We already know many of the environmental reasons for impaired brain
function in children. These include deficiencies of essential nutrients,
especially of zinc, during development and the effects of common social
poisons which include alcohol, tobacco smoking and toxic metal exposures.
Since lead-free petrol became available, blood lead levels in my patients
have fallen. However, alcohol use, smoking and steroid hormone use in
younger women in the form of contraceptives or hormonal medications,
before their first pregnancies, and during pregnancy or at birth to
“protect” the lungs of a premature child, have been increasing.
Inexplicably, dental mercury amalgams continue to be inserted into the
mouths of future parents.
John McLaren-Howard’s biochemical findings in 61 autistic children
give an important perpective into why childhood illnesses have increased
so dramatically. Most of the autistic children had zinc and copper
deficiencies and superoxide dismutase (SODase) dysfunction. 16 had DNA-
adducts in leucocytes to malondialdehyde, 12 to cadmium, 9 to nickel, 3 to
mercury and one to lead. Even if only 5% of autistic children show
evidence of signs of mercury exposures, this still means large numbers of
children are adversely affected by mercury but the main source is likely
to be parental dental amalgams. It could be that any extra mercury in a
vaccination is “the straw that breaks the camel’s back” for some
vulnerable children.
The relation between environmental factors and brain development and
function has been investigated for decades. In 1982 Tanaka and colleagues
discovered a beneficial effect of supplementary zinc on foetal growth in
rats which could possibly help preventing the CNS dysfunctions of Foetal
Alcohol Syndrome. They also noted that the effect of zinc supplementation
was not as good compared to the results in the control animals not given
alcohol.
In 1994 Nishida and colleagues determined copper, zinc-superoxide
dismutase (Cu,Zn-SOD) activities in 22 human brains from fetuses to
adults. Cu/Zn-SOD activity of the cerebral cortex and white matter
increased from 15% in fetuses to 50% of adult levels in neonates. The
activity of the white matter was higher than that in the cortex in the
foetal period, but was essentially the same as those of the cortex in the
postnatal period. Cu/Zn-SOD activity in the central nervous system was
highest in the spinal cord and higher in the order pons, medulla oblongata
> cerebellum, midbrain, thalamus > putamen, pallidum and cerebrum.
These low activities may be related to the vulnerability of cerebral
cortex and white matter in premature infants.
If even a little of the huge amount of money spent on “politically
correct epidemiological studies” was used instead for basic biochemical
investigations, so many of today’s “mysteries” would be unveiled.
2 Tanaka H, Nakazawa K, Suzuki N, Arima M. Prevention possibility for
brain dysfunction in rat with the fetal alcohol syndrome-low-zinc-status
and hypoglycemia. Brain Dev.1982; 4: 429-38.
3 Nishida A, Misaki Y, Kuruta H, Takashima S. Developmental
expression of copper, zinc-superoxide dismutase in human brain by
chemiluminescence. Brain Dev. 1994; 16: 40-3.
Rapid Response:
Environmental reasons for increases in autism
We already know many of the environmental reasons for impaired brain
function in children. These include deficiencies of essential nutrients,
especially of zinc, during development and the effects of common social
poisons which include alcohol, tobacco smoking and toxic metal exposures.
Since lead-free petrol became available, blood lead levels in my patients
have fallen. However, alcohol use, smoking and steroid hormone use in
younger women in the form of contraceptives or hormonal medications,
before their first pregnancies, and during pregnancy or at birth to
“protect” the lungs of a premature child, have been increasing.
Inexplicably, dental mercury amalgams continue to be inserted into the
mouths of future parents.
John McLaren-Howard’s biochemical findings in 61 autistic children
give an important perpective into why childhood illnesses have increased
so dramatically. Most of the autistic children had zinc and copper
deficiencies and superoxide dismutase (SODase) dysfunction. 16 had DNA-
adducts in leucocytes to malondialdehyde, 12 to cadmium, 9 to nickel, 3 to
mercury and one to lead. Even if only 5% of autistic children show
evidence of signs of mercury exposures, this still means large numbers of
children are adversely affected by mercury but the main source is likely
to be parental dental amalgams. It could be that any extra mercury in a
vaccination is “the straw that breaks the camel’s back” for some
vulnerable children.
The relation between environmental factors and brain development and
function has been investigated for decades. In 1982 Tanaka and colleagues
discovered a beneficial effect of supplementary zinc on foetal growth in
rats which could possibly help preventing the CNS dysfunctions of Foetal
Alcohol Syndrome. They also noted that the effect of zinc supplementation
was not as good compared to the results in the control animals not given
alcohol.
In 1994 Nishida and colleagues determined copper, zinc-superoxide
dismutase (Cu,Zn-SOD) activities in 22 human brains from fetuses to
adults. Cu/Zn-SOD activity of the cerebral cortex and white matter
increased from 15% in fetuses to 50% of adult levels in neonates. The
activity of the white matter was higher than that in the cortex in the
foetal period, but was essentially the same as those of the cortex in the
postnatal period. Cu/Zn-SOD activity in the central nervous system was
highest in the spinal cord and higher in the order pons, medulla oblongata
> cerebellum, midbrain, thalamus > putamen, pallidum and cerebrum.
These low activities may be related to the vulnerability of cerebral
cortex and white matter in premature infants.
If even a little of the huge amount of money spent on “politically
correct epidemiological studies” was used instead for basic biochemical
investigations, so many of today’s “mysteries” would be unveiled.
1 Grant ECG, McLaren-Howard J. Re: The effects of toxic metals in
autistic children. http://bmj.com/cgi/eletters/329/7466/588-b#74117, 13
Sep 2004
2 Tanaka H, Nakazawa K, Suzuki N, Arima M. Prevention possibility for
brain dysfunction in rat with the fetal alcohol syndrome-low-zinc-status
and hypoglycemia. Brain Dev.1982; 4: 429-38.
3 Nishida A, Misaki Y, Kuruta H, Takashima S. Developmental
expression of copper, zinc-superoxide dismutase in human brain by
chemiluminescence. Brain Dev. 1994; 16: 40-3.
Competing interests:
None declared
Competing interests: No competing interests