Protandim Science Update: Nutrigenomics and DNA Explained

Protandim Science Update: Nutrigenomics and DNA Explained

Elite Academy 5, June 11, 2010

Dr. Joe McCord addressed a group of Protandim distributors to bring them up to date on the science involving Protandim.  He explained the term Nutrigenomics, the study of how dietary components — the foods we eat — interact with human DNA to regulate the 25,000 genes that make up our genome to regulate gene expression.  Our genome sequence is the blueprint that makes us uniquely who we are.  Nutrigenomics studies how what we ingest interacts with our genome.

Dr. McCord explains that describing Protandim as  antioxidant generator is no longer adequate, to explain what Protandim is.  Protandim is a Nrf2 Activator in the nutrigenomics arena.

Nrf2 is one of the key proteins in every cell of our bodies that has the function of regulating the genome.  Of the 25,000 genes that make up our genome, Nrf2 controls about 2% of those, or nearly 500 that are known as survival genes.  These are genes that help our bodies react to certain threats.  Nrf2 is referred to as the master regulator of our survival genes.  These genes are responsible for regulating or encoding antioxidant enzymes, anti-inflammatory genes and antifibrotic genes.

The latter set of genes are associated with scar tissue formation.  Scar tissue formation to heal skin cuts is a good thing, but scar tissue formation in internal organs can be fatal.  Scar tissue in the lungs, for example, leads to pulmonary fibrosis, a deadly disease.  We now understand that Protandim has an impact on the genes controlling the formation of scar tissue.

Dr. McCord’s presentation goes on to talk about 3 new topics, Protandim’s influence on addictive behavior, metabolic syndrome, and Muscular Dystrophy.

1. Can Protandim help break addictive behavior, such as smoking?

This question came about in response to widespread experience among Protandim users that they seemed better able to overcome addictive behavior, including smoking.

Dr. McCord attributed the new-found interest in the potential of Protandim to help overcome addiction because of anecdotal evidence brought to his attention by Protandim distributors.  Having studied this further, Dr. McCord discussed some of the reasons Protandim can have such an effect not only on nicotine addiction, but also addiction to cocaine. The process that causes addiction to nicotine at the cellular level is not fundamentally different than that causing addiction to cocaine, or even food addictions, for that matter.

He explained the role of the brain’s pleasure center, scientifically known as the nucleus accumbens.  Brain cells communicate with each other by releasing neurotransmitters such as glutamate.  The nucleus accumbens is an area of the brain where such activity takes place.

A gene known as the cystine-glutamate exchange transporter gene is described by Dr. McCord as a turnstile.  As it allows cystine to enter the cell, at the same time, glutamate is released.  The problem is that certain addictive substances inhibit production of glutamate by the cystine-glutamate exchange protein in cells by blocking this exchange, resulting in the body being starved of glutamate.

This causes basal glutamate levels to drop as the cells are starved of glutamate, thus creating a sense of longing for the drug of choice.  In the short term, when one takes a hit of the drug (nicotine or cocaine, etc.), there is a brief elevation of glutamate, thus satisfying the craving — but this effect last only for a matter of minutes.  This describes the mechanism of addiction.

It turns out, however, that the cystine-glutamate exchange transporter gene is among those most responsive to Protandim.  This may account for  Protandim having shown to increase the cystine-glutamate exchange by as much as 640% — thus countering the body’s craving for the Nicotine or Cocaine.  This phenomenon is further explained by a study entitled, “The Role of Cystine-Glutamate Exchange in Nicotine Dependence in Rats and Humans.”

Protandim is now also known to elevate GSH levels, and to also elevate xCT.  Elevating GSH has been shown efficacious in humans in breaking addictive behavior to both cocaine an nicotine, because GSH helps maintain basal glutamate concentration in the nucleus accumbens of the brain.

This may how Protandim can moderate the body’s drug-seeking behavior, and why it may be easier for Protandim users to quit smoking.  Dr. McCord cautions that at this point only anecdotal evidence from Protandim users suggests that Protandim may be a useful adjunct, and that clinical trials to prove the hypothesis may be appropriate in order to answer the question definitively.

2. Human Clinical Trial on Metabolic Syndrome

Dr. McCord announced a major new human clinical trial on Protandim and the Metabolic Syndrome at the University of Colorado Denver.  The principal investigator is Robert Eckel, MD, one of the foremost endocrinologists studying studying heart disease and metabolic syndrome, former President of the American Heart Association.

Metabolic syndrome is a combination of medical disorders that increase the risk of developing cardiovascular disease and diabetes.  It affects one in five people, and prevalence increases with age.  Some studies estimate the prevalence in the U.S. to be up to 25% of the population, characterized by central obesity, elevated triglycerides, low HDL levels, hypertension, and hyperglycemia.

3. New Peer-Reviewed Study on Protandim and Muscular Dystrophy

Also discussed is a new peer-reviewed study published in June of 2010, showing how the dietary supplement Protandim decreases plasma osteopontin and improves markers for oxidative stress in Muscular Dystrophy.  While done on mice, it has a close biochemical model to human Duchenne Muscular Dystrophy.  Results of the study show that Protandim decreased TBARS by 48%.  Protandim also decreased osteopontin, a profibrotic factor, by 57%.  Protandim also increased by 33% a major protective anti-atherosclerosis enzyme known as PON1 and associated with HDL, the good cholesterol.  This enzyme prevents the oxidation of LDL, the bad form of cholester0l.  This is linked to TBARS in that elevated TBARS limits paraoxonase (PON1).  It has been previously demonstrated that low serum PON1 activity can foreshadow serious coronary events.  A 2003 study concluded that, “Low serum PON1 activity toward paraoxon is an independent risk factor for coronary events in men at high risk because of preexisting disease or other CHD risk factors.”  Clinical trials for Protandim showed that Protandim contributes to elevated PON1 activity.


In a mouse model of muscular dystrophy this peer-reviewed study demonstrated the following:

  • Protandim decreased TBARS,
  • Protandim decreased OPN, a pro-fibrotic factor,
  • Protandim increased paraoxonase (PON1), a protective anti-atherosclerosis enzyme
  • Protandim decreased anomalous MRI signals in leg muscles


Playing time: 38 minutes.