A Tale of Three Metals and The Fate of Western Civilization

A Tale of Three Metals and The Fate of Western Civilization

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Biff: LET’S DIG UP TOXINS, PURIFY THEM, AND INJECT THEM INTO OURSELVES! AND BABIES! AND PREGNANT WOMEN! AND LET’S PUT THEM INTO PAINT THAT WE USE IN OUR HOMES WE LIVE IN, AND PUMP THEM INTO THE AIR WE BREATHE! AND LET’S MAKE SURE THAT THE WATER WE DRINK COMES INTO OUR HOMES IN PIPES THAT LEACH LEAD!
Buff: ARE YOU MAD?
Biff: NO, BUT WE WILL BE!

The Romans drank beverages prepared in lead vessels, and brought spring water into their homes through lead pipes. Lead poisoning undoubtedly hastened the fall of the Roman empire. So when we think about the evidence that we are harming ourselves, and our children, with lead in the water, mercury in the air, mercury in flu vaccines, and aluminum in many other vaccines, one has to wonder: what are the likely effects on society?

  1. African Americans will suffer the most. Due to Vitamin D deficiency, African Americans at northern latitudes can be expected to be most sensitive to toxins because they rely on dietary Vitamin D to drive their cellular detoxification systems. The fix? Measure blood Vitamin D levels, and absent any mutation that would preclude increased doses of Vitamin D, improve brain health via addition Vitamin D supplementation.
  2. Young adults (millenials) will have different sociality, and higher rates of early-age psychological disorders such as schizophrenia. They may also experience higher rates of early age of onset Parkison’s disease, Alzheimer’s disease, and other neurodegenerative diseases. The fix? Filter aluminum out of the water, try silica-rich mineral waters, silica drops, with a preference for sources with the more biologically available silicic acid. In short, detoxify their food, water, and everything in their environment, and more (see below).
  3. Young children with special education needs will tend to be more violent and brain studies will show increased presence of amyloid precursor protein, the kind responsible for Alzheimer’s disease.
  4. There will be a population-wide downward shift in IQ.
  5. There will be a plague of multiple chemical sensitivity.
  6. Academics will be stretched thin and the curriculum dumbed down to the point where schools will have to stop giving grades. When 20% of the class can no longer function academically to take and exam, the rest will be asked to “help” their classmates learn.
  7. Families will become increasingly stressful social units. Divorce rates will skyrocket.
  8. People will become increasingly dependent on the State (Nanny State).
  9. Those most able to withstand the toxic effects of accumulating neurotoxins will become increasingly taxed because their income and property will have to sustain an increasingly demanding medico-government empire.
  10. When they, too, begin to fall apart, the tax base will falter.
  11. Violence will become increasingly common. Those most damaged will tend to kill and injure those who are capable.
  12. America will tear itself apart from within.

This doomsday scenario is not inevitable. So what can we do to prevent this?

  1. Listen to the mothers. They have experience in what works. NIH has avoided real research on neurodevelopment disorders that address neurotoxic metal exposure since the CDC worked so hard to defraud the public on the vaccine/autism link. They gambled, lost, and we now pay the cost.
  2. These solutions must be tested in combinations in clinical studies to insure safety, and also to validate them (if they do help). They must be studied NOW, before it’s too late.

Option 1. Environmental Detoxification. Remove all neotoxins from your home. Use reverse osmosis water filters, and use filtered water for everything – even cooking – because aluminum is used to condition the water coming from the tap. Fluoride is another issue, and your filtration should also remove fluoride. Eat organic foods and nothing out of aluminum containers. Certainly never cook in aluminum pots.

Option 2. Get the Aluminum Out. Consider using high silicic acid mineral water, or adding silicic acid drops to your filtered water to bind any aluminum from food. Other possibilities include malic acid, magnesium, and acetoacetic acid:

Principles of Orthomolecularism. R.A.S. Hemat: “Aluminum can be effectively complexed and excreted with silicon, a complex of malic acid and mg, and acetoacetic acid.”

Precise combinations that work best and are safe are not yet determined. That’s why we need studies.

Doctor Toni Bark, MD informs me that ketogenic diet can also help reduce brain inflammation and reduce the effects of toxic metals from the body and the brain – including the reduction of brain amyloid. And Dr. Richard Frey’s research on intranasal insulin and intranasal deferoxamine seems very promising for the actual removal of iron and aluminum from the brain. Care should be taken to conduct any such research under the direct care of a physician.

Option 3. Up the Vitamin D3, watch the A, Avoid Folic Acid. Dr. Keith Baggerly, MD, has determined that the FDA flubbed in it recommended daily Vit D intake. As a result, most Americans are Vit D deficient. Increased Vitamin D3 can be expected to improve many aspects of health by helping our cells properly fold proteins. Vits A and D are antagonistic, and so watch all sources of Vit A and make sure you and your child are not taking in too much Vitamin A. Read The Big Vitamin D Mistake. and Grant Genereux’s resources on Vit A toxicity [1] [2].

Much of our population has MTHFR mutations that cause problems with Folic Acid. Moms taking prenatal vitamins should seek methyl folate or folinic acid instead of folic acid. Children’s vitamins with methyl folate are also available.

Option 5. Reduce Brain Inflammation. Chronic low-grade inflammation is a hallmark of autism. Powerful brain antioxidants include N-acetylcysteine and glutathione. It seems likely that everyone with a brain could benefit from less brain inflammation.

Option 6. Improve the Gut. The commensal (helpful) bacteria in the large intestine can become significantly altered after antibiotic use to treat ear infections, most likely caused by harm from to the immune system from thimerosal. Pro-biotics may help, as will eating organic.

Option 7. Keep This Handy for Bad Head Days. Brain dysfunction from metal-induce excitotoxicity involves high glutmate levels in the brain. Oxaloacetate can reduce blood glutamate levels, allowing the excess glutamate in the brain to spill into the blood. Oxaloacetate is used after stroke to reduce the exitotoxic brain injury. Research is needed to determine if it should be used after vaccination to reduce the incidence of vaccine-induced excitotoxicity. And aluminum should be removed from vaccines because the schedule results in toxic doses in infants.

Option 8. HBOT is HOT. Consider Hyperbaric Oxygen Therapy (HBOT). HBOT can increase de novo neurogenesis. If the brain has suffered a loss of neurons due to toxic exposure, increased neurogenesis – at the right time in development – could ultimately be shown to increase IQ.

Option 9. Avoid Thimerosal. If you choose to use a flu vaccination, ask the doctor for the type of flu shot that does not contain thimerosal.

Option 10. Tell Congress You Want Research Reform.

No studies of the synergistic toxicity of aluminum, lead and mercury have been conducted at doses reflecting the vaccine schedule and daily exposure due to leaching of lead from pipes into homes.

We know which homes have lead pipes. Departments of Health should consider telling parents of children in those homes to avoid exposures to mercury and to aluminum – in other words, to skip vaccines that contain these neurotoxic metals. The children will become more educated, better behaved, make better decisions, commit fewer crimes, and overall have better lives. Toxicity of lead, aluminum and mercury is synergistic.

No studies of the options and combinations of options listed above have been conducted to determine if we could improve overall brain health in children and adults. This research is badly needed. YOU can make it happen.

Make an appointment with your Congressional Representative and ask them to create the Brain Health 2030 initiative designed to reverse the ill effects of the past 30 years of industry and medicine on brains, and on our childrens’ brains. These interventions are not intrusive. Studies could be done also with the Department of Education to determine whether reports of violence decrease, grades increase, drop-out rates decrease if entire SCHOOLS – including administrators – are enrolled in Healthy Brain programs, which could incorporate aspects of mindfulness.

You can join the Neurodevelopment Research Reform group on Facebook where ideas on the Brain Health 2030 initiative are shared. And you can support our efforts to compile the most promising evidence-based approaches to improving brain health by supporting IPAK’s Neurodevelopment Research Reform Initiative.

This article is a call for research reform. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Check with your physician before changing any mode of medical treatment for your child, or yourself.

Further Reading:

Lyons-Weiler, J and R. Ricketson. 2018. Reconsideration of the Immunotherapeutic Pediatric Safe Dose Levels of Aluminum. Journal and Trace Elements in Medicine and Biology 48:67 73.

https://www.sciencedirect.com/science/article/pii/S0946672X17300950

Thanks to Tim Lundeen for the Vit A information and of course to the outstanding medical doctor, Dr. Toni Bark, MD for permission to cite her expertise.

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My Journey from Ignorance

WHILE RETURNING from the United Nations building where I heard NYU Professor Mary Holland (School of Law) nail the issues of constitutional and international law on the right to informed consent to the floor, to a standing ovation, I received an email from Mary ( To my delight). I read, in part:

“I  started reading your Ebola book last night.  Wow, you have evolved a lot in your thinking on vaccines in a VERY short period, based on your definition of ‘antivaxxers’ at bottom of 206, top of 207.  Have you written up how your views evolved so quickly?  It might be a helpful roadmap towards turning others around.  Was this all in connection with the autism book, or did your views changing precede that book?”

Looking at my book this morning, I turned to page 206, with trepidation, to find the younger, knowing me, trying to save the world by chiding and deriding people whom I have come to learn much more about in the past two years:

“Again and again with Ebola we see, from Guinea to the US, societies struggling with the ethical problem of the needs (and wants) of a few vs. the safety (and lives) on the many”.

Ok, that’s not too bad.  A bit uppity, but I cannot disagree. But it gets worse.

“With over 100 cases confirmed, the US is, at the time of this writing, at high risk of an epidemic of measles because the herd immunity is lacking due to a dogmatic antivaccination movement”.

I warned you.

Deplorably, I continue:

“The efficacy of the measles vaccine in protecting children against terrible diseases should be reason enough for parents to insist on vaccinating their children, but the so-called ‘anti-vaxxers’ (people who believe vaccines place their children at risk of developing autism) fail to consider the greater good: They put others at risk by not participating in national programs for the greater good.”

I really do not like my former self. Naturally, I continue, because I knew SO much before I actually looked into the studies and the data:

“This perspective is more than mere 20:20 hindsight; such occurrences of cultural and institutional amnesia are certain to recur as our society becomes more reliant and trusting in technology, and we forget to respect the awesome power of biology and Nature”.

I really don’t know this guy, I swear.

Mary Holland will certainly be remembered as one of the most staunch defenders of human rights, well, in the history of abuses in medicine. So back to Mary’s question:

“Have you written up how your views evolved so quickly?  It might be a helpful roadmap towards turning others around.  Was this all in connection with the autism book, or did your views changing precede that book?”

Here’s how and why my views have changed. First, I was really rather upset about the fact that CDC Director Thomas Freiden stated in his testimony to Congress that there were no mutations in the Ebolavirus that was driving the epidemic.  I was upset because I had the 396 mutations on my laptop at the very moment he testified to Congress.  I capture that moment in “Ebola“. My anger at the CDC increased when I attended a secret White House conference call, held by the Ebola Czar, in which I asked about the 396 mutations – whether they influenced the ability of tests to detect Ebola, or altered its virulence or transmissibility. In that call, the entire scientific community was lied to again by a CDC Scientist who claimed that the virus was “99.9999% identical to the strain from Zaire in 1995”, which was not true at all.  I capture both of those events in “Ebola”, as well as how the White House then asked the Associated Press to stop covering potential cases of Ebola in the US.  I even ask in that book whether that was “fascism”.

Fast forward a couple of months to where I had decided to write “Cures vs. Profits“. I felt that we had bungled our response to Ebola so badly that I wanted to cheer myself up and write a book on the successes in biomedical research.  Having participated in so many studies over the past two decades, I knew of many reasons that the public should continue to support biomedical research, and I was going to share all that I knew, and discover more. The first two chapters deal with “the bad stuff” – the doctors who cheat at medicare fraud, which robs other patients of needed funds for real medicine – and the biomedical researchers who cheat at their research studies.

I wrote my chapters out on grapefruit, on cancer vaccines, on prostate cancer robotic surgery, and then something happened: I wrote a chapter on ADHD overdiagnosis. I tell the story of the destruction of a promising career of Dr. Gretchen Watson.  Pharma sent a “Key Opinion Leader” to EVMS to debate her over her study, and the next day she was told her case load was canceled, that her colleagues were told that she no longer worked at EVMS, and that she was to expected to resign.  She refused, and won an appeal to HR.  But then someone floated a rumor that she manipulated her data in the 1996 study showing overdiagnosis.

The investigation revealed no flaw – well, a typo in an appendix – but the damage to her career was done. The good news is that Dr. Watson has decided to write of book of her own after reading my chapter on ADHD.  She now also serves on the Board at IPAK.

When I finished writing the rest of “Cures“, including chapters on the history of hormone receptor status in breast cancer, chemosensitivity assays, characteristics of good research scientists, and cancer vaccines, I found the book missing something.

So I decided to write a chapter on Vaccines.

I’ll let the chapter on vaccines speak for itself- it begins with tales of how wonderful vaccines are, how they save lives.  I went back to review the autism/vaccine link, fully expecting to review the Andrew Wakefield issue briefly, how his claims that MMR were linked to vaccines. I read the retracted study.

I found that Andrew Wakefield never claimed that the MMR might cause autism.  Instead, I found the study to suggest that it was a question worth looking into.

My digging around then led to my discovery of reports that someone at CDC had revealed that CDC had manipulated data on the studies designed to disprove Wakefield by omitting results with a positive association.

The more I dug into the issue, and then into the literature, the more I found the science of vaccines falling far short of the science needed to insure public health via any medical procedure given to millions. And this is where I leave the issue in “Cures“. I added an addendum that reviews four open controversies in vaccines that cause me to question whether vaccines can be called an unmitigated success in translational research.

In retrospect, I see that position as something of an understatement.

My understanding of vaccines was (obviously) limited, and I needed to grasp the risks involved. I needed resolution. So after I completed “Cures“, I began writing about what I had learned. I spoke with people with an open mind. I started to listen not only to what these evil, selfish “anti-vaxxers” had to say, I started to really think about the consequences of the additives. I began to question the over-arching claims of safety.

And via some new contacts, I made connection with Tony Lyons of Skyhorse Publishing. After a few chats, he, Louis Conte and I agreed that I should write a book on the Genetics of Autism. (I love Louis – and knowing what I know of him now, my bet is that he thought I was a good prospect – but somehow I can hear him telling Tony that Jack has ‘a way to go, but I think he’ll get there’. Thank you Louis for the confidence.

So in I dove, into 3,000 research articles on autism.  Not on vaccines – on autism.  I wanted to know if the basic science could in any way reasonably support a hypothesis that vaccines or their additives cause autism. The answer is a resounding “Yes, yes, and yes”. Other articles in this blog will give you an idea of some of the evidence that exists on the role of chronic microglial activation and autism, for example.

To the readers of “Ebola” who feel confused or hurt by my, and others’ ignorance, please remember that there is a Great Unknowing, even among professionals.  Think about it – all “Anti-vaxxers” with vaccine-injured children were once pro-vaccine. As I advised some 500 participants at the VIALs Health Summit in Atlanta, GA, do not argue with them – educate them. Your anger and frustration is warranted, but help them move from ignorance to awareness and understanding.

I took it upon myself to consider 3,000 articles on autism for “Causes” (available at Amazon.com and in your local Barnes and Noble or indie bookstore).  (I skimmed 3,000, read >2,000, and cite >1,000). Look at what knowledge can do to a scientist who themselves feel cheated and lied to, someone who entrusted the CDC to perform objective science (See “The Tyranny of Pseudoscience“):

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The author at a CDC Rally, April 22nd, 2016.

 

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Educating the public and calling for Congress to Subpoena Dr. William Thompson at the CDC on the true nature of so-called “Science” conducted at the CDC on the link between vaccines and autism.

To My Fellow Scientists and Medical Health Care Professionals

I wrote “Ebola” in good faith, assuming that the position of the CDC on vaccines was based on sound science. It was unfathomable to me that

-Upon finding positive associations, CDC would routinely over-analyze data from studies until they could make associations go away, and when they could not succeed in doing that, they would simply omit the results;

-CDC would suspend an employee who drew these practices to the attention of then CDC Director Dr. Julie Gerberding (who subsequently took a position in charge of vaccine development at Merck);

-After CDC published these studies they called for an end to research on vaccine safety with regard to potential links to autism;

-CDC would ignore nearly all of the basic science that shows mechanisms of how neurotoxins in vaccines (not just MMR) could reasonably be expected to cause autism in some people;

-CDC’s position is based on ecological association studies, not randomized prospective clinical studies with proper controls.

-Our knowledge of vaccine safety is based on post-market surveillance;

-CDC would ignore all of the post-market surveillance on vaccine safety, claiming that the passively collected data in VAERS did not provide causal evidence;

-CDC would lie repeatedly under oath to Congress about the State of Science on the link between vaccines and autism;

-No one has ever conducted a vaccinated vs. unvaccinated study for association with negative health outcomes, including autism.

-CDC would communicate to the public that “Vaccines Do Not Cause Autism” on their website knowing full well that 6/12 vaccines on the schedule before the age of 7 have 0 studies one way, or the other, on whether they indeed may (or may not) contribute to the risk of autism.

I, like the rest of the world, relied on the CDC to be a reliable source of information on vaccine safety.  Yes, I vaccinated my children. I will not allow them to get the HPV vaccine. Here is why.

To the Parents of Vaccine-Injured Children who Regressed Into Autism

Your observations are the basis of a new era in vaccine science.  All science begins with observations. Help and relief is on the way. And there is nothing that can stop it.

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Dr. Lyons-Weiler (right) meets Marcella Piper-Terry (left) at the 2016 CDC Rally.
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Fellow Vaccine Risk Aware Protestors Calling for Congress to Subpoena Dr. Thomspson
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Dr. Lyons-Weiler meets the future Director of the CDC.

After the Rally, we enjoyed a summit at Life University hosted by VIALS. Here was our audience:

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Here I presented the CDC Schedule as backed by “Magic”, because no science exists on any link between 6 vaccines and autism, whereas some vaccines do, in fact have some studies that support association:

no science 2no science

That was a good day in Atlanta, GA. Here are the slides to share with your pediatrician:

VIALs health summit slides James LyonsWeiler MAGIC

CDCSCHEDULE
“MAGIC!!!”

 

 

Next stop, the United Nations:

 

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Dr. Lyons-Weiler attends a UN Session on Toxins in Our Children, April 26th, where Dr. Thompson’s revelations were shared with the world.


 

Mary Holland standing up for your rights to refuse medical procedures as a basic human right. To watch the unprecedented UN Session on Toxic Contamination of Children (4/26/2016), follow this link.

Mary Holland’s question to me was an important one:like many, if not most other professionals, I had argued my position on the vaccine/autism question from a position of ignorance.  They simply have not done their homework, and many have bought the CDC’s lies hook, line and sinker. They count on CDC to be honest and forthright. This include the AAP, the AMA, and, very likely, your pediatrician.

Most of them probably have not read a single study. They likely have never read the following words that Dr. William Thompson said to Dr. Hooker:

Thompson: “They don’t really want people to know that this data exists.”

Thompson: “…among the blacks, the ones that were getting vaccinated earlier, were more likely to have autism.”

Thompson: “It appears in the final publication is that race in general is downplayed. Of course it is.”

Thompson: “I actually think the most interesting results are the isolated, ones that don’t have their co morbid conditions. The effect is where you would think it would happen.”

Thompson: “I was just looking at—I was like, oh my God, I cannot believe we did what we did. But we did.”

Thompson: “The higher ups wanted to do certain things and I went along with it. In terms of chain of command, I was number four out of five. “

Thompson: “…Literally, everyone else got rid of all their documents, and so the only documents that exist right now from that study are mine.”

Thompson: “There are things that I haven’t even shared with you because I can’t prove it, and that’s what I struggle with. I don’t want to share things with you that I can’t prove, that there aren’t hard records. I am worried that the other four people will collude and say no, that’s not true.”

Thompson: “That’s what I keep seeing again, and again, and again where these senior people just do completely unethical, vile things and no one holds them accountable. “

Thompson: “The reason you don’t see anything else circulating on the study, it was five of us behind closed doors for two years.”

Thompson: “It’s the lowest point in my career that I went along with that paper.”

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Dr. William W. Thompson

My book “Cures vs. Profits” tells more of the story of Dr. Thompson and Hooker. At this point, I am willing to go on the record and say that I have zero – ZERO confidence in any science coming out of the CDC Immunization Safety division. And no one else should trust their research, either.

In fact, nothing they publish can be trusted. Not merely because of what Thompson said.

I’ve read their studies.

They are atrociously unsafe ventures in data cooking, model overfit, sad excuses for “control variables”, use of multicollinear variables, the product of repeated data analysis to a desired result (no association). They are a mess.

The individual people in question include

RADM Anne Schuchat, Principal Deputy Director of CDC

Dr. Frank DeStefano, Director of the Immunization Safety Office

Dr. Coleen Boyle Director, National Center on Birth Defects and Developmental Disabilities (NCBDDD)

Dr. Poul Thorsen (co-author on suspect CDC studies, wanted by HHS for embezzling over $1Million in funds that were to be used for autism research, living openly in Denmark).

and others.

In my research, I strive to remain objective. However, since 2004, when the research fraud at the CDC occurred, there have been over 1,000,000 cases of autism that potentially could have been prevented simply by splitting up the MMR into three vaccines, spacing the vaccines out, giving non-adjuvanted vaccines with 1 adjuvanted, screening for safe epitopes, removal of mercury from all vaccines, giving medical exemptions to parents who already have one autistic child (to avoid the genetic x environment interaction), dropping HepB until adulthood… so many simple things that could have been done to reduce early exposures to toxins. Where is the science for biomarkers to indicate which children might be most at risk of ASD due to vaccines?  Not done.  CDC called for no more science.

We Want Evidence-Based Public Health Policies, not Policies Based on Subjective Belief (aka “Magic”)

Right now, the so-called “Anti-vaxxers” I so woefully admonished in “Ebola” are not all “Anti-Vaxxers”. They do consist partly of some people who believe no safe vaccine could ever exist. I respectfully remind them that until the science is done to show that non-adjuvanted vaccines without mercury, aluminum, formaldehyde, etc are tested, their knowledge claim is an untested generalization about all vaccines. Out of well-deserved distrust, they call for no more science on vaccine safety – because they know that some will be injured by that very research.

But the Vaccine Risk Aware movement also includes people who are 100% Pro-Vaccine Safety. They suspect that safe and effective antigen presentation systems can be designed, that use exposure at the skin (microdermal abrasion), with epitopes that do not induce autoimmunity. They believe that taking the toxins out will likely make vaccines safer. But they do not make such claims.  They call for more science, not less, but on newer options for inducing immunity.

To watch my presentation at the VIALS Health Summit State of Science on Vaccine Safety: Autism, in which I explain how the CDC’s claims that vaccines do not cause autism must be based on magic, follow these links: (Part 1, Part 2, Part 3).

Calls for Retraction of CDC “Studies”

Because CDC committed scientific fraud, the studies they performed should be retracted. IPAK has informed the journals of this, and we have sent them copies of “Vaccine Whistleblower, by Kevin Barry, Esq.

I urge all of my colleagues to view the movie #Vaxxed.  Call your local theater and ask them to screen the movie. If you consider yourself an objective scientist, read “Whistleblower“, and RFK jr.’s book, “Thimerosal: Let the Science Speak“.  Order “Master Manipulator” by James Grundvig, which tells the story of Poul Thorsen, a CDC collaborator wanted for absconding with autism research cash (given what CDC would have done with the money, Thorsen may be a hero, for all we know).  For a deeper timeline view on how long corporate corruption has eroded science in our most esteemed institutions like the CDC, read “Science for Sale” by David Lewis.

I ask my professional colleagues from all walks of science and medicine then to join us in our calls for retraction of the CDC’s false studies: DeStefano et al., Madsen et al., and Verstraeten et al.  I will not stop educating professionals about the fraud because we need evidence-based medicine, not medicine based on guesses, or hopes, or magic.  Babies are dying in the womb due to mercury in flu vaccine reserved for pregnant women; babies are born autistic due to immunoneuroexcitotoxicity; they are born with seizure disorders; toddlers regress into autism after learning language. And yes, it may be due to cumulative and interactive effects of toxic chemicals from agriculture, industry, our home, etc.  But we can reduce the toxins we expose our children to.  Right now, autism risk is 1 in 68, up from 1 in 3000 in the 1970’s.  Let’s have #theconversation.

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Acknowledgements. I have literally thousands of people to thank for helping move from ignorance to awareness.  You know who you are. Thank you.

Please support VIALs with a generous donation.  Tell them Jack sent you!
To support Dr. Lyons-Weiler and his research associates at IPAK, visit ipaknowledge.org

VIALs health summit slides James LyonsWeiler MAGIC

causes

Aluminum, Alzheimer’s and Autism

TO THE READER: IMPORTANT DETAILS HAVE EMERGED FROM STUDIES ON THE CAUSES OF BRAIN DYSFUNCTION FROM STROKE AND ALZHEIMER’S DISEASE THAT LEAD DIRECTLY TO HOPE FOR EFFECTIVE AMELIORATION OF THE BRAIN-CELL DESTROYING PROCESSES IN AUTISM. READ THE ARTICLE ALL THE WAY THROUGH TO LEARN ABOUT TWO NUTRIENTS THAT CAN HAVE BEEN FOUND TO REDUCE BRAIN GLUTAMATE LEVELS, WHICH CAUSES CHRONIC MICROGLIAL ACTIVATION (CMA). CMA IS KNOWN TO OCCUR IN THE BRAINS OF AUTISTICS FROM AGE 4-44. THE POSSIBILITIES ARE IMMENSE. MORE RESEARCH IS URGENTLY NEEDED. -JLW (April 8, 2016)

THERE ARE TWO MAIN KNOWN PROCESSES involved in the onset of autism. The first is susceptibility to environmental toxins via mitochondrial dysfunction, which can be the combined result of environmental insults and mutations in mitochondrial genes and genes that directly influence mitochondrial function.  This combination of factors exists in as many as 20% of cases of autism.

The second is chronic microglial activation (CMA). Microglia are amazing nerve cells that serve as shepherds of learning, fostering connections at the synapse during reinforcement learning. They also play the role of the white blood cells (WBCs) of the brain, becoming activated due to injury or infection. Upon dying, brain cells release chemicals calls cytokines that activate microglia from tending shepherds to armed killers. They consume bacteria, viruses, and cellular debris, clearing the brain of the dead and dying cells. The eat impaired dendrites in their activated state.

Other cells called astrocytes mop up the chemical signals that cause microglial activation via molecules called receptors. One of these signals is glutamate.  CMA occurs when something causes glutamate build-up in the brain.  CMA can occur in autism patients with or without mitochondrial dysfunction, and both processes may be at work and interrelated in any given patient with autism.

Causes of Excess Glutamate in the Brain

Many environmental factors can cause excess glutamate. Eating it (MSG) is one way to upset the balance between glutamate in the blood and the brain. The higher the concentration of glutamate in the blood, the less able the brains glutamate pumps are able to dump excesses into the blood. Mercury and aluminum, both additives found in vaccines, can cause chronic microglial activation by harming astrocytes’ ability to uptake glutamate. Chronic microglial activation is found in people with autism from age 5 to 44 (Vargas et al., 2005).

Researchers at the Johns Hopkins University in the Neuroimmunopathology lab studied autistics aged 5-44 and found that their brains had widespread microglial hyperactivation and sensitivity to astrocytes, reflecting IL-6 cytokine mediated inflammation (Vargas et al., 2005). The chronic inflammatory conditions were most pronounced in the cerebellum, anterior cingulate and the medial frontal gyrus. The fact that the hyperactivated state persisted for decades is a critical observation from this study.

Reducing Brain Glutamate and Brain Damage from Stroke

A series of important studies have shown that techniques that clear excess glutamate from the brain during stroke reduces brain damage.  Campos et al. (2011a), demonstrated the effectiveness of oxaloacetate  (a known blood glutamate scavenge) in treating rats in which a stroke was induced. The found that intravenous injection of oxaloacetate decreased both blood and brain glutamate levels. This led to an astounding  80% reduction volume of the brain infarct, dramatically reducing brain edema. The neuroprotective effects of oxaloacetate are due to the depletion of blood glutamate levels – which occurs as a consequence of the activation of a blood-resident enzyme glutamate-oxaloacetate transaminase (GOT) (Gottlieb et al, 2003). When blood glutamate levels are low, the gradient across the blood-brain barrier is in the correct ratio to allow rapid glutamate clearing. This will result in a shut-down of microglial activation.

Similar results were found in human studies by the same team. Campos et al (2011b) studied a cohort of several hundred stroke victims at two hospitals. Using the same inclusion and exclusion criteria, they found that blood glutamate levels at the time of admission to the hospitals was a good predictor of outcome from stroke. (Read more at “GOT to ride the body of excess glutamate“.

These studies confirm earlier findings that both oxaloacetate and pyruvate are effective at reducing brain glutamate levels (Boyko et al., 2012).

Read this exciting study in the abstract from Castillo et al. (2015):

“Glutamate excitotoxicity is a primary contributor of ischemic neuronal death and other cellular components of the neurovascular unit. Several strategies have been developed against glutamate excitotoxicity, however none of them have not shown positive results in the clinical practice so far. Nowadays, the concept of blood/brain glutamate grabbing or scavenging is well recognized as a novel and attractive protective strategy to reduce the excitotoxic effect of excess extracellular glutamate that accumulates in the brain following an ischemic stroke. The main advantage of this novel therapeutic strategy is that it occurs in the blood circulation and therefore does not affect the normal brain neurophysiology, as it has been described for other drug treatments used against glutamate excitotoxicity. In this work we report all experimental data from the beginning of our studies, focused on stroke pathology, and we describe new findings about the potential application of this therapy. Future clinical trials will allow to know the real efficacy of this novel therapeutic strategy in stroke patients.”

Microglia, Glutamate and Alzheimer’s Disease

One of the most vocal minds pointing to CMA as a major process involved in autism was Dr. Russell Blaylock, MD.  The abstract above  reads just like studies from autism by Blaylock and others (substitute “stroke” with “autism”). Blaylock’s various writing and videos of his presentations have awakened many to the fact that autism is a medical condition, not a neurodevelopmental disorder per se. The medical aspects of autism mean that reversing the causes of the disorder, such as shutting down chronic microglial activation, should be possible. An important part of that is diet. Some foods (such as those containing MSG) will exacerbate brain trauma caused by the excitotoxicity cycle set up by immunotoxins in vaccines (aluminum and mercury). Tylenol should be avoided as it depletes glutathione, a necessary component of microglial glutamate reduction.

It has only more recently been found that immunoneuroexcitotoxicity is at the causal center of Alzheimer’s disease.  A rich literature exists that shows that CMA is found as a causal factor in Alzheimer’s disease, with specific causal links demonstrated between excess glutamate, and microglial dysfunction.

Here is an example from Solito and Sastre (2012):

Contrary to early views, we now know that systemic inflammatory/immune responses transmit to the brain. The microglia, the resident “macrophages” of the brain’s innate immune system, are most responsive, and increasing evidence suggests that they enter a hyper-reactive state in neurodegenerative conditions and aging. As sustained over-production of microglial pro-inflammatory mediators is neurotoxic, this raises great concern that systemic inflammation (that also escalates with aging) exacerbates or possibly triggers, neurological diseases (Alzheimer’s, prion, motoneuron disease). It is known that inflammation has an essential role in the progression of Alzheimer’s disease (AD), since amyloid-β (Aβ) is able to activate microglia, initiating an inflammatory response, which could have different consequences for neuronal survival. On one hand, microglia may delay the progression of AD by contributing to the clearance of Aβ, since they phagocyte Aβ and release enzymes responsible for Aβ degradation. Microglia also secrete growth factors and anti-inflammatory cytokines, which are neuroprotective. In addition, microglia removal of damaged cells is a very important step in the restoration of the normal brain environment, as if left such cells can become potent inflammatory stimuli, resulting in yet further tissue damage. On the other hand, as we age microglia become steadily less efficient at these processes, tending to become over-activated in response to stimulation and instigating too potent a reaction, which may cause neuronal damage in its own right. Therefore, it is critical to understand the state of activation of microglia in different AD stages to be able to determine the effect of potential anti-inflammatory therapies. We discuss here recent evidence supporting both the beneficial or detrimental performance of microglia in AD, and the attempt to find molecules/biomarkers for early diagnosis or therapeutic interventions.

One of the leaders in this area is Israeli scientist Dr. Vivian Teichberg, Ph.D., who proposed that clearing glutamate from the blood might cause a release of glutamate from the brain into the blood.  In a series of clever studies, researchers at the Weizmann Institute found that transforming glutamate in the blood into another form causes glutamate in the brain to exit – providing protection against glutamate storms associated with stroke.  (Read: “Protecting the Brain from A Glutamate Storm“). More on this exciting epiphany, below.

Aluminum, Alzheimer’s, and Glutamate Uptake

Aluminum has long been suspected to be a plausible causal contributing factor to the risk of Alzheimer’s disease. Geographic correlations of aluminum levels in drinking water (Martyn, et al., 1989), and the finding of high amounts of aluminum in the brains of some patients who died from Alzheimer’s disease (just one example, see Exley and Vickers (2014)  were initial indicators. More recent studies seem to confirm the link. A metaanalysis found a 71% increase in the risk of Alzheimer’s disease in individual with chronic exposure to aluminum (Wang et al., 2016). As people age, their microglia become less efficient at clearing Aβ deposits from the brain parenchyma (Thériault et al., 2015).

Chronic Microglial Activation and Aluminum from Vaccines

Nine of 11 available studies reviewed by Flaten et al. (2001) concluded that Alzheimer’s disease incidence was increased regions with highest aluminum in residential drinking water. Measures of inflammation, particularly in the brain, were also seen to be increased when aluminum was high in drinking water (Campbell et al., 2004) – and, importantly, activated microglial cells were also increased. Aluminum in vaccines is almost certainly a causal factor in chronic microglial activation.

Aluminum is found in most vaccines, and is a serious neurotoxin, in spite of a thwarted misinformation campaign to the contrary (Read “Paging Dr. Offit! Your Aluminum Neurotoxicity Reading Assignments are Ready!“). In mice, subcutaneous aluminum injections resulted in significantly increased apoptosis of motor neurons and increases in reactive astrocytes and microglial proliferation within the spinal cord and cortex Shaw CA et al., 2013). Reduced spatial memory capacity and impairment of motor function was observed after six doses (Shaw et al., 2009). Aluminum also influences other cells than microglia; it results in altered mitochondrial metabolism, globular astrocyte shape and astrocyte dysfunction (Lemire et al., 2009).

Olmos-Alonso et al. (2016) found increased proliferation of microglial cells in human Alzheimer’s disease. Stanford University researchers have reported that a drug called EP2 can reverse microglial activation.

1

Chronic microglial activation  (CMA) leads to damage to synapses, loss of neural precursor cells, and neuronal death. The same process of CMA is seen in autism from ages 4-25 (Vargas et al.). Image modified from  Morales et al., 2014. Neuroinflammation in the pathogenesis of Alzheimer’s disease. A rational framework for the search of novel therapeutic approaches. Front Cell Neurosci. 8:112. doi: 10.3389/fncel.2014.00112. eCollection 2014.).


Now The Most Exciting Part: Oxaloacetate and Pyruvate Supplements Clear Excess Glutamate from the Brain

Oxaloacetate is found in nature – and has numerous healthy benefits. It is non-toxic (similar toxicity to vitamin C) and is found in apples, pears, bananas, and spinach. (Read NDX USA’s easy-to-digest article “Oxaloacetate“.

Pyruvate is also found in nature. Foods containing it include red apples, cheese, dark beer, and red wine.  Here is a well-informed article  by Maia Appleby at SFGate on pyruvate supplements (“What Is Pyruvic Acid?”).

Both Oxaloacetate and Pyruvate are available in capsule form, however, the doses required to replicate the effects per body weight conducted in the studies showing their effects on glutamate levels in the brain are very high.  Here are some sources:

Oxaloacetate Supplement, 250 mg, by Natural Dynamix at Amazon.com

[Oxaloacetate (Oxaloacetic Acid) Mental Health Daily Link]

Pyruvate Supplement, 1000 mg, by Piping Rock Health Products at Amazon.com

According WebMD,  our bodies produce pyruvate when it breaks down sugar (glucose), and is used for weight loss and obesity, high cholesterol, cataracts, cancer, and improving athletic performance.  [WebMD Link]

[Disclaimer: These links are provided to the reader to inform on availability, are not meant as a recommendation. No health claims are made by the author, nor any recommendations. High doses of any supplement can have side effects. Check with your doctor before adding any supplements to your diet].

Conclusion

Chronic and acute microglial activation leads to brain trauma in stroke, Alzheimer’s and autism. By reasonable inference, supplements that reduce glutamate-induce chronic microglial activation in Alzheimer’s are very likely to have the same effects on some patients with autism.  Studies are urgently needed to determine if dietary oxaloacetate and pyruvate supplementation provide neuroprotection against chronic microglial activation in persons with autism.  Studies of glutamate levels and injection of oxaloacetate during severe neurological distress following vaccination should be undertaken immediately.

Dr. Lyons-Weiler is the President and CEO of The Institute for Pure and Applied Knowledge, which conducts basic, translational and clinical research in the public interest (without profit motive), and is author of three books, “The Environmental and Genetics Causes of AutismThe Environmental and Genetics Causes of Autism“,  “Cures vs. Profits“, and “Ebola: An Evolving Story“.

References

Boyko M et al., 2012. The effect of blood glutamate scavengers oxaloacetate and pyruvate on neurological outcome in a rat model of subarachnoid hemorrhage. Neurotherapeutics. 9(3):649-57. doi: 10.1007/s13311-012-0129-6.

Campos F, Sobrino T, Ramos-Cabrer P, Argibay B, Agulla J, Pérez-Mato M, Rodríguez-González R, Brea D, Castillo J. 2011. Neuroprotection by glutamate oxaloacetate transaminase in ischemic stroke: an experimental study. J Cereb Blood Flow Metab. 2011 Jun;31(6):1378-86. doi: 10.1038/jcbfm.2011.3. Epub 2011 Jan 26.

Campbell A et al., 2004. Chronic exposure to aluminum in drinking water increases inflammatory parameters selectively in the brain. J Neurosci Res. 75(4):565-72.

Campos F, Sobrino T, Ramos-Cabrer P, Castellanos M, Blanco M, Rodríguez-Yáñez M, Serena J, Leira R, Castillo J. High blood glutamate oxaloacetate transaminase levels are associated with good functional outcome in acute ischemic stroke. J Cereb Blood Flow Metab. 2011 Jun;31(6):1387-93. doi: 10.1038/jcbfm.2011.4. Epub 2011 Jan 26.

Castillo J et al. 2015. A novel mechanism of neuroprotection: Blood glutamate grabber. J Cereb Blood Flow Metab. 2016 Feb;36(2):292-301. doi: 10.1177/0271678X15606721.

Exley C, Vickers T. 2014. Elevated brain aluminium and early onset Alzheimer’s disease in an individual occupationally exposed to aluminium: a case report. J Med Case Rep. 8:41. doi: 10.1186/1752-1947-8-41.

Flaten TP, 2001. Aluminium as a risk factor in Alzheimer’s disease, with emphasis on drinking water. Brain Res Bull. 55(2):187-96.

Gottlieb M, Wang Y, Teichberg VI. 2003. Blood-Mediated Scavenging of Cerebrospinal Fluid Glutamate. Journal of Neurochemistry  87: 119–126.

Lemire J et al., 2009. Aluminum-induced defective mitochondrial metabolism perturbs cytoskeletal dynamics in human astrocytoma cells. J Neurosci Res.;87(6):1474-83. doi: 10.1002/jnr.21965.

Olmos-Alonso A et al., 2016. Pharmacological targeting of CSF1R inhibits microglial proliferation and prevents the progression of Alzheimer’s-like pathology. Brain 139(Pt 3):891-907. doi: 10.1093/brain/awv379.

Martyn, C. 1989. Geographical relationship between Alzheimer’s disease and aluminum in drinking water. Lancet 1:59.

Shaw CA and MS Petrik. 2009. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration. J Inorg Biochem. 103(11):1555-62. doi: 10.1016/j.jinorgbio.2009.05.019.

Shaw CA et al., 2013. Administration of aluminium to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes. J Inorg Biochem. 128:237-44. doi: 10.1016/j.jinorgbio.2013.07.022.

Solito E, Sastre M. 2012. Microglia function in Alzheimer’s disease. Front Pharmacol. 3:14. doi: 10.3389/fphar.2012.00014. eCollection 2012.

Thériault, P et al. The dynamics of monocytes and microglia in Alzheimer’s disease Alzheimer’s Research & Therapy 20157:41 DOI: 10.1186/s13195-015-0125-2.

Vargas DL et al., 2005. Neuroglial activation and neuroinflammation in the brain of patients with autism. Ann Neurol. 57:67-81.

Wang Z et al., 2016.  Chronic exposure to aluminum and risk of Alzheimer’s disease: A meta-analysis. Neurosci Lett. 2016 Jan 1;610:200-6. doi: 10.1016/j.neulet.2015.11.014. Epub 2015 Nov 27.

Zlotnik A, Gurevich B, Tkachov S, et al. 2007. Brain Neuroprotection by Scavenging Blood Glutamate. Experimental Neurology 203: 213–220.

Books by Dr. Lyons-Weiler

Ebola: An Evolving Story (2015, World Scientific)

Genetic and Environmental Causes of Autism (2016, Skyhorse Publishing)

causes

Cures vs. Profits: Successes in Translational Research (2016)

Related Abstracts

Bondy SC. 2016. Low levels of aluminum can lead to behavioral and morphological changes associated with Alzheimer’s disease and age-related neurodegeneration. Neurotoxicology. 52:222-9. doi: 10.1016/j.neuro.2015.12.002. 

Abstract
Aluminum (Al) is a very common component of the earth’s mineral composition. It is not essential element for life and is a constituent of rather inert minerals. Therefore, it has often been regarded as not presenting a significant health hazard. As a result, aluminum-containing agents been used in the preparation of many foodstuffs processing steps and also in elimination of particulate organic matter from water. More recently, the reduced pH of bodies of water resulting from acid rain has led to mobilization of aluminum-containing minerals into a more soluble form, and these have thus entered residential drinking water resources. By this means, the body burden of aluminum in humans has increased. Epidemiological and experimental findings indicate that aluminum is not as harmless as was previously thought, and that aluminum may contribute to the inception and advancement of Alzheimer’s disease. Epidemiological data is reinforced by indications that aluminum exposure can result in excess inflammatory activity within the brain. Activation of the immune system not initiated by an infectious agent, typifies the aging brain and is even more augmented in several neurodegenerative diseases. The origin of most age-related neurological disorders is generally not known but as they are largely not of genetic derivation, their development is likely triggered by unknown environmental factors. There is a growing and consistent body of evidence that points to aluminum as being one such significant influence. Evidence is presented that reinforces the likelihood that aluminum is a factor speeding the rate of brain aging. Such acceleration would inevitably enlarge the incidence of age-related neurological diseases.

Fanne RA, Nassar T, Heyman SN, Hijazi N, Higazi AA.. 2011. Insulin and glucagon share the same mechanism of neuroprotection in diabetic rats: role of glutamate. Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R668-73. doi: 10.1152/ajpregu.00058.2011. 

Abstract
In patients with acute ischemic stroke, diabetes and hyperglycemia are associated with increased infarct size, more profound neurologic deficits and higher mortality. Notwithstanding extensive clinical and experimental data, treatment of stroke-associated hyperglycemia with insulin is controversial. In addition to hyperglycemia, diabetes and even early prediabetic insulin resistance are associated with increased levels of amino acids, including the neurotoxic glutamate, in the circulation. The pleiotropic metabolic effects of insulin include a reduction in the concentration of amino acids in the circulation. In this article, we show that in diabetic rats exposed to transient middle cerebral artery occlusion, a decrease of plasma glutamate by insulin or glucagon reduces CSF glutamate, improves brain histology, and preserves neurologic function. The neuroprotective effect of insulin and glucagon was similar, notwithstanding their opposite effects on blood glucose. The therapeutic window of both hormones overlapped with the short duration (~30 min) of elevated brain glutamate following brain trauma in rodents. Similar neuroprotective effects were found after administration of the glutamate scavenger oxaloacetate, which does not affect glucose metabolism. These data indicate that insulin and glucagon exert a neuroprotective effect within a very brief therapeutic window that correlates with their capacity to reduce glutamate, rather than by modifying glucose levels.

Pogue AI, Lukiw WJ. 2016. Aluminum, the genetic apparatus of the human CNS and Alzheimer’s disease (AD). Morphologie. 2016 Mar 8. pii: S1286-0115(16)00024-2. doi: 10.1016/j.morpho.2016.01.001.

Abstract
The genomes of eukaryotes orchestrate their expression to ensure an effective, homeostatic and functional gene signaling program, and this includes fundamentally altered patterns of transcription during aging, development, differentiation and disease. These actions constitute an extremely complex and intricate process as genetic operations such as transcription involve the very rapid translocation and polymerization of ribonucleotides using RNA polymerases, accessory transcription protein complexes and other interrelated chromatin proteins and genetic factors. As both free ribonucleotides and polymerized single-stranded RNA chains, ribonucleotides are highly charged with phosphate, and this genetic system is extremely vulnerable to disruption by a large number of electrostatic forces, and primarily by cationic metals such as aluminum. Aluminum has been shown by independent researchers to be particularly genotoxic to the genetic apparatus, and it has become reasonably clear that aluminum disturbs genetic signaling programs in the CNS that bear a surprising resemblance to those observed in Alzheimer’s disease (AD) brain. This paper will focus on a discussion of two molecular-genetic aspects of aluminum genotoxicity: (1) the observation that micro-RNA (miRNA)-mediated global gene expression patterns in aluminum-treated transgenic animal models of AD (Tg-AD) strongly resemble those found in AD; and (2) the concept of “human biochemical individuality” and the hypothesis that individuals with certain gene expression patterns may be especially sensitive and perhaps predisposed to aluminum genotoxicity.

Image for online ads (<20% text)

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Neuroprotection in Strokes, Alzheimer’s Disease, and Autism

TO THE READER: DETAILS HAVE EMERGED FROM STUDIES ON THE CAUSES OF BRAIN DYSFUNCTION FROM STROKE AND ALZHEIMER’S THAT LEAD DIRECTLY TO HOPE FOR EFFECTIVE AMELIORATION OF THE BRAIN-CELL DESTROYING PROCESSES IN AUTISM. READ THE ARTICLE ALL THE WAY THROUGH TO LEARN ABOUT TWO NUTRIENTS THAT CAN HAVE BEEN FOUND TO REDUCE BRAIN GLUTAMATE LEVELS, WHICH CAUSES CHRONIC MICROGLIAL ACTIVATION (CMA). CMA IS KNOWN TO OCCUR IN THE BRAINS OF AUTISTICS FROM AGE 4-25. THE POSSIBILITIES ARE IMMENSE. MORE RESEARCH IS URGENTLY NEEDED. -JLW (April 8, 2016)

THERE ARE TWO MAIN KNOWN PROCESSES involved in the onset of autism. The first is susceptibility to environmental toxins via mitochondrial dysfunction, which can be the combined result of environmental insults and mutations in mitochondrial genes and genes that directly influence mitochondrial function.  This combination of factors exists in as many as 20% of cases of autism.

The second is chronic microglial activation (CMA). Microglia are amazing nerve cells that serve as shepherds of learning, fostering connections at the synapse during reinforcement learning. They also play the role of the white blood cells (WBCs) of the brain, becoming activated due to injury or infection. Upon dying, brain cells release chemicals calls cytokines that activate microglia from tending shepherds to armed killers. They consume bacteria, viruses, and cellular debris, clearing the brain of the dead and dying cells. The eat impaired dendrites in their activated state.

Other cells called astrocytes mop up the chemical signals that cause microglial activation via molecules called receptors. One of these signals is glutamate.  CMA occurs when something causes glutamate build-up in the brain.  CMA can occur in autism patients with or without mitochondrial dysfunction, and both processes may be at work and interrelated in any given patient with autism.

Causes of Excess Glutamate in the Brain

Many environmental factors can cause excess glutamate. Eating it (MSG) is one way to upset the balance between glutamate in the blood and the brain. The higher the concentration of glutamate in the blood, the less able the brains glutamate pumps are able to dump excesses into the blood. Mercury and aluminum, both additives found in vaccines, can cause chronic microglial activation by harming astrocytes’ ability to uptake glutamate. Chronic microglial activation is found in people with autism from age 5 to 44 (Vargas et al., 2005).

Researchers at the Johns Hopkins University in the Neuroimmunopathology lab studied autistics aged 5-44 and found that their brains had widespread microglial hyperactivation and sensitivity to astrocytes, reflecting IL-6 cytokine mediated inflammation (Vargas et al., 2005). The chronic inflammatory conditions were most pronounced in the cerebellum, anterior cingulate and the medial frontal gyrus. The fact that the hyperactivated state persisted for decades is a critical observation from this study.

Reducing Brain Glutamate and Brain Damage from Stroke

A series of important studies have shown that techniques that clear excess glutamate from the brain during stroke reduces brain damage.  Campos et al. (2011a), demonstrated the effectiveness of oxaloacetate  (a known blood glutamate scavenger) in treating rats in which a stroke was induced. The found that intravenous injection of oxaloacetate decreased both blood and brain glutamate levels. This led to an astounding  80% reduction volume of the brain infarct, dramatically reducing brain edema. The neuroprotective effects of oxaloacetate are due to the depletion of blood glutamate levels – which occurs as a consequence of the activation of a blood-resident enzyme glutamate-oxaloacetate transaminase (GOT) (Gottlieb et al, 2003). When blood glutamate levels are low, the gradient across the blood-brain barrier is in the correct ratio to allow rapid glutamate clearing. This will result in a shut-down of microglial activation.

Similar results were found in human studies by the same team. Campos et al (2011b) studied a cohort of several hundred stroke victims at two hospitals. Using the same inclusion and exclusion criteria, they found that blood glutamate levels at the time of admission to the hospitals was a good predictor of outcome from stroke. (Read more at “GOT to ride the body of excess glutamate“.

These studies confirm earlier findings that both oxaloacetate and pyruvate are effective at reducing brain glutamate levels (Boyko et al., 2012).

Read this exciting study in the abstract from Castillo et al. (2015):

“Glutamate excitotoxicity is a primary contributor of ischemic neuronal death and other cellular components of the neurovascular unit. Several strategies have been developed against glutamate excitotoxicity, however none of them have not shown positive results in the clinical practice so far. Nowadays, the concept of blood/brain glutamate grabbing or scavenging is well recognized as a novel and attractive protective strategy to reduce the excitotoxic effect of excess extracellular glutamate that accumulates in the brain following an ischemic stroke. The main advantage of this novel therapeutic strategy is that it occurs in the blood circulation and therefore does not affect the normal brain neurophysiology, as it has been described for other drug treatments used against glutamate excitotoxicity. In this work we report all experimental data from the beginning of our studies, focused on stroke pathology, and we describe new findings about the potential application of this therapy. Future clinical trials will allow to know the real efficacy of this novel therapeutic strategy in stroke patients.”

Microglia, Glutamate and Alzheimer’s Disease

One of the most vocal minds pointing to CMA as a major process involved in autism was Dr. Russell Blaylock, MD.  The abstract above  reads just like studies from autism by Blaylock and others (substitute “stroke” with “autism”). Blaylock’s various writing and videos of his presentations have awakened many to the fact that autism is a medical condition, not a neurodevelopmental disorder per se. The medical aspects of autism mean that reversing the causes of the disorder, such as shutting down chronic microglial activation, should be possible. An important part of that is diet. Some foods (such as those containing MSG) will exacerbate brain trauma caused by the excitotoxicity cycle set up by immunotoxins in vaccines (aluminum and mercury). Tylenol should be avoided as it depletes glutathione, a necessary component of microglial glutamate reduction.

It has only more recently been found that immunoneuroexcitotoxicity is at the causal center of Alzheimer’s disease.  A rich literature exists that shows that CMA is found as a causal factor in Alzheimer’s disease, with specific causal links demonstrated between excess glutamate, and microglial dysfunction.

Here is an example from Solito and Sastre (2012):

Contrary to early views, we now know that systemic inflammatory/immune responses transmit to the brain. The microglia, the resident “macrophages” of the brain’s innate immune system, are most responsive, and increasing evidence suggests that they enter a hyper-reactive state in neurodegenerative conditions and aging. As sustained over-production of microglial pro-inflammatory mediators is neurotoxic, this raises great concern that systemic inflammation (that also escalates with aging) exacerbates or possibly triggers, neurological diseases (Alzheimer’s, prion, motoneuron disease). It is known that inflammation has an essential role in the progression of Alzheimer’s disease (AD), since amyloid-β (Aβ) is able to activate microglia, initiating an inflammatory response, which could have different consequences for neuronal survival. On one hand, microglia may delay the progression of AD by contributing to the clearance of Aβ, since they phagocyte Aβ and release enzymes responsible for Aβ degradation. Microglia also secrete growth factors and anti-inflammatory cytokines, which are neuroprotective. In addition, microglia removal of damaged cells is a very important step in the restoration of the normal brain environment, as if left such cells can become potent inflammatory stimuli, resulting in yet further tissue damage. On the other hand, as we age microglia become steadily less efficient at these processes, tending to become over-activated in response to stimulation and instigating too potent a reaction, which may cause neuronal damage in its own right. Therefore, it is critical to understand the state of activation of microglia in different AD stages to be able to determine the effect of potential anti-inflammatory therapies. We discuss here recent evidence supporting both the beneficial or detrimental performance of microglia in AD, and the attempt to find molecules/biomarkers for early diagnosis or therapeutic interventions.

One of the leaders in this area is Israeli scientist Dr. Vivian Teichberg, Ph.D., who proposed that clearing glutamate from the blood might cause a release of glutamate from the brain into the blood.  In a series of clever studies, researchers at the Weizmann Institute found that transforming glutamate in the blood into another form causes glutamate in the brain to exit – providing protection against glutamate storms associated with stroke.  (Read: “Protecting the Brain from A Glutamate Storm“). More on this exciting epiphany, below.

Aluminum, Alzheimer’s, and Glutamate Uptake

Aluminum has long been suspected to be a plausible causal contributing factor to the risk of Alzheimer’s disease. Geographic correlations of aluminum levels in drinking water (Martyn, et al., 1989), and the finding of high amounts of aluminum in the brains of some patients who died from Alzheimer’s disease (just one example, see Exley and Vickers (2014)  were initial indicators. More recent studies seem to confirm the link. A metaanalysis found a 71% increase in the risk of Alzheimer’s disease in individual with chronic exposure to aluminum (Wang et al., 2016). As people age, their microglia become less efficient at clearing Aβ deposits from the brain parenchyma (Thériault et al., 2015).

Chronic Microglial Activation and Aluminum from Vaccines

Nine of 11 available studies reviewed by Flaten et al. (2001) concluded that Alzheimer’s disease incidence was increased regions with highest aluminum in residential drinking water. Measures of inflammation, particularly in the brain, were also seen to be increased when aluminum was high in drinking water (Campbell et al., 2004) – and, importantly, activated microglial cells were also increased. Aluminum in vaccines is almost certainly a causal factor in chronic microglial activation.

Aluminum is found in most vaccines, and is a serious neurotoxin, in spite of a thwarted misinformation campaign to the contrary (Read “Paging Dr. Offit! Your Aluminum Neurotoxicity Reading Assignments are Ready!“). In mice, subcutaneous aluminum injections resulted in significantly increased apoptosis of motor neurons and increases in reactive astrocytes and microglial proliferation within the spinal cord and cortex Shaw CA et al., 2013). Reduced spatial memory capacity and impairment of motor function was observed after six doses (Shaw et al., 2009). Aluminum also influences other cells than microglia; it results in altered mitochondrial metabolism, globular astrocyte shape and astrocyte dysfunction (Lemire et al., 2009).

Olmos-Alonso et al. (2016) found increased proliferation of microglial cells in human Alzheimer’s disease. Stanford University researchers have reported that a drug called EP2 can reverse microglial activation.

1

Chronic microglial activation  (CMA) leads to damage to synapses, loss of neural precursor cells, and neuronal death. The same process of CMA is seen in autism from ages 4-25 (Vargas et al.). Image modified from  Morales et al., 2014. Neuroinflammation in the pathogenesis of Alzheimer’s disease. A rational framework for the search of novel therapeutic approaches. Front Cell Neurosci. 8:112. doi: 10.3389/fncel.2014.00112. eCollection 2014.).

 


 

Now The Most Exciting Part: Oxaloacetate and Pyruvate Supplements Clear Excess Glutamate from the Brain

Oxaloacetate is found in nature – and has numerous healthy benefits. It is non-toxic (similar toxicity to vitamin C) and is found in apples, pears, bananas, and spinach. (Read NDX USA’s easy-to-digest article “Oxaloacetate“.

Pyruvate is also found in nature. Foods containing it include red apples, cheese, dark beer, and red wine.  Here is a well-informed article  by Maia Appleby at SFGate on pyruvate supplements (“What Is Pyruvic Acid?”).

Both Oxaloacetate and Pyruvate are available in capsule form, however, the doses required to replicate the effects per body weight conducted in the studies showing their effects on glutamate levels in the brain are very high.  Here are some sources:

Oxaloacetate Supplement, 250 mg, by Natural Dynamix at Amazon.com

[Oxaloacetate (Oxaloacetic Acid) Mental Health Daily Link]

Pyruvate Supplement, 1000 mg, by Piping Rock Health Products at Amazon.com

According WebMD,  our bodies produce pyruvate when it breaks down sugar (glucose), and is used for weight loss and obesity, high cholesterol, cataracts, cancer, and improving athletic performance.  [WebMD Link]

[Disclaimer: These links are provided to the reader to inform on availability, are not meant as a recommendation. No health claims are made by the author, nor any recommendations. High doses of any supplement can have side effects. Check with your doctor before adding any supplements to your diet].

Conclusion

Chronic and acute microglial activation leads to brain trauma in stroke, Alzheimer’s and autism. By reasonable inference, supplements that reduce glutamate-induce chronic microglial activation in Alzheimer’s are very likely to have the same effects on some patients with autism.  Studies are urgently needed to determine if dietary oxaloacetate and pyruvate supplementation provide neuroprotection against chronic microglial activation in persons with autism.  Studies of glutamate levels and injection of oxaloacetate during severe neurological distress following vaccination should be undertaken immediately.

Dr. Lyons-Weiler is the President and CEO of The Institute for Pure and Applied Knowledge, which conducts basic, translational and clinical research in the public interest (without profit motive), and is author of three books, “The Environmental and Genetics Causes of AutismThe Environmental and Genetics Causes of Autism“,  “Cures vs. Profits“, and “Ebola: An Evolving Story“.

References

Boyko M et al., 2012. The effect of blood glutamate scavengers oxaloacetate and pyruvate on neurological outcome in a rat model of subarachnoid hemorrhage. Neurotherapeutics. 9(3):649-57. doi: 10.1007/s13311-012-0129-6.

Campos F, Sobrino T, Ramos-Cabrer P, Argibay B, Agulla J, Pérez-Mato M, Rodríguez-González R, Brea D, Castillo J. 2011. Neuroprotection by glutamate oxaloacetate transaminase in ischemic stroke: an experimental study. J Cereb Blood Flow Metab. 2011 Jun;31(6):1378-86. doi: 10.1038/jcbfm.2011.3. Epub 2011 Jan 26.

Campbell A et al., 2004. Chronic exposure to aluminum in drinking water increases inflammatory parameters selectively in the brain. J Neurosci Res. 75(4):565-72.

Campos F, Sobrino T, Ramos-Cabrer P, Castellanos M, Blanco M, Rodríguez-Yáñez M, Serena J, Leira R, Castillo J. High blood glutamate oxaloacetate transaminase levels are associated with good functional outcome in acute ischemic stroke. J Cereb Blood Flow Metab. 2011 Jun;31(6):1387-93. doi: 10.1038/jcbfm.2011.4. Epub 2011 Jan 26.

Castillo J et al. 2015. A novel mechanism of neuroprotection: Blood glutamate grabber. J Cereb Blood Flow Metab. 2016 Feb;36(2):292-301. doi: 10.1177/0271678X15606721.

Exley C, Vickers T. 2014. Elevated brain aluminium and early onset Alzheimer’s disease in an individual occupationally exposed to aluminium: a case report. J Med Case Rep. 8:41. doi: 10.1186/1752-1947-8-41.

Flaten TP, 2001. Aluminium as a risk factor in Alzheimer’s disease, with emphasis on drinking water. Brain Res Bull. 55(2):187-96.

Gottlieb M, Wang Y, Teichberg VI. 2003. Blood-Mediated Scavenging of Cerebrospinal Fluid Glutamate. Journal of Neurochemistry  87: 119–126.

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Books by Dr. Lyons-Weiler

Ebola: An Evolving Story (2015, World Scientific)

Genetic and Environmental Causes of Autism (2016, Skyhorse Publishing)

Cures vs. Profits: Successes in Translational Research (2016)

Related Abstracts

Bondy SC. 2016. Low levels of aluminum can lead to behavioral and morphological changes associated with Alzheimer’s disease and age-related neurodegeneration. Neurotoxicology. 52:222-9. doi: 10.1016/j.neuro.2015.12.002. 

Abstract
Aluminum (Al) is a very common component of the earth’s mineral composition. It is not essential element for life and is a constituent of rather inert minerals. Therefore, it has often been regarded as not presenting a significant health hazard. As a result, aluminum-containing agents been used in the preparation of many foodstuffs processing steps and also in elimination of particulate organic matter from water. More recently, the reduced pH of bodies of water resulting from acid rain has led to mobilization of aluminum-containing minerals into a more soluble form, and these have thus entered residential drinking water resources. By this means, the body burden of aluminum in humans has increased. Epidemiological and experimental findings indicate that aluminum is not as harmless as was previously thought, and that aluminum may contribute to the inception and advancement of Alzheimer’s disease. Epidemiological data is reinforced by indications that aluminum exposure can result in excess inflammatory activity within the brain. Activation of the immune system not initiated by an infectious agent, typifies the aging brain and is even more augmented in several neurodegenerative diseases. The origin of most age-related neurological disorders is generally not known but as they are largely not of genetic derivation, their development is likely triggered by unknown environmental factors. There is a growing and consistent body of evidence that points to aluminum as being one such significant influence. Evidence is presented that reinforces the likelihood that aluminum is a factor speeding the rate of brain aging. Such acceleration would inevitably enlarge the incidence of age-related neurological diseases.

Fanne RA, Nassar T, Heyman SN, Hijazi N, Higazi AA.. 2011. Insulin and glucagon share the same mechanism of neuroprotection in diabetic rats: role of glutamate. Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R668-73. doi: 10.1152/ajpregu.00058.2011. 

Abstract
In patients with acute ischemic stroke, diabetes and hyperglycemia are associated with increased infarct size, more profound neurologic deficits and higher mortality. Notwithstanding extensive clinical and experimental data, treatment of stroke-associated hyperglycemia with insulin is controversial. In addition to hyperglycemia, diabetes and even early prediabetic insulin resistance are associated with increased levels of amino acids, including the neurotoxic glutamate, in the circulation. The pleiotropic metabolic effects of insulin include a reduction in the concentration of amino acids in the circulation. In this article, we show that in diabetic rats exposed to transient middle cerebral artery occlusion, a decrease of plasma glutamate by insulin or glucagon reduces CSF glutamate, improves brain histology, and preserves neurologic function. The neuroprotective effect of insulin and glucagon was similar, notwithstanding their opposite effects on blood glucose. The therapeutic window of both hormones overlapped with the short duration (~30 min) of elevated brain glutamate following brain trauma in rodents. Similar neuroprotective effects were found after administration of the glutamate scavenger oxaloacetate, which does not affect glucose metabolism. These data indicate that insulin and glucagon exert a neuroprotective effect within a very brief therapeutic window that correlates with their capacity to reduce glutamate, rather than by modifying glucose levels.

Pogue AI, Lukiw WJ. 2016. Aluminum, the genetic apparatus of the human CNS and Alzheimer’s disease (AD). Morphologie. 2016 Mar 8. pii: S1286-0115(16)00024-2. doi: 10.1016/j.morpho.2016.01.001.

Abstract
The genomes of eukaryotes orchestrate their expression to ensure an effective, homeostatic and functional gene signaling program, and this includes fundamentally altered patterns of transcription during aging, development, differentiation and disease. These actions constitute an extremely complex and intricate process as genetic operations such as transcription involve the very rapid translocation and polymerization of ribonucleotides using RNA polymerases, accessory transcription protein complexes and other interrelated chromatin proteins and genetic factors. As both free ribonucleotides and polymerized single-stranded RNA chains, ribonucleotides are highly charged with phosphate, and this genetic system is extremely vulnerable to disruption by a large number of electrostatic forces, and primarily by cationic metals such as aluminum. Aluminum has been shown by independent researchers to be particularly genotoxic to the genetic apparatus, and it has become reasonably clear that aluminum disturbs genetic signaling programs in the CNS that bear a surprising resemblance to those observed in Alzheimer’s disease (AD) brain. This paper will focus on a discussion of two molecular-genetic aspects of aluminum genotoxicity: (1) the observation that micro-RNA (miRNA)-mediated global gene expression patterns in aluminum-treated transgenic animal models of AD (Tg-AD) strongly resemble those found in AD; and (2) the concept of “human biochemical individuality” and the hypothesis that individuals with certain gene expression patterns may be especially sensitive and perhaps predisposed to aluminum genotoxicity.

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