I am very concerned about the safety of genetically modified (GM) foods and strongly believe far more research is required before humans should regard them as safe, either for themselves or for future generations. This research should be completed before we are FORCED to live on GM foods, there being no longer any choice.

GM foods have already been marketed for public consumption without proper research or discussion into their long term effects.

The food we eat is broken down into Ôfood fractionsÕ which are absorbed and used by the body. GM foods may possibly contain toxic fractions which could have a serious effect not only on the immediate health of some individuals but also on the health of future generations.

It is entirely possible that these toxic fractions could affect us in many ways, for example:

Is it possible that they could act like prions, causing illnesses such as Mad Cow Disease (BSE/CJD) to appear years later ?

The frightening prospect is not that there will be an immediate epidemic or illnesses but that we may have caused an irreversible reversal of human life in, say, 50 yearsÕ time, when teenagers start to die of coronary artery disease, diabetes becomes rampant, and old age arrives before the age of 50. Blighted ova or sperm, damage done in utero, can possibly cause innumerable life-threatening conditions.

We already see the effects of autoimmune diseases, many of which should be renamed "toxic lectinopathy" (or poisonous allergies / sensitivities / reactions to food fractions and chemicals). These are not always recognized as such, even today. If, or when, we have damaged ourselves with a totally genetically modified food chain, there will be no time for recognition or reversal. It will already be too late. The damage will have been done. 

Our greatest asset < our children < will be born with short telomeres and short futures. We may be introducing a threat with GM crops and foods greater than plagues, wars, volcanoes, earthquakes, global warming, ozone depletion or a stray asteroid. 

Remember what happened to Pottenger's Cats? Three generations of eating junk and they went "down the tube".

(Originally published SOMA NEWSLETTER October 2000, Vol.22, No.2. Reprint by request.)


Since 1980 I 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 sensitivities / 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. B1, B2, B6, C, A, Folic Acid and, less often, B 12. They often have anaemia due to the above deficiencies but may have sideropaenia < low iron without anaemia.
Many have low serum zinc, and hair analysis shows low calcium, 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/film, 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 of Endomysial IgA, Gluten IgA and IgG or alpha-gliadin IgA and IgG, reticulin antibodies and IgM to see if these are raised, nor do they look for low C3, C4 and raised immune complexes as seen in coeliac disease, IgM can be raised-to-low also in coeliac disease.

An extremely high percentage of CFS/MCSS patients are MISSED COELIACS and about 5% are MISSED SLE <which is not usually even considered.
All 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 to confirm/diagnose SLE.

Many patients with CFS show white dots in their nails which is associated with low B6, zinc and pyroluria with kryptopyrroles in the urine, and if these levels are high there is high risk for acute intermittent poryphyria, 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. These 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/complicating their treatment. These pathogens need to be identified and killed off.

High levels of aluminium, copper and , less often, lead and mercury are seen in CFS/MCSS patients and show especially on hair analysis. They also have low serum cortisol +/- low serum DHEAS, 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 become hypyglocaemic. Severe amino acid deficiencies are common in my experience (also refer Newcastle University research) and may have low Vit B3 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 Roberts et al of Newcastle University). They also have abnormal metabolites in the urine (and Kryptopyrolles / pyroluria ).


(a) I have seen moribund patients with severe pellagra who were called "hysterical" and not allowed to have Vit. B3. (Pellagra is a Vit. B3 deficiency). One patient at the Cummins Unit of Royal North Shore Hospital crawled out of hospital and caught a taxi to Manly Hospital where she made a rapid recovery with B3 treatment, etc.

(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 tardive 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 ill. I saw her regularly while she was on high dosage IMI 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 again did well on extra nutrients, special diet and minimal Melleril. The evidence supporting increased investigation into causes of symptoms in CFS and MCSS is overwhelming.


(Originally published SOMA NEWSLETTER, October 1999, Vol.21, No.2.    Reprint by request.)