEAST i.e- adrenal exhaustion,

and many are hypothyroid. Most have a marked tendency to hypoglycaemia and need to eat protein

two-hourly in order not to becorne hypyglocaemic. Severe amino acid deficiencies are common in my

experience (also refer Newcastle University research) and may have low vit 83 in addition to nutrient

deficiencies mentioned above. High levels of pesticides/herbicides are common in CFS/MCSS patients (work

of Dr Mark Donohoe and Tim Rob,erts et al of Newcastle University). They also have abnormal metabolites in

the urine (and Kryptopyrotles / pynoluria ).

(a) I have seen moribund patients with severe

have Vit. 83. (Pellagra is a Vit. B3 deficiency)'

Hospital crawled out of hospital and caught a taxi

83 treatment, etc.

pellagra who were called 'hysterical' and not allowed to

One patient at the Cummins Unit of Royal North Shore

to Manly Flospital where she made a rapid recovery with

(b) Another with severe pallor/weakness at Camperdown Children's Hospital with severe CFS picture

was called hysterical until I showed the treating psychiatrist she had antibodies to alpha-casein, alpha-

lactalbumin, proving she had severe cow's milk sensitivity/intolerance. The ice-cream and milk products they

were giving her out of kindness were making her seriously ill and moribund. off all diary products she

rapidly recovered.

(c) Another patient with tarclive dyskinesia due to Serenace, and wrongly diagnosed as schizophrenic

instead of toxic encephalopathy/chloropyrifos poisoning, etc., did well for many months on extra nutrients and

food allergy-free diet, etc., and no neuroleptics at all, or minimal Melleril, until she came into contact with

more spraying with pesticides/herbicides. She was hospitalized and given high amounts- of -neuroleptics,

making her very illr r saw her regularly while she was on high dosage IMr neuroleptic weekly for her Acute

Brain Syndrome which had severe side-effects, agitation, depression. This was to be her treatment

indefinitely, all her complaints about side-effects being ignored. Each day off the neuroleptics she rapidly

improved. Fortunately, she agaiin did well on extra nutrients, special diet and minimal Melleril' The

evidence supporting increased investigation intb causes of syrnptoms in cFS and MCSS is overwheliltr

(originally published soMA NEWSLETTER, October 1999,Vo1.21, No'2' Reprint by request')