A common X-linked inborn error of carnitine biosynthesis may be a risk factor for nondysmorphic autism
Patrícia B. S. Celestino-Sopera,1, Sara Violanteb,c,1, Emily L. Crawfordd, Rui Luoe, Anath C. Lionelf, Elsa Delabyg, Guiqing Caih, Bekim Sadikovica, Kwanghyuk Leea, Charlene Loa, Kun Gaoe, Richard E. Persona, Timothy J. Mossa, Jennifer R. Germana, Ni Huangi, Marwan Shinawia,j,2, Diane Treadwell-Deeringj,k, Peter Szatmaril, Wendy Robertsm, Bridget Fernandezn, Richard J. Schroero, Roger E. Stevensono, Joseph D. Buxbaumh, Catalina Betancurg, Stephen W. Schererf,m, Stephan J. Sandersp, Daniel H. Geschwinde, James S. Sutcliffed, Matthew E. Hurlesi, Ronald J. A. Wandersb, Chad A. Shawa, Suzanne M. Leala, Edwin H. Cook, Jr.q, Robin P. Goin-Kochela,j,r, Frédéric M. Vazb,1, and Arthur L. Beaudeta,j,r,1,3
Departments of aMolecular and Human Genetics, kPsychiatry, and rPediatrics, Baylor College of Medicine, Houston, TX 77030; jTexas Children’s Hospital, Houston, TX 77030; bLaboratory Genetic Metabolic Disease, Departments of Clinical Chemistry and Pediatrics, Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands; cMetabolism and Genetics Group, Research Institute for Medicines and Pharmaceutical Sciences (iMed.UL), Faculdade de Farmácia, Universidade de Lisboa, 1649-003 Lisbon, Portugal; dDepartment of Molecular Physiology and Biophysics, Center for Molecular Neuroscience, Vanderbilt University, Nashville, TN 37232; eDepartment of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; fCentre for Applied Genomics and Program in Genetics and Genome Biology, mHospital for Sick Children, Toronto, ON, Canada M5G 1X8; gInstitut National de la Santé et de la Recherche Médicale U952, Centre National de la Recherche Scientifique Unité Mixte de Recherche 7224, and Université Pierre et Marie Curie, University of Paris 6, Paris 94010, France; hSeaver Autism Center for Research and Treatment, Department of Psychiatry, and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY 10029; iWellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, United Kingdom; lThe Offord Centre for Child Studies, McMaster Children’s Hospital and Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, Canada L8S 4L8; nDisciplines of Genetics and Medicine, Memorial University of Newfoundland, St. John’s, NF, Canada A1B 3V6; oGreenwood Genetic Center, Greenwood, SC 29646; pProgram on Neurogenetics, Child Study Center and Departments of Psychiatry and Genetics, Yale University School of Medicine, New Haven, CT 06520; and qInstitute for Juvenile Research, Department of Psychiatry, University of Illinois, Chicago, IL 60608 This article is part of the special series of Inaugural Articles by members of the National Academy of Sciences elected in 2011. Edited by Helen H. Hobbs, University of Texas Southwestern Medical Center, Dallas, TX, and approved March 27, 2012 (received for review December 20, 2011)
We recently reported a deletion of exon 2 of the trimethyllysine hydroxylase epsilon (TMLHE) gene in a proband with autism. TMLHE maps to the X chromosome and encodes the first enzyme in carnitine biosynthesis, 6-N-trimethyllysine dioxygenase. Deletion of exon 2 of TMLHE causes enzyme deficiency, resulting in increased substrate concentration (6-N-trimethyllysine) and decreased product levels (3-hydroxy-6-N-trimethyllysine and γ-butyrobetaine) in plasma and urine. TMLHE deficiency is common in control males (24 in 8,787 or 1 in 366) and was not significantly increased in frequency in probands from simplex autism families (9 in 2,904 or 1 in 323). However, it was 2.82-fold more frequent in probands from malemale multiplex autism families compared with controls (7 in 909 or 1 in 130; P = 0.023). Additionally, six of seven autistic male siblings of probands in male-male multiplex families had the deletion, suggesting that TMLHE deficiency is a risk factor for autism (metaanalysis Z-score = 2.90 and P = 0.0037), although with low penetrance (2–4%). These data suggest that dysregulation of carnitine metabolism may be important in nondysmorphic autism; that abnormalities of carnitine intake, loss, transport, or synthesis may be important in a larger fraction of nondysmorphic autism cases; and that the carnitine pathway may provide a novel target for therapy or prevention of autism.
http://www.pnas.org/content/early/2012/05/01/1120210109.full.pdf+html?sid=82ea54dd-51ad-4840-8232-f77cbd1e65ee
Researchers link mild autism with red meat intake
By Michael Fielding on 5/16/2012
The deletion of part of a gene that plays a role in the synthesis of carnitine – an amino acid derivative that helps the body use fat for energy – leads to an imbalance in carnitine in the body, says a group of researchers led by those at Baylor College of Medicine and Texas Children's Hospital.
Meat eaters receive about 75 percent of their carnitine from their diet. However, dietary carnitine levels are low in vegetarians and particularly in vegans. In most people, levels of carnitine are balanced by the body's ability to manufacture its own carnitine in the liver, kidney and brain, starting with a modified form of the amino acid lysine.
Carnitine deficiency has been identified when not enough is absorbed through the diet or because of medical treatments such as kidney dialysis. Genetic forms of carnitine deficiency also exist, which are caused when too much carnitine is excreted through the kidneys.
The gene deletion may play a role in milder forms of autism, they say.
"How it is associated with the causes of autism is as yet unclear. However, it could point to a means of treatment or even prevention in some patients," said Dr. Arthur Beaudet, chair of molecular and human genetics at BCM and a physician at Texas Children's Hospital, and the senior author of the report that appears online in the Proceedings of the National Academy of Sciences.
Beaudet and his international group of collaborators believe the gene deletion
The TMLHE gene includes the genetic code for the first enzyme in the synthesis of carnitine (TMLHE stands for trimethyllysine epsilon which encodes the enzyme trimethyllysine dioxygenase).
"TMLHE deficiency itself is likely to be a weak risk factor for autism, but we need to do more studies to replicate our results," Beaudet said. He estimated that at the rates found in his study, the deficiency might be a factor in about 170 males born with autism per year in the United States. This would equate to about one-half of one percent of autism cases.
Studies in the laboratory that identified the deletion were led by Dr. Patricia B.S. Celestino-Soper, as a graduate student in Beaudet's laboratory at BCM, and by Dr. Sara Violante, a graduate student in the laboratory of Dr. Frédéric M. Vaz of the Academic Medical Center in Amsterdam.
Beaudet and his colleagues tested male autism patients who were the only people with the disorder in their families.
"We believe that … the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," Beaudet explained.
http://www.meatingplace.com/Industry/News/Details/33029
======================================
Patrícia B. S. Celestino-Sopera,1, Sara Violanteb,c,1, Emily L. Crawfordd, Rui Luoe, Anath C. Lionelf, Elsa Delabyg, Guiqing Caih, Bekim Sadikovica, Kwanghyuk Leea, Charlene Loa, Kun Gaoe, Richard E. Persona, Timothy J. Mossa, Jennifer R. Germana, Ni Huangi, Marwan Shinawia,j,2, Diane Treadwell-Deeringj,k, Peter Szatmaril, Wendy Robertsm, Bridget Fernandezn, Richard J. Schroero, Roger E. Stevensono, Joseph D. Buxbaumh, Catalina Betancurg, Stephen W. Schererf,m, Stephan J. Sandersp, Daniel H. Geschwinde, James S. Sutcliffed, Matthew E. Hurlesi, Ronald J. A. Wandersb, Chad A. Shawa, Suzanne M. Leala, Edwin H. Cook, Jr.q, Robin P. Goin-Kochela,j,r, Frédéric M. Vazb,1, and Arthur L. Beaudeta,j,r,1,3
Departments of aMolecular and Human Genetics, kPsychiatry, and rPediatrics, Baylor College of Medicine, Houston, TX 77030; jTexas Children’s Hospital, Houston, TX 77030; bLaboratory Genetic Metabolic Disease, Departments of Clinical Chemistry and Pediatrics, Academic Medical Center, University of Amsterdam, 1105 AZ, Amsterdam, The Netherlands; cMetabolism and Genetics Group, Research Institute for Medicines and Pharmaceutical Sciences (iMed.UL), Faculdade de Farmácia, Universidade de Lisboa, 1649-003 Lisbon, Portugal; dDepartment of Molecular Physiology and Biophysics, Center for Molecular Neuroscience, Vanderbilt University, Nashville, TN 37232; eDepartment of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; fCentre for Applied Genomics and Program in Genetics and Genome Biology, mHospital for Sick Children, Toronto, ON, Canada M5G 1X8; gInstitut National de la Santé et de la Recherche Médicale U952, Centre National de la Recherche Scientifique Unité Mixte de Recherche 7224, and Université Pierre et Marie Curie, University of Paris 6, Paris 94010, France; hSeaver Autism Center for Research and Treatment, Department of Psychiatry, and Friedman Brain Institute, Mount Sinai School of Medicine, New York, NY 10029; iWellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, United Kingdom; lThe Offord Centre for Child Studies, McMaster Children’s Hospital and Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, Canada L8S 4L8; nDisciplines of Genetics and Medicine, Memorial University of Newfoundland, St. John’s, NF, Canada A1B 3V6; oGreenwood Genetic Center, Greenwood, SC 29646; pProgram on Neurogenetics, Child Study Center and Departments of Psychiatry and Genetics, Yale University School of Medicine, New Haven, CT 06520; and qInstitute for Juvenile Research, Department of Psychiatry, University of Illinois, Chicago, IL 60608 This article is part of the special series of Inaugural Articles by members of the National Academy of Sciences elected in 2011. Edited by Helen H. Hobbs, University of Texas Southwestern Medical Center, Dallas, TX, and approved March 27, 2012 (received for review December 20, 2011)
We recently reported a deletion of exon 2 of the trimethyllysine hydroxylase epsilon (TMLHE) gene in a proband with autism. TMLHE maps to the X chromosome and encodes the first enzyme in carnitine biosynthesis, 6-N-trimethyllysine dioxygenase. Deletion of exon 2 of TMLHE causes enzyme deficiency, resulting in increased substrate concentration (6-N-trimethyllysine) and decreased product levels (3-hydroxy-6-N-trimethyllysine and γ-butyrobetaine) in plasma and urine. TMLHE deficiency is common in control males (24 in 8,787 or 1 in 366) and was not significantly increased in frequency in probands from simplex autism families (9 in 2,904 or 1 in 323). However, it was 2.82-fold more frequent in probands from malemale multiplex autism families compared with controls (7 in 909 or 1 in 130; P = 0.023). Additionally, six of seven autistic male siblings of probands in male-male multiplex families had the deletion, suggesting that TMLHE deficiency is a risk factor for autism (metaanalysis Z-score = 2.90 and P = 0.0037), although with low penetrance (2–4%). These data suggest that dysregulation of carnitine metabolism may be important in nondysmorphic autism; that abnormalities of carnitine intake, loss, transport, or synthesis may be important in a larger fraction of nondysmorphic autism cases; and that the carnitine pathway may provide a novel target for therapy or prevention of autism.
http://www.pnas.org/content/early/2012/05/01/1120210109.full.pdf+html?sid=82ea54dd-51ad-4840-8232-f77cbd1e65ee
Researchers link mild autism with red meat intake
By Michael Fielding on 5/16/2012
The deletion of part of a gene that plays a role in the synthesis of carnitine – an amino acid derivative that helps the body use fat for energy – leads to an imbalance in carnitine in the body, says a group of researchers led by those at Baylor College of Medicine and Texas Children's Hospital.
Meat eaters receive about 75 percent of their carnitine from their diet. However, dietary carnitine levels are low in vegetarians and particularly in vegans. In most people, levels of carnitine are balanced by the body's ability to manufacture its own carnitine in the liver, kidney and brain, starting with a modified form of the amino acid lysine.
Carnitine deficiency has been identified when not enough is absorbed through the diet or because of medical treatments such as kidney dialysis. Genetic forms of carnitine deficiency also exist, which are caused when too much carnitine is excreted through the kidneys.
The gene deletion may play a role in milder forms of autism, they say.
"How it is associated with the causes of autism is as yet unclear. However, it could point to a means of treatment or even prevention in some patients," said Dr. Arthur Beaudet, chair of molecular and human genetics at BCM and a physician at Texas Children's Hospital, and the senior author of the report that appears online in the Proceedings of the National Academy of Sciences.
Beaudet and his international group of collaborators believe the gene deletion
The TMLHE gene includes the genetic code for the first enzyme in the synthesis of carnitine (TMLHE stands for trimethyllysine epsilon which encodes the enzyme trimethyllysine dioxygenase).
"TMLHE deficiency itself is likely to be a weak risk factor for autism, but we need to do more studies to replicate our results," Beaudet said. He estimated that at the rates found in his study, the deficiency might be a factor in about 170 males born with autism per year in the United States. This would equate to about one-half of one percent of autism cases.
Studies in the laboratory that identified the deletion were led by Dr. Patricia B.S. Celestino-Soper, as a graduate student in Beaudet's laboratory at BCM, and by Dr. Sara Violante, a graduate student in the laboratory of Dr. Frédéric M. Vaz of the Academic Medical Center in Amsterdam.
Beaudet and his colleagues tested male autism patients who were the only people with the disorder in their families.
"We believe that … the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," Beaudet explained.
http://www.meatingplace.com/Industry/News/Details/33029
======================================
shot the messenger
im stunned. by playing into corporate interest here, we the consumers just witnessed corporate science at it's best $$$"We believe that the most attractive hypothesis at this time is that the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," said Beaudet.http://www.sciencedaily.com/releases/2012/05/120507154101.htm
• shoot the messenger
•
a perfect example of 'shoot the messenger'. yes, indeed, pull the article. some times the meat of the matter is just impossible to digest. throw these findings in the trash. burn them, no, burn michael at the stake for even bringing this study to meatingplace and or the media mainstream. it would be a sin to find the cause of these autistic children, even if it did mean the implications of the meat industry. better yet, just do as the usda mad cow debacle does, lie about it. ... CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Terry Singeltary
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• Reply Edit Delete
"We believe that the most attractive hypothesis at this time is that the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," said Beaudet.
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This would equate to about one-half of one percent of autism cases. Oh yeah lets spend billions on this puppy, better yet lets make this the next battle cry and turn it into a gazillion dollar charity. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | read on! Reply
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This is mostly a thinly disguised stab at the red meat industry, it is unfortunate that Meating Place has allowed themselves to be sucked into the mix. Quote from the article; "how it is associated with the causes of autism is as yet unclear", which means obviously they don't have a clue. Therefore the article is just another piece of propaganda aimed at the red meat industry. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Third Rock Reply
• After reading that quote, I stopped reading the article and read the comments. Which always prove to be more interesting. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | A Reply
• I read the study
. . . and although I am not a genetecist it is pretty clear that the absence of the TMLHE gene (which helps to create carnitine in the body) is a factor in mild autism. Which would lead one to believe (although the authors do not directly state this) that additional dietary supply of carnitine from red meat (hence the name) might play a role in preventing this form of autism. The headline above is true (there is possibly a link) but the implication that almost everyone would draw from it (red meat causes autism) is not. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Andrew Clifton Reply
• Pull the article
Meatingplace needs to pull this article and re-write it. Sorry Michael but very confusing. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Meater Reply
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Here is the actual article, folks:
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I do not have time to read it in detail, but upon skimming the article, I can find no real discussion of meat eating or diet in general. The research focuses on carnitine deficiency as it relates to genetic predisposition. Citing previous research, the authors note
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"If penetrancefor autism is influenced by carnitine intake during infancy,the risk for autism associated with TMLHE deficiency may begreater in countries with a high frequency of vegetarian diets andlower meat or beef intake. China, India, and South Korea areall countries where some studies of the incidence of autism areavailable (22, 33, 34) and there is a more vegetarian diet and/ormuch lower beef intake."
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The article posted at meatingplace is a gross misinterpretation of this research. Please note, however, that this research also does NOT show a connection between diet and autism. The quote above offers a testable hypothesis and suggests a direction for research, but that research was not done here. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Holli Reply
• Terrible title!
This is a terrible and misleading title! The article itself provides no definitive means by which meat intake, or lack thereof, will result in mild autism. It simply states that meat provides high levels of carnitine, while dietary carnitine is low in vegetarians and vegans. It does not state the level of production of carnitine within the body based on diet either. I think this article was written more as a scare tactic rather than as a source of scientific knowledge! CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Brendan Corrigan Reply
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I am waiting/wondering if the editors of MeatingPlace or the author of this article will respond to the comments being made? I think they should and hope they will - accountablity folks!! CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Wonderng Reply
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Ummm.... This makes no sense. Not only is there no mention of how diet is connected, but there is a clear mistake in the text:"Beaudet and his international group of collaborators believe the gene deletion..."Huh? CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Holli Reply
• Misleading title
What? The article is confusing, contradictory and has no place on MP. I would have thought that MP would at least not jump on the media hype band wagon with titles whose sole purpose is to elicit an emotional response. Another one of these and I'm dropping my subscription! CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Old Bastard Reply
• There is a way to fix this.
Michael, a hot pot of high octane coffee has a beneficial mind clearing effect. Always write articles after consuming at least 4 full cups. Add a little 2% sweet milk, no creamers. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Douglas Craven Reply
• Confusing Article
What a confusing article. I still don't know if they are saying red meat prevents or casuses autism. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Jason Newman Reply
• Agree with comment below...misleading title and poorly written article
When I started reading the article, I was waiting for the link between read meat consumption and autism to be made. However, that did not happen. This title is misleading and could cause a lot of confusion and undue attention. What the article sounds like it is saying is that increasing dietary intake of red meat may help mildly autistic children with the TMHLE gene deletion. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Reply
• Red Meat and Autism
If you don't have some one with a science background, you should hire one to review an article like this one, before it is broadcasted around the globe. A good communicator, should consult a specialist with expertise in the subject matter before and after writing such an article. You managed to confuse the majority of your readers today. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | AIA Reply
• damaging title
Just one more example of how people that are supposed to be a part of meat industry contribute to the negative perception toward red meat. Right up there with "cook it stupid" when an outbreak has multiple children on dialysis. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | roger stone Reply
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MP once again joins the ranks of mainstream media with misleading head lines. Why would a so-called industry media source do this? Keep it up MP and you will soon loose subscibers and advertisers!!!! CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Again Reply
• Misleading Title and body of article
The way the article reads it sounds as if carnitine defficiency is the cause of the autism. Since you get carnitine from red meat in the diet, it looks like a diet including red meat would provide some protection against autism. The article says its the vegans that normally have low levels of it. If the gene is deleted where they cannot manufacture their own carnitine from lysine pre-cursor then they would have lowest levels of carnitine and be most susceptible to the effects of carnitine deficiency. Either the title is wrong or we are not given enough of the article to be clear in what they are saying. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | SPC Reply
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Please correct the title. Many people scan titles and don't read the entire article. The title is misleading. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Dan Buskirk Reply
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So the intake of red meat would be part of a treatment plan for boys with mild autism??Why not title this article..Red meat helps autism? CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Jason Rainey Reply
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I believe what the study is saying is that NOT eating enough meat is the link, not eating meat. Also, they believe it only accounts for a very small percentage of autism cases. Solid reading, bird. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | anon Reply
• Mild autism associated with red meat intake
The article has one sentence that might be about meat consumption and this form of autism. Why the misleading and inflammatory title? This article is about genetics of autism and should be titlled as such. CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Mark Walton Reply
• I agree! That is a terrible title! It's misleading. CancelSubmit Cancel Submit
Wednesday, May 16, 2012 | DeWitt Reply
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The following sentence was not completed in the article. "Beaudet and his international group of collaborators believe the gene deletion". After reading this article, is the title correct? I read this to mean that some meat consumption will provide the carnatine (or precursors) that will prevent autism? CancelSubmit Cancel Submit Wednesday, May 16, 2012 | Hog Man Reply
SEE NEW TITLE WITH NEW STORY LINE NOW ;
Industry News – AM
Red meat intake may offset autism risk factor: researchers (updated)
By Michael Fielding on 5/16/2012
The deletion of part of a gene that plays a role in the synthesis of carnitine – an amino acid derivative that helps the body use fat for energy – could play a part in the development of a mild form of autism, researchers say. The consumption of red meat, especially among very young children, could in turn reduce the chance of autism developing.
It works like this: A group of researchers at Baylor College of Medicine and Texas Children's Hospital found that patients who lacked the gene in question had an "imbalance" in their carnitine levels. That is, without the gene they could not manufacture sufficient levels of carnitine from within their own bodies. In turn, the lack of carnitine may play a role in milder forms of autism, according to researchers.
Carnitine deficiency has been identified when not enough is absorbed through the diet or because of medical treatments such as kidney dialysis. Genetic forms of carnitine deficiency also exist, which are caused when too much carnitine is excreted through the kidneys.
On the other hand, taking in more carnitine through diet could help off-set the effects of the deleted gene. Meat-eaters get about 75 percent of their carnitine from their diet, and the amino acid tends to exhibit low dietary levels in vegetarians and, especially, vegans.
"How it is associated with the causes of autism is as yet unclear. However, it could point to a means of treatment or even prevention in some patients," said Dr. Arthur Beaudet, chair of molecular and human genetics at BCM and a physician at Texas Children's Hospital, and the senior author of the report that appears online in the "Proceedings of the National Academy of Sciences."
"[The gene] deficiency itself is likely to be a weak risk factor for autism, but we need to do more studies to replicate our results," Beaudet said. He estimated that at the rates found in his study, the deficiency might be a factor in about 170 males born with autism per year in the United States —about one-half of one percent of autism cases.
"We believe that … the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," Beaudet explained.
This news item has been re-edited to better reflect the research findings.
shot the messenger
im stunned. by playing into corporate interest here, we the consumers just witnessed corporate science at it's best $$$"We believe that the most attractive hypothesis at this time is that the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," said Beaudet.http://www.sciencedaily.com/releases/2012/05/120507154101.htm
"We believe that the most attractive hypothesis at this time is that the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," said Beaudet.
Sources
[edit] Food
The highest concentrations of carnitine are found in red meat and dairy products. Other natural sources of carnitine include nuts and seeds (e.g. pumpkin, sunflower, sesame), legumes or pulses (beans, peas, lentils, peanuts), vegetables (artichokes, asparagus, beet greens, broccoli, brussels sprouts, collard greens, garlic, mustard greens, okra, parsley, kale), fruits (apricots, bananas), cereals (buckwheat, corn, millet, oatmeal, rice bran, rye, whole wheat, wheat bran, wheat germ) and other "health" foods (bee pollen, brewer's yeast, carob).[citation needed]
Product
Quantity
Carnitine
Beef steak
100 g
95 mg
Ground beef
100 g
94 mg
Pork
100 g
27.7 mg
Bacon
100 g
23.3 mg
Tempeh
100 g
19.5 mg
Cod fish
100 g
5.6 mg
Chicken breast
100 g
3.9 mg
American cheese
100 g
3.7 mg
Ice cream
100 ml
3.7 mg
Whole milk
100 ml
3.3 mg
Avocado
one medium
2 mg[24]
Cottage cheese
100 g
1.1 mg
Whole-wheat bread
100 g
0.36 mg
Asparagus
100 g
0.195 mg
White bread
100 g
0.147 mg
Macaroni
100 g
0.126 mg
Peanut butter
100 g
0.083 mg
Rice (cooked)
100 g
0.0449 mg
Eggs
100 g
0.0121 mg
Orange juice
100 ml
0.0019 mg
In general, 20 to 200 mg are ingested per day by those on an omnivorous diet, whereas those on a strict vegetarian or vegan diet may ingest as little as 1 mg/day.[24] No advantage appears to exist in giving an oral dose greater than 2 g at one time, since absorption studies indicate saturation at this dose.[citation needed]
[edit] Other sources
Other sources may be found in over-the-counter vitamins, energy drinks and various other products. Products containing L-carnitine cannot be marketed as "natural health products" in Canada. L-Carnitine products and supplements are not allowed to be imported into Canada (Health Canada).[25] However, the Canadian government has issued an amendment in December 2011 allowing the sale of L-carnitine without a prescription [26]
[edit] See also...snip...end
“We’ve begun to realize the range of social, economic and health benefits for Albertans that are waiting to be discovered through prion research,” said Doug Horner, Minister of Alberta Advanced Education and Technology. “For instance, researchers have found that there may be common factors between prion diseases and other human diseases such as autism and Alzheimer’s. Not only can this research help us find solutions to global social and health issues, but it will also enhance the growth of Alberta’s Next Generation Economy.”
Dr. David Westaway, University of Alberta Extending the spectrum of prionopathies to amyotrophic lateral sclerosis (ALS) and autism Dr. Westaway’s study aims to extend the boundaries of what is considered prion disease. His project takes the chemistry of the prion protein into the territory of nervous system diseases such as ALS (Lou Gehrig’s disease) and socialization disorder diseases such as autism. These brain diseases are at least 1,000 times more common than diseases currently accepted as prion related.
Dr. Westaway hypothesizes that a different type of protein misfolding may operate in brain diseases such as Lou Gehrig’s and autism. This type of protein misfolding may occur in response to stresses in the brain. Unlike misfolded prions, other misfolded proteins may be noninfectious and not viable outside of the affected animal. Dr. Westaway’s research team will investigate these hypotheses by inducing changes in the brain cells of laboratory mice, measuring the resulting electrical impulses in the animals’ nervous systems and analyzing the effect on behaviour. Because nervous transmission by electrical impulse can be measured in isolated brain cells, adding small amounts of toxins to the fluids bathing the cell cultures will make it possible to study the effect of stress. The results could lead to new ways of thinking about nervous system disorders.
• Are some commoner types of neurodegenerative disease (including Alzheimer's disease and Parkinson's disease) also transmissible? Some recent scientific research has suggested this possibility
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
Proposal ID: 29403
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both disease, and it’s variants, in many cases are merely names of the people that first discovered them. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer than the TSE prion disease. Symptoms are very similar, and pathology is very similar. I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
Conclusions
There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics let science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already. what’s the use of science progressing human life to the century mark, if your brain does not work?
combined cannot exceed 350 Words
shortened to proper word count ;
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
Tuesday, October 4, 2011
Molecular Psychiatry
advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. Keywords: amyloid; prion; protein misfolding; disease transmission
see more here ;
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
snip...end
Thank You for accepting my submission
# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? and the opportunity to present it, at the Alzheimer’s Association International Conference 2012 (AAIC), as a poster presentation. However, with great sadness, I must regretfully decline the invitation due to a medical reasons, and traveling to Canada, of which is not possible. ...
Thank You,
With Kindest Regards,
I am sincerely,
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
From:
Sent: Saturday, April 07, 2012 8:20 PM
To: Terry S. Singeltary Sr.
Subject: RE: re-submission
Dear Terry,
Yes, your proposal was accepted as a poster presentation. Please decline the invitation if appropriate.
Best Regards,
______________________________________
Alzheimer’s Association – National Office
225 North Michigan Avenue – Floor 17
Chicago, Illinois 60601
=============snip...end...source reference...# 29403==========
14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Human Prion Diseases in the United States
Robert C. Holman1*, Ermias D. Belay1, Krista Y. Christensen1, Ryan A. Maddox1, Arialdi M. Minino2, Arianne M. Folkema1, Dana L. Haberling1, Teresa A. Hammett1, Kenneth D. Kochanek2, James J. Sejvar1, Lawrence B. Schonberger1
1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-borne and Enteric Diseases, Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services (USDHHS), Atlanta, Georgia, United States of America, 2 Division of Vital Statistics, National Center for Health Statistics, Centers for Disease Control and Prevention (CDC), U.S. Department of Health and Human Services (USDHHS), Hyattsville, Maryland, United States of America
Abstract
Background
Prion diseases are a family of rare, progressive, neurodegenerative disorders that affect humans and animals. The most common form of human prion disease, Creutzfeldt-Jakob disease (CJD), occurs worldwide. Variant CJD (vCJD), a recently emerged human prion disease, is a zoonotic foodborne disorder that occurs almost exclusively in countries with outbreaks of bovine spongiform encephalopathy.
This study describes the occurrence and epidemiology of CJD and vCJD in the United States.
Methodology/Principal Findings
Analysis of CJD and vCJD deaths using death certificates of US residents for 1979–2006, and those identified through other surveillance mechanisms during 1996–2008. Since CJD is invariably fatal and illness duration is usually less than one year, the CJD incidence is estimated as the death rate. During 1979 through 2006, an estimated 6,917 deaths with CJD as a cause of death were reported in the United States, an annual average of approximately 247 deaths (range 172–304 deaths). The average annual age-adjusted incidence for CJD was 0.97 per 1,000,000 persons. Most (61.8%) of the CJD deaths occurred among persons ≥65 years of age for an average annual incidence of 4.8 per 1,000,000 persons in this population. Most deaths were among whites (94.6%); the age-adjusted incidence for whites was 2.7 times higher than that for blacks (1.04 and 0.40, respectively). Three patients who died since 2004 were reported with vCJD; epidemiologic evidence indicated that their infection was acquired outside of the United States.
Conclusion/Significance
Surveillance continues to show an annual CJD incidence rate of about 1 case per 1,000,000 persons and marked differences in CJD rates by age and race in the United States. Ongoing surveillance remains important for monitoring the stability of the CJD incidence rates, and detecting occurrences of vCJD and possibly other novel prion diseases in the United States.
Citation: Holman RC, Belay ED, Christensen KY, Maddox RA, Minino AM, et al. (2010) Human Prion Diseases in the United States. PLoS ONE 5(1): e8521. doi:10.1371/journal.pone.0008521
Editor: Mick F. Tuite, University of Kent, United Kingdom
Received: July 21, 2009; Accepted: October 30, 2009; Published: January 1, 2010
Holman et al. This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.
Funding: The authors have no support or funding to report.
Competing interests: The authors have declared that no competing interests exist.
* E-mail: rholman@cdc.gov
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
Most recent response on 02 Jan 2011 at 20:00 GMT
re-Human Prion Diseases in the United States
Original Article
Human Prion Diseases in the United States
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
snip...
Confucius is confused again? how in 1996 and earlier can the 28 sporadic CJD victims and the one-in-a-million there from, how can it still be one in a million in 2008, with the sporadic CJD count rising to 205, still be one-in-a-million? and the years in-between, steady rise just about every year, and it still be only one-in-a-million, year after year after years? I suppose just more of that fuzzy math, which you can see here;
Tuesday, November 08, 2011
Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper
Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.
The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.
Provider Details
Creutzfeldt-jakob Disease Foundation
Summary
Contact Information
More Information
Description:
CJD is a rare, fatal brain disorder. The statistical incidence of CJD cases in the US has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty five percent of the cases are sporadic, meaning there is no known cause at present.Toll free in state: (800) 659-1991, Main: (330) 665-5590
Service Categories
Brain Injury, Dementia/Alzheimer's, Donations, Mental Health
Contact Information:
Phone: (330) 665-5590
Last Update Date: 07/23/2010
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.
Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.
Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.
Re: vCJD in the USA * BSE in U.S.
15 November 1999 Terry S Singeltary, NA
In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.
Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.
My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.
The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?
CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.
So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.
No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;
Since 1990 the U.S. has raised 1,250,880,700 cattle;
Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;
There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;
Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;
Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.
I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.
Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.
It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........
The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.
Terry S. Singeltary Sr.
P.O. Box 42, Bacliff, Texas 77518 USA
Competing interests:None declared
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000 Terry S Singeltary
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.
Considering all this, the sheep to cow ration is meaningless.
As I said, it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
Competing interests:None declared
Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD
+ Author Affiliations
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
Reply to Singletary
Ryan A. Maddox, MPH Ermias D. Belay, MD, Lawrence B. Schonberger, MD Centers for Disease Control and Prevention Atlanta GA
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication).
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans.
full text ;
atypical L-type BASE BSE
Friday, May 11, 2012
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
***In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.
Tuesday, May 1, 2012
BSE MAD COW LETTERS TO USDA (Tom Vilsack, Secretary of Agriculture) and FDA (Magaret Hamburg, Commissioner of FDA) May 1, 2012
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH
Friday, May 4, 2012
May 2, 2012: Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States
Sunday, March 11, 2012
APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations
Wednesday, April 4, 2012
Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68
Sunday, May 6, 2012
Bovine Spongiform Encephalopathy Mad Cow Disease, BSE May 2, 2012 IOWA State University OIE
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010 2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
Tuesday, March 16, 2010
COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA
COMMONWEALTH OF AUSTRALIA
Proof Committee Hansard
RRA&T 2 Senate Friday, 5 February 2010
RURAL AND REGIONAL AFFAIRS AND TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association CARTER, Mr John Edward, Director, Australian Beef Association CHAIR—Welcome. Would you like to make an opening statement? Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so: You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heinemann variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:
snip...see full text 110 pages ;
for those interested, please see much more here ;
Tuesday, January 17, 2012
Annual report of the Scientific Network on BSE-TSE EFSA-Q-2011-01110 Issued: 20 December 2011
Friday, January 6, 2012
OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:
Comments on technical aspects of the risk assessment were then submitted to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
Monday, January 2, 2012
EFSA Minutes of the 6th Meeting of the EFSA Scientific Network on BSE-TSE Brussels, 29-30 November 2011
SPONTANEOUS ??? NOT...
How the California cow got the disease remains unknown. Government officials expressed confidence that contaminated food was not the source, saying the animal had atypical L-type BSE, a rare variant not generally associated with an animal consuming infected feed.
However, a BSE expert said that consumption of infected material is the only known way that cattle get the disease under natural conditons.
“In view of what we know about BSE after almost 20 years experience, contaminated feed has been the source of the epidemic,” said Paul Brown, a scientist retired from the National Institute of Neurological Diseases and Stroke.
BSE is not caused by a microbe. It is caused by the misfolding of the so-called “prion protein” that is a normal constituent of brain and other tissues. If a diseased version of the protein enters the brain somehow, it can slowly cause all the normal versions to become misfolded.
It is possible the disease could arise spontaneously, though such an event has never been recorded, Brown said.
Senior Layperson
Terry S. Singeltary Sr.
Bacliff, Texas USA
Wednesday, May 16, 2012
A common X-linked inborn error of carnitine biosynthesis may be a risk factor for nondysmorphic autism
SNIP...
"We believe that … the increased risk of autism is modified by dietary intake of carnitine from birth through the first few years of life," Beaudet explained.
tss
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