Comments on: WXYZ and bad “investigative” reporting http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/ Autism news and opinion Thu, 09 Feb 2012 06:34:44 +0000 hourly 1 http://wordpress.org/?v=3.0.1 By: Liz Ditz http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51844 Liz Ditz Mon, 14 Jul 2008 18:46:47 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51844 Please be sure to read David Gorski's Science-Based Evidence post on Wilson's inaccurate, irresponsible "Investigative Report" http://www.sciencebasedmedicine.org/?p=71 You may, if you wish, craft a letter of your own to send to the station manager, Bob Sliva Vice President/General Manager WXYZ-TV 20777 West Ten Mile Road Southfield, MI 48037 Please be sure to read David Gorski’s Science-Based Evidence post on Wilson’s inaccurate, irresponsible “Investigative Report”

http://www.sciencebasedmedicine.org/?p=71

You may, if you wish, craft a letter of your own to send to the station manager,

Bob Sliva
Vice President/General Manager
WXYZ-TV
20777 West Ten Mile Road
Southfield, MI 48037

]]> By: Science-Based Medicine » When “investigative reporting” becomes anti-vaccine propaganda http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51838 Science-Based Medicine » When “investigative reporting” becomes anti-vaccine propaganda Mon, 14 Jul 2008 13:01:53 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51838 [...] WXYZ and bad “investigative” reporting [...] [...] WXYZ and bad “investigative” reporting [...]

]]> By: Joseph http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51785 Joseph Sat, 12 Jul 2008 03:28:21 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51785 <i>Are you sure? ABSOLUTELY? Your privilege. I am not and there are many scientists that don´t.</i> So you believe it's possible for something to be a poison at any dose, e.g. 0.00000001 micrograms? Or are you saying something else, like there's no dose-response relationship. Who are the many scientists that don't and what is the argument exactly? Are you sure? ABSOLUTELY?
Your privilege. I am not and there are many scientists that don´t.

So you believe it’s possible for something to be a poison at any dose, e.g. 0.00000001 micrograms?

Or are you saying something else, like there’s no dose-response relationship.

Who are the many scientists that don’t and what is the argument exactly?

]]> By: María Luján http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51783 María Luján Sat, 12 Jul 2008 01:15:16 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51783 <b>Because it’s true in this case. The dose makes the poison</b> Are you sure? ABSOLUTELY? Your privilege. I am not and there are many scientists that don´t. and that was the topic of two of the manuscripts I posted, especially on mercury. <a href="http://www.animalaid.org.uk/images/pdf/booklets/sbt.pdf" rel="nofollow">Link</a> We need SBT applied to the problem of toxic elements (potential) bioaccumulation in ASD as a CMP to the diagnosis (for now I have found this the best terminology)- in mechanism, testing, diagnosis and treatment, IMHO. It all depends of the expert you hear. I consider that there are a lot of experts in classic toxicology and there are very few knowledge in the mechanisms of toxic exposures- and these are worlds of difference-please see the reference above (Do you know the work of Dr Zalups on molecular mimicry; Dr Ballatori?). There is a lot of dogmatic aspects being discussed and a growing body of published evidence showing that things are different and complex in toxicology. <b>Otherwise everyone would be dead with a single atom of mercury ingested. That would mean, no one would be born, because we all are born with some amount of mercury. Sorry, but your links do not address that issue. One of your links notes micromolar concentrations of mercury. Great. The Omnibus case rests on nanomolar concentrations, and that seems to be only implicated in one paper, written by a PSC expert.</b> Please Sullivan, Can we discuss this in other tone? I have never said something about one single atom (?) Thanks The links I posted addressed the problem of the delay time and the dogma of classic toxicology in acute exposure You mentioned the nanomolar concentrations, Do you know this new manuscript? Biochem Biophys Res Commun. 2008 Jul 25;372(2):341-5. Heavy metal ions are potent inhibitors of protein folding. Sharma SK, Goloubinoff P, Christen P. Biochemisches Institut, Universität Zürich, CH-8057 Zürich, Switzerland. Environmental and occupational exposure to heavy metals such as cadmium, mercury and lead results in severe health hazards including prenatal and developmental defects. The deleterious effects of heavy metal ions have hitherto been attributed to their interactions with specific, particularly susceptible native proteins. Here, we report an as yet undescribed mode of heavy metal toxicity. Cd2+, Hg2+ and Pb2+ proved to inhibit very efficiently the spontaneous refolding of chemically denatured proteins by forming high-affinity multidentate complexes with thiol and other functional groups (IC(50) in the nanomolar range). With similar efficacy, the heavy metal ions inhibited the chaperone-assisted refolding of chemically denatured and heat-denatured proteins. Thus, the toxic effects of heavy metal ions may result as well from their interaction with the more readily accessible functional groups of proteins in nascent and other non-native form. The toxic scope of heavy metals seems to be substantially larger than assumed so far. The chaperons <a href="http://www.tulane.edu/~biochem/med/hsp.htm" rel="nofollow">Link</a> There are 5 class of chaperons hsp100, hsp90, hsp70, hsp60 and smHsp-hsp is heat shock protein and the number is the molecular weight in kilodaltons (that is 100 is 100000) Cell Stress Chaperones. 2007 Autumn;12(3):245-54. Heat shock protein 70 regulates cellular redox status by modulating glutathione-related enzyme activities. Guo S, Wharton W, Moseley P, Shi H. (Hsp) 70 has been reported to protect various cells and tissues from ischemic damage. However, the molecular mechanisms of the protection are incompletely understood. Ischemia induces significant alterations in cellular redox status that plays a critical role in cell survival/death pathways. We investigated the effects of Hsp70 overexpression on cellular redox status in Madin-Darby canine kidney (MDCK) cells under both hypoxic and ischemic conditions with 3 different approaches: reactive oxygen species (ROS) measurement by a fluorescence probe, redox environment evaluation by a hydroxylamine spin probe, and redox status assessment by the glutathione/glutathione disulfide (GSH/GSSG) ratio. Results from each of these approaches showed that the redox status in Hsp70 cells was more reducing than that in control cells under either hypoxic or oxygen and glucose deprivation (OGD) conditions. In order to determine the mechanisms that mediated the alterations in redox state in Hsp70 cells, we measured the activities of glutathione peroxidase (GPx) and glutathione reductase (GR), two GSH-related antioxidant enzymes. We found that OGD exposure increased GPx and GR activities 47% and 55% from their basal levels (no stress) in Hsp70 cells, compared to only 18% and 0% increase in control cells, respectively. These data, for the first time, indicate that Hsp70 modulates the activities of GPx and GR that regulate cellular redox status in response to ischemic stress, which may be important in Hsp70's cytoprotective effects. Again I am not doing quantum leaps here I am wondering why this topic is not more properly researched with the amount of published citations on glutathion abnormal status and findings of abnormal levels of toxic elements in ASD. Or why has not been discussed in the Omnibus? Now, why do you think that the current status of SBT, continuously evolving I would say, has not been presented in the OH by experts in the classical toxicology?Who presented the discussion of toxicogenomics and polymorphisms in glutathione cycle/thioredoxins/chaperons? Do you think that this could be noted by classical epidemiology?Where is the discussion of the impact of nanomolar concentration of Hg in chaperons (some of them heat shock proteins) and the status in ASD subgroups? You can tell me well, this has not been studied yet…and you will be right . The next month/year some finding may give other light to the very complex problem of bioaccumulation of toxic elements but the current status of the knowledge does not allow to have absolute conclussions. This is why I still think that the scientific ASD questions are not going to be answered in a court room or in an epi study but in a lab. I wonder what is the importance of this in ASD?Where are the studies on polymorphisms in chaperons in ASD and the impact of toxic elements in them, for example? <b>The model for mercury causing autism is that it is caused by the inorganic mercury in the brain left over after the breakdown of the organic mercury. So, yes, there are differences depending on species and ingestion method. But, in the end, any method of ingestion of either ethyl or methyl mercury should cause autism. It doesn’t.</b> 1-Please do not consider ethyl and methyl mercury similar because the published evidence says that they are not; because methyl and ethyl mercury ( that are ions therefore they need a counterion and this is not a minor topic MEHg+ and EtHg+) have different metabolism . 2-I was not discusssing the model of mercury causing autism- I do not think in THAT terms-, what I wanted to discuss without success is the problem of a CMP to an ASD related to toxic elements management and the lack of research on transport, metabolism and excretion systems in ASD subgroups. <b>And, yes, epidemiology is important. If you wish to brush it aside, go ahead. The whole reason why we are having this discussion is because armchair epidemiologists thought that the increase in the administrative prevalence of autism coincided with the increase in vaccinations and mercury. The fact that people are now discounting epidemiology—in the face of a huge increase in the adminstrative prevalence of autism—tells me that people don’t really care about the increase. It was just a tool to promote the vaccine/autism concept. Now that it is counterproductive to that argument people either say “epidemiology isn’t useful” or, worse yet, ignore the fact that the epidemiology is against them and continue with the epidemic arguments. Lastly, autism and mercury poisoning are not the same. I’ll take the word over Dr. Rodier over Sallie Bernard any day.</b> OK, your privilege; but there are many MANY aspects of Dr Rodier testimony that I do not understand based on the published evidence-non controversial. If you are interested I may present a link where I presented what are these aspects. I´ll take the search for the truth (properly and scientifically – but not dogmatic) over the word of anyone. The problem is that any time that I have tried to discuss this, it becomes a straw “woman” :). My point is that you still goes to causation –Epidemiology discussion as if I am trying to dismiss the value of epi BUT the point of collaboration in CMPs in ASD is not even discussed properly.Epidemiology has its importance but it has strong limitations-especially in terms of collaboration in multicausal heterogeneous individualized conditions. Please do not defend aspects that I have not attacked. I care about the increase; I care about many aspects. I consider that it should be analyzed differently. <b>So, while I appreciate your input in this, I still find it unconvincing.</b> OK, I am not trying to convince you but to present that there are other aspects that are not been analyzed. However, if you are not interested, it is OK. Because it’s true in this case. The dose makes the poison
Are you sure? ABSOLUTELY?
Your privilege. I am not and there are many scientists that don´t. and that was the topic of two of the manuscripts I posted, especially on mercury.
Link
We need SBT applied to the problem of toxic elements (potential) bioaccumulation in ASD as a CMP to the diagnosis (for now I have found this the best terminology)- in mechanism, testing, diagnosis and treatment, IMHO.
It all depends of the expert you hear. I consider that there are a lot of experts in classic toxicology and there are very few knowledge in the mechanisms of toxic exposures- and these are worlds of difference-please see the reference above (Do you know the work of Dr Zalups on molecular mimicry; Dr Ballatori?). There is a lot of dogmatic aspects being discussed and a growing body of published evidence showing that things are different and complex in toxicology.
Otherwise everyone would be dead with a single atom of mercury ingested. That would mean, no one would be born, because we all are born with some amount of mercury.
Sorry, but your links do not address that issue. One of your links notes micromolar concentrations of mercury. Great. The Omnibus case rests on nanomolar concentrations, and that seems to be only implicated in one paper, written by a PSC expert.
Please Sullivan, Can we discuss this in other tone? I have never said something about one single atom (?) Thanks
The links I posted addressed the problem of the delay time and the dogma of classic toxicology in acute exposure
You mentioned the nanomolar concentrations, Do you know this new manuscript?
Biochem Biophys Res Commun. 2008 Jul 25;372(2):341-5.
Heavy metal ions are potent inhibitors of protein folding.
Sharma SK, Goloubinoff P, Christen P.
Biochemisches Institut, Universität Zürich, CH-8057 Zürich, Switzerland.
Environmental and occupational exposure to heavy metals such as cadmium, mercury and lead results in severe health hazards including prenatal and developmental defects. The deleterious effects of heavy metal ions have hitherto been attributed to their interactions with specific, particularly susceptible native proteins. Here, we report an as yet undescribed mode of heavy metal toxicity. Cd2+, Hg2+ and Pb2+ proved to inhibit very efficiently the spontaneous refolding of chemically denatured proteins by forming high-affinity multidentate complexes with thiol and other functional groups (IC(50) in the nanomolar range). With similar efficacy, the heavy metal ions inhibited the chaperone-assisted refolding of chemically denatured and heat-denatured proteins. Thus, the toxic effects of heavy metal ions may result as well from their interaction with the more readily accessible functional groups of proteins in nascent and other non-native form. The toxic scope of heavy metals seems to be substantially larger than assumed so far.
The chaperons
Link
There are 5 class of chaperons hsp100, hsp90, hsp70, hsp60 and smHsp-hsp is heat shock protein and the number is the molecular weight in kilodaltons (that is 100 is 100000)
Cell Stress Chaperones. 2007 Autumn;12(3):245-54.
Heat shock protein 70 regulates cellular redox status by modulating glutathione-related enzyme activities.
Guo S, Wharton W, Moseley P, Shi H.
(Hsp) 70 has been reported to protect various cells and tissues from ischemic damage. However, the molecular mechanisms of the protection are incompletely understood. Ischemia induces significant alterations in cellular redox status that plays a critical role in cell survival/death pathways. We investigated the effects of Hsp70 overexpression on cellular redox status in Madin-Darby canine kidney (MDCK) cells under both hypoxic and ischemic conditions with 3 different approaches: reactive oxygen species (ROS) measurement by a fluorescence probe, redox environment evaluation by a hydroxylamine spin probe, and redox status assessment by the glutathione/glutathione disulfide (GSH/GSSG) ratio. Results from each of these approaches showed that the redox status in Hsp70 cells was more reducing than that in control cells under either hypoxic or oxygen and glucose deprivation (OGD) conditions. In order to determine the mechanisms that mediated the alterations in redox state in Hsp70 cells, we measured the activities of glutathione peroxidase (GPx) and glutathione reductase (GR), two GSH-related antioxidant enzymes. We found that OGD exposure increased GPx and GR activities 47% and 55% from their basal levels (no stress) in Hsp70 cells, compared to only 18% and 0% increase in control cells, respectively. These data, for the first time, indicate that Hsp70 modulates the activities of GPx and GR that regulate cellular redox status in response to ischemic stress, which may be important in Hsp70’s cytoprotective effects.
Again I am not doing quantum leaps here I am wondering why this topic is not more properly researched with the amount of published citations on glutathion abnormal status and findings of abnormal levels of toxic elements in ASD. Or why has not been discussed in the Omnibus?
Now, why do you think that the current status of SBT, continuously evolving I would say, has not been presented in the OH by experts in the classical toxicology?Who presented the discussion of toxicogenomics and polymorphisms in glutathione cycle/thioredoxins/chaperons? Do you think that this could be noted by classical epidemiology?Where is the discussion of the impact of nanomolar concentration of Hg in chaperons (some of them heat shock proteins) and the status in ASD subgroups?
You can tell me well, this has not been studied yet…and you will be right . The next month/year some finding may give other light to the very complex problem of bioaccumulation of toxic elements but the current status of the knowledge does not allow to have absolute conclussions. This is why I still think that the scientific ASD questions are not going to be answered in a court room or in an epi study but in a lab.
I wonder what is the importance of this in ASD?Where are the studies on polymorphisms in chaperons in ASD and the impact of toxic elements in them, for example?
The model for mercury causing autism is that it is caused by the inorganic mercury in the brain left over after the breakdown of the organic mercury. So, yes, there are differences depending on species and ingestion method. But, in the end, any method of ingestion of either ethyl or methyl mercury should cause autism. It doesn’t.
1-Please do not consider ethyl and methyl mercury similar because the published evidence says that they are not; because methyl and ethyl mercury ( that are ions therefore they need a counterion and this is not a minor topic MEHg+ and EtHg+) have different metabolism .
2-I was not discusssing the model of mercury causing autism- I do not think in THAT terms-, what I wanted to discuss without success is the problem of a CMP to an ASD related to toxic elements management and the lack of research on transport, metabolism and excretion systems in ASD subgroups.
And, yes, epidemiology is important. If you wish to brush it aside, go ahead. The whole reason why we are having this discussion is because armchair epidemiologists thought that the increase in the administrative prevalence of autism coincided with the increase in vaccinations and mercury.
The fact that people are now discounting epidemiology—in the face of a huge increase in the adminstrative prevalence of autism—tells me that people don’t really care about the increase. It was just a tool to promote the vaccine/autism concept. Now that it is counterproductive to that argument people either say “epidemiology isn’t useful” or, worse yet, ignore the fact that the epidemiology is against them and continue with the epidemic arguments.
Lastly, autism and mercury poisoning are not the same. I’ll take the word over Dr. Rodier over Sallie Bernard any day.
OK, your privilege; but there are many MANY aspects of Dr Rodier testimony that I do not understand based on the published evidence-non controversial. If you are interested I may present a link where I presented what are these aspects. I´ll take the search for the truth (properly and scientifically – but not dogmatic) over the word of anyone.
The problem is that any time that I have tried to discuss this, it becomes a straw “woman” :). My point is that you still goes to causation –Epidemiology discussion as if I am trying to dismiss the value of epi BUT the point of collaboration in CMPs in ASD is not even discussed properly.Epidemiology has its importance but it has strong limitations-especially in terms of collaboration in multicausal heterogeneous individualized conditions. Please do not defend aspects that I have not attacked. I care about the increase; I care about many aspects. I consider that it should be analyzed differently.
So, while I appreciate your input in this, I still find it unconvincing.
OK, I am not trying to convince you but to present that there are other aspects that are not been analyzed. However, if you are not interested, it is OK.

]]> By: Sullivan http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51780 Sullivan Fri, 11 Jul 2008 23:30:29 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51780 <blockquote>Absolutely? Why so many people is so glad with the use of this word?</blockquote> Because it's true in this case. The dose makes the poison. Otherwise everyone would be dead with a single atom of mercury ingested. That would mean, no one would be born, because we all are born with some amount of mercury. Sorry, but your links do not address that issue. One of your links notes micromolar concentrations of mercury. Great. The Omnibus case rests on nanomolar concentrations, and that seems to be only implicated in one paper, written by a PSC expert. <blockquote>Yes, but the management is different if it is inhalated, ingested, injected...</blockquote> The model for mercury causing autism is that it is caused by the inorganic mercury in the brain left over after the breakdown of the organic mercury. So, yes, there are differences depending on species and ingestion method. But, in the end, any method of ingestion of either ethyl or methyl mercury should cause autism. It doesn't. And, yes, epidemiology is important. If you wish to brush it aside, go ahead. The whole reason why we are having this discussion is because armchair epidemiologists thought that the increase in the administrative prevalence of autism coincided with the increase in vaccinations and mercury. The fact that people are now discounting epidemiology--in the face of a huge increase in the adminstrative prevalence of autism--tells me that people don't really care about the increase. It was just a tool to promote the vaccine/autism concept. Now that it is counterproductive to that argument people either say "epidemiology isn't useful" or, worse yet, ignore the fact that the epidemiology is against them and continue with the epidemic arguments. Lastly, autism and mercury poisoning are not the same. I'll take the word over Dr. Rodier over Sallie Bernard any day. So, while I appreciate your input in this, I still find it unconvincing.
Absolutely? Why so many people is so glad with the use of this word?

Because it’s true in this case. The dose makes the poison. Otherwise everyone would be dead with a single atom of mercury ingested. That would mean, no one would be born, because we all are born with some amount of mercury.

Sorry, but your links do not address that issue. One of your links notes micromolar concentrations of mercury. Great. The Omnibus case rests on nanomolar concentrations, and that seems to be only implicated in one paper, written by a PSC expert.

Yes, but the management is different if it is inhalated, ingested, injected…

The model for mercury causing autism is that it is caused by the inorganic mercury in the brain left over after the breakdown of the organic mercury. So, yes, there are differences depending on species and ingestion method. But, in the end, any method of ingestion of either ethyl or methyl mercury should cause autism. It doesn’t.

And, yes, epidemiology is important. If you wish to brush it aside, go ahead. The whole reason why we are having this discussion is because armchair epidemiologists thought that the increase in the administrative prevalence of autism coincided with the increase in vaccinations and mercury.

The fact that people are now discounting epidemiology—in the face of a huge increase in the adminstrative prevalence of autism—tells me that people don’t really care about the increase. It was just a tool to promote the vaccine/autism concept. Now that it is counterproductive to that argument people either say “epidemiology isn’t useful” or, worse yet, ignore the fact that the epidemiology is against them and continue with the epidemic arguments.

Lastly, autism and mercury poisoning are not the same. I’ll take the word over Dr. Rodier over Sallie Bernard any day.

So, while I appreciate your input in this, I still find it unconvincing.

]]> By: Amanda http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51777 Amanda Fri, 11 Jul 2008 21:45:20 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51777 I've actually had people go as far as to insist that the so-called "regression" I had starting around puberty must've been from the tetanus boosters. So I <em>have</em> heard that crap before. (Of course everyone seems to have their theories about that one, no matter how many hard facts I give them about the most likely reality.) I’ve actually had people go as far as to insist that the so-called “regression” I had starting around puberty must’ve been from the tetanus boosters. So I have heard that crap before. (Of course everyone seems to have their theories about that one, no matter how many hard facts I give them about the most likely reality.)

]]> By: María Luján http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51776 María Luján Fri, 11 Jul 2008 21:33:29 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51776 Sorry Kev, my last post citing several manuscripts was for the author - Sullivan. Sorry Kev, my last post citing several manuscripts was for the author – Sullivan.

]]> By: Sullivan http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51774 Sullivan Fri, 11 Jul 2008 21:25:14 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51774 Patrick, one of them is even called, "Tetanus Toxoid Adsorbed Adult Use" Pretty disingenuous of him to include that (as well as all the others, but this one is so obvious) in a discussion of whether vaccines cause autism in children. Sorry, but there are people who get stories wrong. This guy seems to have worked hard at doing so. Patrick,

one of them is even called,
“Tetanus Toxoid Adsorbed Adult Use”

Pretty disingenuous of him to include that (as well as all the others, but this one is so obvious) in a discussion of whether vaccines cause autism in children.

Sorry, but there are people who get stories wrong. This guy seems to have worked hard at doing so.

]]> By: María Luján http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51775 María Luján Fri, 11 Jul 2008 21:25:14 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51775 Kev, things are not so simple and in absence of knowledge based on data there is no real useful report, only opinions. Ok, let´s see <blockquote>1)the dose makes the poison. Absolutely. There has to be a dose small enough that it would not cause toxicity.</blockquote> Absolutely? Why so many people is so glad with the use of this word? There is an increasing amount of evidence looking at the impact of low doses- even very low doses- correlated to toxicogenomics. Some clues 1- <a href="http://www.ncbi.nlm.nih.gov/pubmed/18501191?ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" rel="nofollow">Link</a> 2-From <a href="http://www.ehponline.org/members/2002/suppl-5/851-854weiss/weiss-full.html" rel="nofollow">Link</a> <blockquote>“This concept may be applied to explain the second type of latency period for methylmercury. A toxic dose of mercury will cause an initial cell loss, which may or may not reduce the number of target cells to the point at which overt symptoms appear. Over time, the aging process will further reduce the number of cells until those that remain are too few to sustain function, and overt effects then erupt. In this situation the higher the initial dose, the greater the loss of cells due to the action of mercury. This will in turn reduce the latency period due to aging. This model explains the dose dependency of the second type of latency period” “To some degree, it mimics the process presumed to underlie Parkinson disease. Most observers agree that the appearance of clinical signs is merely the ultimate phase of a neurodegenerative process whose inception might even be traced to events occurring during early development (19). The clinical signs are believed to emerge after the death of 60-90% of the pigmented, dopamine-producing cells in the substantia nigra pars compacta. The long latency is attributed to the ability of the remaining cells to compensate for the functions of the vanished cells (20)” “The puzzle arises from the prolonged latency before the onset of unequivocal neurotoxicity, which covered a period during which blood and hair levels fell continuously. The dose did not, in this instance, make the poison, so to speak, in apparent violation of a cherished principle of traditional toxicology.” </blockquote> 3- <a href="http://www.ncbi.nlm.nih.gov/pubmed/1751790?ordinalpos=61&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum" rel="nofollow"> Link</a> <a href="http://jasn.asnjournals.org/cgi/reprint/2/4/866" rel="nofollow">Link</a> <blockquote> The toxicity of inorganic mercury was determined by titration. Perfusion with 1 microM inorganic mercury produced necrosis. The pathological features appeared to be the same as those resulting with 18.5 microM inorganic mercury </blockquote> <b>Now then the dose is not making the poison?</b> <blockquote>“The commonalities are obvious: manifestations of damage emerge only after compensatory processes have been exhausted.” “it is that the conventional tenets of toxicology need to be observed with a considerable degree of skepticism. We should be convinced, not by dogma, but by a deep understanding of mechanisms.”</blockquote> from the work presented in link 2) What about Thimerosal and inorganic mercury mechanisms of transport and metabolism and ex cretion- and others such as Al and Pb in children considering the injection route in the case of thimerosal and other coexposures ? <blockquote>2) mercury is everywhere. It was in the organic cinnamon-applesauce cup I just ate. It was in the organic lemonade juicebox I just drank. (sounds like I am the one on the playground, eh?).</blockquote> Yes, but the management is different if it is inhalated, ingested, injected or by dermal contact and affected by nutrition status and individual physiology and (epi)genomics- together with coexposures. 3) Epidemiology again? 4) RhoGam Why one of potential several are going to demonstrate a correlation, especially if it is only a collaborator? Int J Hyg Environ Health. 2007 Dec 20. [Epub ahead of print] Links Principal component analysis and discrimination of variables associated with pre- and post-natal exposure to mercury.Marques RC, Bernardi JV, Dórea JG, Bastos WR, Malm O. Fundação Universidade Federal de Rondônia, Porto Velho, RO, Brazil; Instituto de Biofísica Carlos Chagas Filho,Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil. The variance of variables associated with neurodevelopment at 180 days, pre-natal variables (Hg in placenta, blood and hair) and post-natal Hg exposure (including Thimerosal-containing vaccines, TCV) were examined in 82 exclusively breastfed infants using principal component analysis (PCA). This multivariate method was applied to identify hierarchy and sets of interrelated variables. The PCA yielded a two-factor solution, explaining 92% of variance and summarizing most of the relevant information in the dataset matrix: the first component represented birth weight and vaccine (first doses of Hepatitis B and DTP) variability and explained 57% of variance; the second component represented a gradient of neurodevelopment (Gesell scores) and explained 35% of variance. The third component explained only 3% of the remaining 8% variance. Beside CNS priming by breastfeeding, infant development (birth weight) and time of immunization with TCV should be considered in epidemiological studies. PCA can classify sets of variables related to vaccination and neuromotor development schedules, clearly discriminating between earlier and later TCV exposures of exclusively breastfed infants. In conclusion, the incommensurable concept of the chance of toxic risk caused by TCV-EtHg exposure against the proven benefit of immunization is in no way disputed here. However, infant neurodevelopmental (ND) disorders linked to Thimerosal-Hg stands in need of proof, but PCA points to the possibility of identifying exposure risk variables associated with ND schedules. 5) More epidemiology 6) Autism symptoms by? Things are much more complicated to compare- for yes or not-especially in the absence of knowledge of the above. Kev, things are not so simple and in absence of knowledge based on data there is no real useful report, only opinions.

Ok, let´s see

1)the dose makes the poison. Absolutely. There has to be a dose small enough that it would not cause toxicity.

Absolutely? Why so many people is so glad with the use of this word?
There is an increasing amount of evidence looking at the impact of low doses- even very low doses- correlated to toxicogenomics.
Some clues
1-
Link

2-From
Link

“This concept may be applied to explain the second type of latency period for methylmercury. A toxic dose of mercury will cause an initial cell loss, which may or may not reduce the number of target cells to the point at which overt symptoms appear. Over time, the aging process will further reduce the number of cells until those that remain are too few to sustain function, and overt effects then erupt. In this situation the higher the initial dose, the greater the loss of cells due to the action of mercury. This will in turn reduce the latency period due to aging. This model explains the dose dependency of the second type of latency period”
“To some degree, it mimics the process presumed to underlie Parkinson disease. Most observers agree that the appearance of clinical signs is merely the ultimate phase of a neurodegenerative process whose inception might even be traced to events occurring during early development (19). The clinical signs are believed to emerge after the death of 60-90% of the pigmented, dopamine-producing cells in the substantia nigra pars compacta. The long latency is attributed to the ability of the remaining cells to compensate for the functions of the vanished cells (20)”
“The puzzle arises from the prolonged latency before the onset of unequivocal neurotoxicity, which covered a period during which blood and hair levels fell continuously. The dose did not, in this instance, make the poison, so to speak, in apparent violation of a cherished principle of traditional toxicology.”

3-
Link

Link

The toxicity of inorganic mercury was determined by titration. Perfusion with 1 microM inorganic mercury produced necrosis. The pathological features appeared to be the same as those resulting with 18.5 microM inorganic mercury

Now then the dose is not making the poison?

“The commonalities are obvious: manifestations of damage emerge only after compensatory processes have been exhausted.”
“it is that the conventional tenets of toxicology need to be observed with a considerable degree of skepticism. We should be convinced, not by dogma, but by a deep understanding of mechanisms.”

from the work presented in link 2)
What about Thimerosal and inorganic mercury mechanisms of transport and metabolism and ex cretion- and others such as Al and Pb in children considering the injection route in the case of thimerosal and other coexposures ?

2) mercury is everywhere. It was in the organic cinnamon-applesauce cup I just ate. It was in the organic lemonade juicebox I just drank. (sounds like I am the one on the playground, eh?).

Yes, but the management is different if it is inhalated, ingested, injected or by dermal contact and affected by nutrition status and individual physiology and (epi)genomics- together with coexposures.
3) Epidemiology again?
4) RhoGam
Why one of potential several are going to demonstrate a correlation, especially if it is only a collaborator?
Int J Hyg Environ Health. 2007 Dec 20. [Epub ahead of print] Links
Principal component analysis and discrimination of variables associated with pre- and post-natal exposure to mercury.Marques RC, Bernardi JV, Dórea JG, Bastos WR, Malm O.
Fundação Universidade Federal de Rondônia, Porto Velho, RO, Brazil; Instituto de Biofísica Carlos Chagas Filho,Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.

The variance of variables associated with neurodevelopment at 180 days, pre-natal variables (Hg in placenta, blood and hair) and post-natal Hg exposure (including Thimerosal-containing vaccines, TCV) were examined in 82 exclusively breastfed infants using principal component analysis (PCA). This multivariate method was applied to identify hierarchy and sets of interrelated variables. The PCA yielded a two-factor solution, explaining 92% of variance and summarizing most of the relevant information in the dataset matrix: the first component represented birth weight and vaccine (first doses of Hepatitis B and DTP) variability and explained 57% of variance; the second component represented a gradient of neurodevelopment (Gesell scores) and explained 35% of variance. The third component explained only 3% of the remaining 8% variance. Beside CNS priming by breastfeeding, infant development (birth weight) and time of immunization with TCV should be considered in epidemiological studies. PCA can classify sets of variables related to vaccination and neuromotor development schedules, clearly discriminating between earlier and later TCV exposures of exclusively breastfed infants. In conclusion, the incommensurable concept of the chance of toxic risk caused by TCV-EtHg exposure against the proven benefit of immunization is in no way disputed here. However, infant neurodevelopmental (ND) disorders linked to Thimerosal-Hg stands in need of proof, but PCA points to the possibility of identifying exposure risk variables associated with ND schedules.

5) More epidemiology
6) Autism symptoms by? Things are much more complicated to compare- for yes or not-especially in the absence of knowledge of the above.

]]> By: Patrick http://leftbrainrightbrain.co.uk/2008/07/wxyz-and-bad-investigative-reporting/#comment-51772 Patrick Fri, 11 Jul 2008 19:17:16 +0000 http://leftbrainrightbrain.co.uk/?p=927#comment-51772 Oh, I did find the link at the bottom of the Text version to the 11 vaccines, but only counted 10 that showed a value. Oh, I did find the link at the bottom of the Text version to the 11 vaccines, but only counted 10 that showed a value.

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