MAY 10 2018 – #lessonfive

Most citations used are taken from the NLM database and are in the public domain.

UNDERSTANDING EPIGENICS/NUTRIGENOMICS

Abstract

“One of the most challenging questions in neuroscience is to dissect how learning and memory, the foundational pillars of cognition, are grounded in stable, yet plastic, gene expression states. All known epigenetic mechanisms such as DNA methylation and hydroxymethylation, histone modifications, chromatin remodelling, and noncoding RNAs regulate brain gene expression, both during neurodevelopment and in the adult brain in processes related to cognition. On the other hand, alterations in the various components of the epigenetic machinery have been linked to well-known causes of intellectual disability disorders (IDDs). Two examples are Down Syndrome (DS) and Fragile X Syndrome (FXS), where global and local epigenetic alterations lead to impairments in synaptic plasticity, memory, and learning. Since epigenetic modifications are reversible, scientists believe it is theoretically possible to use epigenetic drugs as cognitive enhancers for the treatment of DS.

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Epigenetic/Nutrigenomic treatments act in a context specific manner, targeting specific regions and state specific chromatin accessibility, FACILITATING THE ESTABLISHMENT OF “LOST” BALANCE.”

The following full text article speaks mostly of drugs, however, it also discusses the ability of EGCG in DS to down regulate DYRK1a. The point is, the ability to manipulate gene over expression in DS is recognized as not just theoretical but completely possible.

Drug therapies can focus only on one gene at a time due to the restrictive nature of pharmaceuticals and dangerous interactions with each other. A single target protocol will never produce hoped for results. 

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Recently, a study on a GABA antagonist was halted for young children with Down syndrome because there were no lasting benefits shown in adults. I didn’t expect this drug to work, not because it wasn’t effective, but because so much more than simply GABA imbalance is wrong with the neuro biochemistry in the Down syndrome brain. You cannot expect a single thing to provide continuing benefits when so many other proteins are countering the hoped for results.

Here then, is the beauty of food or food extracts. Nature has designed its own pharmaceuticals to work in synergy with each other.

You cannot use just anything in nature because many natural products do the opposite to neuro biochemistry in DS than it would in a typical brain. For instance, many products on the market are known antioxidants. It’s a fact that people with DS suffer from oxidative stress. So why not just grab every single natural antioxidant and give it to them? Big mistake. In every cell there is an antioxidant triad of enzymes that function together to change hydrogen peroxide into water and oxygen for the cells usage. But, many of these products, or combination products, work by upregulating the genes in this triad. They have no true antioxidant properties of their own. In DS, the gene for one part of this enzyme triad, Superoxide Dismutase 1 (SOD1) is over expressed. The balance is so disrupted that it simply doesn’t function. Without this enzyme triad functioning your child’s cells have a very short life. This leads to cognitive decline and paves the way for Alzheimer’s disease and premature death. So you must be extremely careful what you give your child because what is beneficial for typical people can be dangerous for people with Down syndrome.

While it is not possible to down regulate SOD1 nature does provide certain foods that will not effect SOD1 but upregulate the other two triad enzymes to restore the balance of the antioxidant enzyme system. This was proven in the Miguid study on Nutrivene published in 2001. In that study, SOD1 was NOT effected by the protocol but Catalase and Glutathione Peroxidase were significantly elevated.

In this case nutrients were used to directly target Catalase and Glutathione Peroxidase to instruct the genes to create more of those enzymes. While, at the same time, avoiding anything that would effect SOD1. The  partial restoration of the antioxidant triad in DS was significant.  (See Magid Study http://trisomy21research.org/2017/09/19/the-miguid-study-on-nutrivene/).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4980517/#!po=12.1429

THE FDA PROHIBITS EVEN INDIVIDUALS FROM MAKING MEDICAL CLAIMS FOR NUTRITIONAL SUPPLEMENTS. MENTION OF NUTRIONAL SUPPLEMENTS IS PROVIDED BASED ONLY ON THE ATTACHED RESEARCH TO EXPLAIN HOW THE HUMAN GENOME RESPONDS TO FOOD SUBSTANCES AND IS NOT INTENDED AS MEDICAL OR CURATIVE ADVICE.