http://www.healthfreedoms.org/vaccines-dont-work-here-are-the-facts/

NEEDHAM, MA — Research sponsored by the National CFIDS

Foundation was formally announced at the International Symposium on Toxins and Natural Products in Okinawa, Japan on November 17-19, 2002 by Dr.Yoshitsugi Hokama. The research, for the first time, discovered ciguatoxin, a potent neurotoxin, in the blood of Chronic Fatigue Syndrome patients.

“Chronic ciguatera poisoning has already been suggested as a scientific model for Chronic Fatigue Syndrome (CFS),” stated Dr. Hokama. Ciguatoxins are potent, heat stabile, non-protein, lipophilic sodium channel activator toxins and are recognized as some of the most potent biological toxins known. They produce dramatic neurological manifestations, such as peripheral sensory or motor symptoms (including paresthesias, pain, burning, tingling, numbness), central symptoms such as headache, autonomic dysfunction and also affect multiple body systems (gastrointestinal, immune, hepatic, cardiovascular) and the muscles.

Many CFS patients in the study had higher levels of the toxin than the patients with cancer, hepatitis or acute ciguatera poisoning.

Quantitative assay results range from 1:5, the lowest toxin level, to 1:160, the highest toxin level. All CFS samples gave titres of at least 1:20, with the majority of titres from 1:40 to 1:160.

Dr. Hokama presented his preliminary findings in a lecture titled “Acute phase lipids in sera of various diseases: Chronic Fatigue Syndrome, ciguatera, hepatitis, and various cancer with antigentic epitope resembling ciguatoxin as determined with Mab-CTX.”

Dr. Hokama is a Professor in the Department of Pathology at the John A. Burns School of Medicine at the University of Hawaii at Manoa. He is a world expert in the area of fish toxins with hundreds of peer reviewed publications to his credit. Hokama developed the Membrane Immunobead Assay test for patient sera, using a specific monoclonal antibody for ciguatera toxin (Mab-CTX). His current research into Chronic Fatigue Syndrome and a ciguatera toxin connection was funded by the National CFIDS Foundation’s research grant program.

Gail Kansky, President of the National CFIDS Foundation, said, “We believe this to be a significant breakthrough. CFS, which has come to include myalgic encephalomyelitis, is a very severe illness that has not received adequate funding or appropriate medical attention. Although there are still many unanswered questions and much work to be done, research efforts will ultimately turn the tide in the understanding of this disease and allow patients to receive appropriate medical therapies. We are indebted to Dr. Hokama and his colleagues for
providing this monumental first step.”

For more information on this study or Chronic Fatigue Syndrome, please contact:

The National CFIDS Foundation
103 Aletha Rd, Needham Ma 02492
(781) 449-3535 Fax (781) 449-8606

Scotia Pharmaceuticals, Guildford, UK

It has been estimated from government sponsored studies in the UK and the USA that 10% of the population suffer to some extent from dyslexia, and that 4% are severely affected.  In the USA there has been a threefold increase in prevalence between 1976 and 1993.  This costly epidemic affects individual lives and educational budgets.  So it is important that the biological basis of the condition is investigated.  Visual and central processing deficits have been found, particularly in the magnocellular visual subsytem^1,2,3

We measured dark adaptation with a Friedmann Visual Field Analyser 2, set for the dark adaptation function, in ten adults with dyslexia and ten controls.  Dyslexics showed poorer dark adaptation than controls especially in the second part of the curve, which corresponds with rod dark adaptation (p < 0.05).  We subsequently tested the possibility that dark adaptation might be influenced by docosa hexaenoic acid (DHA) supplementation.  For one month, five dyslexics and five controls were given 480 mg of DHA daily with no additional vitamin A or vitamin D.  Dark adaptation was then retested.  In four controls DHA had no effect on dark adaptation, although in one (a strict vegetarian) adaptation clearly improved.  By contrast, in the dyslexics with poor scotopic vision, DHA consistently and significantly improved dark adaptation (p < 0.04)⁴.

Within the retina, DHA is heavily concentrated in the lipids of the rod cells, and within the brain neurons at the synapses.  The rod cells are receptors for the magnocellular system, so it is possible that the central processing deficits of the magnocellular system will also be improved following DHA supplementation.  So far, there is only anecdotal and subjective evidence that improvements in reading ability and behaviour are associated with DHA supplementation in dyslexia.  More formal controlled studies are in progress.

1. Grosser GS, Spafford CS.  Light sensitivity in  peripheral retinal fields of dyslexic and proficient readers.  Perceptual Motor Skills 1990:  71:  467-77.

2. Galaburda A, Livingstone M.  Evidence for a magnocellular defect in developmental dyslexia.  Ann NY Acad Sci 1993; 682:  71-81.

3. Eden GF, VanMeter JW, Rumsey JM, Maisog JM, Woods RP & Zeffiro TA.  Abnormal  processing of visual motion in dyslexia revealed by functional brain imaging.  Nature 382:  66-69: 4 July 1996

4. Stordy BJ.  Benefit of docosahexaenoic acid supplements to dark adaptation in dyslexics.  Lancet 1995; 346:385.

   See dyslexia symptoms

SIR-Makrides and colleagues (June 10, p 1463) provide strong evidence that docosahexaenoic acid (DHA) is an essential nutrient for the optimum neural maturation of term infants as assessed by visual evoked potential acuity.  I have data indicating that DHA supplementation in adult dyslexics improves dark adaptation (scotopic vision) and thus DHA may also be a dietary essential for this condition.

We measured dark adaptation with a Friedmann Visual Field Analyser 2, set for the dark adaptation function, in ten adults with dyslexia and ten controls.  Dyslexics showed poorer dark adaptation than controls, especially in the second part of the curve, which corresponds with rod dark adaptation (figure, a; repeated measures Anova p<0.05).  We subsequently tested the possibility that dark adaptation might be influenced by DHA.  For 1 month five dyslexics and five controls were given 480 mg of DHA daily with no additional vitamin A or vitamin D.  Dark adaptation was then retested (figure, b and c).  In four controls DHA had no effect on dark adaptation, although in one (a strict vegetarian) adaptation clearly improved.  By contrast, in the dyslexics with poor scotopic vision DHA consistently and significantly improved dark adaptation (figure, b; paired t-test on final rod threshold, p< 0.04).

It has long been recognised that dyslexics have both retinal and central processing defects,^1,2 but defective dark adaptation has to my knowledge not previously been reported.  DHA is a key fatty acid in both retina and brain and is usually present in large quantities in these tissues.  In these studies I show the benefit of DHA supplementation for one aspect of retinal function.  I have found that DHA supplements given to dyslexics can also be associated with improvements in reading ability and behaviour.  These reports are anecdotal and subjective but more formal controlled studies are in preparation.

I thank Ms. Katrina Searle, Mr. Liam Trow, and Ms. Katy Wood for technical assistance.

The author has a patent on the use of DHA for dark adaptation.

B Jacqueline Stordy

School of Biological Sciences, University of Surrey, Guildford GU2 5XH, UK

1. Grosser GS, Spafford CS.  Light sensitivity in peripheral retinal fields of dyslexic and proficient readers.  Perceptual Motor Skills 1990; 71:  467-77.
2. Galaburda A. Livingstone M. Evidence for a magnocellular defect in developmental dyslexia.  Ann NY Acad   Sci 1993; 682:  71-81.

Benefit of Docosahexaenoic acid supplements to dark adaptation in dyslexics

SIR-Makrides and colleagues (June 10, p 1463) provide strong evidence that docosahexaenoic acid (DHA) is an essential nutrient for the optimum neural maturation of term infants as assessed by visual evoked potential acuity.  I have data indicating that DHA supplementation in adult dyslexics improves dark adaptation (scotopic vision) and thus DHA may also be a dietary essential for this condition.

We measured dark adaptation with a Friedmann Visual Field Analyser 2, set for the dark adaptation function, in ten adults with dyslexia and ten controls.  Dyslexics showed poorer dark adaptation than controls, especially in the second part of the curve, which corresponds with rod dark adaptation (figure, a; repeated measures Anova p<0.05).  We subsequently tested the possibility that dark adaptation might be influenced by DHA.  For 1 month five dyslexics and five controls were given 480 mg of DHA daily with no additional vitamin A or vitamin D.  Dark adaptation was then retested (figure, b and c).  In four controls DHA had no effect on dark adaptation, although in one (a strict vegetarian) adaptation clearly improved.  By contrast, in the dyslexics with poor scotopic vision DHA consistently and significantly improved dark adaptation (figure, b; paired t-test on final rod threshold, p< 0.04).

It has long been recognised that dyslexics have both retinal and central processing defects,^1,2 but defective dark adaptation has to my knowledge not previously been reported.  DHA is a key fatty acid in both retina and brain and is usually present in large quantities in these tissues.  In these studies I show the benefit of DHA supplementation for one aspect of retinal function.  I have found that DHA supplements given to dyslexics can also be associated with improvements in reading ability and behaviour.  These reports are anecdotal and subjective but more formal controlled studies are in preparation.

I thank Ms. Katrina Searle, Mr. Liam Trow, and Ms. Katy Wood for technical assistance.

The author has a patent on the use of DHA for dark adaptation.

B Jacqueline Stordy

1. Grosser GS, Spafford CS.  Light sensitivity in peripheral retinal fields of dyslexic and proficient readers.  Perceptual Motor Skills 1990; 71:  467-77.
2. Galaburda A. Livingstone M. Evidence for a magnocellular defect in developmental dyslexia.  Ann NY Acad   Sci 1993; 682:  71-81.

Note:  Signal369 contains DHA

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