The Seven Most Common Thinking Errors of Highly Amusing Quacks and Pseudoscientists (Part 2):
Let me begin by apologizing for my prolonged and unannounced absence from the blogosphere – the requirements of job and family prevented me from pursuing my blog for a period of time. With luck (and assuming that grant applications are accepted and funded), I should continue to have “fair sailing” for the next few months.
Thinking Error 3: Post Hoc Correction of Hypotheses:
Before we get into this “thinking error”, I need to make abundantly clear what it is we’re talking about. One of the most fundamental characteristics of real scientists is that they are always revising, modifying and – when necessary – discarding their theories and hypotheses in light of new data. To many people outside of the scientific disciplines, this looks like indecision or just plain waffling – a “bad” thing if you’re a politician trying to stake out a position for legislation or electioneering.
However, a failure to “change with the wind” – as one politician put it – is a certain sign that a researcher has abandoned science and turned their hypothesis into a religion. Real science often means having to abandon a cherished hypothesis, one that you have nurtured and raised from a mere pup of an idea, like it was yesterday’s newspaper – if the data warrant it. To fail in this most solemn duty is to turn down the path to the “dark side” – to pseudoscience and quackery.
At issue here is the basic purpose of a hypothesis or theory. Although many people outside of the sciences (and, regrettably, some inside as well) equate “theory” (and “hypothesis”, if they are acquainted with that term) with “idea”, the fact is that it is much more than that. A hypothesis or theory (more about the difference later) is a model of how the universe works. Now, it may be a model of a very small part of the universe (such as the replication of a virus) or it may be a model of the entire universe (e.g. theBig Bang).
No matter what the scale, the purpose of a hypothesis or theory is to give us a deeper understanding of our world by showing us the workings of the parts we can’t see. Or, sometimes, by explaining why the parts we can see do the things they do. Either way, the model – the proposed explanation – has to conform to the behavior of the real world if it is to survive. And that – in a nutshell – is the difference between a hypothesis and a theory. A hypothesis is a model that has not yet been extensively tested to see if it predicts what the real world does – a theory has already survived a number of tests successfully.
Having survived testing does not necessarily mean that the hypothesis (or theory, if it has gotten to that point) has survived unchanged. In the process of testing even the most inspired hypothesis, discrepancies are found between what the hypothesis predicts will happen and what actually does happen. Sometimes these discrepancies can be explained by flaws in the measurements or data collection, but any consistent difference between what the hypothesis predicts and what the data show must be seen as evidence that the hypothesis – the proposed model of how the world works – needs to be modified or abandoned.
The problem is knowing when a hypothesis or theory should be revised and when it should be abandoned – something that is often difficult to see until enough contradictory data has amassed. But, like that favorite old pair of jeans that you keep patching and patching, eventually a hypothesis becomes more patches than whole cloth and needs to be revamped or rejected. On the other hand, many of today’s solid, tried and tested theories went through a period where they needed some “tweaking” (or even major overhauls) in order to function.
The thinking error of post hoc correction occurs when someone tries too hard to keep a failing hypothesis “in the game”, crossing from legitimate modification of the hypothesis to frantic attempts to keep it alive at all costs. This can be – and probably usually is – done without any intent to deceive. And it can be done by people who have an impeccable record of excellence in science – as the mutual fund people always say, “past performance is no guarantee of future yields”.
The hallmark of post hoc correction is the modification of a hypothesis in response to contradictory data in a way that is:
[a] Not supported by any existing data
[b] Not tested or not testable
Let me make this clearer by two examples – one of a legitimate modification of a hypothesis and one of an illegitimate post hoc correction:
[1] Lost a star but gained a planet.
In the early 1800’s, the French astronomer Alexis Bouvard undertook to publish a corrected table of the orbit of Uranus due to observed discrepancies from the orbital tables published by Jean Baptiste Delambre in 1792. He was unable to get all of the observations to fit into the predicted orbit (predicted by the theory of gravity) and so published his new tables in 1821 with the comment that he was unable to determine if the discrepancy was due to errors in the earlier observations or a “foreign and unperceived cause”.
By 1841, however, it was clear that even Bouvard’s calculations were failing to account for the actual orbit of Uranus. At this point, there were two theories in play, one of which was in need of modification – the theory of gravity or the theory that the Solar System had only seven planets. Although the majority of astronomers at the time were “betting” on the existence of an eighth planet (which we know as Neptune), there were others (i.e. George Airy, the Astronomer Royal) who felt that the theory of gravity was in need of an overhaul.
The British astronomer John Adams and the French astronomer Urbain Le Verrier began a search for a new planet, using the mathematical basis of the theory of gravity to predict where this new planet might be, based on the irregularities in the orbit of Uranus. In 1845, they both (more or less simultaneously) found the planet – despite resistance, reluctance and a good deal of old-fashioned mule-headedness on the part of their more senior colleagues.
To diagram the process:
a. Hypothesis (Theory, actually): Gravitational attraction is proportional to the product of the masses involved and varies with the inverse square of the distance between them.
b. Problem: The orbit of Uranus is not following the course predicted by the Theory of Gravitation.
c. Possible Explanations: The Theory of Gravitation does not apply at large distances from the Sun OR there is another planet beyond Uranus.
d. Resolution: After calculating where a planet would have to be to cause the observed perturbations of Uranus’ orbit, astronomers found a planet – Neptune – in the expected location. The Theory of Gravitation had survived another test!
The “take-home points” of this example are looking for supporting data (the planet Neptune) before deciding which theory to revise and the fact that they did not automatically assume that one theory was “privileged” and therefore not subject to scrutiny.
[2] When low means high
A few years ago, an unlikely group of researchers – a PhD academic chemist, an MD oncologist and an MBA – embarked on a project to prove that mercury caused autism. Since tests on hair, blood and urine had previously failed to show any significant difference in mercury content between autistic children and “normal” controls, they tested hair specimens that had been collected at the child’s first haircut – the so-called “first baby haircut” – and retained as a keepsake. This, they felt, would be the definitive proof that autistic children had been exposed to a significantly higher mercury levels as infants (as stated by one of the researchers, Dr. Holmes, during the 2000 DAN! Conference).
Unfortunately, the mercury levels in the “first baby haircut” samples from autistic children were significantly lower than those from the “normal” controls. This might have proved to be a difficulty, had not the researchers applied a post hoc correction to their hypothesis. They concluded that, based on their data, autistic children are unable to excrete mercury as effectively as their “normal” peers. They made this conclusion despite numerous studies, many dating back a few decades, that showed mercury was passively taken up by hair rather than excreted.
In addition, a later national study showed that the hair mercury levels that they measured in the autistic children were very close to the national average for children of the age when these hair samples were taken (remember, the hair samples were taken when the children were one to two years old – the analysis was performed many years later). In addition, this same national study – which was not studying autism – showed that the hair mercury levels of the “normal” controls was greater than the national average by over fifteen times!
To diagram the process:
a. Hypothesis: Mercury causes autism (subhypothesis: previous studies have failed to demonstrate high mercury levels in autistic children because the mercury “washes out” by the time of diagnosis some years later).
b. Problem: Hair mercury levels in hair taken at the “first baby haircut” of autistic children are lower than those of “normal” controls.
c. Possible Explanations: Mercury is not related to autism (apparently not considered by the authors) OR mercury protects children from autism (supported by the data, but nonsensical) OR children with autism cannot excrete mercury as well as “normal” controls (consistent with their data but not supported by it – also, not consistent with over forty years of data on how mercury and hair interact) OR the laboratory assays were in error.
d. Resolution: Rather than opt for an explanation that is consistent with known physiology, the authors chose an “explanation” that supported their hypothesis that mercury causes autism at the expense of being almost certainly wrong. In short, either dozens of researchers’ work over the past forty years (and more) is wrong or the authors of this “study” are wrong in their conclusion.
The “take home points” of this example are that a hypothesis (e.g. “autistic children cannot excrete mercury as well as non-autistic children, leading to low hair mercury levels”) which contradicts previous well-established hypotheses or theories (e.g. “mercury is not excreted in the hair – the hair mercury concentration merely reflects the blood concentration at the time the hair was formed”) needs to have data supporting it, not merely the assertions of its authors. Additionally, most of the time, many conclusions can be drawn from the data of a single study – the authors of this study were blinded to those alternative explanations by their single-minded desire to “prove” their hypothesis.
In short, post hoc corrections of a hypothesis are those which “save” the hypothesis at the expense of making it unsupported by data. You can properly “save” a hypothesis that fails to correctly predict reality by either changing the hypothesis so that it predicts reality better (as was done when Neptune was added as the 8th planet). Or you can try to change reality itself by asserting that your hypothesis only predicts reality in your laboratory or in the absence of “negative thought energy”. Or you can take the route of adding another unsupported hypothesis to the mix in order to make the whole thing “work”, as the authors of the “study” in example 2 did. The latter two processes are post hoc corrections and only add more unsupported assertions to a hypothesis that is – by definition – already in trouble.
Coming Up: Conspiracy! (or, Et tu, Brute!)
Prometheus
Thinking Error 3: Post Hoc Correction of Hypotheses:
Before we get into this “thinking error”, I need to make abundantly clear what it is we’re talking about. One of the most fundamental characteristics of real scientists is that they are always revising, modifying and – when necessary – discarding their theories and hypotheses in light of new data. To many people outside of the scientific disciplines, this looks like indecision or just plain waffling – a “bad” thing if you’re a politician trying to stake out a position for legislation or electioneering.
However, a failure to “change with the wind” – as one politician put it – is a certain sign that a researcher has abandoned science and turned their hypothesis into a religion. Real science often means having to abandon a cherished hypothesis, one that you have nurtured and raised from a mere pup of an idea, like it was yesterday’s newspaper – if the data warrant it. To fail in this most solemn duty is to turn down the path to the “dark side” – to pseudoscience and quackery.
At issue here is the basic purpose of a hypothesis or theory. Although many people outside of the sciences (and, regrettably, some inside as well) equate “theory” (and “hypothesis”, if they are acquainted with that term) with “idea”, the fact is that it is much more than that. A hypothesis or theory (more about the difference later) is a model of how the universe works. Now, it may be a model of a very small part of the universe (such as the replication of a virus) or it may be a model of the entire universe (e.g. theBig Bang).
No matter what the scale, the purpose of a hypothesis or theory is to give us a deeper understanding of our world by showing us the workings of the parts we can’t see. Or, sometimes, by explaining why the parts we can see do the things they do. Either way, the model – the proposed explanation – has to conform to the behavior of the real world if it is to survive. And that – in a nutshell – is the difference between a hypothesis and a theory. A hypothesis is a model that has not yet been extensively tested to see if it predicts what the real world does – a theory has already survived a number of tests successfully.
Having survived testing does not necessarily mean that the hypothesis (or theory, if it has gotten to that point) has survived unchanged. In the process of testing even the most inspired hypothesis, discrepancies are found between what the hypothesis predicts will happen and what actually does happen. Sometimes these discrepancies can be explained by flaws in the measurements or data collection, but any consistent difference between what the hypothesis predicts and what the data show must be seen as evidence that the hypothesis – the proposed model of how the world works – needs to be modified or abandoned.
The problem is knowing when a hypothesis or theory should be revised and when it should be abandoned – something that is often difficult to see until enough contradictory data has amassed. But, like that favorite old pair of jeans that you keep patching and patching, eventually a hypothesis becomes more patches than whole cloth and needs to be revamped or rejected. On the other hand, many of today’s solid, tried and tested theories went through a period where they needed some “tweaking” (or even major overhauls) in order to function.
The thinking error of post hoc correction occurs when someone tries too hard to keep a failing hypothesis “in the game”, crossing from legitimate modification of the hypothesis to frantic attempts to keep it alive at all costs. This can be – and probably usually is – done without any intent to deceive. And it can be done by people who have an impeccable record of excellence in science – as the mutual fund people always say, “past performance is no guarantee of future yields”.
The hallmark of post hoc correction is the modification of a hypothesis in response to contradictory data in a way that is:
[a] Not supported by any existing data
[b] Not tested or not testable
Let me make this clearer by two examples – one of a legitimate modification of a hypothesis and one of an illegitimate post hoc correction:
[1] Lost a star but gained a planet.
In the early 1800’s, the French astronomer Alexis Bouvard undertook to publish a corrected table of the orbit of Uranus due to observed discrepancies from the orbital tables published by Jean Baptiste Delambre in 1792. He was unable to get all of the observations to fit into the predicted orbit (predicted by the theory of gravity) and so published his new tables in 1821 with the comment that he was unable to determine if the discrepancy was due to errors in the earlier observations or a “foreign and unperceived cause”.
By 1841, however, it was clear that even Bouvard’s calculations were failing to account for the actual orbit of Uranus. At this point, there were two theories in play, one of which was in need of modification – the theory of gravity or the theory that the Solar System had only seven planets. Although the majority of astronomers at the time were “betting” on the existence of an eighth planet (which we know as Neptune), there were others (i.e. George Airy, the Astronomer Royal) who felt that the theory of gravity was in need of an overhaul.
The British astronomer John Adams and the French astronomer Urbain Le Verrier began a search for a new planet, using the mathematical basis of the theory of gravity to predict where this new planet might be, based on the irregularities in the orbit of Uranus. In 1845, they both (more or less simultaneously) found the planet – despite resistance, reluctance and a good deal of old-fashioned mule-headedness on the part of their more senior colleagues.
To diagram the process:
a. Hypothesis (Theory, actually): Gravitational attraction is proportional to the product of the masses involved and varies with the inverse square of the distance between them.
b. Problem: The orbit of Uranus is not following the course predicted by the Theory of Gravitation.
c. Possible Explanations: The Theory of Gravitation does not apply at large distances from the Sun OR there is another planet beyond Uranus.
d. Resolution: After calculating where a planet would have to be to cause the observed perturbations of Uranus’ orbit, astronomers found a planet – Neptune – in the expected location. The Theory of Gravitation had survived another test!
The “take-home points” of this example are looking for supporting data (the planet Neptune) before deciding which theory to revise and the fact that they did not automatically assume that one theory was “privileged” and therefore not subject to scrutiny.
[2] When low means high
A few years ago, an unlikely group of researchers – a PhD academic chemist, an MD oncologist and an MBA – embarked on a project to prove that mercury caused autism. Since tests on hair, blood and urine had previously failed to show any significant difference in mercury content between autistic children and “normal” controls, they tested hair specimens that had been collected at the child’s first haircut – the so-called “first baby haircut” – and retained as a keepsake. This, they felt, would be the definitive proof that autistic children had been exposed to a significantly higher mercury levels as infants (as stated by one of the researchers, Dr. Holmes, during the 2000 DAN! Conference).
Unfortunately, the mercury levels in the “first baby haircut” samples from autistic children were significantly lower than those from the “normal” controls. This might have proved to be a difficulty, had not the researchers applied a post hoc correction to their hypothesis. They concluded that, based on their data, autistic children are unable to excrete mercury as effectively as their “normal” peers. They made this conclusion despite numerous studies, many dating back a few decades, that showed mercury was passively taken up by hair rather than excreted.
In addition, a later national study showed that the hair mercury levels that they measured in the autistic children were very close to the national average for children of the age when these hair samples were taken (remember, the hair samples were taken when the children were one to two years old – the analysis was performed many years later). In addition, this same national study – which was not studying autism – showed that the hair mercury levels of the “normal” controls was greater than the national average by over fifteen times!
To diagram the process:
a. Hypothesis: Mercury causes autism (subhypothesis: previous studies have failed to demonstrate high mercury levels in autistic children because the mercury “washes out” by the time of diagnosis some years later).
b. Problem: Hair mercury levels in hair taken at the “first baby haircut” of autistic children are lower than those of “normal” controls.
c. Possible Explanations: Mercury is not related to autism (apparently not considered by the authors) OR mercury protects children from autism (supported by the data, but nonsensical) OR children with autism cannot excrete mercury as well as “normal” controls (consistent with their data but not supported by it – also, not consistent with over forty years of data on how mercury and hair interact) OR the laboratory assays were in error.
d. Resolution: Rather than opt for an explanation that is consistent with known physiology, the authors chose an “explanation” that supported their hypothesis that mercury causes autism at the expense of being almost certainly wrong. In short, either dozens of researchers’ work over the past forty years (and more) is wrong or the authors of this “study” are wrong in their conclusion.
The “take home points” of this example are that a hypothesis (e.g. “autistic children cannot excrete mercury as well as non-autistic children, leading to low hair mercury levels”) which contradicts previous well-established hypotheses or theories (e.g. “mercury is not excreted in the hair – the hair mercury concentration merely reflects the blood concentration at the time the hair was formed”) needs to have data supporting it, not merely the assertions of its authors. Additionally, most of the time, many conclusions can be drawn from the data of a single study – the authors of this study were blinded to those alternative explanations by their single-minded desire to “prove” their hypothesis.
In short, post hoc corrections of a hypothesis are those which “save” the hypothesis at the expense of making it unsupported by data. You can properly “save” a hypothesis that fails to correctly predict reality by either changing the hypothesis so that it predicts reality better (as was done when Neptune was added as the 8th planet). Or you can try to change reality itself by asserting that your hypothesis only predicts reality in your laboratory or in the absence of “negative thought energy”. Or you can take the route of adding another unsupported hypothesis to the mix in order to make the whole thing “work”, as the authors of the “study” in example 2 did. The latter two processes are post hoc corrections and only add more unsupported assertions to a hypothesis that is – by definition – already in trouble.
Coming Up: Conspiracy! (or, Et tu, Brute!)
Prometheus
posted by Prometheus at 11:30 AM
17 Comments:
Yaaaaay!!!
:-) !!!
So glad you've returned and with a great post no less. Welcome back - you were missed.
I was just here the other day wondering about the length of time since your last essay. I haven't even read this post yet, just wanted to say I'm glad you're back! Now off to read.
To everyone who has welcomed my return to the blogosphere - it is heartwarming to know that I was missed.
To those who had wholeheartedly hoped that I had dropped off the edge of the earth (or, at least, a tall cliff), "I'm baaaaack!"
Prometheus
Welcome back Prometheus. Hope those pecks to your liver have healed and won't prevent you from bringing the light of knowledge to mankind or anything.
Welcome back Prometheus.Hope grant applications not too long to fill and not too many at once to complete ( I know a bit about).
There is a point that can complete the view: the possibility that the approach to the truth has not be hypothesized correctly (1), has not been explored adequately (2), has not been tested properly (3) and therefore is far from solved (4).
A proposal , after yours
a. Hypothesis: Mercury causes autism (subhypothesis: previous studies have failed to demonstrate high mercury levels in autistic children because the mercury “washes out” by the time of diagnosis some years later).
a-Heavy metals in general bioaccumulate in tissues in a subgroup of autistic children because of individual genetics.
b. Problem: Hair mercury levels in hair taken at the “first baby haircut” of autistic children are lower than those of “normal” controls.
b. Problem: how to detect heavy metals ( and light ones such as Al) sequestered in tissues?? How to provoke in a safe and trustable way their presence in body fluids, WITH NO USE of chelators?
c. Possible Explanations: Mercury is not related to autism (apparently not considered by the authors) OR mercury protects children from autism (supported by the data, but nonsensical) OR children with autism cannot excrete mercury as well as “normal” controls (consistent with their data but not supported by it – also, not consistent with over forty years of data on how mercury and hair interact) OR the laboratory assays were in error.
c- Possible explanations: Major problems in management of xenobiotics, metal cations transport and aminoacids/polypeptides/proteins metabolism.
d. Resolution: Rather than opt for an explanation that is consistent with known physiology, the authors chose an “explanation” that supported their hypothesis that mercury causes autism at the expense of being almost certainly wrong. In short, either dozens of researchers’ work over the past forty years (and more) is wrong or the authors of this “study” are wrong in their conclusion.
d. Resolution Because the above hypothesis has not been explored, not studied yet, although there are some clues.
María Luján
OK, I've read now. Your writing is always so wonderfully clear for the layperson. I hope you are in a position to teach students, because you're a natural!
I think I would sum this installment up as "If your hypothesis doesn't work, sprinkle a little magic dust on it." Can't wait for the next one.
Superbly argued – another reference post.
The undead science lives...and so does Prometheus! Great post Prometheus, welcome back.
:*)
Maria,
Regarding your suppositions about "Major problems in management of xenobiotics, metal cations transport and aminoacids/polypeptides/proteins metabolism." Those are also hypotheses unsupported by data, so they add nothing to the resolution of the problem.
In point of fact, any mercury brought into the body would have to be reflected in the hair, for the following reasons:
Mercury injected, inhaled or ingested is taken up from its "portal of entry" by the blood. The blood then returns to the central circulation via venules veins, etc. to the heart (blood from the lungs goes directly to the left ventricle, but otherwise the processes are similar). From the heart, the blood goes into the aorta and a fraction of this blood goes into the carotid and vertebral arteries en route to the brain.
The same "packet" of blood carrying mercury destined for the brain also sends blood to the scalp, where growing hair absorbs (passively) mercury, which is bound to cysteine residues, primarily.
As a result, any process that would deliver mercury to the brain also delivers it to the scalp and hair. Thus the question of how convoluted a process Holmes et al must imagine if they can have the blood bypass the hair follicles and still make it to the brain. It is - quite simply - not consistent with well-established fundamentals of physiology.
A much simpler explanation - and one that does not require a complete reworking of the circulatory system - is that the numbers that Holmes et al got were wrong. Most probably, this error can be laid squarely at the feet of the laboratory they were using.
Prometheus
Hi Prometheus
You said
Regarding your suppositions about "Major problems in management of xenobiotics, metal cations transport and aminoacids/polypeptides/proteins metabolism." Those are also hypotheses unsupported by data, so they add nothing to the resolution of the problem.
If you are interested, I can bring the published clues I mentioned about. For me they do add to the resolution of the problem. Perhaps in this point we must agree in disagreement.
Dr Pichiciero work demonstrated that after thimerosal injection, Hg +2 inorganic is present in blood of children.
Thimerosal can (please see my emphasis can)
a) remain as thimerosal (how much??) not tested
b) converted to Hg+2, following Pichichiero, this happens after vaccination. Tested
c) converted to methylHg by in vivo methylation, from Hg+2 (how much??) Following the hair mercury in children with autism, not much because the problem here seems to be not methyl mercury but inorganic mercury, reaching tissues because of lack of excretion. Tested
d) after b and c, react with Al compounds ( if we consider vaccines, they include Al as sulphate and hydroxide) doing complexes in vivo ( how much??), not tested
I wonder, who is exploring this possibility, in genetically different children from birth, considering the overall vaccination schedule?? Some clues
What about Hg+2, inorganic, in the blood of a child after vaccination, imaging that this child has genetic imbalances related to xenobiotics managements?
In sequence, from the reaction between a xenobiotic and glutathione are involved glutathione S transferase, gama glutamyl transpeptidase,cisteynil glicinase, N acetyl transferase and finally mercapturic acid is formed. This sequence needs adequate levels of essential amino acids, pantothenic acid for Coenzyme A and phosphorus for the synthesis of ATP.
So I wonder if Besides/ beyond glutathione , that needs aminoacids , the transformation to mercapturic acid somewhat can be hindered because of problems in some of these enzymes. There are many biochemical steps that can be altered to have the findings that many researchers have in ASD.
Some References on these topics
References about thimerosal sensitization
Glutathione transferases
1-Westphal G. A. Homozygous gene deletion of the glutation S transferases M1 and T1 are associated with thimerosal sensitizaiton Int Arch Ocxcup Environ Health 2000 Aug 73 (6) 384-388.
2-Muller M Inhibition of erythrocyte glutathione S transferase T1 by Thimerosal Int J Hyg Envrion Health 2001 Jul 203 (5-6), 479-481.-
3- In Autism
BMC Genet. 2006 Feb 10;7(1):8 Analysis of case-parent trios at a locus with a deletion allele: association of GSTM1 with autism.
Buyske S, Williams TA, Mars AE, Stenroos ES, Ming SX, Wang R, Sreenath M, Factura MF, Reddy C, Lambert GH, Johnson WG.
Free article in
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16472391
4-Failure of Hg presence in hair in inorganic mercurialism
Sci Total Environ. 2001 Feb 21;267(1-3):151-68.
The Mt. Diwata study on the Philippines 1999--assessing mercury intoxication of the population by small scale gold mining.
Drasch G, Bose-O'Reilly S, Beinhoff C, Roider G, Maydl S.
The region of Diwalwal, dominated by Mt. Diwata, is a gold rush area on Mindanao (Philippines) where approximately 15000 people live. The fertile plain of Monkayo is situated downstream, where people grow crops such as rice and bananas; locally caught fish is eaten frequently. The ore is dug in small-scale mines and ground to a powder by ball-mills while still in Diwalwal. The gold is then extracted by adding liquid mercury (Hg), forming gold-amalgam. To separate the gold from the Hg, in most cases the amalgam is simply heated in the open by blow-torches. A high external Hg burden of the local population must be assumed. To evaluate the internal Hg burden of the population and the extent of possible negative health effects, 323 volunteers from Mt. Diwalwal, Monkayo and a control group from Davao were examined by a questionnaire, neurological examination and neuro-psychological testing. Blood, urine and hair samples were taken from each participant and analyzed for total Hg. A statistical evaluation was possible for 102 workers (occupationally Hg burdened ball-millers and amalgam-smelters), 63 other inhabitants from Mt. Diwata ('only' exposed from the environment), 100 persons, living downstream in Monkayo, and 42 inhabitants of Davao (serving as controls). The large volume of data was reduced to yes/no decisions. Alcohol as a possible bias factor was excluded (level of alcohol consumption and type, see Section 4.4). Each factor with a statistically significant difference of at least one exposed group to the control group was included in a medical score (0-21 points). In each of the exposed groups this score was significantly worse than in the control group (median control, 3; downstream, 9; Mt. Diwata, non-occupational exposed, 6; Hg workers, 10). In comparison to the surprisingly high Hg concentration in blood (median, 9.0 microg/l; max, 31.3) and in hair (2.65 microg/g; max, 34.7) of the control group, only the workers show elevated levels: Hg-blood median 11.4, max 107.6; Hg-hair median 3.62, max 37.8. The Hg urine concentrations of the occupational exposed and non-exposed population on Mt. Diwata was significantly higher than in the control group: control median 1.7 microg/l, max 7.6; non-occupational burdened median 4.1, max 76.4; and workers median 11.0, max 294.2. The participants, living downstream on the plain of Monkayo show no statistically significant difference in Hg-blood, Hg-urine or Hg-hair in comparison with the control group. The German Human-Biological-Monitoring value II (HBM II) was exceeded in 19.5% (control), 26.0% (downstream), 19.4% (Mt. Diwata, non-occupational) and 55.4% (workers) of the cases, the German occupational threshold limit in 19.6% of the workers. Only some of the clinical data, characteristic for Hg intoxication (e.g. tremor, loss of memory, bluish discoloration of the gingiva, etc.), correlate with Hg in blood or urine, but not with Hg in hair. The medical score sum correlates only with Hg in urine. The poor correlation between the Hg concentration in the biomonitors to classic clinical signs of chronic Hg intoxication may be explained by several factors: Hg in blood, urine and hair do not adequately monitor the Hg burden of the target tissues, especially the brain. Inter-individual differences in the sensitiveness to Hg are extremely large. In this area a mixed burden of Hg species must be assumed (Hg vapor, inorganic Hg, methyl-Hg). Chronic Hg burden may have established damage months or even years before the actual determination of the Hg concentrations in the bio-monitors under quite different burden was performed (Drasch G. Mercury. In: Seiler HG, Sigel A, Sigel H, editors. Handbook on metals in clinical and analytical chemistry. New York: Marcel Dekker, 1994:479-494). Therefore, a 'Hg intoxication', that should be treated, was not diagnosed by the Hg concentration in the bio-monitors alone, but by a balanced combination of these Hg values and the medical score sum. In principle, this means the higher the Hg concentration in the bio-monitors, the lower the number of characteristic adverse effects are required for a positive diagnosis. By this method, 0% of the controls, 38% downstream, 27% from Mt. Diwata, non-occupational exposed and 71.6% of the workers were classified as Hg intoxicated. A reduction of the external Hg burden on Mt. Diwata is urgently recommended. An attempt to treat the intoxicated participants with the chelating agent dimercaptopropanesulfonic acid (DMPS) is planned.
Environ Int. 2001 Oct;27(4):285-90. Related Articles, Links
Mercury pollution in the Tapajos River basin, Amazon: mercury level of head hair and health effects.
Harada M, Nakanishi J, Yasoda E, Pinheiro MC, Oikawa T, de Assis Guimaraes G, da Silva Cardoso B, Kizaki T, Ohno H.
Department of Social Welfare Studies, Kumamoto Gakuen University, Japan.
There is increasing concern about the potential neurotoxic effects of exposure to methylmercury for the 6 million people living in the Amazon, even in regions situated far away from the gold mines (garimpos), considered to be the major source of mercury pollution. In November 1998, a spot investigation on mercury contamination was conducted in three fishing villages (Barreiras, Rainha, and Sao Luiz do Tapajos) on the Tapajos River, an effluent of the Amazon, situated several hundred kilometers downstream from the gold-mining areas. A total of 132 fishermen and their families volunteered for the current study. As was anticipated, the total mercury levels in the head hair collected from the fishing villages were relatively high (14.1-20.8 ppm on the average) and the number of subjects with a high total mercury level over 10 ppm (the least upper bound of a normal value) was 103 (78.0%) in total, along with various symptoms, thereby suggesting wide mercury contamination in the Tapajos River basin. Moreover, in view of the absence of other diseases (e.g., alcoholism or malaria), a high intake of fish containing a methylmercury level, and high hair mercury levels in addition to the various symptoms such as sensory disturbance (especially glove-and-stocking type, which is characteristic of Minamata disease), tremor, failure in two-point discrimination, and slight balancing failure, several subjects examined were diagnosed with mild Minamata disease. The findings obtained suggest, thus, that the mercury pollution in the Amazon should be crucially observed for head hair mercury level and health in a much broader region.
Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92.
Mercury and autoimmunity: implications for occupational and environmental health.
Silbergeld EK, Silva IA, Nyland JF.
Department of Environmental Health Sciences, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Mercury (Hg) has long been recognized as a neurotoxicant; however, recent work in animal models has implicated Hg as an immunotoxicant. In particular, Hg has been shown to induce autoimmune disease in susceptible animals with effects including overproduction of specific autoantibodies and pathophysiologic signs of lupus-like disease. However, these effects are only observed at high doses of Hg that are above the levels to which humans would be exposed through contaminated fish consumption. While there is presently no evidence to suggest that Hg induces frank autoimmune disease in humans, a recent epidemiological study has demonstrated a link between occupational Hg exposure and lupus. In our studies, we have tested the hypothesis that Hg does not cause autoimmune disease directly, but rather that it may interact with triggering events, such as genetic predisposition, exposure to antigens, or infection, to exacerbate disease. Treatment of mice that are not susceptible to Hg-induced autoimmune disease with very low doses and short term exposures of inorganic Hg (20-200 mug/kg) exacerbates disease and accelerates mortality in the graft versus host disease model of chronic lupus in C57Bl/6 x DBA/2 mice. Furthermore, low dose Hg exposure increases the severity and prevalence of experimental autoimmune myocarditis (induced by immunization with cardiac myosin peptide in adjuvant) in A/J mice. To test our hypothesis further, we examined sera from Amazonian populations exposed to Hg through small-scale gold mining, with and without current or past malaria infection. We found significantly increased prevalence of antinuclear and antinucleolar antibodies and a positive interaction between Hg and malaria. These results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired.
Int J Occup Environ Health. 2005 Apr-Jun;11(2):132-137.
Please look at http://www.ijoeh.com/archive_01.html#1102
“Generally, Hg detected in urine is considered the preferred biomarker for inorganic and elemental Hg exposure, while Hg in hair indicates MeHg intoxication that may reflect long term exposure and the level of MeHg in the brain”-page 132.
But after the exposure- and because of the decrease, there can be no signals of Hg intoxication- and however being in tissues.
Therefore
1- Hg in hair is present at high concentrations when the source of Hg is contaminated food ( mainly fish) or the introduction of the Hg is via oral
2- Hg in fluids can be low when inorganic Hg is the source of the poisoning. Hair, blood or urine are not useful in these cases
3- My point:
What if the main problem is the Hg +2 inorganic (not shown in common biomarkers) but not excreted but sequestered in tissues- this has been published yet, as I tried to present above.
4- What about the concomitant problems with xenobiotics cycle management (presented above) with the published studies about the importance of GSMT 1 ( presented above) and oxidative stress ( recent one from July 2006) and the imbalances in aminoacids/proteins/minerals – and you can find here more citations
http://www.kevinleitch.co.uk/forum/viewtopic.php?id=57
http://www.kevinleitch.co.uk/forum/viewtopic.php?id=92
http://www.kevinleitch.co.uk/forum/viewtopic.php?id=40
and metal cation transporters- mainly +2 (Hg+2, Cd+2 and Pb+2) that all can interfiere in Ca+2, Mg+2 and Zn+2 biochemistry ( including all the receptors, second messengers systems, etc).?
Therefore we are talking mainly of specific proteins- with different functions- or specific enzymes (proteins with catalytic activity):
A-of the cycle of the xenobiotics management
B -of the cation+2 metal transporters (that it is not easy) One sample:
Environ Health Perspect. 2002 Oct;110 Suppl 5:689-94.
http://www.pubmedcentral.gov/picrender.fcgi?artid=1241226&blobtype=pdf
Transport of toxic metals by molecular mimicry.
5- Dr Holmes manuscript demonstrated that Hg levels were in the range of normalcy ( because it all depends on what you compare). BUT it can all be considered another published manuscript where the Hg in the form of Methyl mercury is excluded as the source of the contamination, being then to test the inorganic mercury, that is very difficult to prove, especially a lot of time after the exposure.In the case of workers in gold mining for example a) the exposure is constant and b) there are also another sources of oral contamination.
Sincerely
María Luján
PD: Please forgive me because of the inclusion of the abstracts. I know they are long but also there are several interesting citation included that I found interesting to read. I assure you I tried to follow your suggestions but I only included those who complete really the idea, IMHO.
"Thus the question of how convoluted a process Holmes et al must imagine if they can have the blood bypass the hair follicles and still make it to the brain."
CDC-funded, high-powered, neural activity-seeking, mercury beaming devices?
This is a good idea. Based on this, the CDC will be sure to test thimerosal for safety and admit they should have done this 77 years ago.
"mercury protects children from autism (supported by the data, but nonsensical)"
I don't know about that. Apparently, smoking prevents Parkinson's disease.
First, I want to commend you on your choice of topics, and say that I agree with the general thrust of your comments. That said, I'd like to make an observation about your terminology.
What you call "post hoc corrections" might be more accurately called "ad hoc maneuvers." They serve _only_ to salvage a favored hypothesis, without pointing the way toward additional investigations (i.e., they are not fruitful or fecund).
To Bob Koepp:
I agree with you that "ad hoc maneuvers" might be a better and more descriptive term. However, "post hoc correction" is the "official" term for this kind of logical error in the philosophy of science arena.
Don't blame me - blame Alan Chalmers.
Prometheus
Not to split philosophical hairs, but I think you're referring to the informal faclly called "post hoc, ergo propter hoc," which isn't equivalent to what you call "post hoc correction." It doesn't, after all, make a lot of sense to criticize a correction for being post hoc, or after the fact. But I don't know from terminological officialdom ;-)
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