Dr. Gordon’s Comments:

GMO foods are one cause of todays epidemic of poor health contributing to food sensitivities is the tip of the iceberg. Now, there is hope we can stop this monster; truth in labeling will put an end to this travesty.

“Why are there basically no genetically engineered foods or crops anywhere in Europe, while 75 percent of U.S. supermarket foods—including many so-called “natural” foods—are GE tainted?

The answer is simple. In Europe genetically modified foods and ingredients have to be labeled. In the U.S. they do not. Up until now, in North America, Monsanto and the Biotechnocrats have enjoyed free reign to secretly lace non-organic foods with gene-spliced viruses, bacteria, antibiotic-resistant marker genes, and foreign DNA—mutant “Frankenfoods” shown to severely damage the health of animals, plants, and other living organisms in numerous scientific studies.

Monsanto and their allies understand the threat that truth-in-labeling poses for GMOs”

See the attached and know that together consumers do have the power to end Monsanto control of all food.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://articles.mercola.com/sites/articles/archive/2011/10/03/cbi-taking-down-monsanto-gmo-products.aspx?e_cid=20111003_DNL_art_1

Excerpt:

By: Ronnie Cummins
Organic Consumers Association

“If you put a label on genetically engineered food you might as well put a skull and crossbones on it.” – Norman Braksick, president of Asgrow Seed Co., a subsidiary of Monsanto, quoted in the Kansas City Star, March 7, 1994

Monsanto and Food Inc.’s stranglehold over the nation’s food and farming system is about to be challenged in a food fight that will largely determine the future of American agriculture.

From: Jeffrey Smith

Celebrating the Non-GMO Revolution

Dear Garry,

On January 20th Pamm Larry had an epiphany, as she calls it. Why not have a GMO labeling law on the November 2012 ballot in California? She did her research, put a website together, and “came out” on March 20—as a single voice with a big idea. Within six months, there were about 70 state leaders – holding events, showing films, recruiting support, and creating the framework for what may become the pivotal vote to usher GMOs out of our food supply.

Dr. Gordon’s Comments:

This is a bombshell! Autism genetic causation with millions of dollars invested in this wrong direction is all but dead when the world reads the attached in-depth report.

Of course, erroneous ideas hang around in medicine for years, as there is so much money involved in sticking with out-moded concepts. This destroys the “expert” standing of so many autism so-called experts so do not expect overnight acceptance of the environment causation, which to anyone not involved in genetic research will find is clearly the logical explanation for not just autism but the fact that in USA one in four in school today are on drug therapy for some condition, diebetes, asthma, mental issues including depression adhd, obsessive compulsive and so on. 

This latest large study moves the pendulum away from genetic causation back to environment!! This study is carefully reported here in all detail so if you are involved in autism please read the attached in its entirety, as there are important details you will want to express accurately if you are advising patients or teaching.

I have always known that what Andrew Wakefield reported on, see his website and book Callous Disregard, had merit (IE MMR triggered autism in what had seemed to be normal children up until then). I have dealt with many of these families and attended numerous conferences

However, things are not always simple A + B = C and Thiomersal may not be acting alone and there are these Epigenetic issues we know are happening when substances like Bisphenol A impair methylation, as Randy Jirtle at Duke has documented in Agouti mice. Then the issue becomes one of what are the contributing environmental toxins and they may well vary from case to case. Then when you try to study which nutrient deficiencies are contributing to the autism spectrum, you have issue including D, Magnesium etc and now issues around the need for methylation support in order to better handle the load of toxins found in every child’s cord blood (see Ten Americans at www.ewg.org). 

Then the bomb shell of cerebral folate deficiency now reported in NEJM last week where we find that some antigen is blocking the folate receptors in brain and the only hint of nutrient deficiency was documented only in cerebral spinal fluid. Now we have many potential culprits for this new autoimmune disease of the folate receptor – milk protein or whatever you want to implicate to help explain why the folate receptor in brain are blocked and cannot take up folic acid unless in the form of Folinic acid or 5’MTHF and apparently needed by some in significant orthomolecular levels.

Now we have the time line of events and a turning point in the disease was 1988, which we now find is when vaccine manufacturers turned away from egg and incorporated aborted fetal tissue for vaccine production. 

WILL someone ever make sense of all this so that we can stop this epidemic? 

I vote for anyone wanting a healthy baby to start a one or two year aggressive detox program for prospective mom and dad along the lines I advocate with oral chelation including my Power Drink with ZeoGold added along with regular exercise and some sauna exposure to enhance sweating, as a minimum.

Then hopefully start a boycott of all vaccines made on aborted fetal tissue that includes 24 of them today. That would be nice but since that in some countries is met with jail terms and a gun pointed at the prospective recipient of the vaccine, maybe we have to settle for now with trying to decrease the number of adverse outcomes by at minimum using aggressive Vitamin C based oral program. That means using a minimum of one gram per 10# of weight or roughly for year of age, as one program to try to diminish the clear risk I see in associated with current vaccine use in a world population whose immune system is compromised from birth with over 220 known toxins including an average of over 1000 times more lead in tissues than was present 700 years ago (see Cal Tech, Clair Patterson). 

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://www.ageofautism.com/2011/07/new-autism-twin-study-demolishes-decades-long-belief-in-genetic-causation.html

Excerpt:

For over two decades now, so-called “autism experts” have been claiming that autism is more than 90% caused by genes. The influence of these claims on autism policy and research funding is hard to overstate. But few realize that the basis of these claims hangs on a fragile evidence base: two small twin studies–one from Great Britain, the other from Scandinavia–that reported high rates of concordance for autism among identical twins and no concordance at all among fraternal twins. Last week, the largest and most rigorous twin study ever conducted, the California Autism Twin Study (CATS) reported contradictory new evidence that struck a devastating blow to these claims. The CATS identical twins had lower and the fraternal twins higher concordance rates than past studies, a striking finding that suggests that instead of being highly heritable, the vast majority of autism cases stem from environmental causes.

Dr. Gordon’s Comments:

Maternal nutrition ties to autism?  My plan for healthy babies takes on a new sense of urgency with this latest research!! Please read if you have anyone that might go through a pregnancy this year; they need to know this.

This new study about children born less than 1 year after the last child having three times the incidence of autism suggests to me that maternal nutrition is compromised after one child. The second pregnancy following too closely does not give the needed time to
replete nutrients lost during the last pregnancy.

I point out that all planned pregnancies ideally need to be preceded by ideally a year of detoxification. But, now we can see that also we need to build expectant mothers up nutritionally with far higher levels of nutrients found in today’s totally outmoded prenatal supplement formulas.

Just more vitamin D alone would reduce this tragic incidence of autism. My preferred prenatal is Beyond Chelation Improved, as that way we also get the essential fatty acids and the total spectrum of useful minerals while gently chelating out toxins with things like garlic and dl methione and oral EDTA, which alone has 507 references about its efficacy in lowering lead levels even in occupationally exposed workers on mywww.gordonresearch.com website.

Ideally I always also recommend my “power drink” using organic greens and Beyond Fiber and Maca and BioEn’R-G’y C, one slightly heaping tsp of each in 10+ ounces of good mineralized water like Pellegrino. And, for those willing, add Quinton Marine Plasma to that program. Then you can expect to have the healthiest possible baby known as Quinton babies, as putting in ultra trace minerals found only in this sea water based nutrient mineral drink has been shown to save lives of very sick babies so let them get it from their mother while in-utero too.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link: http://online.wsj.com/article/SB10001424052748703667904576072832311108462.html?mod=djemHL_t

Excerpt:

HEALTH INDUSTRY 
•JANUARY 10, 2011, 12:02 A.M. ET 
Closely Spaced Pregnancies Linked to Autism Risk 

By JENNIFER CORBETT DOOREN 
WASHINGTON — Closely spaced pregnancies were associated with an increase in the odds of a second child being diagnosed with autism, according to a study involving California children.

The study, which the journal Pediatrics published online Monday, showed the sooner conceptions followed the prior birth of a sibling, the greater the likelihood of the second child having an autism diagnosis. 

The study looked at more than 660,000 second-born children in California between 1992 to 2002. The study measured the time the second child was conceived relative to the first child, and then looked at autism diagnosis of the second sibling. 

The study found that second children who were conceived less than 12 months after the first child’s birth were three times more likely to be diagnosed with autism than children spaced further apart. Second children conceived less than two years after the first had almost twice the odds of receiving an autism diagnosis.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Full article: http://www.fliqz.com/aspx/permalink.aspxvid=75c53ffb47df42fb85809973823b249d

Excerpt:

Nova
A Tale of Two Mice
In this audio slide show, Dr. Dana Dolinoy of Duke University explains the role that the epigenome, a sort of second genome, plays in regulating the expression of our genes. As Dolinoy notes, we can no longer say with certainty whether genetics or the environment have a greater impact on our health, because the two are inextricably linked through the epigenome.

Posted: July 1, 2008
CHAPTER 1: THE AGOUTI SISTERS

DANA DOLINOY: Hi, I’m Dr. Dana Dolinoy, a post-doctoral research fellow in the laboratory of Randy Jirtle at Duke University. In our laboratory we study epigenetic gene regulation, or how environmental exposures interact with the epigenome to affect long-term health and disease.

So today I’d like to introduce you to two Agouti mice. And as you can see, the yellow mouse is quite obese, and she is also prone to diabetes and cancer. But on the other hand, the brown mouse remains slender and lean and also has a lower risk of developing disease.
But what’s really amazing about these two mice are that they are genetically identical — they are two identical twin sisters from the same mother. So what makes them look so different?

CHAPTER 2: THE EPIGENOME

DANA DOLINOY: Well, it turns out that there’s a second genome called the epigenome. Epigenome literally means, in addition to, or above, the genome, and while the recently completed human genome project identified approximately 25,000 genes, these genes still need instructions for what to do and when to do it and where to do it, and that’s where the epigenome comes into play.

A useful analogy is to think of the epigenome as the software that directs the genomic hardware of a computer. All of our cells contain the same DNA and genes, but it is the epigenome that decides how these genes are expressed and determines how a cell becomes a heart cell, a liver cell or even a hair cell.

Epigenetics consists of molecular switches and markers, such as DNA methylation, that help control gene regulation in which a quartet of atoms called a methyl group attaches to DNA and shuts down genes. And as you can see the red balls here are attaching to the DNA and turning off the gene.

CHAPTER 3: THE ELUSIVE AGOUTI

DANA DOLINOY: So back to the Agouti sisters. In the yellow obese mouse, the Agouti gene is unmethylated and turned on all the time, while in the brown mouse, the gene is completely methylated and shut down. There are also other mice that appear mottled in which half of the cells are methylated and shut down, and the other half are unmethylated and turned on, and these mice appear to be yellow and brown. So the coat colors of these Agouti mice acts like a sensor for the amount of DNA methylation present.

We used the Agouti mice to study how maternal nutrients and environmental factors affect the epigenome. Specifically, we wanted to know whether a mom’s exposure to a contaminant found everywhere in the environment can alter the fetal epigenome, and eventually the long-term fate of her offspring.

In the study, pregnant mothers were exposed to a common chemical found in certain plastics. This chemical is called bisphenol-A, or BPA for short, and it’s present in many commonly used products, including food and beverage containers, baby bottles, dental sealants and the lining of food cans.

About four years ago, the CDC studied approximately 400 people, and in 95 percent of these 400 people, they measured detectable levels of bisphenol-A. And when we fed the pregnant mothers, the mice, BPA, we noticed that the number of offspring with the yellow obese coat color increased dramatically, and we also saw that maternal exposure to this chemical decreased DNA methylation in the offspring and turned this Agouti gene on when it is supposed to be off.

CHAPTER 4: BREEDING HEALTHY PUPS

DANA DOLINOY: So we started a second study in which pregnant mothers were exposed to BPA plus nutritional supplementation such as methyl donors like folic acid or genistein, which is a common ingredient found in soy products. The level of soy that we provided is similar to what a person who eats a high soy diet or an individual living in Asia might eat.
And once we did this, we observed that the offspring were no longer predominantly yellow and more obese, and that there were more offspring with the slender brown coat color phenotype. This indicates that maternal nutrient supplementation can counteract the negative effects of exposure to that chemical.

CHAPTER 5: CONCLUSIONS

DANA DOLINOY: The traditional thinking about human health and disease is that it is affected by genetics and the environment, and whenever identical twins have different disease status, this was often attributed to the environment or different behavioral choices such as smoking status.

But with epigenetic gene regulation, we can see that we can no longer say whether genetics or the environment have a bigger impact, because it may be not only what you were exposed to, but what your mother and potentially grandparents were exposed to as well. And maybe even your father.

These studies with the agouti mice show us that we can no longer say whether genetics or the environment have a greater impact on our health, because the two are inextricably linked through the epigenome. This work suggests in the future that we may be able to protect individuals from negative epigenetic profiles, either by modifying the diet or developing drugs that can affect epigenomic profiles, although we’re several years away from doing this.

Full article: http://journals.lww.com/co-pediatrics/Abstract/2010/04000/What_causes_autism__Exploring_the_environmental.17.aspx

Excerpt:

 Purpose of review: Autism is a biologically based disorder of brain development. Genetic factors – mutations, deletions, and copy number variants – are clearly implicated in causation of autism. However, they account for only a small fraction of cases, and do not easily explain key clinical and epidemiological features. This suggests that early environmental exposures also contribute. This review explores this hypothesis.
Recent findings: Indirect evidence for an environmental contribution to autism comes from studies demonstrating the sensitivity of the developing brain to external exposures such as lead, ethyl alcohol and methyl mercury. But the most powerful proof-of-concept evidence derives from studies specifically linking autism to exposures in early pregnancy – thalidomide, misoprostol, and valproic acid; maternal rubella infection; and the organophosphate insecticide, chlorpyrifos. There is no credible evidence that vaccines cause autism.

Dementia and Geriatric Cognitive Disorders   10/01/2009
Vol. 28, No. 3, 2009   
 
A Prospective Study on the Development of Alzheimer’s Disease with Regard to Thyroid-Stimulating Hormone and Homocysteine
Sylvia Annerboa, Miia Kivipeltoa, b, Johan Lökka

aDepartment of Neurobiology, Care Sciences and Society, and
bAging Research Center, Karolinska Institutet, Stockholm, Sweden
 Abstract

Background/Aim: The combination of elevated total homocysteine (tHcy) levels and low levels of thyroid-stimulating hormone (TSH) are linked to Alzheimer’s disease (AD) in some studies, although the evidence is mixed. Our objective was to prospectively investigate the association between tHcy and TSH and the subsequent development of AD. Methods: A subsample of 200 nondemented subjects was taken from the Kungsholmen Project, a population-based study among people 75 years. Information about tHcy and TSH levels were taken from the baseline investigation of the Kungsholmen Project study. Results: Increased tHcy levels were related to an elevated risk of AD (n = 61) after a mean follow-up time of 6.7 years. People with high tHcy (the 3rd tertile) had more than twice as high a risk of developing AD than those with low tHcy, even after adjusting for age, sex, education, ApoE status, MMSE score and laboratory parameters. tHcy was negatively correlated with TSH (p = 0.02). There was neither an influence of TSH nor an interaction between tHcy and TSH in the development of AD.

 Conclusions: These results suggest that homocysteine, but not TSH, is involved in the development of AD. The connection between elevated tHcy and low TSH levels needs to be studied further.

Copyright © 2009 S. Karger AG, Basel