Seizures and the Immune System – Part 3
By Kent Heckenlively, Esq.
At the entrance to one of the schools at which I teach is a quote from the anthropologist Margaret Mead. It reads, “Never doubt that a small group of thoughtful, concerned citizens can change the world. Indeed, it’s the only thing that ever has.”
In my last article I noted the belief of many DAN practitioners that the problem with autism was one of “infections and toxins.” I questioned whether infections and toxins could produce similar effects in T-cell disruption, leading to immune system over-reaction and causing both autism and seizures. (My first article discussed research showing that a meningitis virus in a mouse led to fatal seizures by causing an overreaction of the animal's immune system.) I was also looking for a possible way to link the infections and toxins, but couldn’t piece together how they might interact.
Then one reader directed me to www.autismcalciumchannelopathy.com/Infectious Agents.html, a web-site at which I found some interesting claims. After first noting that various viruses and other pathogens have been implicated in autism, the author noted, “The best association to date have been made between perinatal (around the time of birth) cytomegalovirus and rubella viruses and autism.”
While I've been researching the possible role of the cytomegalovirus as well as other herpes viruses, the rubella connection brought me back to one of my earliest investigations. It was probably more than five years ago that I picked up a book entitled, “Psychiatric Disorders of Children with Congenital Rubella”, published in 1971 by Drs. Stella Chess, Sam Korn, and Paulina Fernandez. The book recounted the 1964 rubella outbreak and the “wide range of physical and intellectual handicaps” suffered by children who were exposed to the virus during pregnancy.
One of the striking findings was a high number of autistic children in this population. Of the 243 children in the study, 10 were classified as autistic, while 8 showed partial symptoms of autism. Two of the paragraphs in the conclusion of the chapter on the autistic children made a strong impression on me.
“The high prevalence of autism in this series of 243 children with congenital rubella inevitably raises the vexed question of the etiology of childhood autism. Our study did not attempt to probe this question, and we cannot offer a conclusive judgment. Nevertheless, there is an inescapable implication in this data. Our findings would appear to support the argument in favor of an organic etiology as against other lines of inquiry.” (P. 122)
“In our series, the existence of congenital disorder in unequivocally established. The exact mechanism by which organic damage manifests itself behaviorally as autism remains to be determined. But the association between congenital rubella and autism is striking. One is led to wonder to what extent this link was ignored in the past, especially before the 1964 epidemic made pediatricians and child psychiatrists more aware of the sequale of rubella.” (P. 123)
Dr. Stella Chess was one of the great figures of child psychiatry, founding the New York Longitudinal Study in 1956, which established the idea of a child’s natural temperament and how that affected their later life. Two years earlier, in 1954 she was the first professor of child psychology at New York Medical College, later founding the pediatric psychiatry unit at Bellevue Hospital, and becoming a long-time professor at NYU.
After reading her book I thought I’d try to contact her. Surprisingly, even though she was in her late 80s she was still at NYU. I was actually a little shocked when a strong, older woman’s voice answered the phone and I explained I was looking for Stella Chess.
“This is Dr. Chess,” she replied.
I quickly explained who I was and she seemed to tolerate me so I asked my question. “Dr. Chess, you wrote about children whose mothers were infected with the rubella virus during pregnancy and the high rate of autism. That seems to clearly show a viral exposure prior to birth leading to autism. But is there any reason why an infant with a poorly functioning immune system might not react the same way? If this infant had a poorly functioning immune system, is there any reason why exposure to rubella, possibly through the MMR (measles, mumps, and rubella) shot, wouldn’t do the same thing?”
She paused. “We never considered that question.”
“But is it a reasonable question to ask?”
“It’s reasonable,” she agreed.
Dr. Chess died in 2007 at the age of 93. The staff at NYU found out she’d died when she didn’t show up for work that week.
Between the medical literature Stan Kurtz found on PubMed showing links with autism and the herpes virus going back to 1981, the work of Dr. Andrew Wakefield on the measles virus, and Dr. Chess’ work implicating the rubella virus contributing to autism from 1971, it seems clear that some infectious agent is at work. But then how do the toxins come into play?
Going back to www.autismcalciumchannelopathy.com/Infectious Agents.html may provide a potential answer. In the section entitled “Other Issues for Consideration” is the following paragraph. “A series of murine and (other) studies pointing to links between viral infections and absorption and tissue/organ distribution of environmental toxins may be of great relevance. It has been observed for example that the intestinal absorption of cadmium increases during a common viral infection. In the infected animals the absorption of the metal was increased by 70% at low doses and was tripled at high doses compared to non-infected animals. The increased absorption also enhanced the accumulation of cadmium in all studied organs. Redistribution of trace elements already in the body has been noted, with brain levels of mercury increasing twofold during viral infection.”
“Mercury was also shown to change virally-induced myocarditis in a direction compatible with the development of chronic disease and allow increased persistence of virus, indicating theta heavy metals may interact and adversely affect viral replication and development of inflammatory disease.”
Viral infections can lead to increased retention of heavy metals. According to Dr. Isaac Pessah of UC Davis, thimerosal interferes with the ability of the immune system to work properly, theoretically meaning they can't effectively fight viruses and other pathogens. It seems we keep coming back to this unholy duo of infections and toxins.
If we’re able to understand how these two interact with each other in autism I think we’ll be able to change the world. At least the world of our children. And maybe even Keith Olbermann will do a story on it.
Kent Heckenlively is Legal Editor of Age of Autism
I had the Depoprovera* birth control shot right after my son was born. I was breastfeeding so they said that the shot was the only "safe" method that wouldn't harm my baby while nursing. It just struck me while reading this that I have NO IDEA what is in those shots. Obviously, what ever was injected in to me went straight in to my son as well. He is now almost 5 years old with mild autism. Anyone know what or where you can find out what is in that shot? Did anyone else have the same experience by chance that I did?
Posted by: Gabriel's Momma | February 14, 2009 at 09:51 PM
Truly amazing insights. The connections between viruses, metals, and immune function do indeed seem to all be so closely interrelated that it appears that viruses make heavy metals worse, and heavy metals make viruses worse, and both weaken the immune system.
Since metals and viruses seem so closely intertwined, it makes me wonder if you have to treat both problems (infections and metals) simultaneously to get the best results??
Now I'm wondering if maybe using both Enhansa and the protocol for mitochondrial disorders would be the most beneficial?
Enhansa both increases intracellular glutathione AND is an anti-viral medicine. So it sounds like it would treat both parts of the problem (by fighting the viruses and removing heavy metals).
But, we're exposed to viruses and metals (and other toxins) every day, so that's why I'm thinking you need to have good mitochondrial health in order to preemptively protect against these daily stressors.
Particularly, children with autism should be checked for mitochondrial disorders because:
"Recent research has supported a role for mild mitochondrial dysfunction among ASDs.[40-42] Investigators reported that levels of free and total carnitine and pyruvate were significantly reduced, while ammonia and alanine levels were considerably elevated, in ASDs. These are suggestive of mild mitochondrial dysfunction.[40]"
http://www.medscape.com/viewarticle/584398_6
For information on mitochondrial disorders, see this amazing link:
http://biochemgen.ucsd.edu/mmdc/ep-3-10.pdf
On page 7, there is a table that lists the "Vitamin and Cofactors for the Treatment of Mitochondrial Disease".
Also, on page 5 there is a chart that lists "atypical" symptoms of a disease that are suggestive of mitochondrial dysfunction. For example, typically cerebral palsy does not get worse with infections. So if a child's cerebral palsy does get worse with infections, that indicates that the child may have mitochondrial disease. AND, this chart also lists seizures as an "atypical feature" of autism. So while not all children with autism have seizures, those who do have seizures should probably be checked for mitochondrial disease.
**But I'm not a doctor. Ask your child's doctor before making any medical decision. It's especially important to ask a doctor about which supplements to use because while many supplements are vital to good health, they can also be toxic in too high of an amount. Also there are different forms of mitochondrial disorders. So a doctor could help determine which form of mitochondrial disease your child has (if any) and then be able to prescribe the best supplements for him or her.
Posted by: CM | February 12, 2009 at 09:08 AM
More good puzzle pieces to fit together,, Thanks Kent (and Natasa for autismcalciumchannelopathy). I agree on the mercury - virus connection. There is a process going on that we are starting to figure out. Some other good research in this area-
1: Sci Total Environ. 2007 Aug 1;381(1-3):88-98. Epub 2007 Apr 30.Click here to read Links
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.
PMID: 17467775 [PubMed - indexed for MEDLINE]
1: Environ Res. 2007 Sep 20 [Epub ahead of print]Click here to read Links
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.
PMID: 17888900 [PubMed - as supplied by publisher]
Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis).
Ilbäck NG, Wesslén L, Fohlman J, Friman G.
Pharmacia and UpJohn, Helsingborg, Sweden.
A myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice was used to investigate the effects of 12 weeks of methyl mercury (MeHg) exposure (3.69 mg/g diet) on inflammatory heart lesions, virus in the heart, the cytokine response, i.e. cachectin/TNF-alpha and gamma-interferon (IFN-gamma) levels in plasma, and on disease complications and mortality. This dose of MeHg did not influence mortality in this infection model. The inflammatory and necrotic lesions in the ventricular myocardium 7 days after the inoculation covered 2.2% of the tissue section area in infected control mice. This damage was increased (n.s.) by 50% (to 3.3% of the tissue section area) in MeHg-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was corroborated using an immune histological technique. MeHg treatment tended to increase (2.2-fold, n.s.) the number of Mac 2+ cells (macrophages) in the heart muscle in this infection. Plasma levels of both TNF-alpha and IFN-gamma increased on day 3 of the infection in MeHg-treated as well as in non-MeHg-treated mice, but the mean IFN-gamma response was more pronounced in the MeHg-treated mice. On day 7 of the infection, when most animals still showed clinical signs of disease, cytokine levels were back to normal. MeHg-exposure in non-infected mice did not affect cytokine levels. In situ hybridization of virus RNA in myocardial tissue showed remaining virus in those mice who had the lowest plasma IFN-gamma levels. A 20% increased (P < 0.05) lymphoproliferative response to the T cell mitogen Con A was observed as a result of the MeHg treatment. Even heart tissue lesions and virus persistence tended to be influenced by MeHg in a direction compatible with the development of chronic disease.
Selenium and mercury are redistributed to the brain during viral infection in mice
Nils-Gunnar Ilbäck1, 2 Contact Information , Ulf Lindh3, Ren Minqin4, Göran Friman1 and Frank Watt4
(1) Section of Infectious Diseases, Department of Medical Sciences, Uppsala University Hospital, Uppsala, Sweden
(2) Toxicology Division, National Food Administration, Uppsala, Sweden
(3) Research in Metal Biology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden
(4) Centre for Ion Beam Applications, Department of Physics, National University of Singapore, Singapore
Received: 24 February 2005 Revised: 1 March 2005 Accepted: 17 March 2005
Abstract As part of the general host response to coxsackievirus B3 (CB3) infection, the concentration of essential and nonessential trace elements changes in different target organs of the infection. Essential ( e.g., Se) and nonessential (e.g., Hg) trace elements are known to interact and affect inflammatory tissue lesions induced by CB3 infection. However, it is unknown whether these changes involve the brain. In the present study, the brain Hg and Se contents were measured through inductively coupled plasma-mass spectrometry and their distribution investigated by means of nuclear microscopy in the early phase (d 3) of CB3 infection in normally fed female Balb/c mice. Because of the infection, the concentration of Hg ( 4.07±0.46 ng/g wet wt) and Se (340±16 ng/g wet wt) in the brain increased twofold for Hg (8.77±1.65 ng/g wet wt, p<0.05) and by 36% for Se (461±150 ng/g wet wt, ns). Nuclear microscopy of brain sections from mice having elevated Se and Hg concentrations failed to find localized levels of the elements high enough to make detection possible, indicating approximately homogeneous tissue distribution. Although the pathophysiological interpretation of these findings requires further research, the increase of Hg in the brain during infection might have an influence on the pathogenesis of the disease.
Influence of mercuric chloride on resistance to generalized infection with herpes simplex virus type 2 in mice.
Christensen MM, Ellermann-Eriksen S, Rungby J, Mogensen SC.
Department of Medical Microbiology and Immunology, University of Aarhus, Denmark.
The effect of mercuric chloride on resistance to generalized infection with herpes simplex virus type 2 (HSV-2) in mice was studied. The severity of the infection was evaluated by the amount of infectious virus in the liver. Mercury at a single dose of 20 micrograms aggravated the infection, and neither increasing the single dose to 80 micrograms nor giving repeated doses of 20 micrograms further intensified the infection. Examination of the course of infection after mercury exposure revealed an increased virus replication and dissemination during the first days of the infection, indicating that the early, nonspecific defence mechanisms were affected. Virus clearance and elimination, which is mediated by specific immunity, seemed not to be influenced. Examination of cells from the peritoneal cavity and of livers from virus-infected mice showed that mercury detectable by autometallography was exclusively found in mature peritoneal macrophages and in Kupffer cells of the liver. Inflammatory cells, recruited to the peritoneal cavity or infiltrating the infectious foci of the liver, did not show any mercury deposits. Attempts to demonstrate an effect in vivo of mercury on potential antiviral macrophage functions like interferon-alpha/beta (IFN-alpha/beta) and tumour necrosis factor-alpha (TNF-alpha) secretion and oxidative burst capacity were not successful, possibly because recruited, inflammatory cells, which have not been exposed to the high mercury concentrations at the site of injection, take over these functions of intoxicated macrophages.
PMID: 8931761 [PubMed - indexed for MEDLINE]
Posted by: Teresa Conrick | February 11, 2009 at 11:29 PM
Kent, thanks for this series. 3 wks ago, my daughter had a febrile seizure, and she came home early today, spiking a fever and vomiting at school.
She is laying next to me on the couch, her heart racing, and temp of 103.
I am so pissed off that if she gets worse, and I take her to a hospital, no doctor is going to know wtf to do. We took her in to the ER 3 wks ago after her seizure. We told them she has primary immunodeficiency. Although she had a temp of 104, and just had a seizure, they didn't bother to perform any labs, not even a strep test. We went on to spend a week fighting off a 105 temp.
I wonder why the lack of care, because we told them she has autism, and that she is not up to date w/ vaccines due to a medical exemption?
My daughter, who's reaction was likely to the varicella vax (erythema multiforme/ her first seizure/ fever 21 days post vax), showed hardly any (not enough for protection) antibodies to the vaccine, yet the actual varicella in her system quadrupled in a 2 yr period.
I wish I knew what was going on in her little body, and could fix it. I am pissed off that the doctors just don't get it. It's times like this when I really want to spit in Offit's face. He is standing in the way of healing my daughter's immune system.
Just a thought, perhaps the thimerosal induced T-cell disruption is causing inflammation, as well as altered immune response to viruses. When removing these toxins through chelation, T Cell function is restored, and inflammation diminishes.
Makes sense why chelation doesn't work for all kids, maybe they have genetic T Cell dysfunction.
Posted by: Monica | February 11, 2009 at 05:58 PM
Very interesting! My son had one MMR at 12 months, his titers 4 years later were still more than 4x reference range for rubella, double for mumps and measles. And absolutely NO titers measured for varicella, despite having had the vaccine (5 months after the MMR, back when I was still really dumb). Wouldn't it be great to do a comparative study on titers between vaccinated NT and non-NT kids? I bet everyone -- doctors included -- would be shocked to learn the true variability in efficacy and immune response.
Posted by: Garbo | February 11, 2009 at 04:57 PM
If the president of the peanut corporation can send contaminated salmonella and not think twice about it (this was proven), then, why would we think this is not happening on a much grander scale in our vaccine production facilities? The FBI is going to ask the president to partake of his own products...let's see what he will do heh? Just thought, maybe that should be the angle, get the FBI in there, and have them do the same thing...if they think vaccines are so safe, then by dose and weight, they should agree to be shot up...and their family members. Of course, I don't think that's ethical, but it may be after what I have been through?
For crying out loud, these people are liars, and they know they cause seizures, autism, and so many other illnesses...
Posted by: Kathy Blanco | February 11, 2009 at 03:34 PM
If you refer to Dr. Amy Yasko, she said that the rubella virus was the hardest to grow on male cells. After many failed attempts (hey there could be a message there but don't expect Big Pharma to get it!) they finally got it to culture on aborted female fetal tissue. There is definitely a problem with ALL the components of the MMR.
I also don't trust the FDA's say so that vaccines are safe, in particular the MMR. We ran stories here on AoA that specifically said that vaccine manufacture was tainted and there were unexplained fibers in the MMR vaccine vials. And the FDA certainly wasn't looking for it, was it? They can't even keep the food supply safe. How in the world do you expect them to keep things that are injected directly into your bloodstream sterile and safe?
Posted by: Is the FDA working at all? | February 11, 2009 at 11:00 AM
I believe the study Maggie is referring to was done by Dr. Yazbak regarding MMR vaccination surrounding pregnancy. His study is found here:
http://www.vacinfo.org/researchers.htm
Posted by: Diane F. | February 11, 2009 at 10:17 AM
Kent,
There was a study done showing breastfeeding women who were postnatally vaccinated with rubella had a VERY high rate of children with autism. I can't find the study right now. It's hard to find anything on the internet anymore that's against vaccines. Anyway, I was vaccinated with rubella at the same time my son got Hep B in 1999 when it was full of mercury. I breastfed for a whole year. I'm sure lots of live rubella virus was excreted in the breast milk. All his vaccines had mercury in 1999 and 2000 - nobody even tries to deny that. Perfect setup for autism. I believe the practice of vaccinating women postnatally is still going on. I was able to warn my sister about this and she refused the postnatal rubella vaccine and guess what - no autism. BAD, BAD idea to vaccinate postnatally breastfeeding mothers with a LIVE virus. I was naive and trusting but the doctors should have known. Why didn't they?
Posted by: Maggie | February 11, 2009 at 09:54 AM
Thank you very much for this article. This is another clear explanation of what I know happened to me when I told my OB/GYN my husband and I wanted to start a family, and she immediately measured my rubella titers. When the titers came back negative, she told me to get an MMR (no separate vials available, and of course I was naive and trusted her) and wait four months before conception. I waited longer than that, but obviously in my case the vaccine had the same affect as my being infected with the rubella virus while pregnant. My son was breech, tangled in his cord, and I had to have a C-Section. (I've since attributed all of that to the fact he gestated with live viruses) He had some breathing problems at birth and was in the NICU, where they gave him the Heb B vaccine, which in 1997 was filled with thimerosal. He then went on to be diagnosed with autism at age 2. I believe our case is a clear example of your article.
Also, as I commented on the second in your series of these articles, my son has PLEVA, which is definite T-cell disruption leading to immune system over-reaction in plain sight.
http://tinyurl.com/c2rn22
http://tinyurl.com/d8djmp
Posted by: Diane F. | February 11, 2009 at 09:25 AM
This is so interesting. Thanks Kent.
mentioning Keith Olbermann...How very disappointing to see his regurgitation of misinformation about Dr Wakefield. Unfortunately, my cousin saaw that piece and called me asking if I had seen the story, "about teh Dr who falsified documents to make vaccines look like the culprit....?"
AAhhhhh.... et tu, Keith?
Posted by: kathleen | February 11, 2009 at 06:09 AM
Hi Kent, I am the author of the paper on autismcalciumchannelopathy, thanks for quoting it, do contact me if you wish to discuss more recent findings that have not been added on there yet.
Posted by: Natasa | February 11, 2009 at 05:56 AM