I didn't understand why this "lumberjack guy" was talking to all of us parents about trees, Lignasan, and ethylmercury. My daughter became sickly and regressed in skills after vaccines -- many with the vaccine mercury called thimerosal. Bacterial and viral infections were then to be constant unwanted parasites in her life as her immune system took a direct hit. Meg was diagnosed with autism shortly after and just recently has been diagnosed with an autoimmune disorder. Dan seemed to me to be on the wrong trail. It took me a while to connect the research and see that these clues Dan, along with Mark Blaxill, had been discussing and writing about for quite some time were the first "puzzle" pieces to autism.
So on that September night, I was grateful and excited to finally meet with Dan. He had contacted me as he was coming into town to visit his sister, and wanted to know if I could meet them for dinner. I had become entranced with those children of the 1930s, those first canaries in the debut of mercury-containing vaccines, who were subsequently declared to have "Autistic Disturbances of Affective Contact". I had e-mailed Dan and Mark over the years as they researched their book, The Age of Autism -- Mercury, Medicine and a Man-made Epidemic. My father had been an ophthalmologist and surgeon from the 1940s until the 1980s, and thimerosal, the ethylmercury preservative, was a heavily used medical product in that field, too, and in his own office.
Over dinner, after we shared stories and tears about my daughter's descent
into illness after vaccines and the ultimate reality of severe autism, Dan
pulled out a crisply, folded copy from his jacket pocket of Leo Kanner's 1971
paper, "Follow-up Study of Eleven Autistic Children Originally Reported in
Dan and his sister, Rosie, were both so encouraging as he invited me to make
history and help trace the roots of autism. It was an easy answer for me,
"Yes!" Dan and Mark had already found some of the "original
11," so I knew it could be done and I was ready for the challenge.
Finding the clues to how autism first appeared was like trying to hit a bullseye; slowly, we got closer and closer. To find the cause, we had to go back -- back to the start.
Dan also shared about GPI, General Paralysis of the Insane, a horrific neurodegenerative disease that had quite an interesting story. GPI historically was seen as the end result of the sexually transmitted disease syphilis, a sly spirochete bacteria very similar to the spirochete of Lyme bacteria today, sickening the brain and rendering its victim slowly insane, finally losing the ability to talk, walk or recognize anyone. Yet Dan and Mark's research showed that GPI only seemed to occur in syphilis patients who had been treated with mercury, a standard of care for centuries up to the era of antibiotics that arrived with penicillin in the 1940s. Like acrodynia in childhood, a disease connected to mercury in teething powders, GPI began to disappear when antibiotics took over as the treatment of choice. It seemed to be a possible interaction between the microbe of syphilis and mercury that sparked GPI. State mental institutions around the country had thousands of GPI patients, often for years, as their insanity whittled them down to a shell of their former selves.
By Teresa Conrick, Dan Olmsted and Mark Blaxill
We found her.
Eight years after setting out to identify the 11 children in the first medical report of autism, we have found “Virginia S.”, the eldest child in that landmark paper -- and thus the first-born child of the Age of Autism.
Her real name: Vivian Ann Murdock. Born in 1931, Vivian was placed in a Maryland institution at age 6 and died in a state-run home in 1987, age 56. She was the daughter of a prominent Baltimore psychiatrist, Harry M. Murdock, and his wife, Margaret.
The key to finding her real name was the recent online publication of the 1940 U.S. Census – allowing one of us (Teresa) to test her hunch about the institution to which"Virginia" had been committed as a child: The Rosewood School in Owings Mills. The hunch was correct; the Census listed an "Inmate" there named Vivian Murdock, age 8 in 1940, who we conclusively identified as "Virginia S."
In Dan and Mark's The Age of Autism – Mercury, Medicine, and a Man-made Epidemic, published in 2010, we described the seven children we'd identified to that point, and wrote of “Virginia”: “We continue to search for this eldest child of the Age of Autism and whatever clues her identity may hold.”
Now, having spoken with family members, and pored over countless records and archives, we believe her identity does offer important clues, ones remarkably consistent with the other cases in that first report -- exposure to new mercury compounds in their families.
Vivian was directly in the path of at least three mercury vectors:
-- the first use of mercury-preserved vaccines in Baltimore -- a drive to vaccinate every infant with those shots began the month she was born;
-- her parents' avocation of orchid growing and breeding, which required intensive application of chemicals including mercury;
-- and her father’s psychiatric career, which brought him – and probably his family through second-hand exposure – in contact with mercury treatments for a common form of insanity.
Mercury is no longer used in agriculture or mental health treatment. But each year, 100 million children worldwide get vaccines containing thimerosal, the ethylmercury preservative first used in those shots in Baltimore. In the United States, flu shots, most of which contain mercury, are recommended for pregnant women and for infants beginning at 6 months of age.
Our research on Vivian and the other first cases of autism suggests that is a very bad idea.
Vivian’s identity also offers insight into how the damaging idea of “refrigerator parents” – supposedly cold and neglectful mothers and fathers responsible for causing their children's disorder -- got its start. We will explain these clues and conclusions in detail, but first the basics about the discovery of Vivian Murdock.
Seventy years ago this month, in April 1943, a psychiatry journal called The Nervous Child published an article titled “Autistic Disturbances of Affective Contact.” Written by Leo Kanner, a Johns Hopkins child psychiatrist who is widely considered the founder of the field, it begins:
“SINCE 1938, there have come to our attention a number of children whose condition differs so markedly and uniquely from anything reported so far, that each case merits -- and, I hope, will eventually receive -- a detailed consideration of its fascinating peculiarities.” Elsewhere, he called it "a behavior pattern not known to me or anyone else theretofore."
The three of us have always found those words remarkable, coming as they did from an acknowledged authority who eight years earlier had catalogued every known childhood mental disability in his landmark 500-page book “Child Psychiatry.” Those pages contained not a whisper of autism, or anything that in retrospect looks similar.
Our own research convinced us the autism rate before 1930 was effectively zero (it is now 1 in 50). A handful of cases over several centuries might conceivably qualify, but there was nothing approaching the cluster of children whose worried parents brought them to see Leo Kanner in the years between 1938 and 1943.
Curious whether the family backgrounds of those first 11 cases might point to common environmental exposures, we began trying to identify them in 2005. The eight boys and three girls were described in the paper only by a first name and last initial. But because Kanner gave birth years for each child, we knew that “Virginia S.” was the oldest; her birthday was listed as September 13, 1931. Even as the number of autistic children seen by Kanner rose in later years, none appears to have been born earlier. (In a 1955 update, Kanner revisited his first 42 cases. The oldest autistic person at that point was 24 -- born in 1931 and presumably Virginia S.)
We began our hunt with Kanner’s original 1943 "Autistic Disturbances" report and a follow-up paper he wrote in 1971. (In the latter paper, he slipped once and referred to “Virginia S.” by what we now know is her real first name, Vivian.) In “Autistic Disturbances,” he quoted a psychologist noting that Virginia “could respond to sounds, the calling of her name, and the command, ‘Look!’
“She pays no attention to what is said to her,” the psychologist said, “but quickly comprehends whatever is expected. Her performance reflects discrimination, care, and precision. … She is quiet, solemn, composed. Not once have I seen her smile. She retires within herself, segregating herself from others. She seems to be in a world of her own …”
By Teresa Conrick
It's official. According to a press release, today April 22nd, Moleculera Lab's website will be live, to start sharing information about testing for Pandas/Pans. I have been writing about PANDAS and PANS for the past few years as they seem related to Autism, and for many of our children, much suffering.
From their website - What is PANDAS and PANS, and now--- CANS?:
"PANDAS is an acronym for "Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococci". PANDAS was first reported over a decade ago by Dr. Susan Swedo at the NIH, and affects children abruptly after streptococcal infections. Childhood Acute Neuropsychiatric Symptoms (CANS) and Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) are proposed as a new, broader classification that would expand both the etiological infectious agents and the clinical manifestations, to the current description of PANDAS. This is an important development since there are reported cases of patients fulfilling the clinical criteria of PANDAS but laboratory studies are negative for a recent group A streptococcal infection. Published reports have postulated that stress as well as other types of infections can result in neuropsychiatric conditions, which include Borrelia burgdorferi (Lyme disease), Mycoplasma pneumonia, herpes simplex, common cold and varicella viruses."
How will testing help PANDAS/PANS/CANS and many childen also with an AUTISM diagnosis?
"Moleculera Labs provides personalized clinical testing services for individuals suspected of suffering from PANDAS/PANS, which are treatable neurologic conditions that may be associated with motor tics, obsessive compulsive disorders (OCD) and sometimes Autism Spectrum Disorders. This perplexing neurologic condition is believed to be associated with an autoimmune response triggered by commonly occurring infections which result in a patient’s antibodies targeting neurologic receptors in the body.."
This is very good news, and I am very thankful to Dr. Cunningham and her lab. Since Megan has an Autism diagnosis, an autoimmune diagnosis, and has had symptoms of PANDAS/PANS over the years, it is significant to finally be able to connect the many children and young adults who have tics, ocd, issues with eating, food and GI pain, rashes, agitation, aggression, sleep issues, enuresis, anxiety, hallucinations, regression in behaviors, regression in academics, and the gut wrenching effect of all of this on the families. Real medical treatments are essential.
By Teresa Conrick
The damage that mercury can cause to a body, continues to grow. This recent study, Mercury Exposure in Young Adulthood and Incidence of Diabetes Later in Life: The CARDIA trace element study, shows us the insidious nature of this poisonous toxin. Mercury compounds are known for their acute effects but less has been studied on long term effects. This study did just that and the results are alarming, yet not surprising to those of us who have been sounding our own alarm about mercury's danger here, at Age of Autism.
Some caveats from the abstract:
- Laboratory studies suggest that exposure to methylmercury at a level similar to those found in fish may induce pancreatic islet β-cell dysfunction.
- We examined whether toenail mercury levels are associated with incidence of diabetes in a large prospective cohort.
- A prospective cohort of 3,875 American young adults, aged 20-32 years, free of diabetes in 1987 (baseline), were enrolled and followed six times until 2005.
- A total of 288 incident cases of diabetes occurred over 18 years of follow-up.
- ....toenail mercury levels were positively associated with the incidence of diabetes.
The full study is only available with a subscription/purchase so I was able to read that for more information. The authors do describe how mercury is a toxin with widespread effects in both the organic and inorganic form. They also commented that it is fish consumption and amalgam fillings that are the major sources of exposure. They further elaborated that the mercury in fish consumption are at levels that can induce oxidative stress. That seems very significant and they do say that is the reason for the pancreatic islet b-cell dysfunction. They actually showed in a mouse that even low levels of mercury can cause pancreatic islet b-cell dysfunction. This should be national news as the devastating health effects have been shown.
Managing Editor's Note: Teresa Conrick reports below on the confluence of brain disorders in America as a report showed that a third of our seniors have Alzheimers at time of death and another report stated that 1 in 50 American school kids has autism. That's a pretty frightening bracket of life to use a March Madness phrase. Teresa asks, yet again, are these lkife altering"A" diagnoses related?
By Teresa Conrick
One out of three seniors is now dying with Alzheimer's disease. That's a frightening fact. We've reported here, on Age of Autism, that both Alzheimer's and Autism have connections with biomarkers and treatments (see Cuckoo for Coconut Oil.)
Coincidentally, about 30-40 percent (one out of three) adults receives an influenza vaccine. Is that a coincidence or is it a clue? Since both Autism and Alzheimers are each frequently quoted as being " A MYSTERY," is there a pattern to their well kept secrets? Alarmingly, there is much evidence that mercury, and Thimerosal, the kind of mercury in most flu shots, can cause immune and autoimmune issues . Is there a connection to immune issues and Alzheimers? We know Autism has numerous connections to the immune system, with many children and young adults also receiving an autoimmune diagnosis.
“Since 1938, there have come to our attention a number of children whose condition differs so markedly and uniquely from anything reported so far that each case merits—and, I hope will eventually receive—a detailed consideration of its fascinating peculiarities...."
By now, we all know that famous introduction to the paper, by Dr. Leo Kanner, which introduced Autism to the world.
"Since the 1930s, it [Thimerosal] has been widely used as a preservative in a number of biological and drug products, including many vaccines...."
Add in these studies which show adverse outcomes of immune and autoimmune effects through exposure to mercury/thimerosal:
"Low concentrations of HgCl(2) affect immune function in human cells by dysregulation of cytokine signaling pathways, with the potential to influence diverse health outcomes such as susceptibility to infectious disease or risk of autoimmunity."
"The different forms of mercury differ in the type and range of immune disorders, and ethylmercury (thimerosal) and inorganic mercury are similar in that they cause systemic autoimmunity, characterized by a marked increase of IgE and systemic immune-complex deposits "
"This study provides further evidence that mercury exposure may lead to autoimmune dysfunction and systemic inflammation in affected populations."
"mercury compounds may cause immunosuppression or immunostimulation, autoimmune reactions, or hypersensitivity."
"Evidence is emerging that exposure to mercury (Hg) may elicit many pathological manifestations, including immunomodulation."
"Hg was shown to actively increase the reactivity of the immune system in rodents. This immunostimulation led to the development of immunotoxic problems such as allergeric responses and autoimmune disease."
"..mercury exposure has been associated with cellular autoimmunity and mercury accumulates in the thyroid gland. "
"low-level, nontoxic iHg preexposure may interact with other risk factors, genetic or acquired, to promote subsequent autoimmune disease" development.
By Teresa Conrick
My beautiful daughter, Megan, will be 20 years old on March 2nd. The real heroes are the children, and now soon to be adults of this Autism Epidemic, who live each day in the shadow of pain. Meg is one of them. I write a lot about Autism, not to complain of my struggles, but to share the hope that we are turning the corner from the days of Autism being some type of "mental mystery," to its proper position --- an immune-mediated disease, that can present as neuropsychiatric and/or neurodegenerative. The "spectrum" that so many love to describe would be, in reality, a gauge of illness, of infection, and autoimmunity, and not some psycho-babble yardstick.
A recent article in the UK, Guardian, by Kristina Chew, a mother of a son with an Autism diagnosis, caught my eye recently, and also hammered in my head and heart, that there are definitely different opinions regarding Autism. While it is fine to have and share an opinion, it is another to add in questionable facts and information. From Ms. Chew:
"Do we really need a cure for autism? I've grappled with whether it's morally or medically right to talk about 'curing' autism.......Currently there is no known biomarker for autism, and the disorder is diagnosed based on observations by teams of experts. Most scientists agree that autism is of genetic origin and begins to develop while a child is in the womb. ......Autism is a lifelong disability that cannot be cured in a medical sense."
The link she provides for "autism is of genetic origin' will take you to the CDC website, with a hodge-podge of archaic gene/chromosome bullet points, put out by the same folks who walk the walk and talk the talk of the pharmaceutical/medical industry. Close your eyes and it is 1975, and we are hearing the defense of toxic leaded gasoline and the denial of environmental injury. I am not quite sure why CDC or Ms. Chew do not report this more recent study from Stanford regarding autism and genes:
"A new Stanford University School of Medicine study of twins suggests that non-genetic factors play an unexpectedly large role in determining autism risk, turning upside down recent assumptions about the cause of this common, disabling developmental disorder......It found that genes account for 38 percent of autism risk, with environmental factors explaining the remaining 62 percent.
"It took me a bit by surprise that the heritability of autism was so much lower than previous studies calculated," said Joachim Hallmayer, MD, the first author of the new paper...
The finding that autism risk is strongly influenced by environmental factors should alert scientists to the need to study risk factors they haven't been considering, the researchers said. In recent years, autism research has been focusing more on genetics."
I think that is a better and more current analysis of where we are now concerning any genetic connections in Autism. The focus does need to be on the environment, including vaccines, something we, here at Age of Autism, have been saying since our inception.
Do we need a cure for Autism? I think that is a disturbing question, kind of like saying do we need to stop pain and suffering? Do we need to stop Alzheimer's, Parkinson's or Cancer? Why yes, we do! There are thousands of children and young adults now, who wake each day in pain. Then the issue of morally, if we really look at what that means - decent, ethical, honest, honorable vs the opposite - dishonest, evil, unethical, wicked. Well, I'll take heaps and seconds on the former, as it seems morally reprehensible that these individuals should not be able to live and function in a body that feels good.
By Teresa Conrick
There have been numerous studies over the years, attempting to show a connection from maternal flu to autism. The original studies seemed to develop from the idea that those mothers who had flu during their pregnancy went on to have babies who later developed schizophrenia:
"Pregnant women who contract the flu may increase the risk that their child will develop schizophrenia later in life, according to a recent addition to a growing body of research along these lines. The study, published in the August 2004 Archives of General Psychiatry, “is not definitive but is the strongest evidence thus far that a prenatal virus may be a risk factor [for schizophrenia],” says lead investigator Ezra Susser, head of epidemiology at Columbia University’s Mailman School of Public Health.
“Influenza infection during pregnancy appears to be a risk factor,” agrees Johns Hopkins University neurovirologist Robert Yolken, who adds it is probably one of many risk factors for developing schizophrenia..... Until more study is completed, the Mailman team still advocates that pregnant women get the flu shot. Susser says, “The very safest thing would be to get vaccinated against the flu virus before becoming pregnant.”
At the bottom of that page, we are shown a picture of a woman sneezing, with this caption next to her:
"A cold now, catastrophe later. Having the flu while pregnant may pave the way for future schizophrenia in children."
From this concept, research then on Autism having a connection to prenatal influenza was born. If you go on Pubmed and type in "Autism" and "influenza," 42 studies will pop up, the earliest in 1995, interestingly stating there is NO connection.
There were also studies showing no evidence in schizophrenia as well:
As we approach the one month anniversary, the terror and the possible future solutions to prevent mass killings, continue to keep the internet busy. I read two articles written by two different psychiatrists that I wanted to share, as each has a very different analysis of this horrible incident. Since my recent writing here on Age of Autism concerned Adam Lanza and the "P/M" factor [Psychiatry/Medication] I continue to read about this tragedy. I worked at a psychiatric hospital for 15 years, and therefore, I have a personal interest in the connection to Psychiatry.
Psychiatric Times sent out to their email subscribers, this article written by H. Steven Moffic, MD:
"Amidst all the initial speculation on the reasons for the tragedy, my wife noticed an e-mail from a psychiatrist that struck us as possibly revealing deeper issues, some perhaps indirectly relevant. The subject was “Autism not a Mental Illness.” Autism was one of the initial diagnoses associated with this killer. Beyond such premature diagnostic speculations, the e-mail was reacting to a CNN coverage in which a physician and a reporter discussed that autism may not be an illness, since NIMH was considering autism and other mental conditions as “neurogenerative.” Perhaps, the e-mailer suggested, if autism was not considered to be a mental illness, would that be better because then, if the murderer did not have a mental illness, mental illness could not be blamed for the mass murder."
"If indeed the perpetrator of the Newtown tragedy fell on the Autism spectrum, how often does a mass murderer have that diagnosis?"
"The more impersonal ways of relating on the internet may veer us more toward the social deficits and lack of empathy that is characteristic of the Autism spectrum."
"That is when I began to think more seriously of evil, as did many in the aftermath of this recent tragedy"
Soon after the tragedy, one of the fathers of a child killed tearfully pleaded for society to learn from what happened in order to prevent future mass murders. Here’s what I think psychiatry can contribute:
Here at Age of Autism, we have been sharing with our readers the realities of the increasing numbers of children being diagnosed with an Autism Spectrum Disorder. With that comes many topics, including vaccine injury and regression, school issues, adult housing and also various treatments. I have a daughter diagnosed with severe Autism and recently, an autoimmune disorder. Megan regressed in health and skills after vaccinations. With the continuing surreal killings in public settings over the years - schools, college campuses, malls and even a movie theater, the media has had a history of attempting to link some of these cases to Autism or Aspergers. You can read our recent statement Age of Autism Responds to Newtown Tragedy as this point is important: " Age of Autism mourns the deaths of all innocent victims of this awful crime and offers its deepest condolences to their families. Additionally, we are deeply disturbed by the association of the perpetrator of this awful crime by various media outlets to a vulnerable community - the autism community - with rumors that he was on the autism spectrum. Regardless of whether or not the shooter truly is on the autism spectrum, we wish to make it clear that autism spectrum disorders (ASDs) are in no way associated with criminal violence."
It is important then to look at reality and root causes because without them, it can be hard to find a solution. I would like to share some important data about these tragedies since we are all in the midst of a recent, gut-wrenching inciden,t but to do so, we have to go back in time, to look at patterns, something we think is important here on AoA.
On May 20th,1988,
Laurie Dann walked into an elementary school in Winnetka, Illinois and shot
five students, killing one. She was to kill herself later that day. I remember
vividy hearing about that as I was working at a psychiatric hospital about 15
miles away. It was a shocking reality to know that a school could become a
sitting duck to a violent mind. Here was a recent article about that horrific
day, the young boy killed, and the fact that school shootings keep increasing:
"Since then, there has been a school or campus shooting somewhere in the United States almost every year. In many years, there have been three or four campus or school shootings."
On Friday, December 14th, 2012, Adam Lanza, an unknown name to the world on December 13th, allegedly forced his way into Sandy Hook Elementary School, in Newtown Connecticut. There he allegedly shot and killed 26 victims, 20 young children and 6 female adults. He is also believed to have killed his mother before this attack and then killed himself after the attack. If you google his name today, you will see 517 million hits. A monster? What do these two cases have in common? Weapons? Murder? Yes, both were tragic crimes but also with another commonality -- the perpetrator had been treated by a psychiatrist. Another clue, is the lesser discussed use of medications that may have a bigger piece, in not only these two cases but in other savage and senseless deaths of innocent people:
School Shooters Under The Influence Of Psychiatric Drugs
"Despite 22 international drug regulatory warnings on psychiatric drugs citing effects of mania, hostility, violence and even homicidal ideation, and dozens of high profile school shootings/killings tied to psychiatric drug use, there has yet to be a federal investigation on the link between psychiatric drugs and acts of senseless violence."
"At least fourteen recent school shootings were committed by those taking or withdrawing from psychiatric drugs resulting in 109 wounded and 58 killed (in other school shootings, information about their drug use was never made public—neither confirming or refuting if they were under the influence of prescribed drugs.) The most important fact about this list, is that these are only the shooters where the information about their psychiatric drug use was made public. To give an example, although it is known that James Holmes, suspected perpetrator of a mass shooting that occurred July 20, 2012, at a movie theater in Aurora, Colorado, was seeing psychiatrist Lynne Fenton, no mention has been made of what psychiatric drugs he may have been taking. Also note that all these mass shootings didn’t just occur in the United States:
1 -- Huntsville, Alabama – February 5, 2010: 15-year-old Hammad Memon shot and killed another Discover Middle School student Todd Brown. Memon had a history for being treated for ADHD and depression. He was taking the antidepressant Zoloft and “other drugs for the conditions.” He had been seeing a psychiatrist and psychologist.
2 -- Kauhajoki, Finland – September 23, 2008: 22-year-old culinary student Matti Saari shot and killed 9 students and a teacher, and wounded another student, before killing himself. Saari was taking an SSRI and a benzodiazapine. He was also seeing a psychologist.
My daughter, Megan, regressed in her physical, mental and social health after vaccinations. Her life forever changed, I am committed to finding out both cause then cure to improve her quality of life, along with so many like her. As a result, I spend a good amount of time reading research and scientific papers to help clarify any connections. Those connections would include immune issues, autoimmunity, mercury and vaccines. Megan has both an Autism and autoimmune diagnosis. Here are some connections:
"Among patients with autism spectrum disorders (ASD) evaluated in our clinic, there appears to be a subset that can be clinically distinguished from other ASD children because of frequent infections (usually viral) accompanied by worsening behavioural symptoms and/or loss/decrease in acquired skills. This study assessed whether these clinical features of this ASD subset are associated with atopy, asthma, food allergy (FA), primary immunodeficiency (PID), or innate immune responses important in viral infections..........Clinical features of the ASD test group were not associated with atopy, asthma, FA, or PID in our study but may be associated with altered TLR responses mediating neuro-immune interactions."
The authors' conclusion, that children with regressive Autism may have altered TLR responses, seems important so I went looking to see why that would happen. You can read about Toll-like receptors here but I also found an interesting dissertation that seemed pertinent:
"Herein we show that mercury administration results in release of endogenous ligands that activate TLR7, an innate immune receptor implicated in the development of systemic autoimmunity."
Interesting but since it was a short dissertation, I needed to find out more and luckliy, I found that dissertation had become a published research study:
Bacterial, viral, and parasitic infections have been implicated in the development and exacerbation of autoimmune diseases(6) . A number of other studies have shown that exposure to chemicals (drugs or heavy metals) can also trigger or exacerbate autoimmune disease (19,20,49,50). However, the effects of infections and chemicals on autoimmune disease have for the most part been studied separately, whereas human patients are likely to be exposed to both factors. Hence, in this study, we tested the effect of a commonly dispersed chemical and an infectious agent on autoimmunity. NKT cell ligand-bearing bacteria of the Sphingomonas strain are abundant soil microbes, and have been detected in the stools of 25% of healthy individuals (51). Although contact levels vary among individuals, mercury exposure is virtually universal because of its natural release in the environment, abundance as a pollutant, and presence in dental amalgams, cosmetics, preservatives, fumigants, and vaccine preparations (7,52). As previously demonstrated, normally maintained immune tolerance is broken by exposure to mercury. Administration of both mercury and bacteria induced pronounced anti-nucleolar reactivity and exacerbated the heavy metal-induced autoimmunity.
By Teresa Conrick
I just finished Susannah Cahalan's superb book, BRAIN ON FIRE - MY MONTH OF MADNESS, chronicling her bizarre and frightening trip into, and then out of the disease, Anti-NMDA Receptor Encephalitis. I have been writing about Anti-NMDA Receptor Encephalitis for the past two years, as it seemed to me, to have connections to my daughter's Autism diagnosis. Megan had, these past years, exhibited odd seizures, strange movements with vocal tics and aggression. Testing did not show antibodies to NMDA receptors but did show antibodies to GAD65, though the two appear connected.
Susannah vividly takes us along her journey from healthy twenty-four-year-old to seizures, hallucinations and entrance into the land of psychosis, with a very possible one-way ticket, to the end of the line. With loving parents and two brilliant neurologists, Josep Dalmau, M.D. and Souhel Najjar.M.D, throwing her a lifeline, Susannah ascends from Dante's hell from the immune treatments targeted at reversing the disease. It is a read that will keep you moving from page to page voraciously as you see the monster coming and want to see how it is ultimately killed. It truly seemed like a miracle as it is a horrific disease, seemingly on the increase and some don't make it out with one hundred percent of themselves, and some don't make it out at all.
Like daffodils in the early days of spring, my neurons were resprouting receptors as the winter of the illness ebbed. Susannah Cahalan p197
I want to thank Susannah for sharing her story and making the plea that so many cases are going unnoticed -- "How many children throughout history have been exorcised and then left to die when they did not improve? How many people are currently in psychiatric wards and nursing homes denied the relatively simple cure of steroids and immune therapy treatments that brought me back from the brink?"
She also brings up Autism and autoimmunity:
Two particular fields of study, schizophrenia and autism, will likely gain the most from this landscaping of the elephant. Dr. Balice-Gordon [Dr. Dalmau's colleague] believes that a percentage, albeit a small one, of those diagnosed with autism and schizophrenia might in fact have an autoimmune disease. Many children ultimately diagnosed with anti-NMDA autoimmune encephalitis were first determined to be autistic. How many children originally first diagnosed with autism weren't able to find their autoimmune diagnosis? p 224
My daughter, Megan, may be one of those children and I know that she is not alone. Some common denominators that I have written about regarding Autism seem to have a possible connection to Susannah's story --- infections, hormones and cancer, with a specific focus on Melanoma. I have discussed Melanoma as some families seem to have a vulnerability to both Autism and Melanoma and how that may be, as they related to glutamate signalling. Owning a cat, something Susannah also did, seems to put people at a higher risk for schizophrenia due to infection with Toxoplasma gondii, a parasite. Susannah had a history of Melanoma, had recently been on hormones via birth control and there was the possibility of a bug bite [bedbug], too, all clues into causation. Hormones seemed to be a trigger for Megan' s symptoms, as well. Susannah, in her book, further describes the changing landscape of autoimmune diagnoses:
Dr. Najjar, for one, is taking the link between autoimmune diseases and mental illnesses one step further through his cutting-edge research, he posits that some forms of schizophrenia, bipolar disorder, obsessive-compulsive disorder, and depression are actually caused by inflammatory conditions in the brain.
By Teresa Conrick
It is not new news that beta amyloid, a protein heavily studied in Alzheimer's disease has also been showing up in Autism:
2006 - High levels of Alzheimer beta-amyloid precursor protein (APP) in children with severely autistic behavior and aggression.
2011 - "The Weigel lab also reported observing secretions of protein called beta-amyloid in brain tissue of children with autism. Interestingly, the level of beta-amyloid related to the severity of autism and aggression".
2011 - Increased Secreted Amyloid Precursor Protein-α (sAPPα) in Severe Autism: Proposal of a Specific, Anabolic Pathway and Putative Biomarker
2011 - Accumulation of Amyloid-Beta Peptide Species In Four Brain Structures In Children with Autism - International Society For Autism Research
What is becoming more evident is that the roots of amyloid beta may be attached to the immune system - literally.
ScienceDaily (Jan. 4, 2012)- Autism May Be Linked to Abnormal Immune System Characteristics and Novel Protein Fragment
"Immune system abnormalities that mimic those seen with autism spectrum disorders have been linked to the amyloid precursor protein (APP)......The amyloid precursor protein is typically the focus of research related to Alzheimer's disease. However, recent scientific reports have identified elevated levels of the particular protein fragment, called, sAPP-α, in the blood of autistic children."
What made this something even on my radar was that I recently wrote about vaccine injuries from the H1N1 vaccine leading to Narcolepsy. I included a study that had this fact - "Beta -amyloid is not only of relevance in dementia processes but is also reported to modulate the response to environmental stressors in the brain, and is supposed to have antimicrobrial properties against different classes of microorganism, including some strains of streptococci." Since we like to connect the accurate dots here at Age of Autism, it seemed relevant that those two factors, beta amyloid and antimicrobrial poperties, may be important.
Consider these important findings in Alzheimer's research as they may then have a significant correlation for children who regress into Autism:
23 March 2010 - Microbes implicated in Alzheimer's
By Teresa Conrick
In 2011, I wrote about how drug makers were thrilled about the money expectations in treating glutamate receptor issues and Autism. Ironically, another new study will be again showing that glutamate receptors [ mGluR1] are not working properly in those who have an Autism diagnosis. This from The Wall Street Journal:
"ZURICH—Changes in the brain caused by autism can be reversed in mice, a new preclinical study showed, opening a potential path to develop a treatment for the incurable disorder.
Roche Holding AG,ROG VX +17% a Swiss drug maker, and the University of Basel's Biozentrum said Friday the study identified a way to reverse a dysfunction in the brain's wiring typically caused by the disorder, which stumps intellectual development and can cause aggressive and anti-social behavior, and becomes evident in early childhood.
The study results will be published in the Oct. 5 issue of Science.
Researchers found that reactivating a gene involved in the formation of synapses, or junctions between nerve cells, can scale down the excessive production of a receptor called mGluR1. In some autistic people this gene is not working. Controlling production of the receptor ultimately makes structural defects in the brain--which are typical of autism—disappear."
Yet we are not told WHY there are changes in the brain. Instead we are whisked off into the land of genes and structural defects. Here's another, from the NYT, heralding the big release of this study AND the money:Competitors Form Partnership to Develop Autism Drugs
"Two of the front-runners in the race to develop drugs to treat mental retardation [WOW - guess Mr. Pollack missed this back in 2010 ] and autism are joining forces, hoping to save money and get to the market sooner......“This deal will establish the biggest effort to date” in autism drugs, Luca Santarelli, head of neuroscience for Roche, said before the announcement. Financial terms are not being disclosed."
...The mechanism that has perhaps shown the most promise, at least in mice, is to damp signaling in the brain by blocking a receptor called mGluR5. [Note that the WSJ said mGluR1]
Roche will provide money to help Seaside complete its clinical trials of arbaclofen. Seaside will halt development of its own mGluR5 antagonist, which it licensed from Merck, and will instead receive royalties on sales of Roche’s drug.
The alliance could pose a challenge to Novartis. “This is No. 2 and No. 3 ganging up on No. 1,” said Dr. Michael Tranfaglia, medical director of the Fraxa Research Foundation, which sponsors research into treatments for fragile X syndrome.
Dr. Randall L. Carpenter, chief executive of Seaside, said the money from Roche was a needed diversification of the company’s funding. Virtually all of the $90 million Seaside has raised has come from the Barony Trust, which is run by Peter Whipp, a British investment manager."
The picture that is emerging is that there is going to be
loads of money - a BONANZA - in treating all of these symptoms! And it's
all GENES! Well, not really though you would not know that from all of
these articles. Autism is a HUGE money ticket for drug development but
the reality is that much of the mechanism of action from many drugs always takes
us back to the scene of the autism epidemic.
I have posted before about certain drugs targeting Autism symptoms and how each also targets MERCURY toxicity and damage:
Namenda (Memantine HCL)
N-acetyl cysteine (NAC) [This is an OTC antioxidant supplement that some companies are hoping to "investigate" for Autism. ]
By Teresa Conrick
Is Autism an autoimmune disease? I think for many it evolves into a disease of the immune system so that may swing that answer to a "yes." I know for my daughter who has an Autism diagnosis, she has tested positive for autoimmunity so the topic of immune functioning is important to me and also many other parents of children with an Autism and/or PANDAS [Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus] diagnosis. Many of us saw both our children's health and behaviors change after vaccination.
Knowing that, it is particularly interesting that in 2010, there was a growing number of vaccine injuries that produced an autoimmune diagnosis, a frightening one -- Narcolepsy and Cataplexy.
The vaccine implicated was the H1N1 flu shot. Here is a group of related research and letters associated with this phenomenon that seems to be related:
Letter to the Editor—Dauvilliers et al, Post-H1N1 Narcolepsy-Cataplexy, SLEEP, Vol. 33, No. 11, 2010
"..The cause of narcolepsy is likely autoimmune based...As for most autoimmune diseases, twin pairs are most often discordant (65% to 80%), and environmental triggers are suspected to play a critical role.1 Most notably, two recent reports have found an association with past streptococcus infections,7,8 leading to the speculation that upper airway infections could be involved in many cases as a cofactor....."
"....In three major centers of reference for narcolepsy—Montpellier, France; Montreal, Canada; and Stanford University, United States—we noticed in the first months of 2010 an unusual increase in abrupt onset narcolepsy-cataplexy diagnosed within a few months of H1N1 onset....Of the 31 cases, 14 post-vaccination cases were identified....The post streptococcal marker ASO was positive in 11 cases
"...Of the 14 post-vaccination cases, 11 cases followed adjuvanated vaccination, while 3 were vaccinated without adjuvant. Delay between vaccination and cataplexy onset in these cases ranged from 2 days (strong local response followed by a generalized reaction following vaccination)to 5 months, although in 9 of the 14 post-vaccination cases the onset occurred 2-8 weeks following vaccination. As the delay between onset and diagnosis is often long,1,13 more cases are likely to be identified in the future."
"How could H1N1 vaccination or infection trigger narcolepsy?.....a specific immune response to H1N1 (and possibly subsequent molecular mimicry) or generalized stimulation of the immune system.....most cases followed vaccination with ASO3. This vaccine has been reported
to be associated with side effects suggestive of stronger immune stimulation.14 In the United States, where vaccination did not contain the ASO3 adjuvant, only 2 post-vaccination cases were documented......Nevertheless, these correlative findings indicate an urgent need for further examination of a possible link..."
By Teresa Conrick
A few months back, I wrote about a calcium-binding protein, S100B, as it had been implicated as a possible biomarker in Autism -- "Autistic children had significantly higher serum S100B protein levels than healthy controls." From that article -- S100B is a calcium-binding protein that is produced primarily by astrocytes. Increased serum S100B protein levels reflect neurological damage.
In my reading and researching, I came upon this sentence- "an increase of serotonin levels by fluoxetine [PROZAC] administration increased S100B concentrations....." which made me wonder if it could be possible that S100B might be a player in research showing that SSRI use in pregnancy might cause Autism. This is not fact -- it is a hypothesis but let's take a look at some points.
July 2011 Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders
."...we found a 2-fold increased risk of ASD associated with treatment with selective serotonin reuptake inhibitors by the mother during the year before delivery.. with the strongest effect associated with treatment during the first trimester ..No increase in risk was found for mothers with a history of mental health treatment in the absence of prenatal exposure to selective serotonin reuptake inhibitors.........no association was seen for the small group of women who were prescribed a non-SSRI antidepressant only.......we found no association between ASD and a history of depression or a history of any mental health disorder..."
The underlining is from me, as emphasis, so you can see a contradiction presented on some sites. First from an Autism Speaks Blog:
"In fact, it’s not clear whether the autism risk associated with taking antidepressants during pregnancy is, in fact, related to the women’s depression rather than the drugs themselves."
I think it's important to emphasize that the writer of this Autism Speaks blog is appearing to state a fact -- that is just not true. She was not the only one. Here from an FDA site:
"This study does not prove that exposure to an antidepressant can cause autism. It is possible that depression, not the medicine, was related to autism risk." Are we seeing a pattern here where blame is being placed on the mother rather than the pharmaceutical product?
Now I think the authors of the SSRI study were clear:
- No association was seen for the small group of women who were prescribed a non-SSRI antidepressant only.
- No association between ASD and a history of depression or a history of any mental health disorder
So it seems that the use of an SSRI [ Fluoxetine hydrochloride -Prozac, Paroxetine hydrochloride -Paxil,
Sertraline hydrochloride - Zoloft and Fluvoxamine maleate - Luvox ] during pregnancy might influence an Autism diagnosis -- but how?
When I read that Prozac, not unlike Risperdal, could cause an increase in S100B, I wondered if SSRI use and S100B could be involved. Let's be clear that this is a small piece to the autism numbers, as the authors state: "The fraction of cases of ASD that may be attributed to use of antidepressants by the mother during pregnancy is less than 3% in our population, and it is reasonable to conclude that prenatal SSRI exposure is very unlikely to be a major risk factor for ASD. Although these findings indicate that maternal treatment with SSRIs during pregnancy may confer some risk to the fetus with regard to neurodevelopment, this potential risk must be balanced with the risk to the mother or fetus of untreated mental health disorders. We recommend that our findings be considered as preliminary and treated with caution, pending results from further studies...."
Here are some connecting dots that I would like to add:
- ....overexpression of S100B has been shown to accelerate Alzheimer disease-like pathology with enhanced astrogliosis and microgliosis (12). Because of these observations, the concept has emerged that S100B, when present in the brain extracellular milieu in relatively high amounts, might act as an unconventional cytokine and/or a damage-associated molecular pattern molecule playing a role in the pathophysiology of neurodegenerative disorders and inflammatory brain diseases..
By Teresa Conrick
It was last year that I reported on Anti-NMDA-Receptor Encephalitis and a connection to Autism. My daughter had some prominent symptoms and I was looking into the dynamics of this increasing medical condition. Meg tested negative and subsequent labs showed that her positive antinuclear antibodies [autoimmunity] to be associated with Gad65 [ glutamic acid decarboxylase (GAD) is an enzyme that catalyzes the decarboxylation of glutamate to GABA and CO2.] It is no coincidence that Megan's symptoms seemed to mirror some of those in Anti-NMDA-Receptor Encephalitis as the two, GAD65 and N-methyl-D-aspartate receptor, are connected.
Below is a study now showing that Anti-NMDA-Receptor Encephalitis has been added into the current Diagnostic and Statistical Manual of Mental Disorders as a true, medical causation to an Autism diagnosis. In other words, an antibody causing autoimmunity can cause regression of behaviors and skills, and then appear to present as a primary psychiatric disorder . Immediate and proper medical care must be given to prevent further damage and permanent disability -- "Patients with early immunotherapy performed significantly better. The most severe deficits were observed with inefficient or delayed initial treatment. " --
Researchers must not be afraid to admit that vaccinations can cause this increasing and horrific medical phenomenon:
Anti-NMDA receptor encephalitis after TdaP-IPV booster vaccination: cause or coincidence?
Researchers must not deny its connection to other childhood immune disorders with cute names:
"In about 50% of the patients Mycoplasma pneumonia serum IgM is positive. Although the significance of this is unknown, infections may trigger an autoimmune encephalitic process akin to PANDAS (pediatric autoimmune neuropsychiatric illness associated with streptococcal infections) mediated by antistreptococcal-antineuronal antibodies."
Researchers must not avoid the Anti-N-methyl-D-aspartate receptor encephalitis connection to research involved in Autism and autoimmunity:
"NR1 and NR2b glutamate receptor immunoreactivity patterns are abnormal in the hippocampi of thimerosal treated SJL mice."
Tijdschr Psychiaty 2012;54(5):475-9.
[Anti-NMDA-receptor encephalitis: a new axis-III disorder in the differential diagnosis of childhood disintegrative disorder, early onset schizophrenia and late onset autism].
[Article in Dutch]
Psychiatrie & Psychologie, Masstricht.
Childhood disintegrative disorder (CDD), early onset schizophrenia (EOS), and late onset autism (LOA) often follow a similar course: initially, development is normal, then there is a sudden neuropsychiatric deterioration of social interaction and communication skills, which is combined with a decline in intelligence and reduction in daily activities. A 9-year-old boy was admitted to the paediatric ward with acute onset of secondary epileptic seizures. It was not long until the boy's symptoms resembled that of patients with cdd, eos and loa. Intensive tests led to the diagnosis of anti-NMDA-receptor encephalitis. Anti-NMDA-receptor encephalitis should be regarded as a possible organic cause underlying the syndromal presentation of CDD, EOS and LOA.
Teresa Conrick is Contributing Editor for Age of Autism.
By Teresa Conrick
There is no escaping the ever increasing research coming out weekly, showing solid science connections behind environmental and vaccine injury causing autism. One only has to read the news and research churning out inconvenient truths in science. Here are some recent examples that are reminders that those who continue to try and deny and dismiss damage to the human body are starting to lose the battle.
This first example originated two years age and is again hitting the news as there is such heated controversy. We'll call this inconvenient truth - blaming the scientist:
December 2, 2010 - Strange Discovery: Bacteria Built with Arsenic
"Menlo Park, Calif. – In a study that could rewrite biology textbooks, scientists have found the first known living organism that incorporates arsenic into the working parts of its cells. What's more, the arsenic replaces phosphorus, an element long thought essential for life. The results, based on experiments at the Stanford Synchrotron Radiation Lightsource, were published online today in Science Express........"It seems that this particular strain of bacteria has actually evolved in a way that it can use arsenic instead of phosphorus to grow and produce life," said SSRL Staff Scientist Sam Webb, who led the research at the Department of Energy's SLAC National Accelerator Laboratory. "Given that arsenic is usually toxic, this finding is particularly surprising."
Surprising as finding measles virus, chronic streptococcus and heavy metals in those diagnosed with Autism. For two years there has been a host of scientists, bloggers and institutions foaming at the mouth to stop this arsenic-bacteria research, yet the initial researcher and her collaborator will not yell "uncle" (good for them!) -- "Her collaborator, Ronald S. Oremland from the U.S. Geological Survey in Menlo Park, California, is glad to see the genome available and, with Wolfe-Simon, still stands behind the 18 words spoken 1 year ago. --- "Our data show evidence for arsenate in macromolecules that normally contain phosphate, most notably nucleic acids and proteins." We have our own heroic researchers and doctors that stand behind their studies, with all of us standing right along side.
Next item is a more recent study that also has hit the news creating quite a furor. This one, we'll call blaming the patient:
"Women infected with the cat parasite Toxoplasma gondii are more likely to attempt suicide than non-infected women, new research finds. The reason for this connection, however, remains mysterious. T. gondii is a protozoa that prefers to infect cats, but can make its home in any warm-blooded animal. Humans can pick up the parasite from contact with cat feces, or by eating undercooked meat or unwashed vegetables. Once ingested, T. gondii can make a home for itself inside the brain and muscle tissues, protected inside cysts that are resistant to attacks by the host's immune system.Some studies have linked infection by this parasite with a variety of mental health and brain problems, including schizophrenia, neurosis and brain cancer.....But in women with infections, they found, the risk of an attempt is 1.5 times greater than in women without.
"We can't say with certainty that T. gondii caused the women to try to kill themselves, but we did find a predictive association between the infection and suicide attempts later in life that warrants additional studies," lead researcher Teodor Postolache, a psychiatrist at the University of Maryland School of Medicine, said in a statement. "We plan to continue our research into this possible connection."
Good for them! More research is reasonable to help these poor people receive proper medical treatments as most have never received anything but psychotropic drugs when indeed, an infection appeared to be causing the behavior.
By Teresa Conrick
On May 31st, it was discovered that the federally funded Harvard Brain Tissue Resource had a problem. A freezer containing one-third of the brains of those who had an autism diagnosis was thawed. Fifty-four brains were now decomposing yet how this happened remains a mystery. Dr. Martha Herbert, MD, PhD, assistant professor of neurology at Harvard Medical School and a pediatric neurologist at Massachusetts General Hospital has also done brain research using brains of those diagnosed with autism. Dr. Herbert was contacted and reported back to us that this was not her lab.
We are reading all over the internet: "The freezer failure came despite two alarm systems that are designed to alert security and staff should there be a malfunction. Both alarm systems are connected to separate circuits, and the room containing the freezer is monitored around the clock, the hospital said. Twice a day temperature gauges on each freezer are inspected. Each freezer was reading normally, at minus 79 degrees centigrade. It was only when the door was opened that it became evident that the freezer had malfunctioned. Freezer failures are not uncommon in research, but for a freezer and two alarm systems to fail simultaneously is perplexing."
Yes, perplexing and heartbreaking as also in May and also recently in the news, a very young boy with an Autism diagnosis tragically died. We learned that Alexi LePoer, like so many children with an autism diagnosis, snuck out of his home and was later found at the bottom of a nearby pool. It happens over and over, the siren call of the lake, pool, pond to the young child and then the last breath of life. It is a nightmare that is increasing right along with the epidemic numbers of children being diagnosed with Autism. The LePoer family described their feelings and thoughts regarding their tragic loss. These wonderful and generous parents decided that donating their son's organs could help others, especially his brain. Alexi was severely impaired and had just started to use a few words and his regression into an Autism diagnosis is all too familiar:
"Like many children later diagnosed with autism, Alexei hit normal developmental benchmarks at first, making his later descent that much harder on the couple. There was no family history of neurological disorders, and the couple thought they were doing everything right.
By Teresa Conrick
Mainstream medicine seems to be toying around with the idea of "borrowing" scientifically sound interventions from the DAN (Defeat Autism Now) movement and other alternative doctors who treat autism. This recent article, Antioxidant shows promise as treatment for certain features of autism, study finds , is an irony on many levels. Some highlights, that we will call -- IRONY #1:
- A specific antioxidant supplement may be an effective therapy for some features of autism, according to a pilot trial
- The antioxidant, called N-Acetylcysteine, or NAC, lowered irritability in children with autism as well as reducing the children’s repetitive behaviors.
- Stanford is filing a patent for the use of NAC in autism, and one of the study authors has a financial stake in a company that makes and sells the NAC used in the trial.
- “One of the reasons I wanted to do this trial was that NAC is being used by community practitioners who focus on alternative, non-traditional therapies,” Hardan said. “But there is no strong scientific evidence to support these interventions
Interesting ..."no strong scientific evidence to support" seems hardly correct. Investigating NAC years ago, I discovered its use in Autism was most probably related to its use as a chelator of toxic metals.
There are 81 studies listed on Pubmed that deal strictly with N-acetyl cysteine and mercury. Here are some good examples:
- N-acetylcysteine as an antidote in methylmercury poisoning
" The present study demonstrates that oral administration of N-acetylcysteine (NAC), a widely available and largely nontoxic amino acid derivative, produces a profound acceleration of urinary methylmercury excretion in mice.....The ability of NAC to enhance methylmercury excretion when given orally, its relatively low toxicity, and is wide availability in the clinical setting indicate that it may be an ideal therapeutic agent for use in methylmercury poisoning."
- N-acetyl cysteine treatment reduces mercury-induced neurotoxicity in the developing rat hippocampus.
"Mercury is an environmental toxicant that can disrupt brain development....Here, based on its known efficacy in promoting MeHg urinary excretion, we evaluated NAC for protective effects in the developing brain. In immature neurons and precursors, MeHg (3 μM) induced a >50% decrease in DNA synthesis at 24 hr, an effect that was completely blocked by NAC coincubation.....Treatment of MeHg-exposed rats with repeated injections of NAC abolished MeHg toxicity. NAC prevented the reduction in DNA synthesis and the marked increase in caspase-3 immunoreactivity. Moreover, the intermediate-term decrease in hippocampal cell number provoked by MeHg was fully blocked by NAC. Altogether these results suggest that MeHg toxicity in the perinatal brain can be ameliorated by using NAC, opening potential avenues for therapeutic intervention."
- Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors
"Thimerosal alone induced approximately 3-fold decrease in cell viability whereas pretreatment with either cystine, glutathione,
or NAC provided significant protection from cell death....It is likely that the extracellular NAC and glutathione provided partial protection by complexing with the Thimerosal in the culture medium as well as by increasing intracellular glutathione levels....The significant protection by NAC and glutathione ethyl ester against Thimerosal cytotoxicity suggests the possibility that supplementation with glutathione precursors might be protective against mercury exposures in vivo. Numerous clinical studies have demonstrated the efficacy of NAC in increasing intracellular glutathione levels and reducing oxidative stress in humans."
By Teresa Conrick
Autism One is always a superb menu of speakers and presentations and this year was no exception. Listening to Dr. Luc Montagnier, co-discoverer of the Human Immunodeficiency Virus (HIV) and the 2008 Nobel laureate for Medicine, was fascinating and hopeful as he stressed how Autism has its roots in INFECTIONS, where bacteria, viruses and heavy metals cause the symptoms and behaviors. For many of us, that is not new information but hearing such a famous and brilliant doctor present data on ill children getting much better and some recovering health and lost skills, was simply amazing. Equally riveting and monumentally important, was hearing Dr. Andrew Wakefield present evidence of GI inflammation/disease and the devastation they produce for so many with an Autism diagnosis. This video, showed how dramatic and miraculous HEALING is when pain can be stopped and learning and functioning can then begin to advance. Dr. Wakefield quoted from his most recent book, this clear association that so many of us know from having ill children with gut pain and the connecting behaviors that manifest -- ....."the bowel bone's connected to the brain bone" .... a fact that most mainstream doctors have not yet fully acknowledged.
As fate would have it, I was to meet another inspiring and heroic man, this one was only seventeen-years-old, yet his mission and message equaled the two I have just described. While I was waiting to talk to a presenter, I watched this young man make his way over to a space near me, talking to a nearby mother, I heard his words - "I am recovering myself from Autism." I looked quickly as he smiled at me and I reached out to shake his hand, while I tried to hide my tears. "How", I asked him, "are you doing this on your own?" He began to tell me his name, "Nicholas Glenski", and that he and his Dad were up from Springfield, MO. (That's he in the photo with AofA's Jake Crosby.) I was so impressed that I asked if we could talk together, maybe I could ask him some questions for a blog about Autism? He smiled again and was very happy to oblige. Saying he was freezing in the air conditioning, with his dad's permission, we sat outside on a strip of warm, narrow grass, with the sun blazing above.
It seemed I was destined to meet this wonderful young man, as he reinforced what so many of us know -- that Autism for many means a sick body accompanied by symptoms and behaviors that wreak havoc for that person. He wanted help and healing from his Autism.
By Teresa Conrick
On Friday, May 25, I will be one of hundreds at The Autism One Conference, who will be listening to Nobel Laureate, Luc Montagnier, M.D., describe how bacteria can be involved in Autism:
"This correlation, which is based on more than one hundred children of European origin, naturally does not prove a causal relationship. However, a therapy first started by a group of independent clinicians and now performed in conjunction with laboratory observations reinforces the idea that systemic bacterial infections play a role in the genesis of symptoms of autism. Our GPs have observed that a long-term therapy consisting of successive antibiotic treatments with accompanying medications induced in 60% of cases a significant improvement -- sometimes even a complete resolution of symptoms. These children can now lead a normal school and family life."
Needless to say, I am very excited to hear his talk and also find out about treatments aimed at helping so many sick children. My daughter is one of them which is why I keep writing about Meg's long history of infections and her recent autoimmune diagnosis. So in keeping with that theme of infections leading to immune dysfunction and autoimmunity, I wanted to share some of what I have found as I continuously search both past and present for clues.
In 1999, as I was seeing my daughter's autism symptoms become more pronounced at age 6, The New England Journal of Medicine came out with an article entitled, "MOLECULAR MIMICRY AND AUTOIMMUNITY". Of course, I never saw it until recently because back in 1999, I had no idea that Megan's Autism diagnosis could be related to her ear infections, Strep and sinus infections, and the many unnamed viral illnesses that were relentless to her body. I would never have predicted that now, at age nineteen, she would have tested positive for an autoimmune diagnosis, so seeing this article made me wonder how was it possible that research and reports on autism since 1999 did not emphasize the IMMUNE SYSTEM? Instead we are bombarded with expensive genetic studies showing little connections to the REAL issues of Autism.
Here then is an excerpt from that 1999 NEJM study showing us a haunting connection to Autism today:
"AUTOIMMUNE disease is the consequence of an immune response against self-antigens that results in the damage and eventual dysfunction of target organs. Although the triggering event in most autoimmune diseases is unknown, an infectious cause has long been postulated to explain the development of autoimmunity. Molecular mimicry is one mechanism by which infectious agents (or other exogenous substances) may trigger an immune response against autoantigens." That would be where my daughter is now. So when I saw this next paragraph, I then realized WHY the issue of the immune system, infections and autism might be minimized and even denied:
With Autism numbers climbing, there are those who look to the profit margin of knowing thousands of children, teens and young adults may need medications to "target behavior." It is unfortunate and incorrect that Autism is still being looked at as a behavioral and developmental disability for many instead of a neuroimmune disease that manifests in repetitive behaviors, anxiety and verbal/social regression. For many, like my daughter, that regression came about after vaccinations. These children tend to be very vulnerable canaries to toxins, thus medications can prove to be problematic for many. It is important to know the mechanism of action in treating symptoms short term, but especially long term as some of these drugs have severe side effects that increase with dosage as well as duration.
Recently, I wrote about a new study showing that over a third of children with an autism diagnosis had high levels of S100B in their blood, a calcium-binding protein that is produced primarily by astrocytes and is indicative of active brain injury. While reading about S100B, I started to realize that some abstracts and research about Risperdal and other anti-psychotic medications were appearing that seemed to show a pattern.
(Note: below is a public video from a parent unrelated to AofA showing her son's Risperdal-related side effect. Her message attached to the video reads, This is my son Nathan he is 13yrs old and started with the neck twitching about 3 months ago. He has been on Risperdal (risperdone) for about 8 years now. I have seen his doctors on a regular basis to discuss the side effects and to see what we can do about weening him off. However he did not say this was Tardive Dyskinasia, he gave me another medication to help with this side effect, but I am not going to keep giving my son medication to solve the problem of a drug side effect. I am trying to get answers, he is scheduled for a Neurologist appt in July and in the mean time we are currently at .05 mg risperdone, he was taking 3 mg before then dropped down to 2, then 1 and now 0.5. I am so confused everything I have looked up on Tardive Dyskinasia shows me that this is what my son has. Nathan is autistic and his doctor recently prescribed us Congentin to help with the neck twitching, but what I have read on Congentin says this is not for patients with Tardive Dyskinesia, its so confusing. All i know is that his twitching gets really bad to where he is so sore from his neck and his doctor also reccomended us taking Benadryl has anyone ever heard of that..???)
Some Facts About the S100B Autism Study
- High S100B levels offer an indicator of cell damage when standard diagnostic procedures are still silent.
- Increased serum S100B protein levels reflect neurological damage.
- Elevated S100B protein may be indicative of active cell injury and can reflect an axonal and glial pathology.
- Serum and cerebrospinal fluid (CSF) levels of S100B protein levels are raised in some autoimmune neuropsychiatric disorders, reflecting the presence of glial cell pathology and continuing neurological damage.
- S100B protein levels were elevated in autistic children, and they were significantly correlated with the degree of the severity of autism
- patients with associated allergic, inflammatory or autoimmune disorders; and patients who were receiving any medications -- were excluded.
I thought it would be helpful to set this up with an "abstract" that is based on studies connecting these dots. Their is a longer version also for any who want to read the corresponding studies:
In a recent NIMH Director's Blog, Dr. Thomas Insel gave yet another update on PANDAS and PANS. Both of those are names describing two similar medical conditions that can evolve from either Streptococcus bacteria for the former, and for the latter- Lyme bacteria, Epstein Barr Virus, or Mycoplasma bacteria , plus "cause unspecified." We have been hearing a lot about these two increasing neuropsychiatric disorders but what really caught my eye was the title and comparisons being made by Dr. Insel. His chosen title for the blog, "From Paresis to PANDAS & PANS" is an ironic twist on what we, here on Age of Autism, have been talking about for years -- the evolution of disorders, especially those with neuropsychiatric features and how mercury has been a big player.
I think it's important to take a clear look at what that means by going back in time with the knowledge that we have today. In 2010, Dan Olmsted and Mark Blaxill's book, "The Age of Autism: Mercury, Medicine, and a Man-Made Epidemic" described in great detail how General Paralysis Of The Insane, Paresis, as Dr. Insel called it, was a devastating and deadly disease. This Paresis, or GPI, was a disease that was directly connected to Syphilis, a truly horrible, sexually-transmitted bacterium that could be dormant for years and then reveal itself in sinister ways.:
For centuries, mercury use was widespread in medicine, and the consequences were disastrous. The greatest plague of Europe and America, spanning five hundred years, was syphilis, and the standard of care (the generally accepted medical treatment of the time) before penicillin was mercury. Our investigation has led us to believe that a man-made mercury compound, interacting with syphilis itself, caused the horrendous affliction called general paralysis of the insane. This illness, also called GPI, is a classic instance of the synergistic dangers of metals, microbes, and man. - p.2,
"The Age of Autism: Mercury, Medicine, and a Man-Made Epidemic" -
Throughout their book, we see examples of this relationship between mercury and microbes right up to our present day, Age of Autism. In reading Dr. Insel's opening paragraph below, from his blog, it should remind us all that it is possible that PANDAS and PANS could too, then have their roots in man-made hands. Knowing that, it will be a kick in the stomach for these sick children if the new DSM-5 tries to embrace their immune-mediated illnesses into its pages of Obsessive Compulsive Disorder. These disorders that often present with neurological and psychiatric features may have immune and autoimmune roots and we know that bacteria and viruses can be triggers, but so can poisons and toxins, like mercury:
General paresis was a form of psychosis with delusions, hallucinations, and memory problems often of rapid onset and thought to be due to a general constitutional weakness. At least that was the explanation until 1913, when general paresis was shown to be caused by syphilitic infection of the brain. The first treatments were awarded a Nobel Prize in 1917. The advent of antibiotics 30 years later led to the virtual eradication of neuro-syphilis, as the disorder came to be called, in this country. The idea that mental or behavioral disorders could be due to infection is, therefore, not new but it remains surprisingly difficult to accept....We may be looking at a similar reluctance to accept an infectious cause of pediatric sudden onset obsessive compulsive disorder (OCD) – in a debate that has been ongoing for almost two decades... The onset has not always been linked precisely with a strep infection and the critical increase in antibodies to strep has not been evident consistently. Nevertheless, immune-based treatments have proven successful, leading to the growing acceptance of the concept of Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus (PANDAS).
A recent study just came out that seemed important. It showed that some children [thirty-six percent] with an Autism diagnosis had significantly higher serum S100B protein levels than healthy controls and that those with severe autism had significantly higher serum S100B protein than children with mild to moderate autism. The study was looking at levels to determine autoimmunity in Autism and since my daughter has both severe symptoms of Autism and has been positive for autoimmunity on the antinuclear antibodies test, this study seemed very relevant. Though 36% does not seem like a huge number, there may be factors involved lowering it. It seemed reasonable to explore this more as to why this would be. More data can be obtained too too, it appears-- "Elevated S100B levels in biological fluids (CSF, blood, urine, saliva, amniotic fluid) are thus regarded as a biomarker of pathological conditions, including perinatal brain distress, acute brain injury, brain tumors, neuroinflammatory/neurodegenerative disorders, psychiatric disorders. In the majority of these conditions, high S100B levels offer an indicator of cell damage when standard diagnostic procedures are still silent."
This S100B, according to the Autism study, "...is a calcium-binding protein that is produced primarily by astrocytes. Increased serum S100B protein levels reflect neurological damage. Autoimmunity may have a role in the pathogenesis of autism in some patients. Autoantibodies may cross the blood–brain barrier and combine with brain tissue antigens, forming immune complexes and resulting in neurological damage......"Furthermore, S100B protein may act as a cytokine [46,50,51], and in vitro studies have shown that, at high levels, S100B protein can induce the neuronal expression and secretion of proinflammatory IL-6. Elevated levels of S100B have been detected in the CSF of MS patients during acute phases or exacerbations of the disease , and it has therefore been proposed that elevated S100B protein may be indicative of active cell injury  and can reflect an axonal and glial pathology."
By Theresa Conrick
Read LeRoy, PANDAS, Autism and EL - Will the real "Mystery Illness" Please Stand Up?- Part 1
So it is possible that medical mysteries may have some common features. A few years ago, The Today Show had a beautiful young girl on who had become famous for an odd and scary reason. She was sneezing thousands of times a day: Nov 11, 2009.
"It began, Lynn Johnson said, when both Lauren and her 10-year-old sister came down with colds in mid-October. The colds ran their course in two weeks and included the expected sneezing — big, nasal, productive sneezes.
“After she had the cold, she seemed to be feeling better for a day,” Johnson said, so she let Lauren go to a friend’s house for a sleepover. She returned home on Nov. 1 — and life suddenly went into gesundheit mode.“She came back from having the sleepover; it became a rhythmic, nonstop, chronic sneeze...
A tic, not a sneeze?
Johnson said that after trying 11 different drugs to no effect, doctors suggested Lauren might have something called “intractable psychogenic sneeze” — a little-understood syndrome that has been identified in only about 40 other people around the world....Snyderman offered her opinion. “If you peel back the layers of the onion and watch Lauren, she’s sneezing through her mouth — not a real, productive, nasal sneeze — which raises the question that perhaps this is more like a tic,” Snyderman said. “You have things like Tourette syndrome. There are things like Munchausen syndrome, where people sort of make things up to gain attention.”
Anyone else wondering if “intractable psychogenic sneeze” is some sort of a Conversion Disorder of the sinuses? Like the LeRoy teen girls, the hysteria diagnosis can affect all different body parts. It is a convenient denial of illnesses that seem to be increasing.
"Snyderman continued: “It’s not that she has chosen not to stop — she can’t,” Snyderman said. “It’s an involuntary tic that has taken over her life. It does bring up the psychological aspect of how you get to that....Snyderman emphasized that Lauren’s sneezes are not caused by a pathogen and are not contagious."
Lynn Johnson shared that Dr. Snydernan later apologized to them after this show. She said that she had made a grave mistake in inferring that there was any psychological or Munchhausen issues and that the family needed real medical help. She had the family stay late that night, the only lights visible at 10 pm that night came from the 13th floor as they met with some of the doctors who emerged to help them. The TODAY show had THOUSANDS of emails from around the world. Dr. Snyderman would devote more time the following day, this time on the air, to clear up the atmosphere of the prior day's "misdiagnosis" of Lauren and focus on a real medical direction:
"NBC's Dr. Nancy Snyderman, along with Today Show viewers,shares some advice for Lauren Johnson, the 12-year-old girl who sneezes more than 1200 times a day."
Sneezing Girl Gets Help from Dr. Nancy Snyderman and Today Show Viewers
By Teresa Conrick
I have always thought that the best research looks not only at the evidence in front of you but takes a look back into the past to see if history holds a key. It is true with Autism, as we saw in Mark Blaxill and Dan Olmsted's chronology of MERCURY and its trail to the first cases of Autism in, The Age of Autism Mercury Medicine and a Manmade Epidemic and similar searching may also be needed for some newer, rising childhood neuropsychiatric disorders, like PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection )- soon to be PANS ( Pediatric Acute-Onset Neuropsychiatric Syndrome infection). In LeRoy, NY, there appears to be a cluster of cases that has evidence pointing to PANDAS/PANS.
Let me elaborate more on the PANDAS to PANS piece. “From Research Subgroup to Clinical Syndrome: Modifying the PANDAS Criteria to Describe PANS (Pediatric Acute-onset Neuropsychiatric Syndrome)”. A group of researchers and clinicians, headed by NIMH investigators, collaborated back in 2010 on the issues of acute onset tics and ocd as factors in PANDAS and especially the fact that many cases of PANDAS were turning up to not be caused by only Streptococcus. As a result, there are new criteria to match the new name for this increasing medical condition. From that White Paper:
Diagnostic Criteria Proposed for Pediatric Acute-onset Neuropsychiatric
Syndrome (PANS). PANDAS to PANS
I. Abrupt, dramatic onset of obsessive-compulsive disorder or severely restricted food intake
II. Concurrent presence of additional neuropsychiatric symptoms, with similarly severe and acute onset, from at least two of the following
seven categories (see text for full description):
2. Emotional lability and/or depression
3. Irritability, aggression and/or severely oppositional behaviors
4. Behavioral (developmental) regression
5. Deterioration in school performance
6. Sensory or motor abnormalities
7. Somatic signs and symptoms, including sleep disturbances, enuresis or urinary frequency
III. Symptoms are not better explained by a known neurologic or medical disorder, such as Sydenham chorea, systemic lupus erythematosus, Tourette disorder or others.Note: The diagnostic work-up of patients suspected of PANS must be comprehensive enough to rule out these and other relevant disorders. The nature of the co-occurring symptoms will dictate the necessary assessments, which may include MRI scan, lumbar puncture, electroencephalogram or other diagnostic tests.
So what does that mean? Here are some possibilities:
1. Not only Strep but also Lyme bacteria, Mononucleosis (Epstein Barr Virus), and Mycoplasma bacteria ("Walking Pneumonia,") are added to the list of infectious triggers. Good news for many who have children who have suffered yet were often lost or dismissed due to absent Strep symptoms.
2. The very important word, "Autoimmune" is now gone from both title and description. "Acute" replaced it which may be problematic, especially as PANS increases in numbers, severity and chronic presentation.
3. A huge change and one I think is significant moving forward - "including not only disorders potentially associated with a preceding infection, but also acute onset neuropsychiatric disorders without an apparent environmental precipitant or immune dysfunction." That further takes old PANDAS away from its immune epicenter, muddying the waters more for those trying to get proper medical treatments (IVIG, antibiotics, antiviral etc) and paving the way to more of a behavioral-targeting drug treatment.
4. This definition may make PANS seem to fit more into a behavioral, psychiatric diagnosis , ie -- DSM-5. That could not only change the perception of immune-mediated disorders but also delay proper research into why so many children are not able to handle illnesses and what types of medical treatments could help. Clearly this is an immune/autoimmune process yet there seems to be a backing away from that direction.
It seems important to keep the focus on the immune system as many of the children's issues originate from that area. Here are some studies that accentuate that point:
- "Infectious and immune factors are broadly implicated in the pathogenesis of childhood neuropsychiatric conditions, including Sydenham’s chorea (SC), Tourette’s syndrome (TS), obsessive-compulsive disorder (OCD), attention-deficit/ hyperactivity disorder (AD/HD) and autism spectrum disorders (ASD).1–5" .......
- "Altered humoral immunity, including higher autoantibody levels, is reported in a wide range of behavioral syndromes,including movement disorders,43,49 schizophrenia, 50,51 autism 52 and neuropsychiatric SLE"......
By Teresa Conrick
I have been following all of the news and reports on the teens and now two adults who have developed sudden onset tics and Tourette-like symptoms in upper NY. It is an unanswered medical phenomenon still and one that is devastating. One thing that seems certain -- the issue of Conversion Disorder vs Immune Disorder needs a further analysis. A report titled, "Investigation of Neurologic Symptoms among Le Roy Jr/Sr High School Students, October 2011 – January 2012" has been made available for viewing and some interesting pieces of information seem worthy of our attention:
All cases were female. Three of the 12 cases were identified as having pre-existing medical conditions associated with tic disorders. Two of the three cases, who were tic free for a period of time, experienced an exacerbation of tic symptoms during this time period. The third case was identified as having a previous diagnosis of Tourette’s disorder and did not have a new onset of tic symptoms, but rather an acceleration of on-going tics during this time period. Onsets of tic symptoms ranged from May 2011 to December 2011 for the nine new onsets.
My good and learned friends here at Age of Autism, Mark Blaxill and Dan Olmsted, have been writing about LeRoy and some of the intriguing (AofA Tics and Toxins A History of Building Woes) and significant environmental factors that may be at play. (AofA Tics and Toxins Playing Fields on FEMA Flood Hazard) Kevin Barry, an avid Age of Autism reader and researcher, also included some historical, pertinent pieces as to what could be making some of the teens so ill. Having my own daughter with similar issues of sudden onset motor and vocal tics, seizures and a history of repeated Strep infections, parasites, and lengthy viral illnesses has made the search for the source of this mystery all the more important to me.
By Teresa Conrick
With tics and Tourette-like illness in the news so much right now due to the increasing number of students at LeRoy HS in NY exhibiting them, it is with irony that P.A.N.D.A.S., a possible medical diagnosis for what we are seeing in LeRoy, is again up for scrutiny and denial somewhere else. Here on Age of Autism, we are keeping up with the dizzying news that is our epicenter of what we are all about here - that many children are suffering with PHYSIOLOGICAL illnesses yet being wrongly diagnosed with PSYCHIATRIC disorders. What is unraveling in Leroy has been happening for YEARS and for those of us with children stricken by regression after vaccination or immune illnesses, like PANDAS, the question that needs to be asked by many professionals denying what we all have known is - why are there so many sick children with immune and autoimmune diseases?
A few weeks back,a study came out, which wasn't really a study but more of an analysis steering an opinion. The name, "Moving from PANDAS to CANS,- unavailable for public access -" was quite a surprise as another name had been decided that would encompass the growing bacterial and viral issues of this increasing, medical misery - PANS," Pediatric Acute-onset Neuropsychiatric Syndrome." PANS would change the criteia from the sole and hated Streptococcus bacteria to other various bacteria and viral infections, showing that not only Strep could trigger neuropsychiatric symptoms. Vickie Blavat, a mother of an affected child with PANDAS and a research marvel on the PANDAS website, did a very nice job analyzing, "Moving from PANDAS to CANS" as well as other good information on this page:
In 2010, the NIMH hosted a think tank of various doctors and researchers to discuss PANDAS and its future. At that meeting, it was determined that a name change was in order and we would experience a shift from PANDAS to a new name…PANS. PANS would stand for Pediatric Acute-onset Neuropsychiatric Syndrome. To date, the new name has been verbally used by Drs. Swedo, Cunningham and others at conferences, symposiums and in layperson articles. They explain how various bacteria and infections, not soley strep, can trigger neuropsychiatric symptoms. We still wait for official confirmation and documentation of the change, diagnostic criteria, and treatment plans. One thing is definite, it was voted on and the name is PANS.......Imagine the PANDAS community’s surprise when a new article surfaces from the often referred to “naysayers” of PANDAS. .......They deem it should be called CANS (Childhood Acute-onset Neuropsychiatric Symptoms). Their CANS would be a very big umbrella for any person that has a sudden onset of neuropsychiatric symptoms, even if the cause is not infection triggered. Example, in addition to infection and autoimmune triggered events, if the cause for the sudden onset is drug induced (including illegal drugs like cocaine), psychogenic, metabolic, trauma, abuse, heavy metals, etc. the person can be diagnosed with CANS. The only prerequisite for a CANS diagnosis would be the sudden onset of symptoms. In other words, their CANS is a dump diagnosis.
So it sounds like the doctors who are listed on this paper, Singer HS, Gilbert DL, Wolf DS, Mink JW, Kurlan R are establishing some sort of new criteria that does not make sense moving forward in helping these ill children. Is it possible that like Autism, there are some folks in the psychiatric world, like in the development of DSM-5, who want to keep fighting the reality of immune illness versus mental illness in our children? They keep trying to prove that their methods are the only treatments and that kids will get better with them. Yet their their big hitter medicines are proven ineffective for a big piece of both Autism and P.A.N.D.A.S.--- REPETITIVE behavior:
- A new multi-center study suggests the prescribed antidepressant citalopram [ Celexa] is no more effective than placebo in altering obsessive features of autism
According to background information in the study, the use of antidepressants in children with autism spectrum disorder took off before there was strong scientific proof about its effectiveness.
In the last decade, its use has grown so that today more than 40 percent of autistic children swallow a daily dose of an antidepressant in an attempt to control spinning, rocking and repetitive behavior.
- These results showed that fluoxetine [PROZAC] was not effective for reducing repetitive behaviors in children and adolescents with Autistic Disorder.
By Teresa Conrick
I have a teen daughter very affected with vocal tics, OCD, enuresis, estrogen-related seizures and a significant past history of streptococcus infections as well as numerous viral illnesses. Her diagnosis in 1995 - AUTISM - and additionally in 2011 - an autoimmune diagnosis - based on two positive results for antinuclear antibodies. Armed with that knowledge, I was lured to an article this week called, Le Roy Parents Want Answers about Mysterious Illness . I was shocked to read a horrific account of twelve high school girls, all from the same school, who had each begun to have severe symptoms similar to Tourette's syndrome, with tics and verbal outbursts. These are familiar symptoms to me and for any parent who has a child who regressed into an immune or autoimmune disease.
I have researched and done much reading about Autism and also P.A.N.D.A.S. (Pediatric Autoimmune Neuropsychiatic Disorders Associated with Streptococcal Infections) because both seem to be related to Megan and to each other, as the immune system seems to be a big, common denominator. Seeing a story that describes previously healthy teens, teen girls, become so ill with movement and vocal tics, should alarm everyone. The many articles on this story offer bits and pieces of clues as we all read it is "a mystery:" Autism and P.A.N.D.A.S. used to be mysteries but over the years, many parents have reported that regression into each often came about due to vaccination or acute illness from bacterial or viral infections. Streptococcus bacteria also known as "Strep Throat" for many, has been implicated often for P.A.N.D.A.S. but parents are also seeing regression and further exacerbation with other infections, such as Lyme (Borrelia bacterium) and Pneumonia ( Mycoplasma pneumonia). Are we seeing a rise in these immune-mediated diseases over the past years of increased vaccinations?
These are some facts:
1- A mysterious disorder which exhibits symptoms similar to Tourette's Syndrome has affected twelve female students at the same high school in LeRoy, NY.
2- Tourette's Syndrome is a neurological disorder defined by involuntary motor and vocal tics.
3- The New York State Department of Health says since September, 12 girls in Le Roy suddenly developed tics. Some are so bad, they had to be pulled out of school and tutored at home.
By Teresa Conrick
Those are my two daughters in 1995. They were watching a favorite Christmas video, The Snowman, based on the UK story by Raymond Briggs. Unlike our giddy, holiday Frosty, the Snowman, the UK version is a beautiful, haunting story of love and loss. The many times I watched it with Meg -- winter, summer, fall,spring -- it didn't matter the season. Nights she woke up crying from gastrointestinal pain or intense, physical distress, she wanted to watch, The Snowman, but she could never, ever watch when he melted. She would leave the room.
Megan, now eighteen, has both an autism diagnosis and an autoimmune diagnosis. Rare? Unrelated? I think not. I believe as we end 2011 and enter into 2012, the upcoming year will bring us more facts and research into the connection between autism and autoimmunity. With that, let's say goodbye to the autism ghosts of Christmas past which gave little hope for meaningful research on preventing new cases of autism (regression) or research on medical treatments for those currently affected (progression) Junky genetic studies, Drosophilia eye-gazing, unknown autism prevalence, and bullshit research has to END. We know that bacteria, viruses and metals can cause autoimmune effects and the research needs to be centered around that.
Going back in time each holiday season, the ghosts of past Christmases can haunt those living with autism and autoimmunity. In 1995, my daughter's autism diagnosis was never related to her ongoing illnesses with Streptoccocus and other bacterial infections as well as numerous viral infections. Labs now have shown IgG quantitative titers for each -- Measles-Mumps-Rubella -- to be elevated. That was the vaccine that dramatically affected my daughter with many days of rash, fever, GI issues, loss of language and then odd visual issues. Brief definition of IgG:
Measles and mumps (rubella) antibodies are virus-specific proteins produced by the immune system in response to an infection by the measles or mumps ( & rubella) virus, or in response to vaccination. There are two types of antibodies produced, IgM and IgG. The first type to appear in the blood after exposure or vaccination is IgM antibodies. Levels of IgM antibodies increase for several days to a maximum concentration and then begin to taper off over the next few weeks. IgG antibodies take a bit longer to appear, but once they do, they stay in the bloodstream for life, providing protection against re-infection..
There are very sick children and young adults with an autism diagnosis, and there seems to be mounting evidence that the MMR (Measles Mumps Rubella) vaccine has quite possibly left its mark in them. So back to high titers and autism. If a toddler is vaccinated at 15 months, what is happening to produce very high titers 18 years later? Why are the Drosophilia scientists not dropping the fruit flies and looking at viral titers -- or Strep in those affected by autism?
By Teresa Conrick
My daughter, Megan's recent diagnosis of an autoimmune condition coupled with an abnormal EEG are big, red flags that help illustrate why she is so ill. Finding that out hardly ends my journey for more answers to help improve her health and her life. The disturbing behaviors and symptoms of vocal tics, dilated pupils, agitation, enuresis, and OCD are a barometer of brain dysfunction. Add in estrogen-induced seizures that developed at age seventeen in tandem to her autoimmune diagnosis and that may be another clue. As a result, I have been exploring more of the issues that connect her to those children who have a P.A.N.D.A.S. (Pediatric Autoimmune Neuropsychiatric Diagnosis Associated with Streptococcal Infections) diagnosis as Megan has had numerous bouts of Strep and other infections that exploded into severe movement and vocal tics over the years. Her original regression into an autism diagnosis slowly happened after vaccinations along with increasing viral and bacterial infections as a toddler, then an acute rash, fever and loss of language after her MMR vaccine. We now seem to be in the land of chronic waxing and waning of symptoms and the most sobering part --- we are not alone.
More parents are finding each other and connecting via their child's medical issues. Autism and P.A.N.D.A.S. may be cousins of a similar origin as there is overlap in symptoms, both behavioral and medical. A good place to learn more about P.A.N.D.A.S. is this informative site. A warrior mother in the P.A.N.D.A.S. trenches, Diana Pohlman, developed it in 2009 as she decided to bring parents, research and researchers together to investigate why their children were becoming acutely affected by a monster that Streptococcus bacteria seemed to awaken. Like so many of us, she saw her son regress into an immune illness that severely affected his mood, behaviors, functioning -- his life. More and more children each year seem to be developing tics, severe anxiety, obsessive compulsions, involuntary movements and psychiatric issues, not randomly, but due to an infection affecting the brain. It is usually Streptococcus, an evil little bacteria that these mothers despise, because it is stealing their children. So Autism parents and P.A.N.D.A.S.parents are beginning to link arms to tackle both cause and cure. As it states on Diana's website above, "Parents Helping Parents," is a key for many families to compare medical issues and treatments.
P.A.N.D.A.S. is a medical diagnosis yet many still do not understand it thus, there is confusion on its causation, how to diagnose it and then appropriate treatments. We in the trenches of Autism are familiar with these issues as we have been dealing with them for too many years. Our toddler or child becomes ill, either through an infection or after vaccination and there is a regression in skills. Odd, perseverative and debilitating behaviors creep in. Life forever changes. Doctors dismiss the cause and labels are given. Precious time is lost then more medical symptoms, more labels. A stinging reality -- lack of proper medical treatments cause worsening behaviors. This continues to happen at an alarming rate.
Some significant research continues to evolve with P.A.N.D.A.S., and the names Cunningham, Swedo and Murphy are becoming instrumental in connecting the hated bacteria to the hosts they have kidnapped. Another interesting development was the apparent acknowledgement from Dr. Tom Insel that P.A.N.D.A.S. was indeed a real, medical illness. For those who do not know him, Dr. Insel is Director of the National Institute of Mental Health (NIMH), the component of the National Institutes of Health "charged with generating the knowledge needed to understand, treat, and prevent mental disorders", per the website, including Autism and now also, P.A.N.D.A.S.
Here is a portion of what he reported a year ago:
By Teresa Conrick
My daughter, Megan, diagnosed sixteen years ago with Autism, has had an intense twelve months of.medical symptoms. I call them "symptoms" but they really are clues as to the true nature of her diagnosis of autism. It began last Fall with seizures, unusual, hormone-related, monthly ones, that had progressed into episodes of behavioral concern. An earlier EEG had showed no seizures but instead, a pervasive and ominous diffuse slowing of the brain waves. Excessive estrogen can trigger mania, agitation and seizures in a typical female, so combine that with a diagnosis of autism and you get a full blown detour into an abyss, frighteningly far, far away from normalcy. More testing had shown "estrogen dominance," another "symptom" in Meg's body. Hormone therapy has not yet stopped the behaviors. Anti-seizure medication has not yet stopped the seizures. An autoimmune diagnosis also has now surfaced, which helped make sense of the increasing irritability, enuresis, plus motor and vocal tics, often screamed out of my lovely daughter's mouth. Her sister, two years younger, has lived in a path of bewilderment, fear and I am quite sure, shame, as the odd and erratic behaviors of her "older", yet really "younger" sister infiltrated our house. No friends or family have been in our home for so long as we have been living a nightmare. The behaviors were not a choice made by Megan, but instead have been a "symptom" of her immune system kidnapping her. For me, it has been a painful reminder of how sinister Autism can be, especially when bacterial and viral infections seem to trigger Meg's body into a twilight zone in which I can't reach her. Was this STILL autism or were we in a new place, like P.A.N.D.A.S. (Pediatric autoimmune neuropsychiatric disorders associated with Streptococci)? It is like watching her regress again, as she did sixteen years ago. Her recent years have been positive for numerous Strep, candida, clostridia, and other viral infections.
It was decided that Meg needed an MRI and a 24-hour, closed circuit televised, EEG. Her neurologist, new since Summer for us, saw how my daughter's behaviors were concerning and listened to my description of aggressions, involuntary movements and vocal tics/yells that I am sure the neighbors down the block could hear. I am thankful that he didn't just see an eighteen year old, severely affected "with autism," and just needing something for the behavioral "symptoms." Going into a hospital with Meg, overnight and away from the safety of home, took my breath away with fear as I thought about it. Meg had a 24 hour EEG at age six but the electrodes were fastened to her head at the hospital, yet we were able to go home with a fanny pack monitor. Other EEGs had been just a few hours long. This EEG was to be video monitored, an important addition as that 24 hour EEG twelve years ago was normal, yet she had just developed generalized tonic clonic seizures at age seventeen. The video would be able to help us determine if there were subclinical seizures causing these scary behaviors.
There were many departments that we had to pass through in our journey. Admissions, Ambulatory Services and then MRI, all before noon. Others were to follow later. More than one (in fact 6 people that day) asked if Meg needed, or if I wanted her to get a flu shot. October in a hospital is a continuous infomercial for Flu and Pneumonia vaccines. I politely declined and wondered if our record had now been flagged, similar to Elaine's from Seinfeld, where it labeled her as a “difficult” patient. I wasn't trying to be difficult but Meg's decline in health started with mercury-containing vaccines and then the fever and full body rash after her MMR significantly hastened that decline with loss of speech, loss of eye contact and loss of relating to us.
My daughter, Megan, diagnosed sixteen years ago this month with autism, has now been diagnosed as having an autoimmune disorder, or -- is it -- an autoimmune disease? Disease sounds profound but with all of her very serious symptoms for years, now worsening, it makes sense in my head, but in my heart --- it is devastating. We have tested twice now, using the antinuclear antibodies test, and both times it came out "positive," showing her body was indeed, fighting itself. Although Lupus has been ruled out, we don't know yet what type of antigen is causing the autoimmune response so for now, it is a nameless monster. We do know that estrogen seems to trigger these episodes for Megan.
Because Meg has had numerous symptoms of other disorders and diseases, such as motor and vocal tics, loss of speech, choreiform movements, agitation, rigid OCD (obsessive-compulsive disorder), enuresis, transient psychotic features, aggression, and then a culminating seizure, I have needed to read, research and try to understand the overlap so we could hopefully find both cause and cure. The key, it appears, is a 10.0, richter scale magnitude quote that Dr. Madeleine Cunningham used in her Autism One presentation recently in Chicago. Dr. Cunningham is a brilliant mind who, according to her website, is focused on, "the study of autoimmunity and behavior which is manifest in diseases such as Sydenham's chorea following group A streptococcal infection. Our study identified antibody mediated neuronal cell signaling as the basis for the choreic movement disorder. Other related movement and psychiatric disorders such as obsessive compulsive disorder, Tourette's Syndrome and Tics are under investigation for subsets that may be related to streptococcal infection and/or to autoantibodies which signal in the brain." She has been on the hunt since 1985 for Streptococcus and its many haunting manifestations. Many families of P.A.N.D.A.S. (Pediatric autoimmune neuropsychiatric disorders associated with Streptococci) children have reported a family history of Strep, Sydenham's Chorea, Rheumatic Fever and other autoimmune diseases. Here is that quote from Dr. Cunningham:
“If autoantibodies are proven to affect behaviors, it will change the way we think about and treat mental disorders forever.”
To me, that significant sentence sums up so much of what I see in Meg, read in the research and believe in my heart. There are other researchers also looking into autoimmunity, behavioral symptoms, and illness. Here was a two part series, long but worth the read. I have taken excerpts that relate to autism, Megan and her autoimmine issues: Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1
By Teresa Conrick
Yet another study has come out to add to the growing list of research showing that autism can be connected with exposure to mercury. This study took the idea of heritability and paired it with a known exposure to mercury, Pink Disease. Also known as Infantile Acrodynia, Pink Disease was a mysterious ailment that affected 1: 500 children. Its origin was teething powders and also worm medicines that contained mercury, given to babies and children, but it took YEARS for that truth to be accepted. Here is a description and opinion from, A REVIEW OF INFANTILE ACRODYNIA ('PINK DISEASE'), NOVEMBER 30, 1949, of the painful and sometimes deadly symptoms seen: NIH Acrodynia
CARDIOVASCULAR: Tachycardia, hypertension; occasionally epistaxis, melaena, gangrene.
EMOTIONAL.: Depression, apathy, fretfulness, perversion of appetite, loss of interest, insomnia.
NERVOUS SYSTEM.:Myasthenia, hypotonia, photophobia; sweating, incontinence; head-banging, rocking and salaaming; paraesthesia, possibly 'thalamic' pain; disturbed temperature regulation; occasionally tremor, convulsions.
SKIN AND MUSCOAE:. Erythema, swelling of hands and feet; ulceration of mouth, loosening of teeth; dystrophy of nails and hair.
METABOLIC:. Hyperglycaemia, glycosuria; loss of weight: increased basal metabolic rate; enlargement of liver.
ENDOCRINE: Cessation of growth; diuresis.
DIGESTIVE: Vomiting, diarrhoea; occasional prolapse of rectum; occasional intestinal spasm, rarely progressing to intussusception.
BLOOD. Neutrophil leucocytosis.
And like Autism, Pink Disease was a "mystery", with many different opinions on causation yet the clues seem so clear now:
"The concept of diet deficiency, for example, has been abandoned, attractive as it seemed at one time, partly because the disease, whether in symptoms or pathology, resembles no known deficiency disease in man, and partly because it is found very frequently in conditions which seem to preclude malnutrition. The limits of age within which authentic cases have been reported are from the third week (Wyllie and Stern, 1931) to the fourth year;.....above this age there are probably a few cases......very rare cases reported in adults...indeed it is unlikely that a disease which appears not to have its origins in prenatal life or birth itself should be confined to the first four years....a lively baby becomes increasingly apathetic, loses interest in its surroundings, ceases to play, sleeps little, cries a lot. Older children cease to stand or walk or talk, and do not resume their progress in activity until the illness is past. No smile can be provoked, and the child resents being lifted or handled unless to be nursed very quietly."
And like Autism, when hard science pokes its way in, that reality may provoke feelings of denial:
By Teresa Conrick
In Part 1 of our examination of Anti-NMDA Receptor Encephalitis, I presented a late-onset case of autism. Similar cases have been shown to be caused by antibodies against NR1–NR2 heteromers of the NMDA receptor. There was really very little about the precipitating event that explained why the 9 year-old boy became a victim of such an extreme medical and behavioral illness. Because of its acute psychiatric manifestation, Anti-NMDA Receptor Encephalitis is often misdiagnosed as a psychiatric issue rather than a neurological-medical disease. Its apparent increase in cases has been debated as -- a true increase or just better diagnosing? I have to say it -- we, in the autism community, really dislike that phrase as it has become a mantra of ignorance in the face of truth.
Some further investigating brought me to another case of Anti-NMDA Receptor Encephalitis that presents with some more tangible facts. Here is the Pubmed excerpt:
J.Neurol 2011 Mar;258(3):500-1. Epub 2010 Sep 30. Anti-NMDA receptor encephalitis after TdaP-IPV booster vaccination: cause or coincidence? Hofmann C, Baur MO, Schroten H.
And that's it. There was no abstract but after some searching, I did find a link:
LETTER TO THE EDITORS
Anti-NMDA receptor encephalitis after TdaP–IPV booster vaccination: cause or coincidence?
Caroline Hofmann • Marc-Oliver Baur • Horst Schroten
Received: 5 September 2010 / Accepted: 13 September 2010 / Published online: 30 September 2010
Anti-NMDA receptor encephalitis is a recently described autoimmune disorder mediated by antibodies to the NR1 subunit of the N-methyl-D-aspartate receptor. It was first
recognized as a paraneoplastic syndrome in young women with ovarian teratoma . Further studies have shown that about 40% of the patients with anti-NMDA receptor
encephalitis do not have a clinically detectable tumor, and men and children are also affected . The mechanisms triggering the disorder, especially in patients without an
associated neoplasm are unknown. The high incidence of prodromal viral-like symptoms suggests a possible infection triggering the autoimmune response . We report about a 15-year-old female patient who was diagnosed with anti-NMDA receptor encephalitis after receiving a booster vaccination against tetanus/diphtheria/pertussis and polio (TdaP-IPV). Within the first 24 h after the injection she developed a low-grade fever and general fatigue. During the following weeks, her family observed an unusual need for sleep. Psychiatric symptoms became apparent 5 weeks after the immunization and included disorganized thinking and hallucinations. Within a few days she became increasingly agitated with orofacial dyskinesia, opistotonic posturing, and choreic movements of the upper extremity. She grew unresponsive to verbal commands and required intensive care treatment due to autonomic instability. The unique pattern of clinical symptoms led to the consideration of anti-NMDA receptor encephalitis, which was confirmed by the detection of anti-NMDAR antibodies in plasma and cerebrospinal fluid. Other possible causes of encephalopathy including intoxication,infectious and metabolic diseases were ruled out; repetitive brain scans showed no abnormalities. After confirming the diagnosis, an extensive tumor search was performed without any proof of malignancy; biopsy of a prominent ovarian cyst revealed no teratoma. The onset of prodromal symptoms shortly after the immunization is intriguing and suggests the vaccination as a possible trigger of anti-NMDA receptor encephalitis. Neurological adverse events including autoimmune disorders have been discussed in literature for many years; a definite causal association between vaccination and disease was seldom established. For example, the 1976 swine influenza vaccine was associated with an increased frequency of Guillain-Barre Syndrome (GBS) . A recent study about the safety of TdaP vaccination in adolescents revealed no increased risk of neurological adverse events , even though rare cases of GBS have been reported. To our knowledge, this is the first possible case of vaccination associated anti-NMDA receptor encephalitis. Therefore, not only infectious agents and tumor antigens but also vaccines should be considered as a possible trigger of immune response in this recently described disorder.
Conflict of interest None.
By Teresa Conrick
My daughter, Megan, continues to be severely affected by both the medical and behavioral symptoms of autism. As a result, I continue to read studies and research that correlate with the symptoms that she has. Some of the factors, if we were to list them like they do in a journal, would be -- seizures, autism, nmda/glutamate dysfunction, cancer signalling, encephalopathy, agitation. Surprisingly, there was a current, case study just out that had many of these key words:
Late onset autism and anti-NMDA-receptor encephalitis The Lancet, Vol 378. Issue 9785, Page 98, 2 July 2011
Caroline Creten, MD, Sanne van der Zwaan BSc, Roos J Blankenspoor BSc, Arien Maatkamp, PhD, Prof Jim van Os PhD, Dr Jan NM Schieveld PhD
In December, 2009, a 9-year-old boy was admitted to our hospital with an acute onset of secondary generalised seizures. He had no medical or psychiatric history and functioned very well socially and academically. He presented with speech and swallowing difficulties, which after 10 days developed into a severely agitated catatonic state with opisthotonic posturing, tonic posturing of limbs, insomnia, and dyskinesia. Initially the electroencephalogram showed a normal background pattern with epileptic discharges, and oligoclonal bands were present in cerebrospinal fluid (CSF). Brain MRI and extensive blood tests were normal. The neurological diagnosis was atypical childhood epilepsy with centrotemporal spikes, for which oral corticosteroids and anti-epileptic drugs were prescribed. His catatonia was treated with benzodiazepines. In January, 2010, our patient presented in a robotic state with complete mutism and negativism, and he did not respond to any form of contact. We provisionally diagnosed acute late onset autism with a differential diagnosis of childhood disintegrative disorder or early onset schizophrenia.
Childhood disintegrative disorder, early onset schizophrenia, and late onset autism often share a final common pathway: previous normal development, followed by sudden neuropsychiatric regression of social interaction and communication skills, and a decline in intelligence and daily activities. 1 The disorders are sometimes misrecognised and collectively called as autistic disorder. Although judged to be functional psychiatric diagnoses, the marked deterioration and poor prognosis suggest an organic cause, especially in children with catatonia, a normal development up to at least 5 years of age, or both1,2. In our patient, late onset autism was considered because: it is associated with neurological disorders; 2 it is a known end stage of acquired brain injury; progression of symptoms was fast and severe, unlike in early onset schizophrenia; the absence of positive symptoms made schizophrenia less plausible; the age of onset and rare prevalence made chronic disintegrative disorder unlikely; 1 and accompanying catatonic features were present. 3 After extensive diagnostic assessments, our patient was finally diagnosed with anti-NMDA-receptor encephalitis on the basis of slightly raised anti-NMDA-receptor antibody titres in serum and highly raised titres in CSF. 4 Clinical characteristics of this condition are acute major neuropsychiatric symptoms including anxiety, aggression, agitation, behavioural changes and catatonia, delusional thoughts, progressive speech deterioration, and hallucinations. Neurological symptoms such as dyskinesia, abnormal seizure-like movements, and diffuse and profound autonomic instability have also been reported.4.5 Anti-NMDA-receptor encephalitis can occur in the context of malignant disease; 4 however for our patient extensive oncological investigations were negative. Electroconvulsive therapy was given for the severe catatonic state, and monoclonal antibody treatment (rituximab) was started because of the unsatisfactory response to the initial treatment with benzodiazepines. The acquired autism gradually subsided, he spoke fluently and was able to draw a happy picture (figure). In June, 2011, he only had some mild cognitive dysfunction.
By Teresa Conrick
In this series on xenobiotic chemicals, like mercury/thimerosal, and their connection to autism, cancer and neurodegeneration, there are indications that some companies and researchers are racing to the "cure" yet avoiding inconvenient truths. As a result, there is a continuation of denial about the environmental and pharmaceutical toxins -- both man made -- that have their fingerprints on many of these cases of regression into disease. Some would say the fingerprints are on both poison and "cure', as mercury, and especially Thimerosal, are shown to be guilty of causing damage that, for example, Riluzole, via clinical trials, is supposed to fix:
Poison "Within a eukaryotic cell there is careful regulation of the levels of phosphorylation which is controlled by the delicate balance between the activity of protein kinases and protein phosphatases......In this study we show that the thiol-reactive heavy metal HgCl2, known to contribute to the development of autoimmune disorders, induces a rapid and robust activation of tyrosine phosphorylation within human myelomonocytic cells."
Poison "Focal adhesion kinase (FAK) is a signaling molecule associated with cell survival. Previously, we showed that thimerosal, a reactive oxygen species (ROS) generator, can acutely induce FAK tyrosine phosphorylation (within minutes) and chronically induce apoptosis (within days)"
"Cure" The Neuroprotective Agent Riluzole Inhibits NMDA-Induced FAK 125 Tyrosine Kinase Phosphorylation in the Rat Hippocampus
Glutamate: a potential mediator of inorganic mercury neurotoxicity. "Exposure to mercury vapor (Hg0) produces neurotoxic effects which are for the most part subsequent to its biotransformation in brain to the mercuric cation (Hg2 +), which has an exceptionally strong affinity towards the SH groups in proteins. However, neurologic symptoms are often encountered in subjects in which Hg+ concentration in the brain remains in the SUBMICROMOLAR range, markedly below the anticipated threshold for direct inhibition of cerebral metabolism and function. In this report we review biochemical and morphological evidence obtained in this and other laboratories in tissue culture studies suggesting that in such instances mercury neurotoxicity may be mediated by excitotoxic activity of GLUTAMATE (GLU)."
David H. Gorski
Drug Discovery and Development
"The research interests of the Gorski laboratory fall into two broad categories. First, we are interested in the transcriptional regulation of vascular endothelial cell phenotype. Our second area of interest is the role of metabotropic glutamate receptors (mGluRs) in breast cancer. These receptors have traditionally been believed to be restricted to the central nervous system, but our collaborators at Rutgers University and Robert Wood Johnson University first serendipitously observed that mGluR-1 induces melanoma in transgenic mice.... we have noted that mGluR1 is expressed on vascular endothelial cells and have preliminary evidence that its inhibition is also antiangiogenic......"
By Teresa Conrick
If you have been following this series (Part 1 and Part 2) on the connections of mercury, both environmental and pharmaceutical, I hope that it has become clear that many diseases appear to be sparked by exposure from both. Viruses, included as xenobiotics, may also be included, as mentioned in Part 3 here: " proteins in the intracellular signaling cascades that are activated by receptor tyrosines were initially isolated as oncogenes in cancer cells or tumor viruses." More specifically to measles, and for Megan and many of her autism peers, the additional regression, loss of language, fevers, rashes, GI disease, encephalopathy and seizures after the Measles, Mumps and Rubella vaccine, changed lives forever: here Tyrosine phosphorylation of measles virus nucleocapsid protein in persistently infected neuroblastoma cells
"The mechanisms governing the establishment and maintenance of a persistent MV infection in brain cells are still largely unknown. To understand the mechanisms underlying MV persistence in neuronal cells, a tissue culture model was studied.... We present data to show augmented protein tyrosine kinase activity in the persistently infected cells."
Is it possible Xenotropic murine leukemia virus-related virus ,XMRV, a virus first found in prostate cancer and now being linked to chronic fatigue syndrome/myalgic encephalomyelitis (ME) and autism, is also involved ? : "XMRV proteins are also homologous to proteins of the growth factor signalling networks (e.g. tyrosine kinases FLT3 and TYRO3) (Table 5) which are relevant to cancer-related growth (Fig 2)." Nature.com.
Since Meg's "estrogen behaviors" are such a drastic conversion of her usual self to a more "manic" state, I decided to look for a biological reason as to why it was happening: Protein Kinase C Inhibition in the Treatment of Mania A Double-blind, Placebo-Controlled Trial of Tamoxifen
By Teresa Conrick
This is a continuing look at a hypothesis, using pertinent pieces of evidence-based research, that connects autism and other neurodegenerative disorders to mercury and also to cancer. Read Part 2 and Part 1. Here is such a study related to mercury and breast cancer:
"Methyl mercury influences growth-related signaling in MCF-7 breast cancer cells" (Pubmed)
"Environmental contaminants have been shown to alter growth-regulating signaling pathways through molecular mechanisms that are mainly unclear. Here we report that within a narrow concentration range (0.5-1 microM) methyl mercury (MeHg) significantly stimulated growth of MCF-7 cells, induced Ca(2+) mobilization, and activated extracellular signal-regulated kinase (1/2) (Erk1/2)."
Here also was a report on research done in 2005 that linked Thimerosal to the glutamate issues of autism and the other diseases we are examining:
Study implicates thimerosal in glutamate dysfunction (ARI Newsletter)
"New research links the mercury-laden vaccine preservative thimerosal to dysregulation of the glutamate system. Glutamate, an excitatory neurotransmitter, is crucial to learning and memory, but when present in excess it can cause widespread neuron damage or death. Glutamate abnormalities are increasingly being implicated as a factor in autism, Fragile X syndrome, and other neurodevelopmental disorders."
Please take a moment to read that entire page as it contain some very interesting information. Note also the story of the boy with an autism diagnosis who improved on cough drops that contain dextromethorphan, a glutamate antagonist, which correlates to the past mention in Part 1 - (HERE)
Journal of Environmental Health, 2010 Antagonism of Dextromethorphan and Riluzole to Neurotoxicity Induced by Methylmercury in Rats. I am not endorsing dextromethorphan or any of the medications mentioned here but pointing out the connection from mercury neurotoxin blockers to an increased pharmaceutical cornucopia of using them as medications directed at neurodegenerative diseases, autism and cancer. There is an irony here that cannot be denied and needs to be examined more closely.
It appears that six years ago, when this ARI newsletter was published, there was a connection to glutamate dysfunction in autism but not yet its connection to ALS, Parkinson's, Alzheimer's, Schizophrenia or cancer. Somewhere, it must have become more obvious, which makes it all the more curious as to why Dr. Gorski would not mention that in his blogs, instead of sarcastic hurls targeted towards so many parents looking for answers about their child's regression into an autism diagnosis.
Here is a good synopsis of where we are in Part 3: the pattern - the hypothesis : toxic exposure (mercury) > glutamate dysfunction > altered protein tyrosine kinase - phosphorylation > regression into disease. The following is research showing how each of the diseases has a common denominator of altered or aberrant protein tyrosine kinases and protein tyrosine phosphorylation:
Protein tyrosine kinases in human breast cancer: kinetic properties and evidence for the presence of two forms of native enzyme (NIH PubMed)
Protein tyrosine kinases in malignant melanoma. (NIH PubMed)
Altered protein tyrosine phosphorylation in Alzheimer's disease. (NIH PubMed)
Mitogen-activated protein kinases (MAPK) in schizophrenia (NIH PubMed) (need to add this study for good visual connection : "Role of reactive oxygen species, mitogen-activated protein kinases and signaling cascade in mercury immunotoxicity" (UGA.edu) "This study indicates that mercury suppresses NO synthesis by inhibition of the nuclear factor .B pathway and modulates cytokine expression by p38 mitogen-activated protein kinase (MAPK) activation"
Protein tyrosine kinase activity in T lymphocytes from patients with systemic lupus erythematosus. (NIH PubMed)
Aberrant protein kinases and phosphoproteins in amyotrophic lateral sclerosis (HERE)
Inhibition of protein tyrosine/mitogen-activated protein kinase phosphatase activity is associated with D2 dopamine receptor supersensitivity in a rat model of Parkinson's disease. (NIH PubMed)
"Brain Region-Specific Decrease In the Activity of Protein Kinase C, and Increase In Activated MAP ( mitogen-activated protein) Kinases In Regressive Autism" (IMFAR)
As these connections become more clear, one does not have to look far to see how medications shown to "attenuate MeHg-mediated cell death by blocking NMDARs" would then be coming to your local Walgreens for diseases on the rise:
Riluzole Clinical Trials
"Review of the use of the glutamate antagonist riluzole in psychiatric disorders and a description of recent use in childhood obsessive-compulsive disorder.
Open-label riluzole in fragile X syndrome.
By Teresa Conrick
In Part 1, I discussed some connections between melanin, autism and cancer. I started on this research road as my red-haired, teen daughter, who regressed after vaccines, is brutally affected with health issues, behaviors of autism and now with extraordinary estrogen dominance and seizures. Those factors kept me challenged into pursuing causation and treatments. I kept coming across more research that connected so many of her health issues -- for example -- (HERE)
"The presence of GluRs in the follicles and the corpus luteum in the ovary of rats and monkeys suggests a possible female sex steroid-GluRs interaction. It is possible that the glutaminergic excitation system may play a role in the up- or down-regulation of estrogen and progesterone."
So I had to keep looking and saw that the metabotropic glutamate receptors are not only involved in autism but also cancer. Looking deeper into their mechanism of action brings us to a closer, more magnified look. What seems to be a pattern is something called protein kinase and phosphorylation. A cell's ability to respond to its extracellular environment involves a complex and highly organized series of events referred to as cellular signalling. "Signalling processes regulate fundamental cellular responses and abrogation of these processes can lead to the development of various human diseases. Tyrosine kinases are important mediators of the signaling cascade, determining key roles in diverse biological processes like growth, differentiation, metabolism and apoptosis in response to external and internal stimuli. Recent advances have implicated the role of tyrosine kinases in the pathophysiology of cancer." Tyrosine kinase – Role and significance in Cancer (HERE)
Now lets take a look at Riluzole at this new magnification. We saw from Part 1 that it is being used for ALS and also now in Clinical Trials via NIH and NCI for breast cancer: David H. Gorski, Barbara Ann Karmanos Cancer Institute/Wayne State University, Detroit MI(HERE) :
Ten years ago, this study was done about Riluzole and its effect on tyrosine phosphorylation which seems very pertinent in this exploration. 2001 Jun - "Effects of riluzole on N-methyl-D-aspartate-induced tyrosine phosphorylation in the rat hippocampus".
"Since increased tyrosine phosphorylation has been observed in response to brain ischemia, we investigated whether riluzole (an inhibitor of glutamate neurotransmission with neuroprotective properties) affects tyrosine phosphorylation stimulated by N-methyl-D-aspartate (NMDA) in rat hippocampal slices. Riluzole produced an extremely potent concentration-related inhibition of NMDA (1 mM)-stimulated protein tyrosine phosphorylation....These results suggest that inhibition of tyrosine phosphorylation may contribute to the neuroprotective effects of riluzole against excitotoxic injury."
This could then be a key into more observations. First a closer look at how mercury is involved in this cellular signaling:
"Low and Nontoxic Inorganic Mercury Burdens Attenuate BCR-Mediated Signal Transduction" HERE 2007 Department of Immunology and Microbiology, Wayne State University, Detroit, MI Department of Pharmacology, Wayne State University, Detroit, MI
"The ubiquitous environmental heavy metal contaminant mercury (Hg) is a potent immunomodulator that has been implicated as a factor contributing to autoimmune disease. However, the mechanism(s) whereby Hg initiates or perpetuates autoimmune responses, especially at the biochemical/molecular level, remain poorly understood. inorganic mercury (Hg+2) interfered with BCR-mediated growth control, suggesting that BCR signal strength was impaired by Hg+2. Extracellular signal-regulated kinase (ERK) 1,2 mitogen-activated protein kinase (MAPK) is responsible for the activation of several transcription factors in B cells. Phosphorylation of ERK serves as an essential node of signal integration Hg+2 does not seem to act directly on ERK-MAPK but rather on an upstream element or elements of the BCR signal transduction pathway, above the level of the key protein tyrosine kinase Syk. Our data suggest that the site of action of Hg+2 may very well be localized on the plasma membrane. These findings support a connection between Hg+2 and attenuated BCR signal strength in the etiology of autoimmune disease."
In 1999, another related study: "Low and nontoxic levels of ionic mercury interfere with the regulation of cell growth in the WEHI-231 B-cell lymphoma" - Institute of Chemical Toxicology, Wayne State University, Detroit, USA "These data suggest that low levels of mercury, which are not toxic, may still contribute to immune dysfunction by interfering with antigen-receptor-mediated and protein-kinase-dependent signal transduction in lymphocytes"
and more evidence:
"Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells" 2000 HERE
Hck is a member of the Src-family of protein tyrosine kinases that appears to function in mature leukocytes to communicate a number of extracellular signals including various cytokines. In this study we show that the thiolreactive heavy metal, mercuric chloride (HgCl2) induces rapid and robust activation of tyrosine phosphorylation within human myelomonocytic cells. ... The ability of HgCl2 to activate Src-family kinases such as Hck in hematopoietic cells may help explain why exposure to the heavy metal is associated with immune system dysfunction in rodents as well as humans. Keywords: autoimmune disease; Src-family kinases; Syk; tyrosine phosphorylation
Having a daughter who regressed into autism compels me to research medical journals because she began having health complications after vaccinations. I have an insatiable hunger for knowledge about mitochondrial dysfunction, inflammatory responses (brain and gut), oxidative stress, immune abnormalities, and hormonal dysfunction causing seizures. Cancer was really not on my radar too much but it has crept up more as Megan's estrogen levels now make her a prime candidate for it, especially breast cancer. You can read about her horrific hormone levels as a causative factor in her catamenial epilepsy HERE. Cancer can be considered a "regression" in healthy cells, most likely due to an environmental cause, yet we don't always hear that.
In a related search last year, I began to examine and write about melanin, and my thoughts about its involvement in autism. It seemed to me that there was a peculiar propensity for an autism diagnosis in those who had red hair, light eyes or just more of a fair complexion, ie - less melanin. Tyrosine, an amino acid needed to make melanin, seemed somehow tied up but I wasn't sure how. Much research backed up the idea that having less melanin did make one more vulnerable to other "neuroregressive" disorders such as ALS, Parkinson's, Alzheimer's, and Schizophrenia, but also Melanoma. Add Melanoma as another Megan health concern I have because she is just so fair, and seems to contain the recipe for these environmental attacks. What brought me closer to these concerns is that by looking at the similarities of these diseases, one can see the pattern emerge. I saw that as I began to look not only at the symptoms but also at the pharmaceutical management - ie - medications being used or contemplated. The first clue was that there seemd to be some pigmentary disorders in children who also happen to have an autism diagnosis. Is that a coincidence or is that showing a mechanism of what may be happening behind the scenes of this historically misunderstood disorder? I hope I can unfold this pattern here so that it can be looked at for further research. It seems that medicine too often develops a pill to treat a symptom while not searching for the roots to the actual diseases and illnesses. Since autism has become a disorder that is increasing at alarming numbers, and with much physical and emotional suffering, it is our duty as a moral and ethical nation to find both cause and cure.
Recently, as I was reading about each - melanin, autism and cancer - certain websites and words kept reappearing - the puzzle pieces were emerging. One of those pieces that I kept running into was medication, initially FDA approved for neurodegenerative conditions, yet interestingly, one was now being considered for use in breast cancer. Since the two seem completely unrelated as diseases, I was intrigued. Now what makes that more compelling is that the same pharmaceutical medication is now being looked at for autism. The key factor that the drugs are working on for each of these diseases are the mGluR, Metabotropic Glutamate Receptors. I wrote about them HERE as many were racing to find a cure with drugs targeting these receptors but hardly any of them seemed to care about the causation or WHY they were implicated. Now cancer is another race for the cure with these glutamate receptors but how is it related to autism? Here was a study that could answer that question:
"Methylmercury Increases N-Methyl-d-Aspartate Receptors On Human SH-SY 5Y Neuroblastoma Cells Leading To Neurotoxicity" 2008 (HERE)
"Methylmercury (MeHg) is a known neurotoxin, yet the mechanism for low dose chronic toxicity is still not clear. While N-methyl-D-aspartate receptors (NMDARs) were found to be induced after exposure to MeHg in a mink model, its role on neurotoxicity is not known. The aims of this study were to investigate the expression and the functional roles of NMDARs on the induction of cell death in the human SH-SY 5Y neuroblastoma cell line after exposure to MeHg. We found a significant increase in NMDARs followed by increased caspase-3 activity after 4 h of exposure to MeHg (0.25-1 microM). Necrotic cell death was found after 4 and 24 h of exposure to MeHg (0.25-5 microM). The NMDAR antagonists dizocilpine ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5,10-iminemaleate [(+)-MK801]) and Memantine (1-amino-3,5-dimethyl-adamantane) (10 microM) completely attenuated MeHg-mediated cell death by blocking NMDARs, thus demonstrating the importance of NMDARs in mercury neurotoxicity.
Two things of importance from that study: 1- From Wikipedia - "Metabotropic glutamate receptors are known to act as modulators of (affect the activity of) other receptors. For example, group I mGluRs are known to increase the activity of N-Methyl-d-Aspartate Receptors (NMDARs), a type of ion channel-linked receptor that is central in a neurotoxic process called excititoxicity."---- meaning that mercury is shown here to be CAUSATIVE to the " (NMDARs) were found to be induced after exposure to MeHg" and 2- Memantine is one of these drugs being used for neurological, regressive diseases and also being investigated for Autism: OSU Medical Center
That seems pertinent on many levels. Some caveats: A significant increase in NMDAR's after exposure to mercury. Memantine weakened that effect by blocking the NMDAR's. The NMDAR's are important in mercury neurotoxicity.
By Teresa Conrick
If you have a preteen or teen daughter(s) with autism - Please Read!
A group of parents who have daughters with an autism diagnosis are networking to form a group for researching the similar health issues our precious girls are having to endure. We want to see the common patterns or differences so that we can gather data to help pinpoint valuable information. A website for this has been developed, a treatment tracking system for autism called ChARMtracker (check it out at http://www.charmtracker.com). It is free to families and there are over 2,000 users worldwide now, all tracking histories, interventions, diets, medications, supplements etc. of their children. The pre-teen/teen girls would be done in a similar fashion but kept together as a group for data and specific age/sex similarities. This is parent-driven and has no connections to any government or pharmaceutical companies. We will be in communication with each other and the researchers as we journey. This will not take the place of a doctor or a medical plan but will hopefully aid in determining any correlations in our girls thus, guide treatment planning.
As I had discussed with my own daughter, Megan, just recently (Autism Estrogen and Seizures) about hormones and seizures, there seems to be some unique and challenging issues that may affect females diagnosed with autism. We would like to explore these ideas by using innovative data-gathering and parental involvement. What better way to the answers than looking at the affected children?
It is our hope that by systematic gathering of testing, data collection and a good source of researchers, we can find the missing answers to health issues that many of our daughters and loved ones suffer with so that treatments can be matched and health outcomes changed for the positive. As seizures seem to represent a very scary reality for our teen girls, we will also be reaching out to parents of girls injured by the Gardasil vaccine http://truthaboutgardasil.org/ to join us in our quest. Please wish us luck as we start on this innovative and trailblazing journey.
Please email me if you are interested:
The treatment category is sponsored by Lee Silsby, the leader in quality compounded medications for autism.
By Teresa Conrick
The sketch you see of my daughter, Megan, was done by my neighbor, Ceil, when Megan was eight. She used a photo as Meg was never able to pose and Ceil wanted to capture the sense of Megan's autism. I think the likeness is stunning and the message haunting. Meg is unable to speak and yet she wants to desperately. Ceil and her family moved in 2004, right as my marriage was moving into divorce court. It was a hard year and honestly, this year may top it.
Megan is now eighteen and as I have written here Hormones Seizures and Autism a Dangerous Mix she began to have Catemenial Epilepsy in the Summer of 2010. It is an extremely unusual type of epilepsy as it comes violently, strikingly and fortunately, only one time monthly, announcing the rise of estrogen and impending ovulation. Megan is a victim of injuries to her body brought on by vaccines as a baby/toddler and this latest assault, like a sniper rising out of the shadows each month, is a reminder of why autism is so very dramatic in its medical and behavioral picture.
We completed a month of hormone testing to be able to get a more comprehensive view of what could be happening to cause Megan to violently convulse into a grand mal type seizure, leaving her incapacitated and then into a deep, deep sleep for hours. Before I share that data and a possible source of this mysterious medical monster, let me describe the behaviors that have been happening, especially since autism has been historically branded as "psychiatric" and the medical horrors downplayed as "anecdotal."
My sweet daughter who has no words is charming and beautiful but this experience has turned her personality into Mr. Hyde as the hormones surge. As we get closer to Meg's period, she begins to snort out of her nose loudly and often. Any professionally-trained DSM follower, would call this a "stim" or possibly "repetitive" behavior but they would be wrong. You see, as Meg's potent levels of hormones begin their crazy climb, estrogen especially, causes nasal swelling:
"ORL J Otorhinolaryngol Relat Spec. 2000 Jan-Feb;62(1):39-42.
Nasal Mucosal Swelling and Reactivity During a Menstrual Cycle.
CONCLUSION: There is a connection between high oestrogen level and nasal mucosal reactivity."
Another "behavior" is wetting and I mean frequent, horribly smelling and like clockwork each month. Again, easy to say that this is autism, a "developmental disability", thus issues of toileting would be included but again, they would be wrong. This is a young woman who knows how to use the toilet but something happens in tandem to the hormone surges. In keeping with the theme:
Tufts Mast Cell Inflammation HERE
"Critical Role Of Mast Cells In Inflammatory Diseases And The Effect Of Acute Stress"
Hormones and Mast Cells
"The bladder has a surprisingly high number of estrogen receptors which make the bladder sensitive to variations in estrogen levels found during the menstrual cycle. Why? The bladder, urethra, vagina and vulva are all part of the urogenital sinus, and began as one small cell in a fetus which later divided to create each organ. Thus it is not suprising that the bladder can be so sensitive to estrogen. High estrogen levels activate mast cells and can cause IC patients to experience an increase in pain, pressure and frequency. Many IC patients endure an increase in bladder symptoms during the times of the month when their estrogen levels are high, particularly in the days before their period"....."These finding could be important in view of the fact that mast cells express estrogen receptors."
Having a child with autism changes your life forever. Mine changed sixteen years ago as I saw my daughter regress and begin to have medical issues that went unanswered and tragically, it is happening more frequently to other parents today. For those reasons, I have become a seeker of truth and healing by reading and examining past and current information regarding autism and the serious medical issues that it includes. For those of us in the trenches of autism, we know how SICK OUR CHILDREN ARE with issues of sensory overload, severe GI dysfunction, immune dysfunction, mitochondrial dysfunction, mast cell/inflammatory dysfunction, toxic encephalopathy, endocrine system dysfunction and seizures. Another factor involved in much of that, is the issue of immune-glutamatergic dysfunction. I know --- more dysfunction, but that is the medical reality of autism.
So a quick -- Immune-Glutamatergic Dysfunction 101 class -- with Wikipedia:
"Glutamate receptors are synaptic receptors located primarily on the membranes of neuronal cells. Glutamate is one of the 20 amino acids used to assemble proteins and as a result is abundant in many areas of the body, but it also functions as a neurotransmitter and is particularly abundant in the nervous system. Glutamate receptors are responsible for the glutamate-mediated post-synaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation. Furthermore, glutamate receptors are implicated in the pathologies of a number of neurodegenerative diseases due to their central role in excitotoxicity and their prevalence throughout the central nervous system."
Pubmed, the website of medical, peer-reviewed journals, is a great way to read about autism and its many medical dysfunctions, including glutamate receptor issues. In doing that, I started with just the key words, "glutamate receptor dysfunction" and Pubmed showed 7,043 studies. I then decided to see what other medical conditions may also be involved with glutamates - glutamate receptor dysfunction plus the word "seizures" gave me 858 studies; glutamate receptor dysfunction and "schizophrenia" showed 641; glutamate receptor dysfunction with "Parkinson's" had 303; and then typing in "autism" with glutamate receptor dysfunction brought me to 29 medical studies. Not very many compared to the others.
One of the first studies, (HERE) "Postmortem brain abnormalities of the glutamate neurotransmitter system in autism'. went back to 2001. Here was the conclusion: "Subjects with autism may have specific abnormalities in the AMPA-type glutamate receptors and glutamate transporters in the cerebellum. These abnormalities may be directly involved in the pathogenesis of the disorder." That sounds important and so I looked at the other 28 studies to read more. What was interesting and maybe disturbing is that about half of the studies done were in the last couple of years. These two specifically caught my attention and seemed to be a trend:
"Fragile X and autism: Intertwined at the molecular level leading to targeted treatments": (HERE)"Research regarding dysregulation of neurotransmitter systems in FXS, including the metabotropic glutamate receptor (mGluR)1/5 pathway and γ aminobutyric acid (GABA)A pathways, have led to new targeted treatments for FXS. Preliminary evidence suggests that these new targeted treatments will also be beneficial in non-fragile X forms of autism."
I usually write about my daughter, Megan, and her many medical issues related to her vaccine injuries. I am detouring you all briefly to describe a recent bout of Shingles that I have been dealing with as it relates to Megan, autism and a pattern that we have seen. Let me also point out that Shingles usually occurs in OLDER folks - and though I am enjoying the last days of my 4th decade - I am not the older that they mean - usually 60+ in years - but hold on to that fact as I'm going to revisit it down below. As vaccine names and amounts have increased, so have disabling idiopathic and chronic conditions brought on by illness and injury. Shingles, (herpes zoster) is a painful, blistering skin rash due to the varicella-zoster virus, the virus that causes chickenpox. Shingles also has been discussed as being directly related to the use in our country of a vaccine to fight varicella zoster - chicken pox, instead of natural immunity.
I am now weeks into this illness, minimal blisters but they are VERY painful and I am dreadfully exhausted! My right side is the affected side (shingles usually stays only on one side) and unfortunately, my eye is involved. As I type this, I have my 2nd appointment tomorrow at the ophthalmologist. I will also add that I am the youngest of seven children and my sibs were generous in passing down to me all their childhood illnesses, including Chicken Pox, back in the day. As I have shared with people about my having Shingles, these two responses show what many in the outside, autism world think - 1) Oh, You must have gotten that because you have so much stress and 2) Oh, I heard about that as it's related to measles. SO Wrong!
In 1995, Merck came out with a slugger of a vaccine. Since the "War on Childhood Infectious Diseases" has proven to be such an effective PR tool for many companies who PROFIT ENORMOUSLY from making vaccines, it was inevitable that Varicella or Chicken Pox, the "chicken" of the "poxes", would be added to the list of mandated vaccines. I remember it well as the campaign on its use seemed targeted at working mothers -- kind of an insurance plan to keep your child chicken pox-less so working moms would not have to be at home for the 5-10 days of their child's illness. I know because I had two little redheads whose doctor convinced their mother that vaccination was the working mother AND loving thing to do. How kind of Merck. Now I know some will say children would die without the vaccine but the possible reality flip-side to that is now many, many more older folks can have a severe illness that also can be horribly painful and long-lasting as well as fatal.
The NYT reported (HERE) in 2005 that it was indeed, very possible that Merck's Varivax was causing a surge of Shingles - "But even as the vaccine protects children, questions are arising about whether its use will increase the incidence of a related disease, shingles, in adults."...."Dr. Vásquez, along with a Yale colleague, Dr. Eugene D. Shapiro, wrote a commentary in the current edition of The New England Journal of Medicine that hailed the effectiveness of the vaccine for chickenpox but urged more study of its effects on shingles." Wow, here was an actual article seriously looking at how this new Chicken Pox vaccine from Merck may be about to cause a huge increase in Shingles. I read on in excitement that the NYT was seemingly allied with many of us who look at safety.
"The vaccine has been somewhat controversial and is not routinely used overseas".."One concern in other countries is whether using the vaccine would increase the rate of shingles in adults. Shingles, evidenced by a rash, blisters and pain, can lead to nerve damage called post-herpetic neuralgia that can last for weeks or months and cause excruciating pain, even from the touch of a shirt against the skin."
By Teresa Conrick
Two years ago, I wrote about my beautiful, vaccine-injured child, Megan, turning 16. March 2nd marks her 18th birthday and boy, has she gotten some horrible gifts! The Supreme Court of our United States declared on February 22nd, (HERE), that she would be unable - EVER - to receive compensation for her childhood vaccine injuries that have detoured her from a healthy, and pain-free life. Her vaccine injuries happened 16 years ago, yet we were never told by any of the professionals back then that autism symptoms can be medically related to brain, gut or mitochondrial injury from vaccines. We are unable to go to those companies who made her vaccines and prove, to a judge and jury, that they were dangerous to her and injured her into "autism."
Now some false autism advocates will try to convince you that autism "just happens", that it's "just genetic", that "we are better at diagnosing it", or that it's such an intense diagnosis that "parents WANT to get their child labeled" for all of the perks and benefits. PERKS & BENEFITS? What a crock! How about this perk- severe medical issues, many of which continue to be ignored or dismissed by the US Medical Establishment.
So back to Megan -- innocent, injured, nonverbal, and now ..... seizures. In August, Megan had a seizure, first in 2 years. She had an initial one back after her 16th birthday and we tested, consulted and waited as her EEG showed no seizure activity. Two years, nothing, thankfully, until this past August of her 17th year. Now like many of the symptoms of autism and many of Megan's medical symptoms, nothing is NORMAL and there always seems to be a puzzle piece begging to be solved. She had that seizure on August 22nd, then the next on September 27th, then October 24th, November 23rd, December 25th, January 27th and now yesterday, February 28th. Do you see the pattern? First, I have to say how thankful that these are a monthly experience as SO many children have numerous, daily and even hourly seizures. They are though of the grand mal/tonic clonic type and so we did initially have her neurologist recommend and start her on anti-seizure medication. She was on this for much of this time while the monthly seizures were not stopped and instead she began to have erratic and concerning behaviors AND also develop a BAD RASH. That was a huge concern and we had to stop the medication, which had unfortunately shown no benefit for her anyway.
So as the trees to the forest showed a picture, hormones became the culprit. Megan is completing hormone testing for a full month to help determine how her hormones might be causing these catamenial seizures. Initial blood testing showed abnormal estrogen and progesterone but could not tell us when or how. I came upon that word, catamenial, as I have been doing a lot of reading on hormones and seizures: (HERE)
"Catamenial (from the Greek kata, by; men, month) epilepsy refers to seizure exacerbation in relation to the menstrual cycle. Traditionally, the term has been used to refer to seizure exacerbation at the time of menstruation. In its purest form, a woman with catamenial epilepsy may have seizures only at the time of menstruation, but this form is not very common". ...... So again, my daughter's medical symptoms exhibit the "not very common." "Menstrually related hormonal fluctuations in estrogen and progesterone underlie the patterns of catamenial seizure exacerbation. Estrogens facilitate seizures, whereas progesterone protects against seizures. During the menstrual cycle, serum levels of estradiol and progesterone fluctuate Estrogens (in particular estradiol, the most important of the different estrogen forms) have potent proconvulsant properties. They exert an excitatory effect on neurons by stimulating the N-methyl-D-aspartate (NMDA)- type glutamate receptor. In women with epilepsy, intravenous administration of conjugated estrogens activates epileptiform discharges and may result in seizures."
Well that seems to be what we are seeing but why? Now it is interesting that words like NMDA and glutamate are at work here as those are also involved in research on autism, like here.."Neuronal glutamate receptor immunoreactivity patterns are abnormal in the hippocampi of thimerosal treated SJL mice" (HERE)
By Teresa Conrick
In 1995 when Megan was diagnosed with PDD-NOS, I thought all would be ok. It wasn't the "AUTISM" word and the neurologist who gave her that diagnosis was famous, and old, so he had to be an expert, right? HA! How naive I was back then. That doctor knew NOTHING about what was wrong with my daughter and she WAS autistic, according to the DSM, but I think he decided that the term PDD, would somehow get him out of the examining room without holding my hand or witnessing my tears. What doctor in their right mind wants to say in 1995, "Your child has AUTISM - a life-long, unknown cause, no treatment, diagnosis?" Two things he DID say have always stayed with me.
This one -- out of absolute denial of the severity of her symptoms (she lost speech, was a robot of perseverating behaviors, fingers in the ears, spinning, GI distress, crying, etc etc) --"Put her in a regular nursery school as being around NORMAL children may help her." Well, I am all for inclusion in the schools BUT my daughter was exhibiting MEDICAL problems that showed up in her behaviors. I don't think hanging out with Suzie or Johnny was going to stop that diarrhea or eliminate her painful auditory dysfunction. The other comment he made that has always lingered with me was this -- "Many of these children are very fair, very pale." It didn't occur to me to probe him on that as I watched my precious child tapping the blocks repeatedly instead of stacking them. She had been counting and stacking them months before and I was fearful that something very bad was happening. I had no idea what was in store.