Update on Tanner on Nutriiveda/interesting new study

[Guest guest]

Hi all!

Well I have been posting to our new BigTent group and am loving it there -but

wanted to share here as well for those of you who have not moved over yet.

First of all for those that don't know - our BigTent group which is free and

private and has way more in the arena of options to make sharing with each other

better is at https://www.bigtent.com/groups/cherab

Tanner has been on the nutriiveda since September but because it was on

backorder until mid October he really has only been on it since mid October. As

I let everyone know it wasn't only us that noticed improvements in Tanner's

speech as we got a call from his head of school who reported not only vast

improvements in speech but in focus, academics -specifically reading as he all

of a sudden was walking around reading books, alert, and not only talking better

-but much more alert and talkative throughout the day -specifically after lunch

when reportedly prior to nutriiveda after lunch he used to be " wiped out " . As

far as weight I know many of the little ones do not need to lose weight, and

this product is fine for them too, but as Tanner got older he appeared to be

putting weight on in his stomach and neck- as Dr. Agin said it looked like

something metabolic was going on (this was in spite of the fact Tanner was

tested for everything under the sun and tested negative) Tanner has always

eaten very healthy too. I just uploaded photos of Tanner to the photo section

here and of course they are on our BigTent group as well. Tanner is now at a

perfect weight for his height -we are thrilled with that but of course even more

with how well he is doing on this product. He lost 12 pounds and grew over an

inch since starting. He is now 5 foot 8 1/2 inches and 150 pounds (13 years

old)

Since Mel is not on any fish oils at all and doing so amazing I found that to be

most interesting. Tanner when I started the nutriiveda was still on his regular

4 ProEFA and 2 ProEPA and in the past if I lowered that in any way he would

regress. Sometime after Thanksgiving I lowered Tanner cold turkey to a 1/2

dosage 2 ProEFA 1 ProEPA just to see if I noticed any regression -I didn't. I

don't want to stop the fish oils as we have heart disease in our family and know

that will help my boys no matter what but do find it interesting that Tanner did

not regress from his dosage being cut in half. I strongly feel this product is

supporting his metabolic system in some way.

For those of you who are friends of mine on fb you will know that in general

Tanner's facial expressions in photo for random photos (not the ones I hand pick

out) he doesn't always have much in the way of facial expressions. What you'll

notice when you look at the photos of Tanner in the uploads is that in every

photo he now has facial expressions. Some of you may not recall but a few years

ago Dr. Jonas and I even tried attaching electrodes to his face to try to

stimulate the nerve endings in his face to try to get his to move his facial

muscles more as his oral apraxia gave him such a blank look too much of the

time. No longer -and how easy was it.

I've been getting such great feedback from parents of children with ADHD too

(mainly teens that are on meds) that we started my son Dakota on it too. If

anyone has interest in this area let me know and I can get you the phone number

of some of the other parents. I currently have an early childhood professional

that is interested in interviewing each of the families to see what she can

learn as to why this appears to be working. She is interested in starting a

blog as well; so look for it at http://www.pursuitofreserach.org under " blogs "

So why? Is it the synergistic blend of ayurveda, protein, amino acids? I don't

know if any of us will know for sure anytime soon but do know that I don't yet

know of one doctor who has not approved this for the kids. Like the fish oils

most say they don't know if it will help in any way -but " can't hurt " So why

perhaps is it working? Well I posted the other day about the amino acid/neuro

improvement link in mice. Today I want to leave everyone with this interesting

study that to me perhaps explains possible links to metabolic/diet and neuro

conditions:

Loss of epigenetic regulators causes mental retardation

Developing neurons don't just need the right genes to guide them as they grow,

they need access to the right genes at the right times. The improper functioning

of one specific protein complex that normally suppresses gene activation is

responsible for a mental retardation-like syndrome in mice, reports a team of

scientists at The Rockefeller University. New findings, published in recent

issues of Neuron and Science, indicate that malfunction of this protein complex

causes mental retardation in mice and humans and may even play a role in

promoting susceptibility to drug addiction. The research also establishes the

complex as a key regulator of neuronal transcriptional identity.

" This research is the result of a close collaboration between our group and that

of Tarakhovsky, which is focused on understanding the role of

epigenetic mechanisms in brain function, such as learning and memory, " says

senior coauthor Greengard, Astor Professor and head of the

Laboratory of Molecular and Cellular Neuroscience. Greengard won the 2000 Nobel

Prize in Physiology or Medicine for research into how neurons communicate.

" Our findings may facilitate the identification of mechanisms responsible for

long-term storage of environmental information in neurons as well as other cell

types, " says senior coauthor Tarakhovsky, professor and

head of the Laboratory of Lymphocyte Signaling. " We now have an animal system

that not only reproduces the human disease but may also enable us to understand

the underlying mechanisms. "

Although genes provide the fixed template that instructs our cells how to grow,

increasing evidence suggests that gene activity is governed by a group of

proteins known as histones. Histones are subjected to chemical modifications

that can permit or prevent genes from becoming active. These modifications are

established by specific enzymes that add well-defined chemical residues to the

amino acids localized within the tails of the histone proteins. Histone

modifications were first identified in the early 1960s by Rockefeller scientist

Allfrey and his colleagues. During the past two decades, research by

Rockefeller University's C. Allis suggested that histone modification

could generate a unique epigenetic " code " that regulates the specific

recruitment of gene expression activators and repressors to individual genes.

The research program of the Greengard and Tarakhovsky labs focuses on GLP/G9a,

an enzyme pair responsible for inducing an epigenetic mark widely known to

silence gene expression in mammals, including humans. By attaching two methyl

chemical groups to a specific amino acid on a specific histone, GLP/G9a

suppresses gene activity. Tarakhovsky and his colleagues, who study GLP/G9a and

its role in epigenetic regulation of inflammatory responses, created a strain of

mice that enables conditional removal of this complex in various cell types,

including neurons in the adult brain.

First author Anne Schaefer, a senior research associate in Greengard's lab,

subjected these mice to a battery of behavioral tests and determined that they

behave much like humans with a mental retardation syndrome called the 9q34

deletion syndrome, in which the region of chromosome 9 that codes for the GLP

genes is missing. The mice lacking GLP/G9a, unlike their normal counterparts,

were not afraid of open space, were lethargic (and as a result, obese) and had

problems learning to adapt to their environment.

The researchers compared the brains of normal mice and the conditional knockouts

and found that there were no structural differences between them. In other

words, the behavioral and learning problems associated with the conditional

knockouts were not due to any kind of damage to the brain's structure or to the

individual neurons.

" This suppressive epigenetic mark completely disappears in these mice, but the

neurons themselves do not die and appear normal, " says Schaefer. " The mice

maintain many of their basal behavioral functions, such as eating and breeding,

but they display abnormal behavior in response to various environmental

signals. "

Schaefer and her colleagues also found that loss of GLP/G9a resulted in

increased expression of genes usually found in muscles and the heart. In

addition to their analysis of genes that change in the different brain regions,

they used a cellular analysis technique developed in labs headed by Rockefeller

scientist iel Heintz and Greengard, called TRAP, which reveals

transcriptional profiles by isolating the RNA messages from structurally and

functionally defined individual cell populations.

" We found that several nonneuronal genes, normally suppressed by the epigenetic

mark, became upregulated in the GLP/G9a conditional knockouts, " says Schaefer.

According to Schaefer and her colleagues, it's also possible that genetically

predetermined or environmentally induced changes of the epigenetic regulators

controlling the methylation mark on histone H3 may be responsible for individual

differences in learning and social adaptation.

The Greengard and Tarakhovsky labs have taken these findings a step further in

collaboration with Nestler's lab at the Mount Sinai School of Medicine. In

research reported in the the January 8 issue of the journal Science, they found

that repeated cocaine administration promotes cocaine preference in mice,

revealing a key role for G9a in drug addiction.

Epigenetic regulators are considered the " last frontier " by pharmaceutical

companies, Tarakhovsky says, because of their position in the chain of events in

cell signaling. " The major excitement of these findings is that there are very

few proteins known to have such key regulatory functions and are structurally

well defined. That means it should be possible to design drugs that specifically

interfere with their activity. "

http://newswire.rockefeller.edu/?page=engine & id=1021

=====