Re: Researchers connect APC protein to autism...and...

[Guest guest]

>

> There is a new study that just came out that linked a protein malfunction to

autism and retardation but of course the studies will only mention those

conditions that funded them- so in my opinion we always need to think outside

the box to those conditions that may also be involved but that do not have the

monies for research as of yet (cof apraxia cof). I just did a quick review of

the protein called APC (adenomatous polyposis coli) and found that it's been

linked to gut issues, colon cancer etc. I know many talk about gut issues with

autism, but as I found with apraxia as well most stick with the same old same

old theories (don't acknowledge that apraxia like autism is totally morphed

since the 1950s) Yet the more brilliant out of the box researchers as you'll

find below look to discover new ways to help, and not just with off label

dangerous side effect drugs or by frying or removing part of our children's

brains with electroshock or surgery.... and to me I'm finding that there is the

benign and healthy discovery of foods, dietary intake (ironically,

scientifically, or through God's sense of humor that points back to NV!)

>

> So getting back to this new study and how this may tie in to how to better

help our children, ourselves...as I have learned and continue to share here -the

body can make the non essential amino acids but not the essential amino acids-

and it's vital for us to consume ALL of them which with restricted diets,

ironically some may be creating more of a problem than the one that they were

trying to solve. Diet and nutrition are complex in that there is a great

science to them -far deeper than what most of us know. If the body does not

have the essential amino acid needed it will create what it can to fill in that

blank -and as you'll read below that has already been linked to cancer when the

essential amino acid lysine is lacking

>

> " One mutation in the APC gene is found in approximately 6 percent of people

with Ashkenazi (eastern and central European) Jewish heritage. This mutation

replaces the amino acid isoleucine with the amino acid lysine at position 1307

in the APC protein (written as Ile1307Lys or I1307K). This change was initially

thought to be harmless, but has been shown to be associated with a 10 percent to

20 percent increased risk of colon cancer. "

> http://ghr.nlm.nih.gov/gene/APC

>

> The mutation of this protein is now also being linked to autism and mental

retardation, and from my findings below is found to be helped by dietary

supplementation of various essential amino acids. Two of the essential amino

acids found to be important for APC are lysine and arginene, both found

naturally through whole food sources in nutriiveda from the whey as again NV

contains ALL of the essential amino acids per serving which is rare (the full

list is Amino Acids: Alanine, Arginine, Aspartic Acid, Cystin, Glutamic Acid,

Glycine, Histidine, Isoleucine, Leucine, Lysine, Methionine, Phenylalanine,

Proline, Serine, Thereonine, Trytophan, Tyrosine, Valine

http://pursuitofresearch.org/ingredients.html

>

> The following are some of the snips I pulled with links to more info all from

credible sources as of course. I can have my theories

http://pursuitofresearch.org/science.html but I want to have a hypothesis based

on previous findings as to why nutriiveda appears to be working for again almost

all that try it.

>

> ~~~~~~~~references, article and scientific findings

>

>

> Essential amino acids

> Humans can produce 10 of the 20 amino acids. The others must be supplied in

the food. Failure to obtain enough of even 1 of the 10 essential amino acids,

those that we cannot make, results in degradation of the body's proteins—muscle

and so forth—to obtain the one amino acid that is needed. Unlike fat and starch,

the human body does not store excess amino acids for later use—the amino acids

must be in the food every day.

>

> The 10 amino acids that we can produce are alanine, asparagine, aspartic acid,

cysteine, glutamic acid, glutamine, glycine, proline, serine and tyrosine.

Tyrosine is produced from phenylalanine, so if the diet is deficient in

phenylalanine, tyrosine will be required as well. The essential amino acids are

arginine (required for the young, but not for adults), histidine, isoleucine,

leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

These amino acids are required in the diet. Plants, of course, must be able to

make all the amino acids. Humans, on the other hand, do not have all the the

enzymes required for the biosynthesis of all of the amino acids.

>

>

> Arginine, an essential amino acid, has a positively charged guanidino group.

Arginine is well designed to bind the phosphate anion, and is often found in the

active centers of proteins that bind phosphorylated substrates. As a cation,

arginine, as well as lysine, plays a role in maintaining the overall charge

balance of a protein.

> http://www.biology.arizona.edu/biochemistry/problem_sets/aa/aa.html

>

> And here a study linking that up in a mice model:

>

> Mol Carcinog. 2006 Feb;45(2):93-105.

> The role of NO synthases in arginine-dependent small intestinal and colonic

carcinogenesis.

>

> Yerushalmi HF, Besselsen DG, Ignatenko NA, Blohm-Mangone KA, Padilla-

JL, Stringer DE, Cui H, Holubec H, Payne CM, Gerner EW.

>

> Gastrointestinal Cancer Program, Arizona Cancer Center, The University of

Arizona, Tucson, Arizona 85724, USA.

> Abstract

>

> Arginine is catabolized by NOS2 and other nitric oxide synthases to form

nitric oxide. We evaluated the roles of dietary arginine and Nos2 in

Apc-dependent intestinal tumorigenesis in Min mice with and without a functional

Nos2 gene. NOS2 protein was expressed only in intestinal tissues of Apc(Min/+)

Nos2+/+ mice. NOS3 expression was higher in intestinal tissues of mice lacking

Nos2, mainly in the small intestine. When diet was supplemented with arginine

(0.2% and 2% in drinking water), lack of Nos2 results in decreased tumorigenesis

in both small intestine and colon. In Nos2 knockout mice, supplemental arginine

(up to 2%) caused a decrease in small intestinal tumor number and size. The

arginine-dependent decrease was associated with an increase in nitrotyrosine

formation and apoptosis in the region of intestinal stem cells. Mice expressing

Nos2 did not show these changes. These mice did, however, show an

arginine-dependent increase in colon tumor number and incidence, while no effect

on apoptosis was seen. These changes were associated with increased

nitrotyrosine formation in epithelial cells. Mice lacking Nos2 did not show

changes in tumorigenesis or nitrotyrosine formation, while demonstrating an

arginine-dependent increase in apoptosis. These data suggest that Nos2 and

dietary arginine have significant effects on intestinal and colonic

tumorigenesis in Min mice. In both tissues, loss of Nos2 is associated with

decreased tumorigenesis when mice are supplemented with dietary arginine. In the

small intestine, Nos2 prevents the arginine-induced decrease in tumor number and

size, which is associated with NOS3 expression and increased apoptosis. In the

colon, Nos2 is required for the arginine-induced increase in tumor number and

incidence.

>

> http://www.ncbi.nlm.nih.gov/pubmed/16329147

>

> Articles:

>

> Researchers connect APC protein to autism and mental retardation

>

> by bjs on August 23, 2010

>

> BOSTON (August 23, 2010) — A clue to the causes of autism and mental

retardation lies in the synapse, the tiny intercellular junction that rapidly

transfers information from one neuron to the next. According to neuroscientists

at Tufts University School of Medicine, with students from the Sackler School of

Graduate Biomedical Sciences at Tufts, a protein called APC (adenomatous

polyposis coli) plays a key role in synapse maturation, and APC dysfunction

prevents the synapse function required for typical learning and memory. The

findings are published in the August 18 issue of The Journal of Neuroscience.

>

> " Both sides of the synapse are finely tuned for efficient transmission; an

imbalance on either side can negatively impact function, resulting in cognitive

deficits. Our study reveals that APC forms a key protein complex in the

postsynaptic neuron that also provides signals to direct synapse maturation in

the presynaptic neuron, ensuring that the two sides of the synapse mature in

concert to provide optimal function, " said senior author Michele H. , PhD,

professor in the department of neuroscience at Tufts University School of

Medicine. is also a member of the cell, molecular and developmental

biology; cellular and molecular physiology; and neuroscience program faculties

at the Sackler School of Graduate Biomedical Sciences at Tufts.

>

> In the in vivo study, the team blocked APC function and found that synaptic

levels of the cell adhesion proteins neuroligin and neurexin dropped

considerably. Without normal levels of these proteins, synapses were less mature

both structurally and functionally. Mutations in the genes for neuroligin and

neurexin are associated with autism in humans, but until now, little was known

about the mechanisms responsible for localizing these proteins at the synapse.

>

> " Our laboratory study is the first to show that APC is needed to recruit

neuroligin and neurexin to the synapse. This finding provides new insights into

the mechanisms required for proper synapse function as well as molecular changes

at the synapse that likely contribute to autistic behaviors and learning

deficits in people with APC loss of function gene mutations, " said .

>

> " Our study also sheds light on a poorly-understood but essential process, the

cross-talk that occurs between presynaptic and postsynaptic neurons. When we

perturbed APC function on the postsynaptic side, we saw changes on both sides of

the synapse, indicating that APC organizes a protein complex that communicates

against the normal flow of traffic, " said first author Madelaine Rosenberg, PhD,

an affiliate of the department of neuroscience at TUSM.

>

> The research team's next step is to examine the behavioral and cognitive

changes that occur when APC is deleted in neurons of the mammalian brain. They

have developed a new mouse model that will allow them to investigate how the

loss of APC function leads to synaptic changes and impaired learning and memory.

>

> Additional authors are Fang Yang, PhD, a research associate in the department

of medicine at TUSM; Mohn, a PhD candidate in the cell, molecular, and

developmental biology program at Sackler and member of 's lab; and

Storer, a PhD candidate in the neuroscience program at Sackler and

member of 's lab.

>

> This study was funded by the National Institute of Neurological Disorders and

Stroke (NINDS), part of the National Institutes of Health, and the Tufts Center

for Neuroscience Research. The Tufts Center for Neuroscience Research, itself,

is supported by the NINDS and by Tufts University School of Medicine and Tufts

Medical Center.

>

> Rosenberg MM, Yang F, Mohn JL, Storer EK, MH. The Journal of

Neuroscience. 2010. (August 18); 30(33): 11073-11085. " The Postsynaptic

Adenomatous Polyposis Coli (APC) Multiprotein Complex Is Required for Localizing

Neuroligin and Neurexin to Neuronal Nicotinic Synapses in Vivo. " Published

online August 18, 2010, doi: 10.1523/JNEUROSCI.0983-10.2010

>

> About Tufts University School of Medicine and the Sackler School of Graduate

Biomedical Sciences

>

>

> Tufts University School of Medicine and the Sackler School of Graduate

Biomedical Sciences at Tufts University are international leaders in innovative

medical education and advanced research. The School of Medicine and the Sackler

School are renowned for excellence in education in general medicine, biomedical

sciences, special combined degree programs in business, health management,

public health, bioengineering and international relations, as well as basic and

clinical research at the cellular and molecular level. Ranked among the top in

the nation, the School of Medicine is affiliated with six major teaching

hospitals and more than 30 health care facilities. Tufts University School of

Medicine and the Sackler School undertake research that is consistently rated

among the highest in the nation for its effect on the advancement of medical

science.

>

> If you are a member of the media interested in learning more about this topic,

or speaking with a faculty member at the Tufts University School of Medicine,

the Sackler School of Graduate Biomedical Sciences, or another Tufts health

sciences researcher, please contact Siobhan Gallagher at 617-636-6586 or, for

this study, at 617-636-2789.

>

> Related posts:

>

> 1. Protein regulates enzyme linked to Alzheimer's disease

> 2. Protein linked to mental retardation controls synapse maturation,

plasticity, CSHL team finds

>

>

http://scienceblog.com/37725/researchers-connect-apc-protein-to-autism-and-menta\

l-retardation/

>

> Also read more here

http://newsfeed.time.com/2010/08/24/new-study-protein-malfunctions-linked-to-aut\

ism/

>

> Please again check http://pursuitofresearch.org/science.html going ahead as

there are a few updates that will be added to this page!

>

> =====

>

[Guest guest]

Has anyone tried just supplementing with the essential amino acids needed?

>

> There is a new study that just came out that linked a protein malfunction to

autism and retardation but of course the studies will only mention those

conditions that funded them- so in my opinion we always need to think outside

the box to those conditions that may also be involved but that do not have the

monies for research as of yet (cof apraxia cof). I just did a quick review of

the protein called APC (adenomatous polyposis coli) and found that it's been

linked to gut issues, colon cancer etc. I know many talk about gut issues with

autism, but as I found with apraxia as well most stick with the same old same

old theories (don't acknowledge that apraxia like autism is totally morphed

since the 1950s) Yet the more brilliant out of the box researchers as you'll

find below look to discover new ways to help, and not just with off label

dangerous side effect drugs or by frying or removing part of our children's

brains with electroshock or surgery.... and to me I'm finding that there is the

benign and healthy discovery of foods, dietary intake (ironically,

scientifically, or through God's sense of humor that points back to NV!)

>

> So getting back to this new study and how this may tie in to how to better

help our children, ourselves...as I have learned and continue to share here -the

body can make the non essential amino acids but not the essential amino acids-

and it's vital for us to consume ALL of them which with restricted diets,

ironically some may be creating more of a problem than the one that they were

trying to solve. Diet and nutrition are complex in that there is a great

science to them -far deeper than what most of us know. If the body does not

have the essential amino acid needed it will create what it can to fill in that

blank -and as you'll read below that has already been linked to cancer when the

essential amino acid lysine is lacking

>

> " One mutation in the APC gene is found in approximately 6 percent of people

with Ashkenazi (eastern and central European) Jewish heritage. This mutation

replaces the amino acid isoleucine with the amino acid lysine at position 1307

in the APC protein (written as Ile1307Lys or I1307K). This change was initially

thought to be harmless, but has been shown to be associated with a 10 percent to

20 percent increased risk of colon cancer. "

> http://ghr.nlm.nih.gov/gene/APC

>

> The mutation of this protein is now also being linked to autism and mental

retardation, and from my findings below is found to be helped by dietary

supplementation of various essential amino acids. Two of the essential amino

acids found to be important for APC are lysine and arginene, both found

naturally through whole food sources in nutriiveda from the whey as again NV

contains ALL of the essential amino acids per serving which is rare (the full

list is Amino Acids: Alanine, Arginine, Aspartic Acid, Cystin, Glutamic Acid,

Glycine, Histidine, Isoleucine, Leucine, Lysine, Methionine, Phenylalanine,

Proline, Serine, Thereonine, Trytophan, Tyrosine, Valine

http://pursuitofresearch.org/ingredients.html

>

> The following are some of the snips I pulled with links to more info all from

credible sources as of course. I can have my theories

http://pursuitofresearch.org/science.html but I want to have a hypothesis based

on previous findings as to why nutriiveda appears to be working for again almost

all that try it.

>

> ~~~~~~~~references, article and scientific findings

>

>

> Essential amino acids

> Humans can produce 10 of the 20 amino acids. The others must be supplied in

the food. Failure to obtain enough of even 1 of the 10 essential amino acids,

those that we cannot make, results in degradation of the body's proteins—muscle

and so forth—to obtain the one amino acid that is needed. Unlike fat and starch,

the human body does not store excess amino acids for later use—the amino acids

must be in the food every day.

>

> The 10 amino acids that we can produce are alanine, asparagine, aspartic acid,

cysteine, glutamic acid, glutamine, glycine, proline, serine and tyrosine.

Tyrosine is produced from phenylalanine, so if the diet is deficient in

phenylalanine, tyrosine will be required as well. The essential amino acids are

arginine (required for the young, but not for adults), histidine, isoleucine,

leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

These amino acids are required in the diet. Plants, of course, must be able to

make all the amino acids. Humans, on the other hand, do not have all the the

enzymes required for the biosynthesis of all of the amino acids.

>

>

> Arginine, an essential amino acid, has a positively charged guanidino group.

Arginine is well designed to bind the phosphate anion, and is often found in the

active centers of proteins that bind phosphorylated substrates. As a cation,

arginine, as well as lysine, plays a role in maintaining the overall charge

balance of a protein.

> http://www.biology.arizona.edu/biochemistry/problem_sets/aa/aa.html

>

> And here a study linking that up in a mice model:

>

> Mol Carcinog. 2006 Feb;45(2):93-105.

> The role of NO synthases in arginine-dependent small intestinal and colonic

carcinogenesis.

>

> Yerushalmi HF, Besselsen DG, Ignatenko NA, Blohm-Mangone KA, Padilla-

JL, Stringer DE, Cui H, Holubec H, Payne CM, Gerner EW.

>

> Gastrointestinal Cancer Program, Arizona Cancer Center, The University of

Arizona, Tucson, Arizona 85724, USA.

> Abstract

>

> Arginine is catabolized by NOS2 and other nitric oxide synthases to form

nitric oxide. We evaluated the roles of dietary arginine and Nos2 in

Apc-dependent intestinal tumorigenesis in Min mice with and without a functional

Nos2 gene. NOS2 protein was expressed only in intestinal tissues of Apc(Min/+)

Nos2+/+ mice. NOS3 expression was higher in intestinal tissues of mice lacking

Nos2, mainly in the small intestine. When diet was supplemented with arginine

(0.2% and 2% in drinking water), lack of Nos2 results in decreased tumorigenesis

in both small intestine and colon. In Nos2 knockout mice, supplemental arginine

(up to 2%) caused a decrease in small intestinal tumor number and size. The

arginine-dependent decrease was associated with an increase in nitrotyrosine

formation and apoptosis in the region of intestinal stem cells. Mice expressing

Nos2 did not show these changes. These mice did, however, show an

arginine-dependent increase in colon tumor number and incidence, while no effect

on apoptosis was seen. These changes were associated with increased

nitrotyrosine formation in epithelial cells. Mice lacking Nos2 did not show

changes in tumorigenesis or nitrotyrosine formation, while demonstrating an

arginine-dependent increase in apoptosis. These data suggest that Nos2 and

dietary arginine have significant effects on intestinal and colonic

tumorigenesis in Min mice. In both tissues, loss of Nos2 is associated with

decreased tumorigenesis when mice are supplemented with dietary arginine. In the

small intestine, Nos2 prevents the arginine-induced decrease in tumor number and

size, which is associated with NOS3 expression and increased apoptosis. In the

colon, Nos2 is required for the arginine-induced increase in tumor number and

incidence.

>

> http://www.ncbi.nlm.nih.gov/pubmed/16329147

>

> Articles:

>

> Researchers connect APC protein to autism and mental retardation

>

> by bjs on August 23, 2010

>

> BOSTON (August 23, 2010) — A clue to the causes of autism and mental

retardation lies in the synapse, the tiny intercellular junction that rapidly

transfers information from one neuron to the next. According to neuroscientists

at Tufts University School of Medicine, with students from the Sackler School of

Graduate Biomedical Sciences at Tufts, a protein called APC (adenomatous

polyposis coli) plays a key role in synapse maturation, and APC dysfunction

prevents the synapse function required for typical learning and memory. The

findings are published in the August 18 issue of The Journal of Neuroscience.

>

> " Both sides of the synapse are finely tuned for efficient transmission; an

imbalance on either side can negatively impact function, resulting in cognitive

deficits. Our study reveals that APC forms a key protein complex in the

postsynaptic neuron that also provides signals to direct synapse maturation in

the presynaptic neuron, ensuring that the two sides of the synapse mature in

concert to provide optimal function, " said senior author Michele H. , PhD,

professor in the department of neuroscience at Tufts University School of

Medicine. is also a member of the cell, molecular and developmental

biology; cellular and molecular physiology; and neuroscience program faculties

at the Sackler School of Graduate Biomedical Sciences at Tufts.

>

> In the in vivo study, the team blocked APC function and found that synaptic

levels of the cell adhesion proteins neuroligin and neurexin dropped

considerably. Without normal levels of these proteins, synapses were less mature

both structurally and functionally. Mutations in the genes for neuroligin and

neurexin are associated with autism in humans, but until now, little was known

about the mechanisms responsible for localizing these proteins at the synapse.

>

> " Our laboratory study is the first to show that APC is needed to recruit

neuroligin and neurexin to the synapse. This finding provides new insights into

the mechanisms required for proper synapse function as well as molecular changes

at the synapse that likely contribute to autistic behaviors and learning

deficits in people with APC loss of function gene mutations, " said .

>

> " Our study also sheds light on a poorly-understood but essential process, the

cross-talk that occurs between presynaptic and postsynaptic neurons. When we

perturbed APC function on the postsynaptic side, we saw changes on both sides of

the synapse, indicating that APC organizes a protein complex that communicates

against the normal flow of traffic, " said first author Madelaine Rosenberg, PhD,

an affiliate of the department of neuroscience at TUSM.

>

> The research team's next step is to examine the behavioral and cognitive

changes that occur when APC is deleted in neurons of the mammalian brain. They

have developed a new mouse model that will allow them to investigate how the

loss of APC function leads to synaptic changes and impaired learning and memory.

>

> Additional authors are Fang Yang, PhD, a research associate in the department

of medicine at TUSM; Mohn, a PhD candidate in the cell, molecular, and

developmental biology program at Sackler and member of 's lab; and

Storer, a PhD candidate in the neuroscience program at Sackler and

member of 's lab.

>

> This study was funded by the National Institute of Neurological Disorders and

Stroke (NINDS), part of the National Institutes of Health, and the Tufts Center

for Neuroscience Research. The Tufts Center for Neuroscience Research, itself,

is supported by the NINDS and by Tufts University School of Medicine and Tufts

Medical Center.

>

> Rosenberg MM, Yang F, Mohn JL, Storer EK, MH. The Journal of

Neuroscience. 2010. (August 18); 30(33): 11073-11085. " The Postsynaptic

Adenomatous Polyposis Coli (APC) Multiprotein Complex Is Required for Localizing

Neuroligin and Neurexin to Neuronal Nicotinic Synapses in Vivo. " Published

online August 18, 2010, doi: 10.1523/JNEUROSCI.0983-10.2010

>

> About Tufts University School of Medicine and the Sackler School of Graduate

Biomedical Sciences

>

>

> Tufts University School of Medicine and the Sackler School of Graduate

Biomedical Sciences at Tufts University are international leaders in innovative

medical education and advanced research. The School of Medicine and the Sackler

School are renowned for excellence in education in general medicine, biomedical

sciences, special combined degree programs in business, health management,

public health, bioengineering and international relations, as well as basic and

clinical research at the cellular and molecular level. Ranked among the top in

the nation, the School of Medicine is affiliated with six major teaching

hospitals and more than 30 health care facilities. Tufts University School of

Medicine and the Sackler School undertake research that is consistently rated

among the highest in the nation for its effect on the advancement of medical

science.

>

> If you are a member of the media interested in learning more about this topic,

or speaking with a faculty member at the Tufts University School of Medicine,

the Sackler School of Graduate Biomedical Sciences, or another Tufts health

sciences researcher, please contact Siobhan Gallagher at 617-636-6586 or, for

this study, at 617-636-2789.

>

> Related posts:

>

> 1. Protein regulates enzyme linked to Alzheimer's disease

> 2. Protein linked to mental retardation controls synapse maturation,

plasticity, CSHL team finds

>

>

http://scienceblog.com/37725/researchers-connect-apc-protein-to-autism-and-menta\

l-retardation/

>

> Also read more here

http://newsfeed.time.com/2010/08/24/new-study-protein-malfunctions-linked-to-aut\

ism/

>

> Please again check http://pursuitofresearch.org/science.html going ahead as

there are a few updates that will be added to this page!

>

> =====

>

[Guest guest]

I shared the following below but feel it's worth sharing again...we need to

consume every single one of the essential amino acids every single day through

our diet:

" Essential amino acids

Humans can produce 10 of the 20 amino acids. The others must be supplied in the

food. Failure to obtain enough of even 1 of the 10 essential amino acids, those

that we cannot make, results in degradation of the body's proteins—muscle and so

forth—to obtain the one amino acid that is needed. Unlike fat and starch, the

human body does not store excess amino acids for later use—the amino acids must

be in the food every day.

The 10 amino acids that we can produce are alanine, asparagine, aspartic acid,

cysteine, glutamic acid, glutamine, glycine, proline, serine and tyrosine.

Tyrosine is produced from phenylalanine, so if the diet is deficient in

phenylalanine, tyrosine will be required as well. The essential amino acids are

arginine (required for the young, but not for adults), histidine, isoleucine,

leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

These amino acids are required in the diet. Plants, of course, must be able to

make all the amino acids. Humans, on the other hand, do not have all the the

enzymes required for the biosynthesis of all of the amino acids. "

http://www.biology.arizona.edu/biochemistry/problem_sets/aa/aa.html

And it's not just supplementation of the essential amino acid it's the body's

ability to digest and utilize what we digest. As many suspect there appears to

be issues with the metabolic systems of our children, and perhaps not just the

children. From what I read in some research they know what essential amino acid

is needed, but it's the issue with the body utilizing it. The purest most

easily digestible as well as balanced form of supplementation is from whole

food. Nutriiveda is a whole food product that contains not only contains ALL of

the essential amino acids per serving, but all the nutrients as well from whole

food sources. This page which I will add to has theories as to why NV is

working for what seems like almost all http://pursuitofresearch.org/science.html

and since funny to me it appears some of the leading research in nutrition is in

the veterinary world....just a thought on that- is that because most know the

overwhelming majority of pet owners just can't or won't be able to spend the

ridiculous amounts of money a month on medications that humans are willing to

spend...like from what I read here 5000 dollars out of pocket money on the off

label medication some are now exploring for autism which has a list of side

effects that could probably kill an elephant!

http://www.latimes.com/news/health/sns-health-autism-drug-treatment,0,2393220.st\

ory

Here is what I'm sure is a great article on the importance of whole food

nutrition from a veterinary publication.

http://www.myhealthsolution.org/pdf/benefitsvetmed.pdf

Don't have time to read it now but if someone else can jump in that would be

great. If not at some point I'll read it -and have to search under every single

one of the essential amino acids and the issues of utilizing them when used as

individual supplements. Also PS -one would believe getting all your essential

amino acids and nutrients into the body from whole food sources daily through a

glass of " chocolate milk " etc

http://pursuitofresearch.org/serving_suggestions.html would be easier than just

about anything else! And beyond easier (and cheaper) what I believe again is

most important to look at in regards to our children -what is safest and most

effective? I believe the answer is clearly going to be whole foods from pure

sources.

=====