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What’s Going On? – The Question of Continuing High Levels of Toxic Metal Excretion

Aluminum bugs By Kent Heckenlively, Esq.

It’s been said that a parent is only as happy as their least happy child.   That saying should probably be reworked for autism parents.  We will be obsessed to the degree of impairment of our least recovered child. 

I’m fortunate that my son Ben had a complete recovery with the quick implementation of the gluten/casein free diet after his 18 month vaccination, but after seven years of bio-medical treatments my daughter Jacqueline is still severely affected with autism and seizures.  It is for her and the parents of other children like her that I write this article.

THE PROBLEM

About four years ago I started tracking my daughter’s toxic metal excretions using the Doctor’s Data lab.  The woman who answers the phone at the lab knows me as the guy who asks if the latest UTM has been completed on “my lovely daughter.”  I’ve got close to 50 of these tests on her and thanks to Jacqueline’s doctor they’ve been charted on graphs.

From the beginning aluminum showed itself to be a problem.  Her excretions have ranged from 8-13 times normal.  In August of 2006 when we were going after strep her aluminum excretion hit a high of 80 times normal.  Her aluminum excretion has ebbed and flowed since that time, but it’s still usually somewhere between 5-10 times normal.  The other metals have also ebbed and flowed, but aluminum has been the most dramatic.

WHAT THE DOCTORS SAY IS THE REASON FOR THE CONTINUED HIGH TOXIC METAL EXCRETION

When I’ve asked her various autism doctors the reason for this continued high toxic metal excretion they tell me to think of my daughter as having a vast, toxic pool inside her which needs to be drained.  Metals sequestered deep in her tissues are now able to be released.  I understand that this explanation may be exactly right.

But something about the explanation seems wrong to me.  Regardless of the amount of metals which she's retained it seems we should have gotten it out by now.  In addition, for all of the metals she’s excreted over the past years I haven’t seen a corresponding increase in cognitive function.  At the age of eleven she’s still in diapers, her speech is very apraxic, and she still has seizures. 

I understand that many DAN doctors claim it’s only when they get near the end of chelation that they see dramatic changes in the kids, but that also raises some additional questions I’ll get to later.

A POSSIBLE EXPLANATION?

I’m part of a weekly conference call on stem cells moderated by Donna Gates (“The Body Ecology Diet”).  Jacqueline went to Costa Rica in August of last year for stem cell treatments.  The treatment didn’t work for her, but I’m aware it has worked for some other children.  (In much the same way the gluten/casein free diet worked for my son, but not my daughter, I’m always interested in new treatments.)

Donna often brings interesting people onto these conference calls whom she thinks might be able to help with autism recovery.  A few months ago she brought on a man named Mark Squibb, a former engineer who now has a web-site which seeks to promote the latest products and ideas in alternative medicine.

I found Mark to be intriguing because he claimed there were some simple tests which could be performed on autistic children to determine their problems, and there were some relatively simple treatments which could help.

I was skeptical because when I’ve put my daughter through medical tests, either in the traditional medical world, or with DAN practitioners, they never find much.  There are no obvious genetic problems, she doesn’t show high in pathogens or other infections, and even the French urinary porphyrin test shows she has only mild mercury toxicity.  I'm out of luck in both worlds!

Mark’s theory was fairly easy to grasp, even if it went far beyond what’s currently accepted in scientific thinking.  It was his claim that the metals suppressed the immune system, let various pathogens use them, and then the pathogens themselves were proceeding to make their own supply of toxic metals, leading to oxygen deprivation. 

The bugs are making metals! 

That’s why kids like Jacqueline were having such long periods of chelation and little recovery.  We were taking metals out, but the bugs (viruses, bacteria, fungi, and molds) were making them faster than we were removing them!  We needed to reach a tipping point where we were getting the metals out faster than the bugs were making them.

Aside from the fact that current scientific thinking would say this was an outlandish theory, it got me thinking.  Was it any crazier than claiming that four years of chelation would still fail to remove sizable amounts of toxic metals from my daughter’s body?  And does the available evidence on my daughter suggest this theory might be right?

Mark also claimed the bugs were using the metals, specifically aluminum, to do something which was essential to their survival.  It let them hunt.  Aluminum is used in treating waste water in order to make particles clump together in a process called flocculation.  (Yes, I did ask, what the flock is that?)  By causing the particles to clump together, it’s easier for the bugs to get their food.

This “clumping” would have system-wide effects which could be measured if you knew where to look.  One of the first places to look was blood-pressure.  These kids would tend to have low blood-pressure, even though their pulse rate would be quite high.  Extremely low blood pressure would also probably result in a seizure.  As a corollary, an extremely high pulse rate could also set off a seizure. 

After one of my daughter’s seizures I took her blood pressure and it was 68/44 with a pulse of 95.  (Normal blood pressure is about 120/80 with a pulse of somewhere around 60.)  Mark said that in the kids he’s tested that very few of them start out with a blood-pressure level above 100. (I used the Omron HEM-650 Wrist Blood Pressure Monitor – About $43 on Amazon)

Another place to look for signs of this clumping would be temperature readings from various parts of the body.  Using an infrared thermometer (Exergen Temporal Scanner - $35 and can be found at Walmart or Toys R Us or on-line) I was supposed to take temperature readings at her temple, her bicep, and the tip of her middle finger.  If the blood was truly “clumpy” it would have trouble moving through the small capillaries found in many parts of the body.  When I measured myself I found my head had a toasty temperature of around 99 degrees, my bicep about 98, and my finger somewhere around 96 degrees.  It was similar for most people I tested.

By contrast, while my daughter had a similar head and bicep temperature, the tip of her finger registered around 70 degrees.  (I know, that pretty much sounds like dead!)  Perhaps that explains why she can’t hold a pencil in her fingers and for years has liked me to hold her hands and clap them together.  Any person who’s ever been freezing knows that by slapping them together you get a little blood flowing into them.

Mark went on to say that this clumping would’ve led to what’s known as “micro-strokes” in the small vessels of Jacqueline’s brain and other parts of her body, a theory pioneered by Dr. Andrew Moulden.  In preparing this article I watched Dr. Moulden’s six-hour DVD “Tolerance Lost” about the issue of micro-strokes throughout the body.  The DVD was enlightening and thought-provoking.

While Jacqueline has had many blood tests the most they’ve revealed is a slight tendency towards anemia.  Mark looked at her blood under a microscope and posted the videos on-line for me to see.  He was most interested in the condition of her red blood cells and I checked out some images of healthy red blood cells to better understand what I was looking at.  My daughter's blood looked like something out of a science fiction movie. 

The majority of her red blood cells were collapsed, meaning they were incapable of carrying oxygen (glad I hadn’t yet tried HBOT), they were clumped together, and there were particles in her blood suggesting leaky gut.  Upon closer inspection of the collapsed blood cells there was evidence of parasites and viral and bacterial infections.

In addition, the pH level between her saliva and urine was inverted, and the surface tension of her urine was lower than anything Mark had ever seen.  When he finished going over the results with me he said, “I hope you don’t mind me saying this, but you’ve got a very sick little girl.”  I replied it was better for him to tell me she was very sick, rather than having both traditional and DAN doctors tell me they couldn’t find anything wrong with her even though she was severely impaired.

Anybody is free to check out Jacqueline’s results, including the narration at www.wholehealthnetwork.com.  You can go to “Research Publications Site” and click on “Autism Cascade” and go to “Case Experiences – By Permission” and click on either “Jacqueline Care Portal” or the other child listed, “Matthew Care Portal”.

If I was to summarize Mark’s belief it’s that the vaccines and their toxic metals give a boost to the body’s bad bugs which then begin to synthesize these metals.  As a result, the blood gets “clumpy” and this presents as a significant problem in the small veins and capillaries as the white blood cells which are so much bigger than the red blood cells, begin to “roll” along the small vessels, blocking off the oxygen-carrying red blood cells, which would in turn take away toxins. 

These kids are “cold” in their extremities, and more importantly, their brains and bodies are deprived of the oxygen necessary to develop.

From my own standpoint it’s a plausible explanation for why Jacqueline’s biggest metal pulls have been when we’ve been going after bacteria, fungi, and viruses, as well as why despite getting out lots of toxic metals it still seems like there’s so much more inside her.  I swear, we’re not feeding her aluminum!

Doing these tests costs money of course, but it’s similar, if not less than what I’ve spent on numerous bio-medical tests which haven’t given me much useful information.  There are some supplements he suggested to increase blood flow, a magnetic mat, and when I went over this with Donna Gates she suggested I also use a Bio-Mat (an infra-red heating pad which costs about $500 dollars.)

The Bio-Mat has been quite interesting as Jacqueline went from being on it for a few hours, to sleeping on it through the whole night.  She loves it!  More importantly, though, when I check the temperature of her middle finger in the morning it’s a toasty 98 or 99 degrees.  I get a warm feeling just imagining all those hours of good blood flow!

Five days into Mark’s protocol I did another UTM on Jacqueline and got a huge aluminum pull (1350, reference range 60), while 4 days later after an EDTA push the aluminum excretion was 250.  The first test was a week and a half away from an EDTA push while the second was mere hours after one.  (Did I just do a big bug-kill?  Did I get to that tipping point?)  Her most recent test after an EDTA push showed aluminum finally down to a near normal level (78), an elevation of lead (3x times normal) and a surprisingly high uranium level (1.7, ref. range .2, or 8.5 times normal). 

With her high uranium levels I know some will wonder if I’m secretly hiding Saddam Hussein’s WMDs.

But in truth, this pattern of excretion is following a similar pattern after Jacqueline did a protocol designed to go after strep in the summer of 2006.  We may have been close to getting the bugs at that point, but they came back.  In that summer her aluminum peak was 4850 (ref. range 60 or 80 times normal) and her uranium was 4.2 (ref. range .2, or 21 times normal).

I’ll continue to do the EDTA and glutathione pushes and monitor.  Hopefully, this will make the chelation period much shorter.  If the next couple tests come up with low excretions I’ll be considering that Mark was right and the metal-making bugs have been defeated.  Maybe it will finally be time to consider HBOT, especially if her red blood cells show an increased ability to carry oxygen. 

If all of this falls apart for some reason, I’ll look for another protocol.

In closing I want to share something my father-in-law said about my wife and I at a recent dinner.  A few days earlier he'd been to the funeral of a Stanford professor and at the reception he got into a conversation with some retired engineering professors who were in their 80s or 90s.  They were extremely animated and lively as they told stories about building the BART train system when people said it couldn’t be done in an urban area with earthquake faults and an already developed infra-structure. 

But these engineers had done it, and the BART system wasn’t the only example of their ingenuity and determination.  They went on to describe how California engineers had built bridges others said couldn’t be built, and how so many “firsts” in engineering had been done here.  My father-in-law then likened that to how Linda and I were so open to trying new things, and then if it doesn’t work we shrug our shoulders and look for the next idea.  He thought our efforts with Jacqueline were an example of that “California spirit.”

I hope that’s how people read these articles.  I’ve written about HHV-6 viruses, high testosterone levels, stem cells, stealth viruses, and God knows what else.  But I've done so in an effort at open inquiry.  It’s never my intention to be the “last word” on a treatment.  If I’m lucky, for many people these articles might be the “first word” on something which might help their child.

Good luck in your own research.  Let me know if you find anything interesting.  I’m always ready to listen.

Kent Heckenlively is Legal Editor of Age of Autism

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I have read your article and i got to say you are an amazing parent, about the bugs, one of the easiest way is Ozone thearapy, you could do IV, or release the ozone gas that is generated from Ozone machine and Oxygen Cylander to her Ear's on both sides for 2 to 3 minutes, for your case I think iv would be a better option.

Gang:

This is a better web address for a bio-mat. https://suzanne.thebiomatcompany.us/home/

Kent.

JulieC,

Sorry for the delay in replying. The answer is not as simple as you would think. If you would like I invite you to go to my website (not finished at this time) and send me your e-mail address. I'll be happy to go into detail. It's just too long for this forum.

Valporic acid or Depokote was what Jett Travolta was on. I am so sorry to have to mention this, since there is so much worry to begin with. My son had low l-carnitine levels from the very beginning, and when they finally dignosed him with epilepsy after 12 long years of undignosed seizures-(starring spells, jerking-doctors claimed he had tourettes, and several grand-mals/with the last one breaking his nose) I shocked the neurologist by refusing his offer of Depokote. Can you imagine low L-carnitine to begin with and then taking Depokote that deleted it further. What was he thinking? We went to Dilantin instead and then seven years of nerve racking med changes; zonnagram,lamictal(great stuff-but allergic),keppra. Just saying - I am nothing- there is no Dr. or MD or RN in front of or behind my name.

I'd consider scheduling a consultation with Dr. Van Merkle sciencebasednutrition.com His work is among the most exciting I've heard in a while. He may have, at the least, some strong insight on your chelation methods. I don't mean to tell you your business - I'm impressed with the amount of effort you've obviously made. Best wishes.
Dr. B.

Dr. Stehen,

You wrote: "Second, a great source of toxic elements almost always overlooked is what a child absorbs from the mother in utero"

My son excreted a lot of aluminum, then excreted a lot of gallium. On his report it listed that one of the resources of gallium comes from agents used in chemotherapy for Hodgkins and non-Hodgkins lymphoma. I was treated for large cell lymphoma 7 years before my son was born and we chelated him when he was 8 years old.

I was so shocked when I read the report. If the toxins from my chemo was transfered to him through my placena, what else was transferred to him?

More info about Valproic Acid:

"It is a known folate antagonist" http://en.wikipedia.org/wiki/Valproic_acid
And this study found that rats who were fed aluminum plus folate had lower levels of aluminum in tissue samples than the rats who were only fed aluminum. Their conclusion was, "folate supplementation might be useful to decrease Al accumulation in its main target organs, i.e., bone, kidney, and brain." http://linkinghub.elsevier.com/retrieve/pii/S0899900704003028

Point being, could the valproic acid be depleting her folate levels thus resulting in increased accumulation of Al in her organs?


Also, I thought you'd want to be aware of these contraindications:
"...end-stage AIDS HIV infection [does this include immune deficiencies due to other causes?], ... urea cycle disorders [imbalances in urine pH can be a sign of urea cycle disorders], and coagulation hematological disorders are absolute contraindications."
http://en.wikipedia.org/wiki/Valproic_acid

And here's just a misc. point, but possibly important:
"Exposure of the human embryo to valproic acid is also associated with risk of autism, and it is possible to duplicate features characteristic of autism by exposing rat embryos to valproic acid at the time of neural tube closure."

Maria L.,

Thanks for the detailed info. Now I have too much night reading for the weekend :)

I'm very interested in this because it sounds like Kent's daughter and Tracy's son are very similar to my son.

Kent - FINALLY I have found one child that is similar to my son Ty! In online discussions with thousands for 5 plus years, noone could relate to my experiences. Jacqueline meet Ty! I also have 3 yrs of UTMs, last count I think was 74, most are graphed. Unlike your daughter, my son is a Mercury excretor (as I have often been known to joke to many DAN Drs. "I swear, I am not breaking thermometers under his bed at night!") because the ongoing dumps have lead them to believe that it must be current exposure. If it is, I can't find it... is there a "mercury bug"? Ironically, malabsorption and bacteria is the one area that we continually have issues on testing, and he is a PANDAS criteria kid through and through, so strep is always an issue. In 2006 we had two clean porphyrin results with "little to no toxicity" and yet 7 days after sending in one of those urine samples to France, we took a UTM with Mercury at a whopping 26 unprovoked! "Little to none", uh, OK??? We did 7 IV EDTA/DMPS combos last Summer and my son excreted very little. My DAN and I agreed we had made a major dent in his toxicity.. and then Fall came and Mercury went back into elevated on unprovoked samples. And while my son is no longer a big sensory kid, he has one issue that has remained throughout his autism, he freaks if you put pressure on his index fingertip, making it very difficult to hold a grip for writing! I also spent 3 hrs on the phone one Sunday with Dr Moulden. I find his theory fascinating, and was prompted to call him because he spoke of the hard knot on the child's thigh as a vaccine reaction and microvascular stroke. That was Ty's first flag that something had happened that fateful day. His shot site swelled, developed red, warm rings around it and stayed that way for a month (he also developed strep two weeks later. Prevnar was one of his vaccines that day). Dr Moulden also reviewed photos of my son before and after his vaccine reaction and noticed several characteristics indicative of microvascular strokes. Through aggressive biomed and lots of detox, we have never had a substantial cognitive gain. Ty remains non verbal and progresses incredibly slow. He is not a seizure kid, but we are awaiting Ann Connolly results now, and scheduling an extended EEG. The more I read about Landau Kleffner, it seems an avenue we should check out at this stage of the journey!
I would LOVE to know how I could test Ty's blood for "clumps" and oxygen saturation. HBOT is one intervention we haven't tried yet, for various reasons, but mainly because it is one of the more costly treatments and Ty has always been a non responder. Much thanks for any info.!
Tracy McDermott


Kent,
Sorry to be redundant, but 2 more things about the valproic acid. I said in a earlier comment that it's not recommended for patients with mitochondrial dysfunction because it depletes carnitine
And I cited a study that found that valproic acid increases oxidative stress (something children with autism already have too much of), and that giving valproic acid to people with mitochondrial disorders may cause hepatoxicity.

But I wanted to mention these points also:
Liver problems are a serious complication of a carnitine deficiency: http://en.wikipedia.org/wiki/Primary_carnitine_deficiency

and
"Carnitine deficiency may impact on energy and lipid metabolism, causing mitochondrial and immune dysfunction."
http://jcn.sagepub.com/cgi/content/abstract/10/2_suppl/2S40

I'm not a doctor, but I'm very concerned that the valproic acid may not be a good treatment for her, and I wonder if it could actually be hindering her recovery since a carnitine deficiency may cause immune dysfunction, mitochondrial dysfunction, and liver problems.
It seems to me that given her symptoms, and the published studies about valproic acid, it would be wise to have her carnitine levels checked, or at least ask her doctor about this.

The Muscular Dystrophy Association recommends carbamazepine as an alternative to valproic acid for people with mitochondrial disease.
http://www.mda.org/Publications/Quest/q65mito.html

Warning to everyone reading this comment:
I'm sure Kent already knows this, but for anyone reading this comment who doesn't already know, don't stop or switch antiepileptic drugs except under the advice of the child's doctor.

Kim:

Here's the web address to buy a bio-mat. https://www.thebiomatcompany.us/home/products/biomat.html

I got the mini-mat ($500 plus S&H), and it's perfect for the kids and a lot less expensive.

All the best,
Kent.

where did you buy a bio-mat?

This is fascinating Kent and your articles are always wonderful. Thank you for sharing your experiences.

I am also very glad that you mentioned Donna Gates, the founder of the Body Ecology diet, in your article. I think she is brilliant and the BED diet deserves more attention from ASD families that are not quite successful with GF/CF/SF diet only, like ours.

We have been doing sequential-integrative homeopathy (from Houston Homeopathic Center) for over a year with our severe ASD kid, with fair success. Then our homeopath told me that she was reviewing her records and found that the kids that have recovered under her care had two things in common, they were all doing sequential-integrative homeopathy AND the body ecology diet.

Needless to say, I jumped right in, got a Body Ecology coach and began the diet. And indeed! My son is reacting beautifully to every clearing we are doing homeopathically since then.

And for the record, every time we clear a vaccine, or we clear parasites, his metal load goes down and we get to see him doing something new that he was not able to do before.

Dr. Stephen,

When you say "Why use IV EDTA as a chelator when it is a nonspecific chelator? There are much more specific and effective methods to control Al so you can then deal with the bigger issues" Can you tell me what they are? I was considering IV-EDTA for my daughter as oral EDTA has not done much to go after the Al and I had always heard that EDTA was good for Al. Thanks

Kent,

I don’t typically respond to these articles, but after reading your story and many of the responses I felt compelled to add to the confusion, for what it’s worth.

First, microorganisms do not synthesize elements. I know it seems like the amount of metals coming out of your daughter is infinite. The truth is, though, it probably is. An analysis I read in a scientific journal many years ago considered a quantitative analysis of the amount of mercury (Hg) absorbed into the body after having amalgam fillings for a few years (didn’t state how many) and calculated every cell of the body could contain approximately 40,000,000 atoms of mercury per cell. That sounds like a fairly substantial amount to me and it correlates with what I find in my metal detoxification procedures. The stronger the therapy, the more you extract. Yes, over time the levels do decrease, but not as one would think as flushing the radiator of a car. That same principle applies to aluminum (Al) and every other element. Think of every cell as its own little universe. Remember, however, the objective is not to eliminate every atom of toxic element from the body (virtually impossible), but to improve function. That’s what it is all about.

Second, a great source of toxic elements almost always overlooked is what a child absorbs from the mother in utero. If the mother had significant exposure to Al throughout her life time then it would be dumped into the fetus to some degree. This is only one of the reasons why some children are more readily affected by vaccines than others. I’m not saying that is the only source besides vaccines, but it can be significant.

Third, Al is a little different than other metals. That’s because it’s a lighter element and thus highly reactive. Unlike heavy metals such as Hg that settle in the cells and their reaction pathways, which tend to require lighter (more reactive) specific elements and higher energy to move them, Al is ready and able to cause damage to organs, glands and systems. Al also has a positive 3 charge and can interfere with phosphorus, which has a negative 3 charge. To fully appreciate the importance of phosphorus to human functioning just pick up any biochemistry book and note its role in producing ATP and critical enzyme functions.

Fourth, you may be inadvertently focused on the lighter element (Al) because it is simply the easiest element for her body to access and eliminate to produce energy if you are not providing the correct specific support for the important pathways necessary to move her past the Al to the heavier elements, which could be the real problem. I could assume that is a possibility since you noted high levels of lead (Pb). Yes, there are the associated microorganisms that need to be addressed along the way, but until you deal with the toxic elements effectively her body will never produce an immune response to cope effectively.

Fifth, EDTA and glutathione pushes may “move” some elements out of the system but does little in the long-run to reduce significantly high levels of cellular toxic loads.

Forgive me for being so forward, but I believe the problem you are facing is you are missing the forest for the trees. Missing the big picture is skewing your details. Anyway, why use IV EDTA as a chelator when it is a nonspecific chelator? There are much more specific and effective methods to control Al so you can then deal with the bigger issues. IV EDTA is good for fast cardiovascular clearing but a very poor method for controlling and eliminating metals on a cellular level in my opinion. The fact you can’t dismiss is that if Al was actually the main issue you should be noting at least some consistent gradual improvement in her seizures with her therapy.

Greg, I hope it's not the lab, we use Doctors Data also.

Kent, HBOT can be life changing. I suggest you try it. The first week of my son on HBOT (3 days/wk) he started riding a bike. ON HIS OWN! Every day we see something new.

Good Luck and we're praying for everyone!
Kevin

Hi Kent
Related to coagulation, there are several recent manuscripts such as:
Inflamm Bowel Dis. 2009 Feb 27. [Epub ahead of print]
Inflammatory bowel disease: A paradigm for the link between coagulation and inflammation.Yoshida H, Granger DN.
Department of Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana.

Inflammatory bowel diseases (IBDs) are associated with platelet activation and an increased risk for thromboembolism. While the mechanisms that underlie the altered platelet function and hypercoagulable state in IBD remain poorly understood, emerging evidence indicates that inflammation and coagulation are interdependent processes that can initiate a vicious cycle wherein each process propagates and intensifies the other. This review addresses the mechanisms that may account for the mutual activation of coagulation and inflammation during inflammation and summarizes evidence that implicates a role for platelets and the coagulation system in the pathogenesis of human and experimental IBD. The proposed link between inflammation and coagulation raises the possibility of targeting the inflammation-coagulation interface to reduce the morbidity and mortality associated with IBD.

Am J Gastroenterol. 2007 Jan;102(1):174-86. Epub 2006 Nov 13. Links
Inflammation and coagulation in inflammatory bowel disease: The clot thickens.Danese S, Papa A, Saibeni S, Repici A, Malesci A, Vecchi M.
Division of Gastroenterology, IRCCS Istituto Clinico Humanitas, Rozzano, Milan, Italy.

Inflammation and coagulation play crucial roles in the pathogenesis of multiple chronic inflammatory disorders. Growing evidence highlights a tight mutual network in which inflammation, coagulation, and fibrinolysis play closely related roles. Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions, characterized by a hypercoagulable state and prothrombotic conditions, and accompanied by abnormalities in coagulation. From a pathophysiological point of view, cells and molecules classically implicated in the physiological process of coagulation have now been shown to behave abnormally in IBD and possibly to also play an active role in disease pathogenesis and/or disease progression. This paper reviews studies performed on the coagulation profile and risk factors for thrombosis in IBD. In particular, an overview is provided of the epidemiology, clinical features, and etiology of thromboembolic complications in IBD. Furthermore, we review hemostatic abnormalities in IBD, as well as the cell types involved in such processes. Finally, we highlight the coagulation system as a dynamic participant in the multifaceted process of chronic intestinal inflammation. Overall, an overview is provided that the coagulation system represents an important, though previously underestimated, component of IBD pathogenesis, and may be a possible target for therapeutic intervention.

Maturitas. 2008 Sep-Oct;61(1-2):122-31.

Republished from:
Maturitas. 2004 Apr 15;47(4):305-14.
Crosstalk between inflammation and thrombosis.Esmon CT.
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Department of Pathology, University of Oklahoma Health Sciences Center, Howard Hughes Medical Institute, Oklahoma City, OK 73104, USA. charles-esmon@omrf.ouhsc.edu

Inflammation shifts the hemostatic mechanisms in favor of thrombosis. Multiple mechanisms are at play including up regulation of tissue factor leading to the initiation of clotting, amplification of the clotting process by augmenting exposure of cellular coagulant phospholipids, inhibition of fibrinolysis by elevating plasminogen activator inhibitor 1 (PAI-1) and decreases in natural anticoagulant pathways, particularly targeted toward down regulation of the protein C anticoagulant pathway through multiple mechanisms. The decreased function of the natural anticoagulant pathways may be particularly problematic because these appear to play a role in dampening inflammatory responses. The protein C anticoagulant pathway provides a useful model for the impact of inflammation on coagulation. This pathway plays a major role in preventing microvascular thrombosis. The pathway is initiated when thrombin binds to thrombomodulin (TM) on the surface of the endothelium. An endothelial cell protein C receptor (EPCR) augments protein C activation by the thrombin-TM complex more than 10-fold in vivo. EPCR is shed from the endothelium by inflammatory mediators and thrombin. EPCR binds to activated neutrophils in a process that involves proteinase 3 and Mac-1 and appears to inhibit leukocyte extravisation. EPCR can undergo translocation from the plasma membrane to the nucleus where it redirects gene expression. During translocation it can carry activated protein C (APC) to the nucleus, possibly accounting for the ability of APC to modulate inflammatory mediator responses in the endothelium. TNF alpha and other inflammatory mediators can down-regulate EPCR and TM and IL-6 can depress levels of protein S in experimental animals. Inhibition of protein C pathway function increases cytokine elaboration, endothelial cell injury and leukocyte extravisation in response to endotoxin, processes that are decreased by infusion of APC. In vitro, APC inhibits TNF alpha elaboration from monocytes and to block leukocyte adhesion to selectins. Since thrombin can elicit many inflammatory responses in microvascular endothelium, loss of control of microvascular thrombin generation due to impaired protein C pathway function probably contributes to microvascular dysfunction in sepsis.

Curr Opin Anaesthesiol. 2009 Apr;22(2):150-4. Links
Link between coagulation abnormalities and microcirculatory dysfunction in critically ill patients.De Backer D, Donadello K, Favory R.
Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles, Brussels, Belgium. ddebacke@ulb.ac.be

PURPOSE OF REVIEW: The current review discusses the role of coagulation in microcirculatory abnormalities and whether anticoagulants may improve microvascular perfusion. RECENT FINDINGS: Microvascular alterations frequently occur in sepsis and ischemia-reperfusion injury. These alterations are due to endothelial dysfunction and interaction of endothelium and circulating cells. Although the activation of coagulation has been extensively shown to occur in these conditions, microthrombosis seems not to be a predominant factor. Nevertheless, the interplay between coagulation, inflammation and the endothelium seems to favor microvascular dysfunction. Several agents with anticoagulant properties, especially activated protein C and antithrombin, improve the diseased microcirculation, but these agents have pleiotropic effects, and it seems unlikely that these beneficial effects are linked to direct inhibition of coagulation. Current evidence does not support the use of pure anticoagulant agents to improve microvascular perfusion. SUMMARY: The activation of coagulation may play an indirect role in microvascular dysfunction, through interplay with endothelium and inflammation.

Curr Atheroscler Rep. 2009 May;11(3):236-42.Links
The wnt pathway: a macrophage effector molecule that triggers inflammation.Pereira CP, Bachli EB, Schoedon G.
Department of Medicine, University Hospital of Zurich, Rämistrasse 100, CH-8091 Zurich, Switzerland.

Wnt proteins are members of the highly conserved wingless family of proteins responsible for cell differentiation and development and for neoplastic and degenerative processes. Recently, Toll-like receptor-mediated Wnt signaling was found to be associated with innate immunity in Drosophila. Upregulation of Wnt5A in human macrophages upon microbial challenge indicated a similar mechanism. Toll-like receptor-mediated Wnt5A expression is a key process for sustained inflammatory macrophage activation through autocrine and paracrine signaling. Downregulation of Wnt5A expression and subsequent attenuation of inflammatory macrophage responses by activated protein C supports the link between inflammation and coagulation, another highly conserved biologic system. Direct evidence for the relevance of Wnt5A in severe systemic inflammation is provided by the finding of higher Wnt5A levels in patients with sepsis than in healthy individuals. The fact that Wnt5A signaling can be modulated by anti-inflammatory mediators makes this effector molecule an attractive target for therapeutic intervention in inflammatory diseases.

Have you considered that the tests results are misleading or the lab is unreliable? If you are still getting high metal counts even after such a long period of treatment try getting a second or third opinion. Also keep in mind that provoked urine tests, in which a chelation drug is given before the urine test and collected over a short time can produce higher than normal levels of metal concentration in the urine and can be misleading. Is your current lab using provoked testing or the normal, and more accurate, non-provoked testing?

Try sending non-provoked urine for testing to several other labs, as well as your normal one, and check the results. Do this with samples from your child and a similar aged child you know that lives nearby that is not effected by autism, sending them to the same labs, but not telling them anything other than you want metal levels checked. If your child's toxic metal levels are truly abnormal then all the labs will show higher levels for your child. If not then there is a flaw in your current lab.

I'm not saying there is a problem with your current lab, only that this would rule it out and could save your child from continuing an ineffective (or even unnecessary) treatment.

Look the fact is that you as a parent are so focused on getting your child better that you may be taken in by unscrupulous persons who prey on the love of a parent for their child. Sometimes you need to step back and just make sure your not being taken advantage of. You're probably not being conned here but wouldn't, for your child's sake, you rather be sure?

Have you looked at the work of Dr. Amy Lasko? She works with more severely affected individuals on the spectrum who do not respond to the other treatments. go to Holisticheal.com there you will find a multitude of information explaining their approach as a multifactorial disease affecting whole body systems. The cost may be a factor, but if you have the time to listen to the many CD's(also access on-line) provided of conferences explaining the microbiology/chemisty and genetic consequences--this may be a path for you to pursue. She addresses specifically the heavy metal burden/viral and bacterial loads that affect cell function(she calls them 'trojan horses') and the aluminum toxicity you are observing. Evidently she has had successes, though the process is long, the outcomes are promising. Dr. Amy also maintains a blog to communicate with you as well as other parents. The information provided is sequential in nature, so start with the recommended recordings of conferences to give you the needed background to understand biochemical pathways/supplementation/testing/analysis. It gets pretty technical...very fascinating..She is quite brilliant, and has recovered her own child, very compassionate. I hope this provides a direction for you. It is not for the faint of heart and can be a long process to restore body systems/functions("marathon and not a race")

Sorry guys, realised that the link below to CFS/infections research does not work. here it is again:
http://www.meactionuk.org.uk/AACFS_2004_Report.htm

Note the parallels btw presentations by Suhadolnik, and later by Freemont on RNase L. Work by Knox also sounds very relevant to autism.

This website here lists research into virally induced seizure disorders http://www.vasera.org/links.html

And videos of many interesting presentations can be viewed through these links: http://www.hhv-6foundation.org/index.html

Maria you said: With the increasing evidence of coinfections in many ASD subgroups (virus, bacteria and fungus) and the amount of Concomitant medical problems- immune linked many of them- more and more published in ASD, this field of research should be more carefully explored.


I've been begging that question for a quite a while, writing to several virologist lately, asking them to ‘please take up autism research’. I'm writing again to say there are funds from AS and that there are good leads to follow on. Countless case studies and a good number of animal studies. Especially the ones of herpes encephalopathies ending up autism. Why on earth is no one following up on those leads for wider autism groups http://autismcalciumchannelopathy.com/Infectious_Agents.html
Also http://autismcalciumchannelopathy.com/HIV_and_Autism.html

There are all top level virologists who have been looking into role of herpesviruses and retroviruses in chronic fatigue, fibro, MS, bipolar, schizophrenia etc.... Autism gets overlooked!! What a shame. We are so close to answers and no one wants to look.

Oh and another thing: so much of this research is also taking a simultaneous look into involvement of those same chronic infection in epilepsy/seizures – which chronic viruses cause which types of seizures, and what are genetic and other predisposing factors. (maybe if more of you guys could write to them also :)

These are the type of research studies that I’d like to see carried over to autism
http://tinyurl.com/q65cn8

Lastly there is plenty of research, mostly by Ilback et al but others also, showing manifold increases in absorption of environmental toxins in chronic infections. Kent, many of our kids are like sponges. It is not only about them not being able to excrete what is already in their systems, but they are likely to pick up much more than healthy people.

Kent, I believe the clumping is called ESR (sedimentation rate). If you do a blood test for ESR, you can get the numbers. This happens in the case of systemic inflammation or autoimmune disease. The clumping reduces the oxygen-carrying capacity of the blood cells. No oxygen = cells cannot function and brain cells cannot grow. The theory about viruses producing heavy metals is a bit far-fetched. Heavy metals are earth elements and viruses can no more produce aluminium than they can produce soil in human cells. I believe that in your daughter's case, widespread inflammation due to a viral infection (from vaccines or whatever) is what's causing the blood to clump. Because the cells cannot get enough oxygen to function, they cannot carry out their regular eliminative functions. If her ESR is high (and I'm sure it's off the charts), then treatment is by anti-virals, antioxidants and anti-inflammatories.

Hi Kent,

I just wanted to let you know that I am a Hyperbaric Technician at a Hyperbaric Oxygen Therapy Clinic in White Rock, BC Canada.

Further to your comments about HBOT - Hyperbarics somewhat disassociates the connection between oxygen delivery and red blood cells. With the increased purity of the oxygen and the most important part, the increased atmospheric pressure we are able to dissolve oxygen into all fluids within the body such as cerebral spinal fluid, lymphatic fluid, as well as blood plasma which makes up 55% of your blood volume and lastly intracellular fluid.

Therfore if the ability of the red blood cells to carry oxygen is impaired or if circulation is impeded we are still able to get vast amounts of oxygen to the hypoxic tissue and therefore encourage the healing process.

I would be happy to discuss hyperbarics with you at your convenience if you require more information. We have treated many children living with Autism with hyperbaric oxygen therapy with great success.

Keep up the great work that you are doing.

Sincerely,
Tracey
o2plus hyperbaric oxygen therapy clinic
Ph: 604-538-2509

Someone told me (wish I could remember who) that a DAN doctor told them (I wish I remembered which one) that EDTA contains aluminum. I have not had the time to confirm this information, but would really like too. If anyone has the time (ha, ha - who am I kidding??) to look into it, I think it would be important info.

"Aside from the fact that current scientific thinking would say this was an outlandish theory..."

You're not alone:
http://www.life-enthusiast.net/ormus/orm_bio_transmut.htm

Actually Kent what is "outlandish" is to think that we what we think we know about physics and chemistry is 100% accurate.

After reading Eric's comment, I must say I agree with the statements that the metals are probably coming from the environment.

Aluminum is one of the most abundant elements in the Earth's crust. Also, aluminum sulfate is used in water purification. To make matters even worse, I've also read that fluoride increases the amount of ingested aluminum that is absorbed by the gut. So you might want to check your water supply, but even if the levels aren't that high, I wonder if 'leaky gut' would be a risk factor for aluminum toxicity? Since usually the majority of ingested aluminum just passes through the gut, would leaky gut syndrome allow large quantities of ingested aluminum to enter the blood stream?

In addition to water, aluminum is in baking powder, and in some foods. The book, Aluminum and Health by Hillel J. Gitelman says "Unintentional aluminum-containing aditives (e.g., aluminum hydroxide, aluminum oleate, etc.) may migrate from paper or paperboard food containers, animal glue and adhesives, cellophane, rubber, or resinous and polymeric coating"
And it's even in cheese, the same book also says, "The basic form of sodium aluminum phosphate is used in processed cheeses and cheese foods as an emulsifying agent to give cheese products a soft texture and to allow easy melting."
And starting on page 74 there is a table that shows how much aluminum is in various foods including fruits, vegetables and nuts.
Some processed foods are prepared on aluminum equipment which contaminates the food.

So long story short, it's everywhere. So I guess the problem and the question is, why is her body storing such high amounts of it.

1. The leaky gut issue is one theory.

2. This study found that citrate increases aluminum and lead absorption:
"Animal models suggest that citrate-containing compounds augment absorption of aluminum from food and tap water, causing aluminum accumulation in bone and brain despite normal renal function. Citrate also enhances lead absorption in animals. "
http://www.ncbi.nlm.nih.gov/pubmed/8091252

3. And back to the link to viruses, remember that study Natasha submitted a while back? I can't remember the specific details, but basically a person who was ill with a virus absorbed more mercury and a higher percentage of mercury was accumulated in the brain. And vice versa. The viruses had a longer lasting and more dangerous effect when higher levels of mercury were present. Since toxins and viruses are always present in the environment, it seems feasible that this connection could create a self perpetuating cycle.

Could it be that in the presence of viruses, the body is less equiped to remove the aluminum, and other metals from the environment, so these metals accumulate in large quantities? That could also explain why the greatest pulls ocurred after going after viruses? (Kind of like what Lisa said about fixing the immune system so it can remove the metals. If the immune system is fatigued from fighting viruses, is it unable to remove both the stored metals and the metals we're exposed to every day?)

4. And another possibility I'm concerned about is the valproic acid. Aluminum causes mitochondrial dysfunction, and valproic acid is contraindicated in people with mitochondrial disorders because it depletes carnitine (a substance required by the body for detoxification.) I realize you have to be very careful when changing anti-epileptic therapy so I wonder if in the meantime, if the new doctor would recommend carnitine supplements? I hope he will be able to switch her to another therapy soon because:

Remember how he said her liver seems stressed. "Oxidative stress has been associated with valproic acid (VPA) treatment, and mitochondrial dysfunction has been implicated in the pathogenesis of VPA-idiosyncratic hepatotoxicity." http://toxsci.oxfordjournals.org/cgi/content/abstract/86/2/436

And
"Fortunately, good treatments do exist for many of the associated complications of mitochondrial disease. For instance, seizures can be managed with antiepileptic medications such as carbamazepine. However, the common antiepileptic valproic acid should be avoided because it depletes the body of carnitine." http://www.mda.org/Publications/Quest/q65mito.html

And
"Valproic Acid Aggravates Epilepsy due to MELAS...Epilepsy is one of the most common presentations of patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). ...Manifestation of epilepsia partialis continua was aggravated by use of valproic acid. Convulsions abated after discontinuation of valproic acid. Our experience suggests that valproic acid should be avoided for the treatment of epilepsy in individuals with mitochondrial disease."
http://www.springerlink.com/content/376k1178p6512738/

Kent,

Another possibility is that one or more of the many supplements or treatments we place our kids on have bad stuff in them.

How can we validate that the long list of stuff on our protocols is all 100% free of the bad stuff? How about the encapsulation, how about the container??

At some level we are trusting allot to those who make, sell, distribute and advocate the use of all these substances. It is an unlikely premise that out air, food, water, carper, furniture, clothing is toxic yet our $30 bottle of super minerals is 100% clean.

My wonderful not high-functioning son is on the protocol, and I start at those bottles of stuff and wonder.

Sincerely
Mike

There are several reports of coinfections in ASD
J Neurosci Res. 2007 Apr;85(5):1143-8.
Evidence for Mycoplasma ssp., Chlamydia pneunomiae, and human herpes virus-6 coinfections in the blood of patients with autistic spectrum disorders.Nicolson GL, Gan R, Nicolson NL, Haier J.
The Institute for Molecular Medicine, Huntington Beach, California 92647, USA. gnicolson@immed.org

We examined the blood of 48 patients from central and southern California diagnosed with autistic spectrum disorders (ASD) by using forensic polymerase chain reaction and found that a large subset (28/48 or 58.3%) of patients showed evidence of Mycoplasma spp. infections compared with two of 45 (4.7%) age-matched control subjects (odds ratio = 13.8, P < 0.001). Because ASD patients have a high prevalence of one or more Mycoplasma spp. and sometimes show evidence of infections with Chlamydia pneumoniae, we examined ASD patients for other infections. Also, the presence of one or more systemic infections may predispose ASD patients to other infections, so we examined the prevalence of C. pneumoniae (4/48 or 8.3% positive, odds ratio = 5.6, P < 0.01) and human herpes virus-6 (HHV-6, 14/48 or 29.2%, odds ratio = 4.5, P < 0.01) coinfections in ASD patients. We found that Mycoplasma-positive and -negative ASD patients had similar percentages of C. pneumoniae and HHV-6 infections, suggesting that such infections occur independently in ASD patients. Control subjects also had low rates of C. pneumoniae (1/48 or 2.1%) and HHV-6 (4/48 or 8.3%) infections, and there were no coinfections in control subjects. The results indicate that a large subset of ASD patients shows evidence of bacterial and/or viral infections (odds ratio = 16.5, P < 0.001). The significance of these infections in ASD is discussed in terms of appropriate treatment.
J Periodontol. 1999 May;70(5):478-84. Links
Relationship between herpesviruses and adult periodontitis and periodontopathic bacteria.Contreras A, Umeda M, Chen C, Bakker I, Morrison JL, Slots J.
Department of Periodontology, School of Dentistry, University of Southern California, Los Angeles 90089-0641, USA.

BACKGROUND: Various mammalian viruses and specific bacteria seem to play important roles in the pathogenesis of human periodontitis. This study examined the relationship between subgingival herpesviruses and periodontal disease and potential periodontopathic bacteria in 140 adults exhibiting either periodontitis or gingivitis. METHODS: A nested-polymerase chain reaction (PCR) method determined the presence of Epstein-Barr virus type 1 and type 2 (EBV-1, EBV-2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) and a 16S rRNA PCR detection method identified Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Bacteroides forsythus, Prevotella intermedia, Prevotella nigrescens, and Treponema denticola. RESULTS: Using a logistic analysis, EBV-1 showed significant positive association with P. gingivalis (odds ratio [OR] 3.37), and with coinfections of P. gingivalis and P. intermedia (OR 4.03); P. gingivalis and B. forsythus (OR 3.84); P. gingivalis and T. denticola (OR 4.17); P. gingivalis, B. forsythus, and T. denticola (OR 4.06); and P. gingivalis, P. nigrescens, and T. denticola (OR 3.29). EBV-1 also showed positive association with severe periodontitis (OR 5.09), with increasing age (OR 1.03), and with periodontal probing depth at the sample sites (OR 1.77). HCMV was positively associated with coinfections of P. gingivalis and P. nigrescens (OR 3.23); P. gingivalis, B. forsythus, and P. nigrescens (OR 3.23); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.59); with severe periodontitis (OR 4.65); and with age (OR 1.03). Patients with mixed viral infections revealed significant associations with P. gingivalis (OR 2.27), and with coinfections of P. gingivalis and B. forsythus (OR 2.06); P. gingivalis and P. nigrescens (OR 2.91); P. gingivalis, B. forsythus, and P. nigrescens (OR 2.91); and P. gingivalis, P. nigrescens, and T. denticola (OR 2.70) with the clinical diagnosis of slight (OR 3.73), moderate (OR 3.82), or severe periodontitis (OR 4.36), and with probing depth at the sample sites (OR 1.39). HSV and EBV-2 showed no significant associations with any of the variables tested. CONCLUSIONS: The results indicate that subgingival EBV-1, HCMV, and viral coinfections are associated with the subgingival presence of some periodontal pathogens and periodontitis. Herpesviruses may exert periodontopathic potential by decreasing the host resistance against subgingival colonization and multiplication of periodontal pathogens.
J Immunol. 1992 Jul 1;149(1):181-7. Links
Modulatory effects of Epstein-Barr, herpes simplex, and human herpes-6 viral infections and coinfections on cytokine synthesis. A comparative study.Gosselin J, Flamand L, D'Addario M, Hiscott J, Stefanescu I, Ablashi DV, Gallo RC, Menezes J.
Laboratory of Immunovirology, Faculty of Medicine, University of Montreal, Quebec, Canada.

Herpesviruses such as EBV, HSV, and human herpes virus-6 (HHV-6) have a marked tropism for cells of the immune system and therefore infection by these viruses may result in alterations of immune functions, leading at times to a state of immunosuppression. We report the results of a comparative study in which we found that EBV, HSV-1, and HHV-6 act differentially on the immune system with regard to their effect on the synthesis of IL-1 beta, IL-6, and TNF-alpha, i.e., three immunoregulatory cytokines mainly secreted by activated monocytes/macrophages. Using the polymerase chain reaction technique, analyses of the mRNA levels for each of the three monokines after viral infection indicated that the effect exerted by each of these herpesviruses on cytokine synthesis by human PBMC was detectable at the transcriptional level. Different amounts of IL-1 beta protein were detected in infected PBMC cultures, HHV-6 being the strongest IL-1 beta up-regulatory among these three herpesviruses. Spontaneous releases of IL-6 and TNF-alpha were found reduced after infection by HHV-6 and EBV, respectively. In comparison to EBV and HHV-6, HSV-1 proved to be a weak monokine enhancer. Results of coinfection studies indicated that virus-induced suppressive effects on cytokine synthesis are dominant. In fact, EBV inhibited TNF-alpha synthesis even in the presence of HHV-6, a strong up-regulator of TNF-alpha synthesis. Similarly, EBV was unable to stimulate IL-6 production in the presence of HHV-6. Viral structural component(s) appeared to be responsible for the up-regulation of IL-6 by both EBV and HSV-1, and of TNF-alpha by HSV-1. Taken together, our observations illustrate that herpesviruses can selectively regulate cytokine synthesis thereby disturbing immune homeostasis; this effect may favor pathogenic events, including the reactivation and/or spread of other infectious agents within the host.

I hope is OK to post these abstracts- Sorry, they are many. But it is VERY frustating to me as the mom of an autistic child suffering from coinfections and their consequences the amount of literature related to coinfections that is available that remains unnoticed, unstudied and ignored by the researchears in the ASD field.
Thank you

J Infect Dis. 2005 Jan 15;191(2):234-7. Epub 2004 Dec 10. Links
Dual infections of the central nervous system with Epstein-Barr virus.Weinberg A, Bloch KC, Li S, Tang YW, Palmer M, Tyler KL.
Department of Pediatrics, University of Colorado Medical School, Denver, CO 80262, USA. adriana.weinberg@uchsc.edu

We describe clinical and laboratory characteristics of 16 patients with central nervous system (CNS) infection caused by Epstein-Barr virus (EBV) and another pathogen. Seven of 10 immunocompromised patients had coinfection with viruses (3 with cytomegalovirus, 2 with JC virus, and 2 with varicella zoster virus) and 3 with nonviral pathogens (2 with pneumococcus and 1 with Cryptococcus species). Three of 6 immunocompetent patients had coinfections with viruses (1 each with herpes simplex virus, varicella zoster virus, and West Nile virus), and 3 had coinfections with nonviral pathogens (2 with Ehrlichia chaffeensis and 1 with Mycoplasma pneumoniae). The EBV load was similar in immunocompromised and immunocompetent patients and in patients with viral and nonviral coinfections. EBV lytic-cycle mRNA was detected in the cerebrospinal fluid of 5 of 6 tested samples, indicating EBV replication in the CNS during coinfection.

This is invasive- and I do think that there are other methods to test-
but I do not understand why not invasive methods are NOT systematically researched in ASD to test for coinfections. With the increasing evidence of coinfections in many ASD subgroups (virus, bacteria and fungus) and the amount of Concomitant medical problems- immune linked many of them- more and more published in ASD, this field of research should be more carefully explored.

More on other viruses
Ann Univ Mariae Curie Sklodowska [Med]. 2003;58(1):291-6.
Copper/zinc ratio in measles patients.Fota-Markowska H, Rolla-Szczepańska R, Modrzewska R, Lis-Tønder J, Borowicz I.
Department of Infectious Diseases, Medical University of Lublin.

The aim of this study was to evaluate the serum copper (Cu), zinc (Zn) levels and Cu/Zn ratio in measles patients in comparison to the control group. The study was conducted on 26 patients. The serum Cu and Zn levels were determined three times using atomic absorbtion spectrometry. The control group included 24 healthy persons. The serum Cu and Zn levels in those persons were determined once. CONCLUSION: in the acute period of the disease, a significant and highly significant increase in Cu/Zn ratio takes place.

Pol Merkur Lekarski. 2004 May;16(95):443-6.Links
[Serum copper and zinc level in patients suffering from infectious mononucleosis and after the regression of clinical symptoms][Article in Polish]


Fota-Markowska H, Rolla-Szczepańska R, Modrzewska R, Kiciak S.
Katedra i Klinika Chorób Zakaźnych Akademii Medycznej w Lublinie. hanna.markowska@futuro.net.pl

The aim of this work was to assess the serum copper (Cu) and zinc (Zn) level and ratio Cu/Zn in the acute, symptomatic period of infectious mononucleosis and during the convalescence period, when no clinical symptoms were present. MATERIAL AND METHODS: We examined 50 persons, including 26 patients (14 women and 12 men) in the age of 16 to 27 years, examined in the acute, symptomatic period of the disease. The diagnosis of infectious mononucleosis was based on the clinical, haematological, biochemical and serologic criteria. Cu and Zn concentration was measured 3 times: on the 1st day and the 2nd week of hospitalisation, and also after the regression of clinical symptoms. The control group consisted of 24 healthy individuals (13 men and 11 women) in the age of 17 to 26 years. Cu and Zn concentration was measured once in this group. All measurements of Cu and Zn serum concentration were done using the method of atomic absorption spectrophotometry (AAS) with AAS-3 spectrophotometer of Carl Zeiss-Jena production, at the wavelength for Cu--324.8, Zn--213.9 nm. We observed the Cu and Zn serum concentration and ratio Cu/Zn in patients with acute, symptomatic infectious mononucleosis and also after the regression of clinical symptoms to be statistically higher that the results from the healthy individuals. CONCLUSION: The statistical significant elevated serum Cu and Zn concentration observed during the course of infectious mononucleosis and after clinical symptoms regression in comparison to healthy persons expressed the perturbation of trace elements homeostasis. If copper to zinc ratio reflects myeloproliferative diseases activity, the practical value for infectious mononucleosis monitoring is the same as copper and zinc serum level measurement.

Sangre (Barc). 1993 Jun;38(3):211-6.Links
[Changes in the hemogram and in the laboratory parameters indicative of iron metabolism in mild viral infections
Olivares M, Walter T, Llaguno S, Osorio M, Chadud P, Velozo L.
Unidad de Hematología, Universidad de Chile, Santiago.

PURPOSE: To assess the duration and intensity of the changes appearing in laboratory values related to iron utilisation during viral infection. MATERIAL AND METHODS: With previous parental consent, 120 eutrophic infants received vaccination with attenuated measles virus or a combination of measles, mumps and rubella viruses as a model of mild viral infection. A number of laboratory tests were performed on day 0 and in two later occasions (4-21, 9-14 or 9-30); these included blood cell counts, ESR, serum iron, total iron binding capacity, transferrin saturation index, free erythrocytic protoporphyrin, serum ferritin, intra-erythrocytic ferritin, direct anti-human globulin test and C-reactive protein. The statistical analyses were done in accordance with ANOVA, Student's t test, Wilcoxon, Kruskall - Wallis, Mann-Whitney and Fisher methods. RESULTS: A significant haemoglobin drop was seen on days 9 and 14 post-vaccination. This descent was > 10 g/L in 8.2% of the cases, and > or = 6 g/L in 19.6%. Serum iron and transferrin saturation decreased significantly, whereas mean corpuscular volume, free erythrocyte protoporphyrin and serum ferritin were significantly increased. All these but protoporphyrin recovered by day 30. Subjects with normal iron metabolism figures on day 0 and those whose thermal variations were above 38 degrees C had greater changes in the figures related to iron metabolism. CONCLUSION: The evaluation of iron metabolism is not reliable if the patient has suffered from infection, although a mild viral one, in the three weeks prior to the study

Pediatrics. 1989 Nov;84(5):851-5.Links
Anemia of a mild viral infection: the measles vaccine as a model.Olivares M, Walter T, Osorio M, Chadud P, Schlesinger L.
Hematology Unit, Universidad de Chile, Santiago.

To define the hematologic changes during a mild viral infection, 93 infants were immunized with live attenuated measles virus and studied prospectively at 0, 4, 9, 14, 21, and 30 days. Hemoglobin concentration decreased significantly by days 9 and 14. The decrease was greater than 1.0 g/dL in 8.6% and greater than 0.6 in 24.3% of the infants. Of the nonanemic infants, 22% became anemic. Serum iron and percentage saturation of transferrin decreased, whereas serum ferritin increased significantly. Mean cell volume, iron-binding capacity, protoporphyrin, and haptoglobin did not show changes. Reticulocyte index and erythropoietin increased significantly at 30 days. Leukocyte counts, Zetacrit, and C-reactive protein did not help to predict the hemoglobin decrease. These results suggest that a mild viral infection in infants induces a significant decrease in hemoglobin that may persist for 14 to 30 days and may be difficult to distinguish from iron deficiency.

Hi Kent-

Please keep researching because like autism itself, unique and so idiosyncratic, what is going on inside the kids must be equally so.

I did a lot of research on biofilm development with Dr. Usman and there is a lot of interesting and comparative issues in not only the environment but in the environment of our children.

Bugs like metals.

here in the environment:

Jinping Cheng1 , Wenchang Zhao1, Yuanyuan Liu1, Cheng Wu1, Caie Liu1 and Wenhua Wang1

(1) School of Environmental Science and Engineering, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, People’s Republic of China

Published online: 5 September 2008

Abstract Biofilms were developed on glass microscope slides in a natural aquatic environment and their mercury adsorption properties were evaluated. Results demonstrated that the biofilms contained a large number of bacterial cells and associated extracellular polymers. Mercury forms detected in the biofilms were mainly bound to residual matter and organic acids. The adsorption processes could be described by a Langmuir isotherm. The optimum conditions for adsorption of mercury to natural biofilm were an ionic strength of 0.1 mol/L, pH 6 and an optimum adsorption time of 40 min. The transformation rate was 0.79 μg gaseous mercury per gram of biofilm.

and here in people:

Metal resistance in Candida biofilms
Joe J. Harrison 1,2 , Maryam Rabiei 1 , Raymond J. Turner 1 , Erin A. Badry 1 , Kimberley M. Sproule 1 & Howard Ceri 1,2
1 Department of Biological Sciences,

KEYWORDS
Candida tropicalis • biofilm • metal tolerance • antifungal resistance • metalloid • extracellular polymeric matrix
ABSTRACT
Yeasts are often successful in metal-polluted environments; therefore, the ability of biofilm and planktonic cell Candida tropicalis to endure metal toxicity was investigated. Fifteen water-soluble metal ions, chosen to represent groups 6A to 6B of the periodic table, were tested against this organism. With in vitro exposures as long as 24 h, biofilms were up to 65 times more tolerant to killing by metals than corresponding planktonic cultures. Of the most toxic heavy metals tested, only very high concentrations of Hg2+, CrO42− or Cu2+ killed surface-adherent Candida. Metal-chelator precipitates could be formed in biofilms following exposure to the heavy metals Cu2+ and Ni2+. This suggests that Candida biofilms may adsorb metal cations from their surroundings and that sequestration in the extracellular matrix may contribute to resistance. We concluded that biofilm formation may be a strategy for metal resistance and/or tolerance in yeasts.


Pediatr Hematol Oncol. 2009 Jan;26(1):57-61.
Coexistence of symptomatic iron-deficiency anemia and duodenal nodular lymphoid hyperplasia due to giardiasis: case report.Kasirga E, Gülen H, Simşek A, Ayhan S, Yilmaz O, Ellidokuz E.
Celal Bayar University Faculty of Medicine, Manisa , Turkey .
Iron-deficiency anemia due to iron malabsorption and duodenal nodular lymphoid hyperplasia (NLH) has been described in children with Giardia intestinalis infection. Also, symptomatic iron-deficiency anemia is rarely encountered in male adolescents. A 14-year-old boy underwent esophagogastroduodenoscopy for investigation of symptomatic iron-deficiency anemia (hemoglobin 5.8 g/dL, mean corpuscular volume 65.3 fL, serum ferritin 5 mg/L) had higher copper and lower zinc/copper ratios than those with low CRP (< or =5 mg/L). Children with HMPV and raised CRP had higher copper and lower zinc concentrations than children with low CRP. Children with RSV/HMPV and raised CRP had higher copper concentrations. Children with RSV/HMPV and raised CRP had higher a alpha-tocopherol concentrations. CONCLUSION: The profiles of micronutrients differ in children with RSV and HMPV and are confounded by CRP. These results may guide strategies for micronutrient supplementation in ARI

Se abnormal, Zn and Cu abnormal, vit A abnormal in certain circunstances....

There are reports of particular circunstances related to Aluminium
Ann Clin Biochem. 2005 Mar;42(Pt 2):149-52. Links
In end-stage renal failure, does infection lead to elevated plasma aluminium and neurotoxicity? Implications for monitoring.Fenwick S, Roberts EA, Mahesh BS, Roberts NB.
Department of Renal Medicine, The Royal Liverpool and Broadgreen University Hospitals, Liverpool L7 8XP, Merseyside, UK.

The well-described long-term effects of sustained exposure to aluminium in patients with end-stage renal failure (ESRF) are a result of uptake and storage of aluminium, leading to cellular toxicity. A case is presented suggesting that this aluminium may be mobilizable, and indicating the consequence of such release. A patient on haemodialysis (HD) presented acutely with infection, a raised CRP, decreased conscious level, impaired cognition and agitation. Subsequent neurological recovery over six to seven days appeared to follow the return of markedly elevated plasma aluminium concentrations to basal (i.e. from 25.2 micromol/L to 2.5 micromol/L; reference range < 0.5 micromol/L), coupled with a resolution of the infection. The patient was on long-term aludrox therapy 3 g/day, and showed relative resistance to the exogenous hormone erythropoietin, resulting in a refractory anaemia and suggesting aluminium toxicity. A series of HD patients (n = 5) presenting with bacteraemia, not on aludrox, showed no appreciable rise in the plasma aluminium mean of 1.3 micromol/L (SD 0.9; range 0.6-2.0 micromol/L). We suggest that infection can result in release of tissue aluminium, leading to acutely elevated plasma aluminium concentrations and signs of neurotoxicity. The amount of tissue storage and resultant aluminium release seemed to be related to the use of aluminium hydroxide as a phosphate binder.


J Toxicol Environ Health B Crit Rev. 2006 Jan-Feb;9(1):63-85.
The speciation of metals in mammals influences their toxicokinetics and toxicodynamics and therefore human health risk assessment.Yokel RA, Lasley SM, Dorman DC.
Pharmaceutical Sciences, College of Pharmacy, and Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, KY 40536-0082, USA.
Chemical form (i.e., species) can influence metal toxicokinetics and toxicodynamics and should be considered to improve human health risk assessment. Factors that influence metal speciation (and examples) include: (1) carrier-mediated processes for specific metal species (arsenic, chromium, lead and manganese), (2) valence state (arsenic, chromium, manganese and mercury), (3) particle size (lead and manganese), (4) the nature of metal binding ligands (aluminum, arsenic, chromium, lead, and manganese), (5) whether the metal is an organic versus inorganic species (arsenic, lead, and mercury), and (6) biotransformation of metal species (aluminum, arsenic, chromium, lead, manganese and mercury). The influence of speciation on metal toxicokinetics and toxicodynamics in mammals, and therefore the adverse effects of metals, is reviewed to illustrate how the physicochemical characteristics of metals and their handling in the body (toxicokinetics) can influence toxicity (toxicodynamics). Generalizing from mercury, arsenic, lead, aluminum, chromium, and manganese, it is clear that metal speciation influences mammalian toxicity. Methods used in aquatic toxicology to predict the interaction among metal speciation, uptake, and toxicity are evaluated. A classification system is presented to show that the chemical nature of the metal can predict metal ion toxicokinetics and toxicodynamics. Essential metals, such as iron, are considered. These metals produce low oral toxicity under most exposure conditions but become toxic when biological processes that utilize or transport them are overwhelmed, or bypassed. Risk assessments for essential and nonessential metals should consider toxicokinetic and toxicodynamic factors in setting exposure standards. Because speciation can influence a metal's fate and toxicity, different exposure standards should be established for different metal species. Many examples are provided which consider metal essentiality and toxicity and that illustrate how consideration of metal speciation can improve the risk assessment process. More examples are available at a website established as a repository for summaries of the literature on how the speciation of metals affects their toxicokinetics.


The fungus sequestrate iron

Mycol Res. 2008 Feb;112(Pt 2):170-83. Epub 2007 Dec 14.

Iron and siderophores in fungal-host interactions.Johnson L.

AgResearch Limited, Grasslands Research Centre, Tennent Drive, Private Bag 11008, Palmerston North, New Zealand.

Most fungi and bacteria express specific mechanisms for the acquisition of iron from the hosts they infect for their own survival. This is primarily because iron plays a key catalytic role in various vital cellular reactions in conjunction with the fact that iron is not freely available in these environments due to host sequestration. High-affinity iron uptake systems, such as siderophore-mediated iron uptake and reductive iron assimilation, enable fungi to acquire limited iron from animal or plant hosts. Regulating iron uptake is crucial to maintain iron homeostasis, a state necessary to avoid iron-induced toxicity from iron abundance, while simultaneously supplying iron required for biochemical demand. Siderophores play diverse roles in fungal-host interactions, many of which have been principally delineated from gene deletions in non-ribosomal peptide synthetases, enzymes required for siderophore biosynthesis. These analyses have demonstrated that siderophores are required for virulence, resistance to oxidative stress, asexual/sexual development, iron storage, and protection against iron-induced toxicity in some fungal organisms. In this review, the strategies fungi employ to obtain iron, siderophore biosynthesis, and the regulatory mechanisms governing iron homeostasis will be discussed with an emphasis on siderophore function and relevance for fungal organisms in their interactions with their hosts.

Some fungus may accumulate toxic elements
Mercury and fungus (between them, Candida species...)

http://www.cfspages.com/mmercmicro.html
Several citations are given
One manuscript
Transformations of inorganic mercury by Candida albicans and Saccharomyces cerevisiae.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2036011

Zentralbl Bakteriol Mikrobiol Hyg [B]. 1983 Jan;177(1-2):57-74.
[Effects of cadmium, zinc, lead and mercury on the growth and accumulating ability of Saccharomyces cerevisiae, Saccharomycopsis lipolytica, Candida tropicalis, and Candida utilis]
...The yeasts tested accumulate heavy metals, especially cadmium, to high concentrations and therefore substrates containing heavy metals are only limited suitable for the scp-production with yeasts.

On redistribution of metals during a viral infection
Sci Total Environ. 2007 Aug 1;381(1-3):88-98. Epub 2007 Apr 30. Virus induces metal-binding proteins and changed trace element balance in the brain during the course of a common human infection (coxsackievirus B3) in mice.Ilbäck NG, Frisk P, Mohamed N, Gadhasson IL , Blomberg J, Friman G.

Infectious Diseases, Department of Medical Sciences, Uppsala University Hospital , Sweden .

Autopsy of the brain has shown a change in trace element balance in some virus-infected individuals, but it is not known whether this event was a result of the infection. In the present study coxsackievirus B3 (CVB3) adapted to Balb/c mice was used to study whether infection induces gene expression of the metal-binding/transporting proteins metallothionein (MT1 and MT3) and divalent-metal transporter 1 (DMT1) and whether it changes the balance of trace elements in the brain. Virus and MT1, MT3, and DMT1 were quantitatively measured by RT-PCR on days 3, 6 and 9 of the infection. Trace elements (13) were measured in serum and the brain by ICP-MS. High numbers of virus were found in the brain on days 3 and 6, but virus counts were decreased and present only in 50% of the mice on day 9. Gene expression of MT1 tended to increase on all days, whereas that of MT3 only showed a minor and not significant increase on day 3. No clear effect was observed in the expression of DMT1. The increase of MT3 was correlated to the brain concentration of Cu. The Cu/Zn ratio in serum increased as a response to the infection. There was a similar decrease in Cd in serum and the brain. On day 6 of the infection, Hg increased in the brain (p<0.05) and was positively correlated to a concomitant decrease (p<0.05) in serum. Virus numbers in the brain were on day 6 positively correlated (p<0.05) to As concentrations. Enteroviral infections may therefore be an underlying factor regarding the changes in essential as well as potentially toxic trace elements in the brain.

and links here

http://www.ncbi.nlm.nih.gov/pubmed/17467775?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Environ Res. 2008 Feb;106(2):178-84. Epub 2007 Sep 21.
Tissue uptake of mercury is changed during the course of a common viral infection in mice.Frisk P, Molin Y, Ilbäck NG.
Research in Metal Biology, Rudbeck Laboratory, Uppsala University , S-751 85, Uppsala , Sweden.


Mercury (Hg) has been shown to have immunotoxic effects and to influence the severity of infection. However, the impact of infection on the normal Hg homeostasis in different target organs involved in the disease process has not been studied. In this study, Hg was measured through inductively coupled plasma-mass spectrometry (ICP-MS) in the intestine, serum, liver, and brain on days 3, 6, and 9 of coxsackievirus B3 (CVB3) infection in female Balb/c mice. The severity of the infection was assessed from clinical signs of disease and the number of virus particles in infected organs. CVB3 and gene expression of metallothionein 1 (MT1) was measured by reverse transcription-polymerase chain reaction (RT-PCR). Gene expression of MT1 increased and peaked on day 3 in the brain (93%, p<0.01) and liver (19-fold, p<0.01) and on day 6 in the intestine (seven-fold, p<0.01). This peak in MT1 in the liver and brain corresponded to the peak in virus numbers in these tissues. Hg in the intestine and serum tended to decrease on all days of infection. The maximum decrease, in comparison with non-infected mice, occurred in the intestine (78%, p<0.001) on day 9 and in serum (50%, p<0.05) on day 6. However, in the brain, Hg increased by 52% (p<0.05) on day 6. Hg went unchanged in the liver. An infection-induced increase of Hg in the brain but unchanged level in the liver may be due to the peak of virus replication and an associated infection-induced expression of MT1. Moreover, the decrease of Hg in serum and the intestine but a concomitant intestinal increase in MT1 on day 6 may reflect a flux and increased retention of Hg to infected organs such as the brain. The pathophysiological interpretation of these preliminary findings requires further research.

Environ Res. 2006 Nov;102(3):308-13.
Iron and copper accumulation in the brain of coxsackievirus-infected mice exposed to cadmium.Ilbäck NG, Lindh U, Minqin R, Friman G, Watt F.

Section of Infectious Diseases, Department of Medical Sciences, Uppsala University Hospital , S-751 85 Uppsala , Sweden.

Cadmium (Cd) is a potentially toxic metal widely distributed in the environment and known to cause adverse health effects in humans. During coxsackievirus infection, the concentrations of essential and nonessential trace elements (e.g., iron (Fe), copper (Cu), and Cd) change in different target organs of the infection. Fe and Cu are recognized cofactors in host defence reactions, and Fe is known to be associated with certain pathological conditions of the brain. However, whether nonessential trace elements could influence the balance of essential trace elements in the brain is unknown. In this study the brain Fe, Cu, and Cd contents were measured through inductively coupled plasma mass spectrometry and their distributions determined by nuclear microscopy in the early phase (day 3) of coxsackievirus B3 (CB3) infection in nonexposed and in Cd-exposed female Balb/c mice. In CB3 infection the brain is a well-known target that has not been studied with regard to trace element balance. The brain concentration of Cu compared with that of noninfected control mice was increased by 9% (P < 0.05) in infected mice not exposed to Cd and by 10% (not significant) in infected Cd-exposed mice. A similar response was seen for Fe, which in infected Cd-exposed mice, compared to noninfected control mice, tended to increase by 16%. Cu showed an even tissue distribution, whereas Fe was distributed in focal deposits. Changes in Cd concentration in the brain of infected mice were less consistent but evenly distributed. Further studies are needed to define whether the accumulation and distribution of trace elements in the brain have an impact on brain function


Maria - Please publish those articles! i had even read that the govt. used bugs to take care of radioactive elements.

In mito disorders, stroke-like episodes are common (I know first hand). I'm guessing they are similar to the micro strokes you mentioned. If you search toxnet for aluminum and mitochondria, you'll find some studies too.

I have more to write on periphery circulation, but am short on time as the PT is leaving.... hopefully more soon.

I'm sorry to say that it's quite impossible that metals are being synthesized by the "bugs", at least in the sense I think you mean. Metals are elements, i.e., they are atoms and not made up of smaller parts. They cannot be synthesized by any known chemical reactions (e.g., the theory of cold fusion turned out to be false). As far as we know, only "hot" nuclear fusion can produce metals from nonmetallic elements--and the only real source of nuclear fusion we know of is the sun!

I would start looking very carefully for hidden sources of metals in your child's surroundings. I agree with the idea that metals can be absorbed through the skin. Alternatively, she may have absorbed more than you thought possible and you just have to be patient waiting for it all to come out...

Hi ObjectiveDad
It is true that bugs can´t "synthesize" toxic elements. As you say, only nuclear reactions can change one element in other.
But with this point clarified, fungus, virus and bacteria have been published to
a-sequester toxic elements (for example mercury in the case of certain fungus)
b-Redistribute toxic elements ( for example in the case of certain virus) and
c-affect the xenobiotics management
Now if chronic infections with fungus, virus- for example herpes- and bacteria coexist therefore the cycle of sequestration may be continuous in time, such as the impact in xenobiotics management.
There are several interesting manuscripts on sequestration redistribution and speciation- that is how chemically a metal is and how affects the human body.Please let me know if you are interested and I may post the abstracts.

I'd like a bunch of bugs that poop platinum... :)

*(it is possible that girls may have androgen problems, which would make them just as susceptible as boys)....

A possible central mechanism in autism spectrum disorders, part 2: immunoexcitotoxicity.Blaylock RL.
Belhaven College, Jackson, Mississippi, USA.

In this section, I explore the effects of mercury and inflammation on transsulfuration reactions, which can lead to elevations in androgens, and how this might relate to the male preponderance of autism spectrum disorders (ASD). It is known that mercury interferes with these biochemical reactions and that chronically elevated androgen levels also enhance the neurodevelopmental effects of excitotoxins. Both androgens and glutamate alter neuronal and glial calcium oscillations, which are known to regulate cell migration, maturation, and final brain cytoarchitectural structure. Studies have also shown high levels of DHEA and low levels of DHEA-S in ASD, which can result from both mercury toxicity and chronic inflammation. Chronic microglial activation appears to be a hallmark of ASD. Peripheral immune stimulation, mercury, and elevated levels of androgens can all stimulate microglial activation. Linked to both transsulfuration problems and chronic mercury toxicity are elevations in homocysteine levels in ASD patients. Homocysteine and especially its metabolic products are powerful excitotoxins. Intimately linked to elevations in DHEA, excitotoxicity and mercury toxicity are abnormalities in mitochondrial function. A number of studies have shown that reduced energy production by mitochondria greatly enhances excitotoxicity. Finally, I discuss the effects of chronic inflammation and elevated mercury levels on glutathione and metallothionein.

Thank you, Kent.

I don't quite know what to make of the idea of "bugs making metals". The whole vaccine injury debacle is out of science fiction anyway, so I tend not to get surprised as easily as I once did. Any bugs which eat metals that we could make use of?

My impression is that our children with efflux are sitting ducks for metal absorbtion and any exposure through air, water, food, skin contact, operates on the old "roach motel" principle-- what gets in never comes out (without help). Our kids had a sudden explosion of arsenic and the question was, was it being dug up in chelation or from recent exposure? Our DAN suggested the obvious--that air quality and pollution exposures differ according to geography. And the cadmium? What's going on is right.

The information about body temp, blood pressure and seizures is quite fascinating.

Whatever the source of the metals (and it is important to figure it out to stop it), I have to agree with you that chelation can improve development in amazing ways. Our twins are making leaps and bounds. I just witnessed something I never thought I'd see-- after a fight over a toy, our son went up to his twin sister (the one who wasn't sharing), looked her in the eye, gave her a hug and a kiss and said "I love you". Of course it came out as "I wuvvoo", but we'll take it. He said his first short sentence less than six months ago. Both twins had lost speech between age one and two and a half, after two flu shots, an MMR and a varicella.

"...the pathogens themselves were proceeding to make their own supply of toxic metals..." This is beyond outlandish. The only way to make Aluminum, or any other metallic element, out of something else is via nuclear fusion. That isn't happening in our childrens' bodies. There must be some other source of Aluminum (either it's still being ingested somewhere or there really is a large pool of it in your/our children -- my son also pulls a lot of Aluminum and little mercury -- anymore anyway).

Kent,
How utterly fascinating this information is. I wonder if the "think tank" has pondered it yet.
Everything you share is always so informative
and I cannot thank you enough for putting it all out there for us to digest.
Both my grandkids(for those who have heard this story-and are bored-stop here) are such perfect examples of the damage vaccines do. Grandchild number 1(I am still trying to recover him at age 11) with vaccines until age 2 was so much more damaged than his younger brother, whose vaccines I halted after his 4 month ones. I recovered him in 2 years even tho he was diagnosed with PDD/NOS at 13 months . Blessings to your daughter and thanks again.
Maurine

http://tinyurl.com/pkvg5f

Not sure if this is at all related: From The Columbus Dispatch.

A microbe that is as old as dirt could one day help keep radioactive metals out of our drinking water.

Shewanella oneidensis bacteria have existed for billions of years, thriving even when the Earth's atmosphere lacked oxygen.

Most forms of life need oxygen to convert food to energy. Shewanella, however, can survive by "breathing" metal.

This process, researchers have learned, also appears to stop groundwater from carrying metals to lakes and streams.

With the help of a special microscope at Ohio State University, Brian Lower, a microbial biogeochemist, and his twin brother, Steven, a microbiologist, say they have figured out Shewanella 's secret.

Their discovery could help clear a path for other researchers to find ways to speed up the organism's breathing process and keep radioactive metals such as uranium at old Cold War nuclear weapons sites from leaking into reservoirs and wells.

How do microorganisms synthesize toxic metals?

Kent,
Thanks for a great post. My own son had toxic metals (7 of them to be exact) that were off the chart when we started on this journey. I was concerned about IV chelation for its invasiveness, and risks of redepositing metals in the brain. Our doctor feels that chelation offers a temporary oxidative benefit, but long term is harsh on kidneys and metals can redeposit and cause more issues. I know this belief is not commonly held in our community because I know a lot of people who chelate. Our doctor also believes if you heal the immune system, the metals will clear naturally. I did not believe him when he told me this in 2007, but put my son on antivirals (both DNA and RNA antivirals- Valtrex, Acyclovir and Tamiflu. Our son does have high titers for HHV6, Varicella, and Parvovirus and Measles. In addition, he had high ASO titers. We also started B12-P5P and folinic acid injections, and supplementation with glutathione, inositol, methionine and other important neurotransmitters. I watched the metals come down over a period of time, and the most recent tox screen shows NO metals except trace lead and aluminum (I called the lab to repeat the test because I was in such disbelief). We also saw a nonverbal child start talking, and an incontinent child start using the toilet and have formed BMs. I now believe our doctor, and his protocol saved us from a lot of chelation. I am not saying this works on all kids, but the antivirals had a dramatic effect for our son. This took about 18 months to occur. Our doctor is an MD who has studied herpetic viruses and how they attack the immune system, and was a former base skull surgeon. He is not a DAN! doctor, but extremely educated on pathogens, toxicology and the immune, vestibular and sensory systems. He has been recovering hundreds if not thousands of kids.
Good Luck and Blessings to you and your family.

Kent in the six years of recovering my son I have learned one thing. Autism is multi-factorial.
You've got to shore up many systems down.
This article makes so much sense to me. Amy Yasko also addresses aluminum in her process and it is widely used in baking and even supplements.
Our kids are so compromised and genetically unprepared, the constant environmental exposure only serves to keep them down.

One can only wonder how nice it would have been if vaccines hadn't pushed them off a cliff at such a young age.

Keep on pressing on. If we waited on research to catch up our kids would be 30 before they made progress.

Wow. Fascinating (as your articles always are). Also a little scary too. My daughter has the factor V lieden clotting disorder so she's already at a higher risk of developing blood clots, and then to think of all the aluminum she was injected with before I knew any better... Prior to reading this article, I had heard a theory stating that aluminum causes "blood sludge". I confess thinking the name sounded outlandish, but the concept behind it made sense since aluminum does cause clumping and dries up moisture (that's exactly why it's in deodorant). So it did seem reasonable to me that enough aluminum in the bloodstream could cause a clot since dehyration can increase the risk of clots.

However, I had no idea that viruses could produce more metals. That's a very interesting hypothesis, and as you've pointed out, your daughter's metal levels seem to indicate its plausibility. Even scientists say that the use of aluminum as a vaccine adjuvant is not very well understood (they don't know why it works, but they use because it invokes a stronger immune response). Could aluminum invoke a stronger immune response because the aluminum helps strengthen the virus by making it "easier for the bugs to get their food"? Just wondering...

As soon as you mentioned the small red blood cells, I immediately thought of Microcytic anemia, which can be caused by many different things including lead toxicity. "Acquired sideroblastic anemia, including lead toxicity" http://en.wikipedia.org/wiki/Anemia
And look what this same page suggests for treatment (which depends on the severity and the cause):

"The diagnosis of iron deficiency mandates a search for potential sources of loss such as gastrointestinal bleeding from ulcers..." [how about inflammatory bowel disease?] "Mild to moderate iron deficiency anemia is treated by iron supplementation with ferrous sulfate or ferrous gluconate. Vitamin C may aid in the body's ability to absorb iron."
And
"Vitamin supplements given orally (folic acid) or subcutaneously (vitamin B-12) will replace specific deficiencies."
And
"Treatment of exceptional blood loss (anemia) is recognized as an indication for hyperbaric oxygen (HBO) by the Undersea and Hyperbaric Medical Society.[16][17]"

Thanks Kent! YAnd good luck on your new path. My goodness how this "topic" leads everywhere.

Wow Kent, this is great info! Keep us posted. It's always interesting to read what you're up to.

:-)

Kent,

God bless you!

I've wondered something similar myself, only not so coherently. In my mind, it was something like, "How can Noah be 80% or 90% better, and we keep doing the things that helped him get better, and yet--he never gets 100%?"

I always figured (wrongly, it turns out, in our case) that once a kid reached a certain point of wellness, wellness would take over completely!

Sickness can be a tricky, complicated thing.

I wish for more and better healing for Jacqueline.

Terri Lewis

My daughter had 8 seizures after her 4-month vaccines and had autism by 5-months old. I started her on CLO but she still had seizures. I gave her nystatin because it helped my son. Looking back her babbling came back and she never seized since. She is 8 today and pretty much recovered.

Hulda Clark also talks about viruses, bacteria and metals all feeding off one another. Her book A Cure for All Diseases helped my kids.

thanks for the info Kent. My twins are similar to your kids. One is nearly recovered, the other has a long way to go still and we're running out of ideas.

ps I love the opening statement, so true!!

Hi Kent loved your article lots of information I have two children of my own with autism and I just moved back to my country in Africa after spending six years in the US persuing biomedical treatments. Like you I never rule out anything. Will definately look into the bio-mat my son never sleeps through the night. Goodluck with your little girl Im off to look for Mark and thankyou for sharing this.
Sutura

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