Zinc deficient, dyslexia, asd

[Guest guest]

Of course, we all know that our kids tend to be deficient in zinc.

I found this article in the BMJ rapid response section. Not only is

this interesting in and of itself, it also cites several sources for

more info. (BTW it was written in response to yet another BMJ

article extolling the safety of vaccines.)

Ellen C G Grant,

physician and medical gynaecologist

Kingston-upon-Thames, KT2 7JU, UK

1. Send response to journal:

Re: 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, , 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