monty1945
Thu, Aug-16-07, 06:16
These are two posts from my site. The exact page is http://gr-
oups.msn.com/TheScientificDebateForum-/general.msnw?action=ge-
t_message&mview=0&ID_Message=1447&all_topics=0
A long article in a major New York City area newspaper,
"Newsday," entitled "Researchers: New understanding of autism
is near," contained several good examples demonstrating why
the "medical establishment" has been so unsuccessful over the
last few decades (the "war on cancer," for instance, was
supposed to be "won" by 1980):
QUOTE: "I had been doing cancer research since I came to the
lab in 1977 and the basic method that we used in cancer was to
ask what's different about the genome of cancer compared with
the normal genome?
"Many of the tools to do that were developed by me," Wigler
said, "so we turned to those tools to ask questions about
autism." UNQUOTE.
And we get the usual vague promises, based on "genetic
understanding," with hints of "therapies" that will make life
more bearable:
QUOTE: Based on his work to date, Wigler surmises a clear
genetic understanding of the numerous ways in which autism
manifests may be tantalizingly close: "I expect that we'll
have a very good bead on a number of the [genetic] causes," of
autism in the not-too-distant future, Wigler said. "And I
suspect there will be a way to treat children to lessen the
symptoms." UNQUOTE.
A non-scientist, however, points out a major flaw in the
notion that this approach will lead to a "cure:"
QUOTE: Alison Singer, executive director of Autism Speaks, a
national advocacy organization... said what's missing in
Wigler's work is the mechanism that causes genes to mutate.
Susceptibility genes, she said, often need an outside stimulus
to set off a genetic chain of events. UNQUOTE.
But then Ms. Singer states: QUOTE: "We want them to pursue the
science wherever it leads," Singer said. "But we don't want to
get into a situation where we blame the parents. When some
parents read stories about older fathers or older mothers,
they can become very sensitive. UNQUOTE.
Source: http://www.newsday.com/news/health/ny-hsauti125331613-
aug14,0,1913106.story
Do we want the scientific method to be followed, or not, Ms.
Singer? There is no way to "pick and choose" - once that
happens, all kinds of influences (social, political, economic,
etc.) can come into play, which can lead to false claims that
are presented to the public as "scientifically proven."
In any case, the key point I'd like to make here is that genes
need to be "turned on," and that since autism is "on the
rise," why are scientists not focusing most if not all of
their research on what is doing this? For example:
QUOTE: Since the 1990s, there's been a dramatic increase in
autismautism among school-age children.
The data are from the U.S. Department of Education, and the
report hints that the increases seen with time are real.
Research has suggested that the rise in autism could be
largely explained by changes in diagnosis, with children who
might have been classified as mentally retarded or speech
impaired before the 1990s now being classified as autistic.
Lead researcher Craig J. Newschaffer, PhD, says the Department
of Education figures do not show this, but he adds that the
increase in autism may never be fully understood.
"I don't know if we are ever going to be in a position
to explain what has gone on over the last decade," he
says. UNQUOTE.
Source: http://www.webmd.com/brain/Autism/news/20050307/study-
-childhood-rise-in-autism-cases-real
It seems that these researchers must be totally ignorant of
the experiments demonstrating that the dietary oils that have
become so common over the last few decades do turn on
transcription factors (which "turn on" genes): QUOTE: It is
concluded that corn oil rapidly activates NF-kappaB in Kupffer
cells via oxidant-dependent mechanisms. UNQUOTE.
Source: Carcinogenesis. 1999 Nov;20(11):2095-100.
Therefore, it only makes sense to start with this simple
dietary intervention, and then just observe if the incidence
of autism decreases substantially. Instead, even if the
researchers can "find the gene," there is no way to know if it
will lead to anything at all. My hypothesis about autism's
cause is a bit more complicated than this, involving what
kinds of polyunsaturated fatty acids are in the children's
mother's cells, but one could certainly see if dietary
intervention beginning at birth would lead to a much lower
rate of autism, and if so, a "cure" for at least autism would
then exist.
One last point that I've made before is relevant on this post,
which is that scientists don't win Nobel Prizes by telling
people what food items they should avoid. In fact, one wonders
if a scientist could do better than teach at the community
college level if he or she made such statements. Fortunately,
I'm an independent scholar who is able to examine large
amounts of evidence, without worrying about what my
"superiors" might think of my conclusions.
In this post, I will cite molecular-level evidence for
my proposal:
QUOTE: ...Biochemical analyses of brain homogenates from PPA
treated rats showed an increase in oxidative stress markers
(e.g., lipid peroxidation and protein carbonylation) and
glutathione S-transferase activity coupled with a decrease in
glutathione and glutathione peroxidase activity.
Neurohistological examinations of hippocampus and adjacent
white matter (external capsule) of PPA treated rats revealed
increased reactive astrogliosis (GFAP immunoreactivity) and
activated microglia (CD68 immunoreactivity) suggestive of a
neuroinflammatory process... UNQUOTE.
Source: Behav Brain Res. 2007 Jan 10;176(1):149-69. Epub
2006 Sep 1.
QUOTE: ...According to the Autism Society of America, autism
is now considered to be an epidemic. The increase in the rate
of autism revealed by epidemiological studies and government
reports implicates the importance of external or environmental
factors that may be changing. This article discusses the
evidence for the case that some children with autism may
become autistic from neuronal cell death or brain damage
sometime after birth as result of insult; and addresses the
hypotheses that toxicity and oxidative stress may be a cause
of neuronal insult in autism... UNQUOTE.
Source: J Toxicol Environ Health B Crit Rev. 2006
Nov-Dec;9(6):485-99.
QUOTE: Autism is a neurological disorder of childhood with
poorly understood etiology and pathology. We compared lipid
peroxidation status in the plasma of children with autism, and
their developmentally normal non-autistic siblings by
quantifying the levels of malonyldialdehyde, an end product of
fatty acid oxidation. Lipid peroxidation was found to be
elevated in autism indicating that oxidative stress is
increased in this disease. Levels of major antioxidant
proteins namely, transferrin (iron-binding protein) and
ceruloplasmin (copper-binding protein) in the serum, were
significantly reduced in autistic children as compared to
their developmentally normal non-autistic siblings. A striking
correlation was observed between reduced levels of these
proteins and loss of previously acquired language skills in
children with autism. These results indicate altered
regulation of transferrin and ceruloplasmin in autistic
children who lose acquired language skills. It is suggested
that such changes may lead to abnormal iron and copper
metabolism in autism, and that increased oxidative stress may
have pathological role in autism. UNQUOTE.
Source: Life Sci. 2004 Oct 8;75(21):2539-49.
QUOTE: It is thought that autism could result from an
interaction between genetic and environmental factors with
oxidative stress as a potential mechanism linking the two.
One genetic factor may be altered oxidative-reductive
capacity. This study tested the hypothesis that children with
autism have increased oxidative stress. We evaluated children
with autism for the presence of two oxidative stress
biomarkers. Urinary excretion of 8-hydroxy-2-deoxyguanosine
(8-OHdG) and 8-isoprostane-F2alpha (8-iso-PGF2alpha) were
determined in 33 children with autism and 29 healthy
controls. 8-iso-PGF2alpha levels were significantly higher in
children with autism. The isoprostane levels in autistic
subjects were variable with a bimodal distribution. The
majority of autistic subjects showed a moderate increase in
isoprostane levels while a smaller group of autistic children
showed dramatic increases in their isoprostane levels. There
was a trend of an increase in 8-OHdG levels in children with
autism but it did not reach statistical significance. There
was no significant correlation between the levels of the
biomarkers and vitamin intake, dietary supplements, medicine,
medical disorders, or history of regression. These results
suggest that the lipid peroxidation biomarker is increased in
this cohort of autistic children, especially in the subgroup
of autistic children. UNQUOTE.
Source: Prostaglandins Leukot Essent Fatty Acids. 2005
Nov;73(5): 379-84.
QUOTE: ...Taken together, these studies suggest increased
oxidative stress in autism that may contribute to the
development of this disease. A mechanism linking oxidative
stress with membrane lipid abnormalities, inflammation,
aberrant immune response, impaired energy metabolism and
excitotoxicity, leading to clinical symptoms and pathogenesis
of autism is proposed. UNQUOTE.
Source: Pathophysiology. 2006 Aug;13(3):171-81. Epub
2006 Jun 12.
oups.msn.com/TheScientificDebateForum-/general.msnw?action=ge-
t_message&mview=0&ID_Message=1447&all_topics=0
A long article in a major New York City area newspaper,
"Newsday," entitled "Researchers: New understanding of autism
is near," contained several good examples demonstrating why
the "medical establishment" has been so unsuccessful over the
last few decades (the "war on cancer," for instance, was
supposed to be "won" by 1980):
QUOTE: "I had been doing cancer research since I came to the
lab in 1977 and the basic method that we used in cancer was to
ask what's different about the genome of cancer compared with
the normal genome?
"Many of the tools to do that were developed by me," Wigler
said, "so we turned to those tools to ask questions about
autism." UNQUOTE.
And we get the usual vague promises, based on "genetic
understanding," with hints of "therapies" that will make life
more bearable:
QUOTE: Based on his work to date, Wigler surmises a clear
genetic understanding of the numerous ways in which autism
manifests may be tantalizingly close: "I expect that we'll
have a very good bead on a number of the [genetic] causes," of
autism in the not-too-distant future, Wigler said. "And I
suspect there will be a way to treat children to lessen the
symptoms." UNQUOTE.
A non-scientist, however, points out a major flaw in the
notion that this approach will lead to a "cure:"
QUOTE: Alison Singer, executive director of Autism Speaks, a
national advocacy organization... said what's missing in
Wigler's work is the mechanism that causes genes to mutate.
Susceptibility genes, she said, often need an outside stimulus
to set off a genetic chain of events. UNQUOTE.
But then Ms. Singer states: QUOTE: "We want them to pursue the
science wherever it leads," Singer said. "But we don't want to
get into a situation where we blame the parents. When some
parents read stories about older fathers or older mothers,
they can become very sensitive. UNQUOTE.
Source: http://www.newsday.com/news/health/ny-hsauti125331613-
aug14,0,1913106.story
Do we want the scientific method to be followed, or not, Ms.
Singer? There is no way to "pick and choose" - once that
happens, all kinds of influences (social, political, economic,
etc.) can come into play, which can lead to false claims that
are presented to the public as "scientifically proven."
In any case, the key point I'd like to make here is that genes
need to be "turned on," and that since autism is "on the
rise," why are scientists not focusing most if not all of
their research on what is doing this? For example:
QUOTE: Since the 1990s, there's been a dramatic increase in
autismautism among school-age children.
The data are from the U.S. Department of Education, and the
report hints that the increases seen with time are real.
Research has suggested that the rise in autism could be
largely explained by changes in diagnosis, with children who
might have been classified as mentally retarded or speech
impaired before the 1990s now being classified as autistic.
Lead researcher Craig J. Newschaffer, PhD, says the Department
of Education figures do not show this, but he adds that the
increase in autism may never be fully understood.
"I don't know if we are ever going to be in a position
to explain what has gone on over the last decade," he
says. UNQUOTE.
Source: http://www.webmd.com/brain/Autism/news/20050307/study-
-childhood-rise-in-autism-cases-real
It seems that these researchers must be totally ignorant of
the experiments demonstrating that the dietary oils that have
become so common over the last few decades do turn on
transcription factors (which "turn on" genes): QUOTE: It is
concluded that corn oil rapidly activates NF-kappaB in Kupffer
cells via oxidant-dependent mechanisms. UNQUOTE.
Source: Carcinogenesis. 1999 Nov;20(11):2095-100.
Therefore, it only makes sense to start with this simple
dietary intervention, and then just observe if the incidence
of autism decreases substantially. Instead, even if the
researchers can "find the gene," there is no way to know if it
will lead to anything at all. My hypothesis about autism's
cause is a bit more complicated than this, involving what
kinds of polyunsaturated fatty acids are in the children's
mother's cells, but one could certainly see if dietary
intervention beginning at birth would lead to a much lower
rate of autism, and if so, a "cure" for at least autism would
then exist.
One last point that I've made before is relevant on this post,
which is that scientists don't win Nobel Prizes by telling
people what food items they should avoid. In fact, one wonders
if a scientist could do better than teach at the community
college level if he or she made such statements. Fortunately,
I'm an independent scholar who is able to examine large
amounts of evidence, without worrying about what my
"superiors" might think of my conclusions.
In this post, I will cite molecular-level evidence for
my proposal:
QUOTE: ...Biochemical analyses of brain homogenates from PPA
treated rats showed an increase in oxidative stress markers
(e.g., lipid peroxidation and protein carbonylation) and
glutathione S-transferase activity coupled with a decrease in
glutathione and glutathione peroxidase activity.
Neurohistological examinations of hippocampus and adjacent
white matter (external capsule) of PPA treated rats revealed
increased reactive astrogliosis (GFAP immunoreactivity) and
activated microglia (CD68 immunoreactivity) suggestive of a
neuroinflammatory process... UNQUOTE.
Source: Behav Brain Res. 2007 Jan 10;176(1):149-69. Epub
2006 Sep 1.
QUOTE: ...According to the Autism Society of America, autism
is now considered to be an epidemic. The increase in the rate
of autism revealed by epidemiological studies and government
reports implicates the importance of external or environmental
factors that may be changing. This article discusses the
evidence for the case that some children with autism may
become autistic from neuronal cell death or brain damage
sometime after birth as result of insult; and addresses the
hypotheses that toxicity and oxidative stress may be a cause
of neuronal insult in autism... UNQUOTE.
Source: J Toxicol Environ Health B Crit Rev. 2006
Nov-Dec;9(6):485-99.
QUOTE: Autism is a neurological disorder of childhood with
poorly understood etiology and pathology. We compared lipid
peroxidation status in the plasma of children with autism, and
their developmentally normal non-autistic siblings by
quantifying the levels of malonyldialdehyde, an end product of
fatty acid oxidation. Lipid peroxidation was found to be
elevated in autism indicating that oxidative stress is
increased in this disease. Levels of major antioxidant
proteins namely, transferrin (iron-binding protein) and
ceruloplasmin (copper-binding protein) in the serum, were
significantly reduced in autistic children as compared to
their developmentally normal non-autistic siblings. A striking
correlation was observed between reduced levels of these
proteins and loss of previously acquired language skills in
children with autism. These results indicate altered
regulation of transferrin and ceruloplasmin in autistic
children who lose acquired language skills. It is suggested
that such changes may lead to abnormal iron and copper
metabolism in autism, and that increased oxidative stress may
have pathological role in autism. UNQUOTE.
Source: Life Sci. 2004 Oct 8;75(21):2539-49.
QUOTE: It is thought that autism could result from an
interaction between genetic and environmental factors with
oxidative stress as a potential mechanism linking the two.
One genetic factor may be altered oxidative-reductive
capacity. This study tested the hypothesis that children with
autism have increased oxidative stress. We evaluated children
with autism for the presence of two oxidative stress
biomarkers. Urinary excretion of 8-hydroxy-2-deoxyguanosine
(8-OHdG) and 8-isoprostane-F2alpha (8-iso-PGF2alpha) were
determined in 33 children with autism and 29 healthy
controls. 8-iso-PGF2alpha levels were significantly higher in
children with autism. The isoprostane levels in autistic
subjects were variable with a bimodal distribution. The
majority of autistic subjects showed a moderate increase in
isoprostane levels while a smaller group of autistic children
showed dramatic increases in their isoprostane levels. There
was a trend of an increase in 8-OHdG levels in children with
autism but it did not reach statistical significance. There
was no significant correlation between the levels of the
biomarkers and vitamin intake, dietary supplements, medicine,
medical disorders, or history of regression. These results
suggest that the lipid peroxidation biomarker is increased in
this cohort of autistic children, especially in the subgroup
of autistic children. UNQUOTE.
Source: Prostaglandins Leukot Essent Fatty Acids. 2005
Nov;73(5): 379-84.
QUOTE: ...Taken together, these studies suggest increased
oxidative stress in autism that may contribute to the
development of this disease. A mechanism linking oxidative
stress with membrane lipid abnormalities, inflammation,
aberrant immune response, impaired energy metabolism and
excitotoxicity, leading to clinical symptoms and pathogenesis
of autism is proposed. UNQUOTE.
Source: Pathophysiology. 2006 Aug;13(3):171-81. Epub
2006 Jun 12.