Dyslexia: a hundred years on
BMJ 1996; 313 doi: https://doi.org/10.1136/bmj.313.7065.1096 (Published 02 November 1996) Cite this as: BMJ 1996;313:1096
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I was astonised when I found that Dyslexia has been identified as
such in 1896. When I was 5 1/2 years of age in 1952 I realised that I was
not keeping up with my peer group. When I was 7 I remember hearing a radio
programm about light beams being bent when passing massive objects. I was
thinking about this when I noticed a fork in a jug of water, being bent by
refraction, a fat stain on a peice of greice proof paper and a planes
vapor trale, I wondered if a star could be leavinf a vapor trale and the
light beam was being bent as was the fork image by some form of stai in
the sky, not bad for a 7 year old. I failed my 11 plus and went to the
local secondary modern, my brother and sister both went to the grammer
school and have achieved high academic success in their chosen
proffessions. The Wiltshire County Council Education Board made no attempt
to screen me for Dyslexia. I found I was Dyslexic at the age of 35. I feel
cheated of my birth right to an education as promised equal to my needs
and requirements under the 1944 Education Act. Margaret Snowling's article
should be required reading for all LEAs My IQ is 140!
Competing interests:
None declared
Competing interests: No competing interests
As the wife of a Dyslexic now age 60 who spent his school years being
treated as a dunce and to this day remains severly affected by the long
term effects I can vouch for an abysmal failure on behalf of the entire
medical or educational profession to even begin to understand the problems
or the inheritance pattern
Grandfather was Dyslexic
Mother 83 is Dyslexic and had severe Endometriosis
Son 60 is Dyslexic and has Hashimotos Thyroiditis
Daughter 29 is Dyslexic and has severe Endometriosis plus Cholysystectomy
age 25 along with Hay fever
One of her Twin daughters age 7 is Dyslexic and has severe Hay Fever
All very clearly have a phonetic problem which has proved
uncorrectable .........eye tracking tests etc are all OK
Years and years of extra specialised tuition for 29 yr old daughter
have done little to help
Years of patient help for 60 yr old has done little to help
Worse still its clear that the 29 yr old is highly likely to be
Thyroid Hormone resistant as is her father and no doubt her daughter
......BUT NO ONE CARES OR EVEN RECOGNISES the problem in the UK because no
tests prove the use or otherwise of Thyroid Hormone at a cellular level
100 years on we are going backwards not forwards
Competing interests: No competing interests
Brain scans on dyslexics such as those conducted by Dr. Posner should
not be accepted at face value because of flawed experimental design and
lack of control of variables such as orthographic or phonic confusion,
indecision, emotional blocking, disengagement and negative reinforcement
of decoding and encoding operations acquired in early learning situations.
Successful decoding and encoding operations by "patients" are generally
ignored by the designers while dysfunctional orthographic signs and their
associated mixed signals are accepted as stable schemata. There cannot be
any halfway dyslexics, sometimes succeeding in their communications and
other times failing. Why would the dyslexic neurological process be
selective in its decoding and encoding operations except that the original
signals were ambiguous, false, misleading or incoherent to begin with
requiring metacognitve tools most "patients" simply do not have, or
coherent and isomorphic resulting in adequate communication? Testing on
transformational generative phonology and its expressions of invented
spelling would be more relevant to visualizing "dyslexic" brain's struggle
for uninhibited communication. More disturbing is the fact that some
dyslexics become "cured," taking hyperliterate titles and professions.
This should not happen without externally altering the defective
neurological stuctures. This would be just another esoteric inquiry except
that this technology has legal and ethical implications for another
generation.
Competing interests: No competing interests
Psychologists ignore treatable biochemical abnormalities in dyslexia.
Psychologist Margaret Snowling failed to mention important and
treatable biochemical abnormalities in dyslexia.1 She chose to ignore
the fact that deficiencies in minerals, vitamins and essential fatty
acids, which are particularly essential for normal brain development and
function, contribute substantially to the problems of children and adults
with dyslexia.
In 1989 we discovered that dyslexic children were severely zinc
deficient in their sweat and had higher toxic metals in their sweat and
hair. The difference between the zinc concentrations in passive sweat of
dyslexic children and their matched controls was highly significant
(p<0.0001).2 These important results have been disregarded by the
dyslexia establishment who favour genetic and neuroimaging studies, and
various “remedial” interventions, while failing to diagnosis and replete
essential nutrient deficiencies.
Zinc deficiency can also be diagnosed from measurements of
concentrations of zinc in white cells and copper deficiency, if also
present, can be diagnosed by a red blood cell test of superoxidase
function. Deficiencies of zinc and copper impair B vitamin functions and
blocks essential phospholipid pathways. In dyslexia there is evidence for
reduced incorporation of docosahexaenoic acid and arachidonic acid into
cell membranes, in contrast to schizophrenia where there an increased rate
of loss of these omega-3 essential fatty acids.3
Animal studies show that zinc deficiency in offspring caused impaired
learning which can be corrected by zinc supplementation. However, maternal
zinc deficiency during early foetal development caused permanent impaired
learning and impaired the offspring’s stress coping mechanisms, which can
increase urinary loss of zinc throughout life in response to stress. Good
nutritional care involves correction of common nutritional deficiencies in
both parents before conception, maintenance of an adequate zinc status
during pregnancy, lactation and growth. This appears to prevent
troublesome dyslexia, even in families with a genetic susceptibility to
the condition. The deleterious effects of numerous genetic conditions, may
be remedied by feeding high dose B vitamins and by ensuring adequate
levels of zinc, folic acid and other essential nutrients.4 A high
inheritance risk of dyslexia is not inevitable.
The fact that children and adults with developmental dyslexia are
likely to continue to have important nutrition deficiencies throughout
their lives, which further impair their already permanently impaired brain
function, is too important to continue to be ignored by dyslexia “experts”
who are mostly psychologists and teachers. Controlled trials find that
vitamin and mineral supplements show improvements in intelligence scores
and brain-function tests and reduce brain wave abnormalities.5
1 Snowling M. Dyslexia: a hundred years on. BMJ 1996; 313:1096-1097.
2 Grant ECG, , Howard JM ,Davies S, Chasty H, Hornsby B, Galbraith J.
Zinc deficiency in children with dyslexia: concentrations of zinc and
other minerals in sweat and hair. BMJ 1989; 296: 607-09.
3 Horrobin DF, Glen AIM, Hudson CJ. Possible relevance of
phospholipid abnormalities and genetic interactions in psychiatric
disorders: the relationship between dyslexia and schizophrenia. Med Hypoth
1995; 45: 605-13.
4 Ames B. A role for supplements in optimising health: the metabolic
tune-up. Arch Biochem Biophys 2004; 423: 227-234.
5 Eysenck HJ, Eysenck SBG. Improvement of I.Q. and behaviour as a
function of dietary supplementation: a symposium. Pers Individual
Differences 1991; 12: 329-65.
Competing interests:
None declared
Competing interests: No competing interests