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MILLIONS of people have been severely disabled (mentally and or physically) by mercury from dental amalgams, and this continues now. A huge pack of LIES has been used to cover this up. The subject gets censored (removed) from various websites. You can see the full research into this in free Chapter 3 at Experts Catastrophe - the catastrophe of official medical charlatanism where you can also see the list of all the references cited below here.However, as Quora prefers long answers to short ones, I'll see how much I can copy in here for you. But I'll first mention that mercury has numerous different effects on brain and body, depending on (a) timing, (b) dose, (c) form of mercury, (d) genetic disposition, (e) interacting factors. My own "peer-reviewed" published evidence also indicates that (in moderation) it causes higher IQ. Furthermore, mercury poisoning expert AH Cutler independently came to the same conclusion as myself, that the current epidemic of "snowflakes" trying to shut down anyone who disagrees with them has also been caused by mercury poisoning. Incandescent anger at divergent viewpoints is one of the most characteristic symptoms of mercury poisoning. I should know because I was there myself in a former life. There is quite a lot more evidence than this answer here will fit in.Oh, and it is all very carefully formatted in the actual book chapters pdfs, whereas here it is a bit of hit and hope.~~~~~~~~~~~~~~~~Before reading this chapter I recommend that you read the first two chapters of this book. Otherwise you may come to it with considerable misconceptions which could make for difficult and unproductive reading here.The main content of this chapter is a scientific paper. I wrote it with the intention of it being accepted in a scientific journal, and so you might find it rather turgid reading and with too many of those citations such as (Authorname, 2012) intruding into my florid prose. On the other hand one journal editor condemned it for (supposedly) appearing to be written like a newspaper article, so maybe there’s hope for non-academic readers nevertheless.You may be wondering whether you can have the competence to make any useful judgement of the soundness or credibility of this article. Wouldn’t the experts perhaps point out all manner of hidden things wrong with it? But I am providing you with a special resource here. In the next two chapters, you can see the world’s top experts telling me (off the record) the reasons why this article is such rubbish that you shouldn’t even be informed of its existence anyway. I suggest that you study those critiques and my rejoinders to them, and (as is always necessary eventually) then decide for yourself who if anyone has the more credibility. I can’t print the re-rejoinders from these experts because none have replied back. Perhaps you could write to these journals yourself to ask them why you shouldn’t be persuaded by what I said in my own replies.Scientific papers normally end with a list of the references cited. In this book I will transfer this paper’s reference list into the list at the end of the book. But this article is unusual in that it contains an appendix which itself contains three further lists of references. I will leave those in place just as they were present in the original documents contained in that appendix. Other than that, what follows after this paragraph is the most updated version of the manuscript I have sent to now eighteen journals. It is usual for scientific papers to begin with a summary called an “abstract”. This gives an overview for those who don’t already have the full text, but may be hard as a non-specialist to follow until you have read that full text, and you shouldn’t let yourself get bogged down by this one here. Also this chapter contains some graphs of disability epidemiology. If you are not already a wizard with such graphs, you may find it useful to jump forward to the section of Chapter 6 which discusses some misuses and abuses of similar sorts of graphs. Lastly, the “p<“ values stated herein indicate the probability of obtaining that result due to random chance.(NOTE: AT NO POINT HAVE I EVER SAID THAT ALL AUTISM IS CAUSED BY MERCURY OR AMALGAMS – See Chapter 7!)Autism, adult disability, and ‘workshy’: Major epidemics being caused by non-gamma-2 dental amalgamsRobin P ClarkeAbstract: It is unknown to most people that the dental amalgams which have been used as standard in recent decades, namely non-gamma-2 dental amalgams, have been substantially unlike those used before the 1970s, in that they constantly emit 20 to 50 times more mercury vapor than the older types. This is the first-ever study of health consequences of non-gamma-2. Following the changeover to non-gamma-2 amalgams, there promptly began a tenfoldish increase of autism, a tenfoldish change of ratio between late onset and early onset, a change from mainly genetic to mainly environmental, and a change from lifelong incurable to sometimes clearly recoverable. Exactly simultaneously there occurred a fourfoldish increase of claims for adult disability in the UK, with disabilities all or mostly of the nature that would be expected from chronic mercury poisoning (including mental disabilities and neurological disabilities). And similarly in the US. These timings cannot be dismissed as coincidence because there are no credible alternative explanations for the increases. Data strongly suggests that non-gamma-2 amalgams are currently by far the main cause of chronic disability in the UK, US, and other such countries, with about 10% of the UK working-age population disabled thereby.An experiment on millions of dis-informed subjectsDental amalgams in patients’ teeth constantly emit mercury vapor, and that vapor is easily measureable. This has been known for decades as indicated in at least 18 published studies (Berglund, 1993; Berglund et al., 1988, Boyer, 1988; Brune et al., 1983; Clarkson et al., 1988; Ferracane et al., 1995; Mackert, 1987; Mahler et al., 1994; Moberg, 1985a, 1985b; Olsson et al., 1989; Olsson and Bergman, 1987; Patterson et al., 1985; Psarras et al., 1994; Svare et al., 1981; Vimy and Lorscheider, 1985a, 1985b, 1990).And yet in stark contradiction of all this clearly established basic science, the UK’s Chief Dental Officer (2009) has publicly asserted, as some supposed fact, that dental amalgams do not constantly emit any mercury vapor (or in his second thoughts on being challenged, at least “not measureably”).Such mercury vapor has been recognised for centuries as one of the most toxic of substances, causing various mental, neurological and physical disabilities. For more than a hundred years prior to the 1970s, strong condemnations were regularly issued against the use of amalgam in dentistry. These warnings were consistently ignored by health authorities, and dismissed with claims that there was no real evidence of harmfulness.Much further evidence of harmfulness of dental amalgam has come to light in recent decades (Mutter, 2011; Hanson, 2004; Homme et al., 2014), not least in thousands of cases of improvement following amalgam removal which cannot be dismissed as merely anecdotal or placebo. Some relatively large-scale trials have been asserted to show amalgam safety, but they have been substantially flawed and in at least one case in reality showed harmfulness rather than safety (as explained by Mutter, 2011 and Homme et al., 2014).In the 1970s a new type of dental amalgam was introduced as the new standard, partly on the basis that it was very much more durable, with far less tendency to corroding and crumbling. This new type was called non-gamma-2.These non-gamma-2 dental amalgams constantly emit 20 to 50 times more of the toxic mercury vapor than the older types (Berglund, 1993; Boyer, 1988; Brune et al., 1983; Ferracane et al., 1995; Mahler et al., 1994; Moberg, 1985a, 1985b; Psarras et al., 1994). The amalgam constantly emitting this neurotoxic mercury vapor is located in a person’s mouth, less than two inches from their brain, and in the pathway to the lungs (where 80% is absorbed at each inhalation). Any notion that the levels of mercury vapor caused by amalgams are very low has to be put in the context of the general outdoor levels being many times lower still at around 0.002 mcg/m3.No safety testing was undertaken before or after it was introduced. Patients and the public in general have still not been informed of the change, let alone of the increased levels of mercury involved. No informed consent has been sought, and no warnings have been given of any possible harmfulness. Indeed, throughout the US it was actually made illegal for dentists to issue such warnings, and Hal Huggins and other dentists were struck off the register of practitioners for doing so.In the UK, a number of untruths were adopted by the NHS and DH such as to prevent people being diagnosed with mercury toxicity and to thereby further reduce any concern about risk. The following untruths have been identified by the author, but it is unlikely that they have been the only ones.1. Untrue assertion that “Chronic mercury poisoning is highly unlikely to present in a psychiatric setting”.2. Use of proven useless urine tests for supposed (dis-) diagnosis of chronic mercury poisoning.3. Use of proven useless blood tests for supposed (dis-) diagnosis of chronic mercury poisoning.4. Chief Dental Officer’s untrue assertion that “no mercury vapor” emits from amalgams, or alternatively “not measureably”.5. Chief Dental Officer’s untrue denial that amalgams are the main source of mercury in the body.6. NHS Chief Executive’s re-insistence on the untruth that dentists have capability for mercury diagnosis whereas doctors do not.The existence of these untruths is authenticated via my Freedom of Information requests as documented partly in an Appendix hereto and more fully via dental mercury falsehoodsDates of introduction and usageNon-gamma-2 amalgams are very much more durable than the previous types. Consequently, declining rates of amalgam install-ation would conceal an increase of prevalence of the amalgams in patients’ mouths. And it is here expected that the key variable would be that rising prevalence rather than the declining rate of installations and replacements.A number of US patents for non-gamma-2 were granted in the mid-1970s. The famous US dentist Hal Huggins states that the changeover to “high copper”, i.e. non-gamma-2, occurred in 1976. In 1986 the ISO standard was changed retrospectively to incorporate them. The non-gamma-2 amalgams took over in the period 1975-79 in Denmark (Hansen et al., 1993). In Germany the use of the earlier types was banned in 1992, making the non-gamma-2 the only option. And according to the manufacturer’s product sheet, Dispersalloy is the most widely used amalgam with over 25 years of proven performance, i.e., since before 1979, but perhaps after their 1974 patent no. 3841860.I have been unable to obtain any numerical data on usage or total prevalence of non-gamma-2 in people’s mouths. The DH have told me they have no such records. And NHS dental records have not recorded the types of amalgam used. It is unlikely that any better information is available in other countries. But we can very reasonably assume that the overall prevalence of non-gamma-2 will have gradually, progressively increased in the decades following its introduction.My epidemiological investigationsHaving become aware of the changeover to non-gamma-2 amalgams, I decided to look to see if there might be epidemiological evidence of any consequences. It appears that no-one has ever done this before.In respect of the following accounts it is important to understand that I have not cherry-picked selected data to prove any point, but instead have used all the best data readily available to me.To avoid undue length here, the reader is referred to consult prior reviews of substantial important other data pointing to similar conclusions as those here, including Hanson (2004), Mutter (2011), Geier et al. (2010), Homme et al. (2014), and others not specifically cited..Is mercury involved in causation of autism?Before presenting the epidemiological findings it will be useful to first show the context of existing evidence from clinical studies on this question.A number of reviews have suggested there is persuasive evidence that mercury is importantly involved in causing of autism (Geier et al., 2010; Bernard et al., 2001; DeSoto and Hitlan, 2010; Kern et al., 2012). And yet the evidence can be shown to be far more decisive than any of these suggest, and indeed beyond all reasonable doubt.In any combinatory review of studies it is necessary firstly to rule out those which lack a sound rationale. A number of studies have used blood mercury or urine mercury as criterion measures, and yet it has been known for decades that these lack merit as indicators of chronic mercury toxicity. Indeed, the most prominent such study, Hertz-Picciotto et al. (2010), stated in its second-last sentence that: “This report did not address the role of prenatal or early-life Hg exposure in the etiology of autism” [i.e., the study could not provide any evidence against causation by mercury].Another danger in meta-reviewing of studies is the merging together of data which should be kept separate. In respect of mercury in autistics’ hair, the most enlightening study is that of Majewska et al. (2010). They found that in younger children autism was associated with markedly decreased hair mercury (p<0.01), whereas in older children autism was associated with markedly increased hair mercury (p<0.01). If they had just lumped all their results together they would have got an entirely unwarranted “no difference” non-result instead. Viewed in the light of Majewska et al, all or most of the other hair mercury studies fall into a coherent pattern. There are several which have smudged together the different ages and therefrom invalidly declared non-results. Meanwhile others strongly reinforce the notion that there are real effects.Holmes et al. (2003) obtained an eightfold difference of mercury in hair, with significance level of 1 in 250,000 (p<0.000004). Some commenters dismiss that study on a basis that it was done by opponents of mercury, and “therefore” their results may have been biased or fraudulent. But one would have expected any bias or fraud to result in a finding that hair mercury was increased in autistics, as that would have been in accordance with the standard rationale for diagnosing toxin exposure from increased hair measurements. They found instead 8﷓fold reduced levels, which strongly suggests that they were instead acting competently and honestly. Their rational-ising notion of paradoxical reductions of measurements in mercury toxic subjects has since been supported by much other evidence that mercury sometimes impairs its own excretion.A study in India (Lakhshmi Priya and Geetha, 2010) found 8-fold increased hair mercury (p<0.001). Another in Kuwait (Fido and Al-Saad, 2005) found 15-fold increased hair mercury (p<0.001).Bradstreet et al. (2003) found that a challenge test with the chelating agent DMSA caused a release of mercury 3.15 times greater in autistic cases than in controls (p<0.0002). That is a 1 in 5000 probability that that excess mercury was just a fluke.The probability of just these results listed above being all due to mere chance is 1/5000 x 1/250000 x 1/100 x 1/100 x 1/1000 x 1/1000, that is one in 12,500,000,000,000,000,000, vastly beyond the standard of proof ever required in any criminal prosecution.And far more than one negative result is required to call into question one significantly positive result. There are far more ways of making a “negative” car that does not move than of making a “positive” one that does. I and thousands of others have lived in the UK for many years and never seen the Queen in all that time, and yet that does not constitute significant grounds for dismissing the testimony of those who claim she has existed. If there were in reality no mercury-autism connection there should be a huge pile of “no-difference-found” results among which these high-significance results would be a small minority. But there is no such pile of null results to speak against the mercury-autism connection.One could seek to interpret all those results with a notion that there could be an unknown factor which both causes autism and also harmlessly causes mercury to vary in hair and other tissues. But that notion is brought into question by the extensive commonalities between autism and mercury toxification (Kern et al., 2012). And it is completely demolished by the observations of the Autism Research Institute which has for decades been surveying the effectiveness of many potential treatments for autism. Of more than 80 treatments tested, the ARI has found that one of the most effective has been removal of mercury by careful chelation. And Blaucok-Busch et al. (2012) obtained highly-significant behavioral improvements even with the rather poor Hg chelator DMSA (p<0.001; p<0.001; p<0.001).Meanwhile, three studies have been promoted as supposedly disproving any mercury-autism thesis. The study by Ip et al. (2004) was shown to be riddled with arithmetical errors, and in reality indicated that there was indeed a mercury connection (DeSoto and Hitlan, 2010). Likewise Soden et al. (2007) actually proved the opposite (DeSoto and Hitlan, 2010). And Hertz-Picciotto et al. (2010) stated in their own second-last sentence that their study did not address causation of autism by prenatal or early-life mercury exposure. Such falsely proclaimed studies are all that stands in supposed defiance of that astronomically large number calculated above. There is even more evidence that merits mention here but it would be superfluous. We can resolutely conclude that mercury is now a major cause of autism. [Updates: Autism association with prenatal SSRI use (Harrington et al., 2014) = amalgam causes both depression of mother and autism of baby. Widespread reports of seizures in 1/3 of autistics = perinatal mercury causes both autism and seizures (Szasz et al., 2002; Klinghardt, 1998).]Increased autism?In academic papers and elsewhere, certain myths about autism are constantly portrayed as self-evident truths, so they must be addressed here. Firstly, the human race does not divide into those “with” autism and those “without” it, or those “on the spectrum” and those “not on the spectrum”. Rather, there is a continuum of variation in the extent to which individuals are more or less autistic (in varying ways). Secondly, there is no scientific basis for a distinction between autism and Asperger’s. It was merely a historical accident that Kanner and Asperger made simultaneous rediscoveries of the syndrome described by JL Down in 1887. Thirdly, there is no scientific basis for the routine references to autism as a “disorder”. Autism can be severely disabling, is often terribly distressing, and may often be a consequence of a disorder (such as maternal infection), but rather than a disorder it is properly considered to be just atypicality (as is genius). [This is now more fully discussed in Chapter 2.]Some researchers with decades of direct experience, such as Bernard Rimland and Lisa Blakemore-Brown, have been of the view that there has been a substantial increase of autistic behaviors, and not just increase of diagnoses.[Update for this book: Significant further discussion of the increase “controversy” is contained in Chapter 2 in the section “The autism increase controversy” (page 68), just before the appendix to that chapter, and also majorly in Chapter 12 and pages 188-189.]The NHS has published a report claiming to show that there has not been any increase, by supposedly showing the prevalence of autism among older adults to be the same as in children (Brugha, 2011). The report detailed the elaborate measures taken to ensure reliability of the autism assessments. And yet it gave no details at all of any measures taken to ensure the validity, that is the (infinitely more important) comparability of the diagnostic procedures as applied to adults relative to applied to children. The reason there were no such details is because there was no way of establishing such validity. And in absence thereof, such a study proves nothing about changing prevalence of autism. I myself have direct knowledge of two older persons given baseless diagnoses of autism by this same NHS that proclaims as expertise the untruths listed on a preceding page here.The Autism Research Institute has a uniquely extensive historical database of cases. Figure 1 [here 3.1] is my re-plot of a graph published by the Autism Research Institute of its own records. Figure 2 shows my extraction from Figure 1 of the time-series of case ratios between late and early onset. Before 1980, onset at birth was twice as frequent as onset in the second year (i.e. regressive autism), whereas after 1990 the later onset rose to become five times more frequent than the onset at birth. The switch-over began at the end of the 1970s and was well under way by 1990. It closely related with the apparent increase of autism illustrated in Figure 3 and elsewhere. Figure 3 shows the data from the California DDS 2003 report (2003), with the earlier 1999 report (1999) (1998 data) re-calculated to the same basis.[Note added to book chapter version: Figure 3 also shows what mathematicians call an exponential increase curve; basically it gets increasingly steeper exactly in proportion to the higher it gets.](Please see free Chapter 3 at Experts Catastrophe - the catastrophe of official medical charlatanism for the graphs, until such time as I can sort out converting them to a form that will load to here. These four graphs are at pages 86 and 87. Also note the free tutorial about use and misuse of such graphs in free Chapter 6.)Fig. 3.1. “U.S. Cases: Autistic children who behaved normally before 18 months vs. those with no normal period.” From Rimland (2000) (replotted)Fig. 3.2. Data from Figure 1 here used to show the changing ratio of cases in respect of age-of-onset. A further datum is from Mrozek-Budzyn et al. (2009) p.109.Fig. 3.3. Autism enrolment in California.Fig. 3.4. Concurrence of California data of Figure 3.3 with total autism implied in Figure 3.2 if onset at birth is assumed to have constant incidence of one unit.In Figure 4 I have added together the two series of Figure 2 such as to give a nominal “total autism” curve based on an assumption that onset at birth has had constant prevalence during those years, and that early onset cases plus late onset cases equals total autism. Figure 4 shows that the increase curves of Figure 3 peculiarly coincided in time with the ratio-change curve of Figure 2. This enables substantial confidence that the conceptually independent Figures 2 and 3 are tracking exactly the same causal phenomenon.The late-onset, regressive autism is much more difficult to overlook than the at-birth autism, as parents are baffled by the regression of their children. Any under-awareness would not have been concentrated on those late-onset cases. And yet it is those which have increased about tenfold, not the more overlookable early-onset. So this data argues against interpretation in terms of mere changing of awareness or diagnostic thresholds. And it cannot be dismissed as due to demise of the diagnosis of “childhood schizophrenia”, because ARI’s survey questionnaire asked about age of onset rather than presumed about it, and indeed the ARI was neutrally called the “Institute for Child Behavior Research” until 1991.These curves strongly suggest that the autism increase was caused by something that started having an effect on children around the end of the 1970s and also caused a tenfold change of ratio of late-onset cases relative to early onset.An overview of autism trends in the US and UK found essent-ially the same trends of increase in both areas and in respect of both autism and “autism spectrum disorders” (Blaxill, 2004). Information about other capitalist countries has been less systematic, but generally similar trends appear to prevail. In respect of Sweden, Gillberg’s three prevalence studies in Gothenburg (Stehr-Green et al., 2003) could have been plotted into Figure 3, but they would have collided impressively with the California data. The data of Denmark is rich in potential for confusion but the careful analysis by Goldman and Yazbak (2004) shows an increase from at least about 1987 onwards. Likewise, the general observation in the other countries is that there has been an increase in recent decades. And the age-of-onset data in Figure 2 follows the same pattern too. (The notion of Bernard (2003) that autism decreased in Denmark after removal of mercury from vaccines is misfounded for various reasons partly explained by Hviid (2004).)So there is here a simple thing to be explained, seemingly beginning around the end of the 1970s.In 1993 there was published “A theory of general impairment of gene-expression manifesting as autism” (Clarke, 1993) (the antiinnatia theory). It remains unchallenged in reasoning and evidence, and unrivalled as the only comprehensive fully satisfact-ory explanation of the supposed mystery of autism. Martha Herbert has recently been arguing that autism is not a brain/behavior condition but rather “whole body”, and also not essentially genetic or developmental and fixed. But the antiinnatia theory already embodied all those notions decades ago.The theory also specified circumstances in which autism would change from a mainly genetic condition to a mainly environmental one. Autism has now indeed markedly changed to a mainly environmental causation (Hallmayer et al., 2011).The 1993 paper made no mention of mercury or an increase of autism (which was only vaguely becoming apparent at the time of writing it). But it did explicitly explain why molecules which randomly, dose-dependently bind to DNA and thereby reduce gene-expression would thereby cause autism. Mercury is now known to do exactly that binding and reducing at levels far below those producing other toxic effects (Ariza et al., 1994; Goyer, 1991; Rodgers et al., 2001; Walter and Luck, 1977).A preceding section here has shown the decisive recent evid-ence of major involvement of mercury in many autistic cases. And thimerosal in vaccines cannot have been a main source of that mercury, for reasons explained in [Chapter 6]. So the question arises of:where else is the source of the mercury that is now so strongly associated with most autism.An update review of the antiinnatia theory was written in 2004-2006, and showed confirmation of various peculiar predictions [Update: including Clarke (2015)], and explained the amalgam-autism causation more fully. But almost all medical researchers have a false presumption about theories, whereby “skepticism” (in reality a prejudice against new ideas) is supposedly a characteristic of intellectual superiority (Eysenck, 1995). And “peer review” systems block from effective publication any ideas that are more than routinely original (Eysenck and Eysenck, 1992).Because readers are deprived of that update review I will outline here just a few of its important points. (1) Many mothers keep their infants close by at all times, and many people keep their homes very unventilated, even installing draught-proofing. The new prediction that autism would be associated with lack of ventilation (of the mercury vapor breathed out by parents or carers then inhaled by infants) has already found significant accidental confirmation (Waldman et al., 2008). (2) The antiinnatia theory points to causation not so much like an overdose “hammer-blow” but rather more like a sustained suppression of genetic data, and thus the every-day inhalation of mercury would be much more impactful than occasional large injections. (3) The tenfold change to predominantly later onset is explained by gradual accumulation when infants regularly inhale the vapor. (4) Any persons who dismiss the antiinnatia theory must logically be supporting one of a handful of utterly absurd alternatives, and this author requests that such “skeptics” kindly state which ones they find so credible: (i) “anti-innatia factors don’t tend to produce biological advantageousness”; (ii) “they don’t exist anyway despite their experimental demon-stration” (genuine flat-earthers will prefer that one); (iii) “they would not tend to become excessive”; (iv) “excess would not manifest as autism”.Some studies have found positive associations between maternal dental amalgams and autism (Holmes et al., 2003; Geier et al., 2009). There have also been some seemingly conflicting findings, such as Adams et al. (2008) compared to Holmes et al. (2003). But rather than concluding from these that the whole mercury or amalgam theories are unsound, or that there has been falsification or error, we may better understand them as reflecting a fact that autism is far from being simply “a novel form of mercury poisoning”, and instead other factors impact in ways not yet known. Even the causation of autism by amalgam vapor alone would be complicated by variables of ventilation, parental habits, galvanic contacts in the mouth, genetics and epigenetics, intake of protective selenium, and other intakes and exposures. That complexity could explain why small cross-sectional studies have given inconsistent results. And meanwhile the time-series data shown in the charts here reflects varying levels of non-gamma-2 applied to whole populations, such that all those confounding variables are evened out, which explains why they show a clear association with the growing prevalence of the non-gamma-2 in adults’ mouths.Increased adult disability?In 2010 I heard on BBC Radio a claim by a government minister that “There certainly hasn’t been a threefold increase of disability”. This suggested to me that perhaps there had indeed been an increase of adult disabilities, threefold or even greater.On investigating this possibility, the most extensive data I could obtain was a chart on page 9 of pathways-presentation.pdf, (DWP, no date a) and online data timeseries (DWP, no date b) from the DWP’s website.(Please see these graphs at page 91 of free Chapter 3 at www.pseudoexpertise.com)Figure 3.5. Autism enrolments (DDS) in California compared with UK adult invalidity benefits claims granted (excluding short-term lower-rate cases and excluding claims denied for policy reasons of “caseload growth now controlled”)Figure 3.6. Autism enrolments under the Individuals with Disabilities Education Act (IDEA)I then took the Figure 4 chart from my (long-obstructed) autism theory update review draft, and removed my data-series derived from age-of-onset ratio-change, leaving only the two data-series of autism enrolment in California. I then added in the data of granted invalidity benefits from the DWP’s chart. I used only zero-baselines, so as to not to misuse the statistics to create artificial alignments. All I did was set the righthand scale such that the first datum of the invalidity benefits data was level with the autism data at that same year, 1979.This showed a close relationship of timing between the two, as shown in Figure 5 here.At this point it will be useful to show you a second chart of the autism increase, this time a different administrative database (IDEA rather than DDS) and covering the whole US, namely Figure 6. This is a more complex graph, with each data-series representing a different age at recording of the cases.With the increasing of age, fewer children from any particular birth-year cohort remain undiagnosed. So in respect of each year on Figure 6, the highest datum is the most accurate estimate to date of the real underlying level. And the falling off at the top of the latest years is due to diagnoses not yet being made.The first important thing that this chart of IDEA data shows is that the increase has been a remarkably uniform exponential sort of curve, with just a moderate decrease of slope after 1992. The other curves, from the California DDS data, can be understood as showing what would be a similarly uniform exponential, but distorted by noticeable “noise” due to smaller samples or mislaid records.Another important thing to understand about all these curves is that we are not here counting clear distinct things like apples or oranges. The number of people granted invalidity benefits in a particular year is a precisely-known integer, but the underlying number of people who were more or less “disabled” is necessarily a debatable, fuzzy one. Likewise with the autism numbers, and this goes some way to explaining why these two autism databases (DDS and IDEA) show significant discrepancies, most obviously in the starting levels before the increase. So we must understand that none of these curves document validly exact measurements of the underlying pathologies in their vertical scales. And therefore we should not be looking for particularly close alignments in the vertical scales; and if we do find such precision it should be considered largely a fluke. Also there is a lack of numerical data on usage or total prevalence of non-gamma-2 in people’s mouths.But these charts nevertheless do give an accurate document-ation on the horizontal scale, of the timing of the increases and of the form of the increases (i.e. not one big jump over a couple of years). And the four series (DDS, IDEA, onset ratio, and invalidity claims) show closely similar timing, of an increase that was gently starting off just before 1980, and then accelerating rapidly through the 1980s and well into the 1990s.Meanwhile, there is also a weight of other facts attesting to the reality of an increase of invalidity.The symptoms of chronic mercury vapor poisoning have been known for centuries, and include most especially all manner of mental and neurological disturbances, but also a variety of other symptoms. The wide variability of the presentation is easily under-stood in terms of the effects of mercury as a general anti-anti-oxidant, and as an antagonist to zinc thereby disrupting hundreds of enzymes, and also binding to the body’s own proteins thereby causing the immune system to identify them as alien and thereby producing auto-immune reactions.Page 14 of pathways-presentation.pdf gives an analysis of diagnoses of the claimants. It shows that 83% of cases are accounted for by those categories especially readily attributable to amalgam illness:Mental disorder 35%Nervous system 10%Musculo-skeletal* 22%Others** 16%(* Which could be mostly fibromyalgia, a modern “mystery” illness commonly sharing features of typical amalgam illness and often cured by amalgam removal.)(** An all-too-likely official label for cases of the amalgam illness which officially does not exist.)[Book update: In David Brownstein’s book Overcoming thyroid disorders, he quotes Dr Derry saying: “Chronic fatigue and fibro-myalgia were non-existent before 1980. So where did these two new diseases come from?” Errm.... no idea, please tell me, folks.]Further evidence supports the reality of the increase. I web-searched for the minister’s words “been a three-fold increase in disability” and found instead that in Finland 1987-1994 there was a threefold increase of disability pensions granted in respect of affective disorders (mainly depression) (Salminen et al., 1997), which is one of the most common effects of amalgam illness.And the disability claimants are now being regularly character-ised by ministers and propagandists as “workshy”, “bogus”, or merely making a “lifestyle choice” of fraudulent leisure.In 2010, the government minister Mark Harper declared on BBC Any Questions that “There are definitely some people in this country—and everyone in every community knows who they are—who are perfectly able to work, and don’t.” and then reiterated with “Everybody knows them, able-bodied people with no barriers to work who choose not to.”Another government minister, George Osborne, asserted that there were a sizeable number for whom claiming disability was a “lifestyle choice”.Meanwhile we are also being told that immigrants are subst-antially more hardworking than the natives of the UK, who appear by contrast to be “workshy”. And indeed employers confirm such a difference.In the real world of disability, the effects of adult mercury vapor poisoning can be far from obvious to “everyone in every community”. As stated in the book Amalgam Illness by Andrew Hall Cutler, at page 78, “Extremely poisoned patients do not look as sick as they are …. they make adequate adrenaline during the stressful time and perform. Then they collapse for a long time while nobody is around.” And at page 13, “One very important note: the patient looks a lot healthier than he is…..It is important to keep in mind that the patient may look well during appointments and yet be unable to conduct day-to-day activities, as well as be experiencing great discomfort on an ongoing basis.”And note also the following 1926 account by the famous chemist Alfred Stock of his own mercury vapor poisoning. Note how easily it could be “known” to be “workshy” were it not that the author was a notable professor.“Mental weariness and exhaustion, lack of inclination and ability to perform any, particularly mental, work, and increased need for sleep. …. My memory, which had previously been excellent, left more and more to be desired and became worse and worse until, two years ago, I suffered from nearly complete memory loss….. I forgot the content of the book or theater play I had just read or seen as well as my own work, which had been published. ….. Obstacles, which formerly I would have overlooked smilingly (and am overlooking again today), seemed insurmountable. Scientific work caused great effort. I forced myself to go to the laboratory without being able to get anything useful accomplished in spite of all efforts. Thought came laboriously and pedantically. I had to deny myself working on solutions to questions beyond the nearest tasks at hand. The lecture that used to be a pleasure became a torture. The preparations for a lecture, the writing of a dissertation, or merely a simple letter caused unending effort in styling the material and wrestling with the language.” (translated by Birgit Calhoun)(Stock, 1926)You can see from all the above that the characteristics ascribed to the allegedly bogus claimants are characteristics of mercury poisoning. With this understanding we can even account for the peculiar observations that workers from Eastern Europe and from more distant countries are found to be more “hardworking” than the native British, who by contrast are accused of being “workshy”. In fact a whole peculiar myth about normal human nature has been deployed here. Any normal healthy person, yourself for instance, would positively want to go out and do things rather than just lie in bed or slump in front of the tv all day every day. The normal healthy person would experience the latter prospect as more like a form of imprisonment than as an agreeable “lifestyle choice”.[[ Update for this book: Here are the words of Frank Field MP speaking on BBC Any Questions (Field, 2012):“London’s got the second highest youth unemployment, and yet it is the mecca for immigrants to come in and work. Now why is it that our schools produce people who cannot work or don’t work, as opposed to other people who at the very same time have work as part of their dna and the best thing in the world they want to do is to actually work? (loud applause).” [He then answers in terms of lazy racist white people, presumably with inferior dna, before continuing....]“It doesn’t take much money to get the kids to school on time, washed, clothed, breakfasted, and to school on time, and it is worrying that something is happening here...” [Indeed, and my own inability to get to the grammar school on time had nothing to do with my family’s shortage of money either.]And here are words about chronic fatigue syndrome from the book Plague (Heckenlively & Mikovits, 2014):“If this had been going on in the fifties and sixties, even if we had discarded it as psychiatric, it would have been written about, and [yet] it’s not in the literature.” ..... “How could we have possibly missed this disease for all these years?”. ....“....by the mid-1980s, distressed doctors and desperate patients had turned the disease into the top category of inquiry at both the CDC and public health departments ....”“Aided by a passive lay press, government scientists have sought to dismiss the disease by labeling sufferers with all manner of deficiencies and malevolent motives. That list has included malingering and cheating welfare systems, .... or people who [had] read about the disease and “wanted to have it”.“By 2009.... patients were denied not merely medical care, payouts on disability claims, and the emotional support that might have been forthcoming from family and friends had they suffered from a “real” disease,..... If they were children, they were denied educations ....” [like don’t I know myself, and see Chapter 8 here] ]]And furthermore, in reality almost all people are desperate to avoid becoming categorised as disabled, going to near-psychotic lengths of denial in the opposite direction. Few people would be pleased to be in any social context, with no better answer to a common question than: “I’ve been chronically disabled for the past five years (mentally rather than physically of course).” Virtually no-one in any society treats mentally disabled people as even near to being social or intellectual equals of themselves (in terms of marriage or educational opportunities for instance) (notwithstanding their pretentions to otherwise).An even greater catastrophe?Notably in line with the UK data, recipients of disability benefits in the US (SSI/SSDI) also increased more than twofold between 1987 and 2007.Here are some further facts. Figure 5 indicates a levelling off at 2.5 million claimants from 1995 onwards. But this must be put in the context of the words of the DWP document those figures came from. It was an internal discussion document about the “Personal Capability Assessment”, and its page 11 was headed “Caseload growth now controlled”. Translating those words from Officialese, they mean that there has been political resistance to the growth of disability claims, and that many thousands of persons genuinely disabled by DH recklessness have been denied the disability benefits they needed for survival, and that if the graph had reflected the real increase of disability it would not have levelled off, but instead would probably have surpassed more like 4 million by 2000 (which is about 10% of the UK’s working-age population). [Update August 2015: “Statistics [reluctantly] released by the DWP on Thursday revealed that 2,380 people died between December 2011 and February 2014 within 14 days of being taken off Employment and Support Allowance because a Work Capability Assessment had con-cluded they were able to work.” (Butler, 2015).][Update November 2015: 590 additional suicides linked to WCA reassessments (Barr et al., 2015; Benefits and Work, 2015).]And yet more. Four of the most characteristic symptoms of chronic mercury vapor poisoning are fatigue, depression, sleep disturbances, and poor memory. And surveys in recent years have found that now a gigantic proportion of the NON-claimant pop-ulation have these very symptoms, as follows.Depression:A survey of 2000 women and girls in England and Wales found 63% had been affected by mental health problems, having “a devastating impact on their lives”, and “48% experiencing mental health problems had stayed in bed or not left the house for a long period as a result” (Platform 51, 2011). Meanwhile, Colin Walker of Mind said his organisation’s research showed men and women experienced mental health problems such as depression and anxiety in roughly equal numbers (Hill, 2011).Insomnia:A report from the Mental Health Foundation (2011) states: “Only 38% of survey respondents (2522 people) were classified as ‘good sleepers’, whilst 36% were classified as possibly having chronic insomnia (2414 people). …. Other estimates of insomnia have put the total figure at around 30% of adults, …. although rates depend upon the criteria used to define it. Of the people reporting insomnia in the survey, over 30% have had insomnia for 2–5 years, and over 25% for over 11 years (figure 4).”The figure 4 in question then shows a distinctly bimodal distribution, in which the larger, longer-term, mode can be reasonably attributed to the effects of the dental amalgam toxicity.Fatigue:In a survey by Pharmaton (2010) in the UK, 24% said they are mentally or physically exhausted every day, 45% say they miss socialising due to tiredness, and 60% of the young are too tired to socialise, compared to 40% in 2002. And that is in line with the widespread experience that immigrants from less-developed countr-ies are substantially more “hardworking” than those who have grown up in the UK, who are conversely “workshy” as discussed on a preceding page here.Memory:Almost everyone nowadays wishes they had “better” memory, by which they mean more remembering rather than less. And yet contrary to the common assumption, memory is not something which natural selection would always be pressuring for more of (such as health or beauty). On the contrary, some persons (e.g. Solomon Shereschevsky) have had more memory than was actually useful for them. And history attests to the powerful memorising abilities of our ancestors.(This chapter continues on the next page.)Update 1All the preceding evidence here was suggesting to me an obvious further question, namely whether the original introduction of amalgams in the 19th century had caused an earlier increase of mental disabilities to the baselines shown here. Subsequent to my writing all the preceding, I learnt of the detailed historical review by Torrey & Miller (2002) of what was then called “insanity”, and the time-series graphs therein (at pages 94, 152, 188, 271, and frontispiece). In Figure 7 here I have re-plotted their data along with dates relating to the introduction of amalgam. Their book makes no mention of amalgam, or dentistry, nor of mercury as a possible cause of that increased morbidity. And yet their graphs show that rates of mental disability steadily increased from the original introduction of amalgams till a century later, by fourteenfold in Ireland and Canada, elevenfold in the US, and fivefold in the UK. These increases occurred in the context of vociferous contemporary condemnations of the use of amalgam due to its causing of mercury toxicity disabilities. The ASDS disbanded and the ADA replaced it because too many dentists preferred making quick profits from poisoning their patients with fillings deceitfully referred to as “silver”.Two curious observations on Figure 7. Firstly, the starting level being much higher in England/Wales, which could be because England was the first industrialised country, and with the main fuel both in houses and factories being mercury-emitting coal, besides which mercury was used for other purposes (such as hat-making). And indeed there is much reference in Torrey & Miller to insanity having been considered “the English disease”.Secondly, the ending level being much higher in Ireland, which could be because Ireland gets high rainfall from the Gulf Stream and consequently people are much more indoors and hence breathing in the amalgam mercury (as per my citation of Waldman et al earlier here). These two reality-harmonious observations suggest that these statistics reflect real increases rather than what some might construe as just some speculated mysterious spontaneous increase of awareness of what was then called insanity.And the Preface of their book states: “It has now been almost thirty years since one of us—E. Fuller Torrey—submitted a paper for publication suggesting that epidemic insanity was a recent phenomenon. .... The paper was summarily rejected by all journals .... and it was never published.... “.And then even my own copy of their extraordinary book had come from being dismissed from a library in Illinois.(Please see page 99 of free Chapter 3 at Experts Catastrophe - the catastrophe of official medical charlatanism for this next graph:)Figure 3.7. Insane persons in relation to the history of amalgams[Update 2 (added to this book chapter, August 2015)[missed out here, see book chapter for full].Conclusions and PredictionsIt is important to bear in mind here the further supporting data reviewed by Mutter (2011), Hanson (2004), Geier et al (2010), Homme et al (2014), and others.There are roughly two alternative viewpoints which may be reached from the data presented here. On the one hand there is a notion which entails that:(1) The heavy involvement of mercury in modern autism has nothing to do with the largest source of mercury input but instead is due to some other mysterious source or process.(2) And these graphs and other observations are mere coincid-ences in time.(3a) And either some mysterious unknown substance caused all these disabilities just so as to resemble the mercury symptoms that Mutter, Hanson, Geier, etc., have long been predicting anyway on entirely different evidence, and just happened to coincide at the right time to neatly confuse the author.(3b) Or there has been either a huge moral degeneration into “workshy” or else millions of people have enthusiastically embraced a “lifestyle choice” of living like a prisoner combined with the social leper dis-status of being mentally disabled, and furthermore these shirkers by some fluke just happened to be getting diagnosed with mercury symptoms even though they knew nothing about mercury toxicity, and by further impressive fluke so closely coincided with the increases of autism diagnoses and non-gamma-2 prevalence. And these “workshy” millions are somehow descendants of the people who hand-built the huge medieval cathedrals in a cold wet small island and then went on to create the largest empire (of hardworking foreigners) in history.(4) And a many-fold increase of mercury burden has not had any harmful effects on the millions thus burdened.(5) And the change of autism from life-long genetic to environmental and recoverable is just another of these mysteries.(6) And those gross untruths from the NHS just happened by fluke to all relate to preventing people getting diagnosed with mercury poisoning (two evidence-defying pseudo-tests, the “birds are highly unlikely to have wings” nonsense, the “see a dentist instead” - “see a doctor instead” nonsense, the review of my non-dental problems complaint exclusively by a dental panel with no toxicological or neurological expertise, the NHS’s own pseudo-study to pretend away the autism increase, and the Chief Dental Officer’s evidence-defying insistence that no mercury vapor comes off anyway).(7) And merely by yet another fluke Torrey’s graphs confirmed my suspicion that there would have been a previous increase of mental disabilities following the original introduction of amalgam 150 years earlier.(8) And merely by yet another fluke there is that observation that most mental disorders start in the 12-25 age-range.Alternatively there is a notion that non-gamma-2 amalgam has been the main cause of a tenfoldish increase of autism and a fourfoldish increase of adult disability including so-called “workshy”. It is the view of this author that this latter interpretation of the data strains credibility very much less than the former. It is hardly a surprising discovery given what Mutter, Hanson, and others have previously predicted on entirely different evidence already.And likewise the data of an increase in the 19th century cannot be lightly dismissed as “merely” coincidence. Some such increase was to be suspected by inference from the later non-gamma-2 data; it is scientifically explainable in terms of known mercury toxicity; and indeed it was very much pre-warned of already by ASDS members 170 years ago. And the ADA then adopted the propaganda language of “silver amalgams” by way of the ongoing cover-up. And I obtained that data from a very detailed review book which did not even mention dental or amalgam, so can hardly be dismissed as some sort of cherry-picking.Editors of putatively scientific medical journals have a duty to ensure that the public is not being kept unaware of evidence of possible serious harm from standard medical practices. It is a serious breach of ethics for such evidence as contained here to be refused publication other than for rigorously justified reasons. If there really are any serious faults in the case presented here, they should be openly published in the scientific literature rather than used as mere excuses to prevent the evidence being raised in the first place.It is here predicted that these increases will tend to correlate together in comparisons between different nations, due to the common causality. It is predicted that these epidemics will only be reversed by reduction of prevalence of non-gamma-2 in victims’ mouths. And meanwhile the risk of autistic disability can be reduced by ensuring adequate ventilation (in practice with a through draught at breathing-level).Appendix: Four Freedom of Information requestsPlease see the actual free book Chapter 3 for continuation - at Experts Catastrophe - the catastrophe of official medical charlatanismAND this is NOT the end of all the evidence by any means. Dental mercury poisoning is the greatest medical catastrophe in history and is the reason why I and you have been and still are constantly LIED to about it. It is almost impossible to get anything published about the subject. Nothing has EVER been published about the catastrophic health effects of non-gamma-2 unless you count this chapter here as being published.Cheers for reading so far and I would be interested to read your thoughts about it.

Out of three questions, first two questions are answered here Surbhi Tripathi's answer to What is the Nipah virus, and how is it transmitted?The last question which is most important one to answer is about government's measures on NiV. As India is one of the member state of World Health Organisation so the preparedness for NiV is recommended by WHO will be apt to apply in India:Surveillance, Prevention and Control ofNipah Virus Infection: A Practical HandbookPage No. 18–354. OUTBREAK OR EMERGENCY PREPAREDNESS AND RESPONSE FOR NiV4.1. PreparednessPreparedness in terms of technical and logistical management of a Nipah outbreak is essential in countries with recurrent outbreaks. The best response to a Nipah outbreak is being able to detect cases as early as possible and prevent further infections.4.1.1. Enhancing surveillance during the NiV transmission seasonSurveillance should be intensified during the Nipah season from January through May, when most Nipah outbreaks have been identified. This will increase the possibility of identifying NiV infection and understanding the characteristics of the virus. Blood, CSF, urine and throat swabs are collected from suspected patients and sent to the reference laboratories.4.1.2. Awareness building in hospitals and raising community awareness• Encourage and train health-care workers to maintain standard infection control precautions, e.g., personal hygiene, use of personal protective equipment(PPE), and manage encephalitis or neurological patients appropriately.• Disseminate information to communities through multimedia, leaflets, posters and meetings (group, community and market) encouraging people:o to stop consumption of raw date palm sap;o not to eat fruit partially eaten by bats;o cover the mouth and nose while caring for unconscious patients;o wash hands with soap and water before and after feeding and taking care of patients.4.1.3. Infection control in health-care settings should be in place• Implement standard infection control precautions.• Acquire and maintain PPE stock and other equipment needed in epidemiological investigations and outbreak response.4.1.4. Planning for outbreak response: some major components4.1.4.1. Formation of a multisectoral team 20Since NiV infection is a zoonosis and outbreaks may be associated with multiple factors such as animal reservoirs, sociocultural practices, food habits and possible human-to-human transmission, a multidisciplinary team is needed, and preparation should be done for pre-outbreak, outbreak and post-outbreak phases.A multisectoral team should be built up at national and local levels for the monitoring, evaluation and response to unusual acute public health events and outbreak response, including Nipah outbreaks. The team should have a holistic, multidisciplinary approach consisting of public health personnel, clinicians and laboratory personnel. The multisectoral team may consist of the following professionals (depending on the evolving and country-specific situation) who would bring relevant expertise in outbreak investigation and response:• epidemiologist• microbiologist• anthropologist and/or social scientist• veterinarian• ecologist.National or subnational level – Rapid Response Team (NRRT): The NRRT should be assigned from institutes at the national/provincial level and partner institutes.District/provincial level – District Rapid Response Team (DRRT): The DRRT consists of the head of health services at the district/provincial level and clinical and laboratory expertise, and other expertise from the public health department.4.1.4.2. Evaluate and ensure the supplies for sample collection, storage and shipment of samples:• Assess PPE in stock;• Assess sample collection instruments;• Assess sample storage capacity in the laboratory;• Evaluate laboratory capacity for NiV testing (e.g., biosafety, quality, skills, human resources and consumables for NiV virus testing);• Evaluate hospital capacities for isolation facilities and ability to treat Nipah patients in Nipah-prone areas.4.2. Alert and outbreak investigationThe outbreak investigation should lead to formulation of an appropriate public health intervention as soon as the source and mode of transmission are known. In the meantime, control measures mitigating known risk factors should be implemented as soon as NiV transmission is suspected.4.2.1. Investigation of a suspected case or cluster of suspect cases:4.2.1.1. Standard Operating Procedures (SOPs) for sample collection and transportation in place:• Surveillance physician will take verbal consent from patient or patient’s family member;• Collect 5 ml venous blood;• If possible, collect 3 ml extra-CSF when appropriate;• Aliquot 1 ml serum and 1 ml CSF samples in 1.8 ml cryovial tube. Try to aliquot serum and CSF samples in three cryovial tubes;• Label the cryovial tube with: type of samples (serum/CSF), patient name and identification number, and date of sample collection;• Store the serum and CSF samples in liquid nitrogen if possible, or −20°C freezer for short-term storage if liquid nitrogen is not available;• Ship samples in liquid nitrogen tank or ice pack to assigned centre for laboratory diagnosis;• Store samples in −70°C freezer for longer-term storage;• A list of potential national or international reference laboratories should be pre-established. There can be several for different purposes: a frontline laboratory would be the WHO Collaborating Centre for laboratory diagnosis of viral diseases with BSL 3 or BSL 4 facilities (see list of WHO Collaborating Centres and other institutions for laboratory diagnosis, surveillance and response in Appendix 4).4.2.1.2. Templates of data collection instruments pre-developed and in place for quick useThese templates should include the following:• line listing of all cases;• case reporting form;• questionnaire for case-control studies or other relevant studies;• forms for sample collection.4.2.1.3. SOP for activating and conducting outbreak investigation teamsThis SOP is commonly country-specific as the process relies on the administrative structures and capacity or resources of a given country. Therefore a country-based manual or protocol for outbreak investigations should be in place in at-risk countries forNipah outbreaks. A more generalized national SOP manual for all emerging or re-emerging infectious diseases of international concern could be developed focusing on a mechanism of response and roles and responsibilities of different parties.The following are some of the key components to prepare a team for outbreak investigation:1) National or Subnational Rapid Response Team (RRT) Should an outbreak of NiV virus disease be suspected and/or reported, the National RRT should be activated and should meet together to:(1) Plan and conduct the investigation;(2) Request further technical support if needed (e.g., further analysis and interpretation, risk communication, initiate control).2) Administrative SOP for field work in place: administrative clearance, organize supplies, travel arrangements:• approval/permission from competent authority;• arrangement for accommodation;• arrangement for security, if needed;• arrange vehicle;• supplies:o medicineso sample collection instrumentso PPEo disinfectants, hand sanitizero basic medical and investigation equipment, e.g., stethoscope, thermometer, GPS instrument, etc.3) SOP for rapid mobilization of additional or experts teamsIf the NiV outbreak is confirmed, an experienced Nipah outbreak investigation team comprising an epidemiologist, clinician, veterinarian and anthropologist or social scientist can move to the field within 24 hours of outbreak reporting.4.2. 1.4. Nipah outbreak investigationThe overall objective of investigating Nipah outbreaks is to control the outbreak and prevent future outbreaks. Any Nipah (or suspicion of) outbreaks should be investigated as the disease is of public health concern with potentially devastating consequences.The specific objectives include the following:• to determine the extent of the outbreak;• to characterize the populations at greatest risk and to identify specific risk factors;• to provide practical recommendations to strengthen control and prevention measures.Key steps when conducting Nipah outbreak investigationStep 1: Activate preparation plan for outbreak investigation (details above).Step 2: Confirm the outbreak.One of the first tasks of the initial investigation team is to verify that a suspected cluster of cases is indeed a real outbreak with common cause. Some will be unrelated cases of the same disease, and others will turn out to be real cases of AES or ALRI but of unrelated diseases. This step consists of confirming the diagnosis through visiting the outbreak affected areas to (1) examine the patients and/or review the medical charts to describe and understand the clinical presentation; (2) collect blood, CSF and throat swab samples at the time of admission/ first contact, and follow-up serum samples 2 weeks after the onset of illness for testing.A Nipah outbreak is defined as the identification of at least one laboratory-confirmed case.Step 3: Define and identify cases.The investigators should develop or adapt standardized case definitions appropriate to the outbreak context (see details in standard case definitions). Testing for NiV infection should be performed when there are: (i) clusters of AES due to an unknown agent or (ii) patients with AES due to an unknown agent living in or near NiV zones.Patients with AES should also be tested for NiV infection when they are exposed to a cluster of unexplained neurological/pulmonary illness in animals, such as horses and pigs.Step 4: Case-findingIn many outbreaks, including Nipah outbreaks, the first cases that are recognized are usually a small proportion of the total number. Retrospective and prospective case-findings are crucial to determine the true magnitude and geographical extent of the outbreak.Active case-finding should be conducted:Among close contacts:• A close contact is defined as “a patient or the person who came in contact with a Nipah case (confirmed or probable cases) AND stayed in the room or veranda or vehicle for at least 15 minutes”.• Record contacts for potential follow-up if need be. They are to be followed up in case of occurrence of illness (up to 18 days). Serum specimens should be collected in case of symptom onseto in high-risk groups or in groups exposed to the sourceo through enhancing surveillance in the outbreak area and the at-risk areas for case-finding in the communityStep 5: Evaluate the outbreak in relation to ‘time, place and person’• establish a line-list of current and previous cases;• draw an epidemic curve;• analyse and interpret the data to identify potential sources of transmission.Step 6: Develop and evaluate hypothesesOnce step 5 has been done, investigators should have some hypotheses regarding the source and/or mode of transmission and the exposures that caused the disease. These hypotheses should be compared with established facts.Step 7: Refine hypotheses and carry out additional studiesIf step 6 is not conclusive, these hypotheses can be refined to look for new modes or vehicles of transmission and be evaluated through conducting case–control studies.Step 8: Implement control and prevention measures (see response section below)Step 9: Communicate findings and information about risks (i.e., outbreak report)• Develop an outbreak report and disseminate to concerned authorities.• Learning from the outbreak includes detailing:o new findingso major limitations during outbreak investigation• Resume the activities of pre-outbreak phase.4.3. Additional considerations with respect to Nipah outbreaksWhen the Nipah outbreak is confirmed, the investigation team needs to:• Immediately inform the local, regional and national authorities.• Inform the partners/stakeholders (notably those involved at local level): treating hospitals, patients’ relatives.• Declare the Nipah outbreak to WHO under the International HealthRegulation 2005 (IHR) via National IHR focal points (see detail below in the response section).Notification and assessment of Nipah outbreak and/or cases to WHO should be based on the following four criteria described in Annex II of IHR 2005. A "yes" to any of the four criteria would lead to notifying WHO under Article 6 of the IHR.• Is the public health impact of the Nipah outbreak and/or cases serious?• Are the Nipah outbreak and/or cases unusual or unexpected?• Is there a significant risk of international spread?• Is there a significant risk of international travel or trade restrictions?4.3.1. Conduct rapid risk assessmentSome of the major risk assessment questions should include the following:• What is the risk of occurrence of further cases from the detected outbreak?• What is the risk of spread of the infection?• What is the risk of major impact of the current outbreak on the health-care system?4.3.2. Evaluate the impact of control measuresEach outbreak should be thoroughly investigated, and lessons learnt from each outbreak should be evaluated and documented so that control measures can be reviewed and modified as required.4.3. 3. Develop further research with the objective of identifying determinants of infection or severity and determining modes and dynamics of infectionThe populations to be investigated would be those exposed to NiV:4.3.3.1. Health-care workers (HCWs)There is evidence of nosocomial transmission in India and Bangladesh, and one nurse was positive to Nipah IgM antibody in Malaysia (3, 4). HCWs are to be trained for infection control and prevention (see below). Surveillance should be in place to detect any suspected cases among HCWs. In addition, a study should be conducted to identify asymptomaticcases among HCWs who provided service to Nipah patients. Among these, positive cases should be subsequently compared with negative ones to determine risk factors for infection and understand the dynamics of transmission. Some components of the study could include:• Make a list of HCWs who provided care to Nipah patients.• Take consent from HCWs.• Interview at-risk HCWs using an exposure questionnaire, about 3 weeks after the last exposure to NiV-infected patients.• Collect 5 ml of blood for serology testing about 3 weeks after the last exposure to NiV-infected patients.4.3.3.2. Communities potentially exposed to NiVThe investigation should encourage involvement of multidisciplinary and multisectoral team using a one-health approach. For instance, investigators should have the support of microbiologists and their laboratories to conduct community-based seroprevalence surveys (detection of recent antibody response) to determine the extent of the outbreak via detecting subclinical and/or asymptomatic cases. Asymptomatic cases could be further compared with controls to identify risk factors for infection.Anthropologists or other social scientists with extensive community-based experience could help propose additional behaviour risk factors to be tested in a case–control study. Anthropologists should work with communication/health promotion specialists to develop communication messages combining both local explanatory models and biomedical models using local terms and languages, and deliver the message in such a way that it is meaningful to the community.Veterinarians and eco-health specialists should join the investigation to conduct studies collecting specimens from animals and the environment in the outbreak settings.Zoonotic and environmental investigations during an NiV outbreak primarily aim to determine the primary reservoir, likely source of the virus, route of transmission and the extent of the spread of the virus in animals. Georeferenced positive specimens could be analysed with positive human cases to better understand the dynamics of transmission.4.4. ResponseAs soon as a Nipah outbreak is confirmed, national authorities should implement control measures based on known risk factors. The interventions should be based on a multisectoral approach and include/understand the following strategic objectives:1. Establishment of a coordination committee for outbreak prevention, and control activities and resources mobilization; the role of this committee is to ensure the general coordination of operations. It must clearly define the responsibilities of the various teams and the route of information during outbreak response operations.2. Setting up partnerships with the media to ensure media monitoring and better risk communication.3. Formation of a referral system with the principal objective of easing transfer of cases to the appropriate case-management health-care settings.a. Active detection for new Nipah cases and their transfer to the case-management ward.b. Follow up all contacts during 18 days after their last unprotected exposure to Nipah patient(s) or infected animal or tissue (e.g., laboratory) and their transfer to the case-management ward if they fall sick.4. Set up a social mobilization and medical education programme whose principal role is to inform the public and promote practices that decrease community transmission of the disease.5. At the foci zone, the medical team should ensure safe case management of Nipah patients by complying with the following guidelines:a. Respect patients and their families’ dignity and rights, in particular their right for information on disease and treatment,b. Set up a specific Nipah case-management ward that ensures biosafety of in-patient care,c. Set up infection prevention and control measures for safe patient care,d. Organize the safe transport of patients from their residence to the ward,e. The express consent of patients is necessary for any hospitalization. In the event of patient’s refusal to be hospitalized, the medical team should organize, temporarily, a patient’s care at home with his/her family support.f. Organize safe burials while respecting the funeral ceremony,g. Set up psychosocial support (patients, family, HCWs).6. Outside the foci zone, to prevent secondary foci, the medical team should reinforce standard infection prevention and control measures in health care in all health centres of the affected district and all hospitals catering to the outbreak zone.7. Establishment of links with the animal health sector to:a. Continue monitoring the cause of disease and death in domestic animals and wildlife.b. Test samples and alert public health authorities as needed.c. Control slaughtering/butchering activities of domestic animals and wildlife, at home, and in markets and slaughterhouses.8. Media and communicationa. Designate a spokesperson in the outbreak team.b. Designate a spokesperson at the national level who communicates with national media.c. Regularly update reports to be sent to assigned authority.d. Conduct regular meetings with press and community.e. Distribute information, education and communication material.4.5. In the aftermath of the outbreak (evaluation)4.5.1. Declare the end of the outbreakThe health ministry declares the end of the outbreak. The date of outbreak end is equal to twice the mean incubation period for Nipah counted from the last infectious contact with a confirmed or probable case.The national authorities should use the announcement of the end of the outbreak to acknowledge national and international field teams as well as the media. They should also formally present their solidarity and their empathy to the victims, their families and the affected populations.4.5.2. Writing a final report of the outbreak control activitiesThe report objective is to describe the activities undertaken during the epidemic as well as constraints and difficulties encountered. It should include technical aspects (final epidemiological analysis, clinical investigations, etc.), as well as administrative and financial aspects. The report should be published to achieve wider dissemination of findings and lessons learnt.4.5.3. Archive outbreak documents and files• Gather all the reports, files, photographs, videos and other documents related to the outbreak management.• Store all the documents in a place accessible for their later use.4.5.4. Evaluate the management of the outbreakThe evaluation of the management of the outbreak response will review the performance of the various components of the strategy: coordination, relationship to the media, surveillance system, social mobilization programme, clinical management and logistics.The aim of the evaluation is to determine lessons learnt to improve the future management of epidemics. This evaluation should be led by a team comprising national and technical partners.4.5.5. To resume activities of the pre-outbreak period

I will begin here with “anecdote” but will continue with vastly more, though in any case anecdote IS data, contrary to the propaganda mangled version usually trotted out in medical brain-damaging schools. So…(first some comments on my autism theory, back at a time when I knew nothing of mercury or the cause of my own life-ruining “mystery” illness).“Robin P Clarke is one of those rare souls with the ability to assimilate and synthesise large amounts of information and generate new and interesting ideas.” – Bernard Rimland, founder of Autism Research Institute, founder of Autism Society of America, debunker of Bettleheim’s theory, and originator of the modern bio/genetic concept of autism.“Well worth publishing” – Hans J Eysenck, most-cited-ever scientist, who did publish it.“Well-written, well-argued, well-documented”– journal’s peer‑reviewer comment.“Get your autism puzzle-pieces here!”– Autism “research” fundraisers.While still at school, I developed a “mystery illness”, severely mentally and neurologically disabling to the extent that I have never been able to complete my formal education, have any sort of career, or any of the normal life that can only follow therefrom.Eventually, the internet was developed, and voluntary people put up free websites of information, and back then there was not the internet censorship and Google manipulation that we have now. Anyone could put anything there. Including the truth. Having thus gained a suspicion that my decades of disability had been caused by dental mercury, I thereafter spent much time studying and becoming more and more knowledgable.Eventually I was able to recover myself from FORTY-EIGHT YEARS of ruinous severe disability. Oh, just a fluke anecdote of course….Dental amalgam is the greatest scientific catastrophe ever. Well, it was when I wrote my book Experts Catastrophe (36 graphs, hundreds of sci refs, 120,000 words). But it has now been overtaken by an even greater triumph of Lysenkoian charlatanism, namely the lockdowns pseudoscience as detailed in http://www.pseudoexpertise.com/clarke-covid3.pdf. Funny, no-one’s ever pointed out that info there before, even though it is the most basic facts of the lockdowns. It just doesn’t fit the MegaBig Money greed agenda so is firmly censored from publication. But you don’t even have to pay me for the work careerless I do. You just have to sneer and censor as we will soon start seeing some doing here.Anyway, enough of my “anecdotes”. I could point you to the definitive review of the amalgam disaster, at http://www.pseudoexpertise.com/ch-3.pdf along with the cheap faceless lies used to prevent publication, at http://www.pseudoexpertise.com/ch-5.pdf and http://www.pseudoexpertise.com/ch-4.pdf. And also to the originating published theory of autism at http://www.pseudoexpertise.com/ch-7.pdf. And for good measure, one of the confirmations of predictions, in this case, the confirmation that mercury pollution has caused the huge rise and fall of IQs known as the Flynn effect (see last link in my profile).But as Quora likes long answers, I will paste in most of that Chapter 3 here. It’s free to read, and free to sneer at, and also free for the proud dentists writing their ignorances here to apologise about. So…~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~From http://www.pseudoexpertise.com/ch-3.pdf (It would better to buy the whole book Experts Catastrophe which you can easily find on Amazon.)3 A suppressed report ofmillions of (non-autistic) victims“Academic journals and societies show an auto-immune response to information that should be the life-blood of medicine.”– Prof. David Healy, author of Pharmageddon“Your paper is important”– mercury expert Dr med. Joachim MutterBefore reading this chapter I recommend that you read the first two chapters of this book. Otherwise you may come to it with consid-erable misconceptions which could make for difficult and unprod-uctive reading here.The main content of this chapter is a scientific paper. I wrote it with the intention of it being accepted in a scientific journal, and so you might find it rather turgid reading and with too many of those citations such as (Authorname, 2012) intruding into my florid prose. On the other hand one journal editor condemned it for (supposedly) appearing to be written like a newspaper article, so maybe there’s hope for non-academic readers nevertheless.You may be wondering whether you can have the competence to make any useful judgement of the soundness or credibility of this article. Wouldn’t the experts perhaps point out all manner of hidden things wrong with it? But I am providing you with a special resource here. In the next two chapters, you can see the world’s top experts telling me (off the record) the reasons why this article is such rubbish that you shouldn’t even be informed of its existence anyway. I suggest that you study those critiques and my rejoinders to them, and (as is always necessary eventually) then decide for yourself who if anyone has the more credibility. I can’t print the re-rejoinders from these experts because none have replied back. Perhaps you could write to these journals yourself to ask them why you shouldn’t be persuaded by what I said in my own replies.Scientific papers normally end with a list of the references cited. In this book I will transfer this paper’s reference list into the list at the end of the book. But this article is unusual in that it contains an appendix which itself contains three further lists of references. I will leave those in place just as they were present in the original documents contained in that appendix. Other than that, what follows after this paragraph is the most updated version of the manuscript I have sent to now eighteen journals. It is usual for scientific papers to begin with a summary called an “abstract”. This gives an overview for those who don’t already have the full text, but may be hard as a non-specialist to follow until you have read that full text, and you shouldn’t let yourself get bogged down by this one here. Also this chapter contains some graphs of disability epidemiology. If you are not already a wizard with such graphs, you may find it useful to jump forward to the section of Chapter 6 which discusses some misuses and abuses of similar sorts of graphs. Lastly, the “p<“ values stated herein indicate the probability of obtaining that result due to random chance.(NOTE: AT NO POINT HAVE I EVER SAID THAT ALL AUTISM IS CAUSED BY MERCURY OR AMALGAMS – See Chapter 7!)Autism, adult disability, and ‘workshy’: Major epidemics being caused by non-gamma-2 dental amalgamsRobin P ClarkeAbstract: It is unknown to most people that the dental amalgams which have been used as standard in recent decades, namely non-gamma-2 dental amalgams, have been substantially unlike those used before the 1970s, in that they constantly emit 20 to 50 times more mercury vapor than the older types. This is the first-ever study of health consequences of non-gamma-2. Following the changeover to non-gamma-2 amalgams, there promptly began a tenfoldish increase of autism, a tenfoldish change of ratio between late onset and early onset, a change from mainly genetic to mainly environmental, and a change from lifelong incurable to sometimes clearly recoverable. Exactly simultaneously there occurred a fourfoldish increase of claims for adult disability in the UK, with disabilities all or mostly of the nature that would be expected from chronic mercury poisoning (including mental disabilities and neurological disabilities). And similarly in the US. These timings cannot be dismissed as coincidence because there are no credible alternative explanations for the increases. Data strongly suggests that non-gamma-2 amalgams are currently by far the main cause of chronic disability in the UK, US, and other such countries, with about 10% of the UK working-age population disabled thereby.An experiment on millions of dis﷓informed subjectsDental amalgams in patients’ teeth constantly emit mercury vapor, and that vapor is easily measureable. This has been known for decades as indicated in at least 18 published studies (Berglund, 1993; Berglund et al., 1988, Boyer, 1988; Brune et al., 1983; Clarkson et al., 1988; Ferracane et al., 1995; Mackert, 1987; Mahler et al., 1994; Moberg, 1985a, 1985b; Olsson et al., 1989; Olsson and Bergman, 1987; Patterson et al., 1985; Psarras et al., 1994; Svare et al., 1981; Vimy and Lorscheider, 1985a, 1985b, 1990).And yet in stark contradiction of all this clearly established basic science, the UK’s Chief Dental Officer (2009) has publicly asserted, as some supposed fact, that dental amalgams do not constantly emit any mercury vapor (or in his second thoughts on being challenged, at least “not measureably”).Such mercury vapor has been recognised for centuries as one of the most toxic of substances, causing various mental, neurological and physical disabilities. For more than a hundred years prior to the 1970s, strong condemnations were regularly issued against the use of amalgam in dentistry. These warnings were consistently ignored by health authorities, and dismissed with claims that there was no real evidence of harmfulness.Much further evidence of harmfulness of dental amalgam has come to light in recent decades (Mutter, 2011; Hanson, 2004; Homme et al., 2014), not least in thousands of cases of improvement following amalgam removal which cannot be dismissed as merely anecdotal or placebo. Some relatively large-scale trials have been asserted to show amalgam safety, but they have been substantially flawed and in at least one case in reality showed harmfulness rather than safety (as explained by Mutter, 2011 and Homme et al., 2014).In the 1970s a new type of dental amalgam was introduced as the new standard, partly on the basis that it was very much more durable, with far less tendency to corroding and crumbling. This new type was called non-gamma-2.These non-gamma-2 dental amalgams constantly emit 20 to 50 times more of the toxic mercury vapor than the older types (Berglund, 1993; Boyer, 1988; Brune et al., 1983; Ferracane et al., 1995; Mahler et al., 1994; Moberg, 1985a, 1985b; Psarras et al., 1994). The amalgam constantly emitting this neurotoxic mercury vapor is located in a person’s mouth, less than two inches from their brain, and in the pathway to the lungs (where 80% is absorbed at each inhalation). Any notion that the levels of mercury vapor caused by amalgams are very low has to be put in the context of the general outdoor levels being many times lower still at around 0.002 mcg/m3.No safety testing was undertaken before or after it was introduced. Patients and the public in general have still not been informed of the change, let alone of the increased levels of mercury involved. No informed consent has been sought, and no warnings have been given of any possible harmfulness. Indeed, throughout the US it was actually made illegal for dentists to issue such warnings, and Hal Huggins and other dentists were struck off the register of practitioners for doing so.In the UK, a number of untruths were adopted by the NHS and DH such as to prevent people being diagnosed with mercury toxicity and to thereby further reduce any concern about risk. The following untruths have been identified by the author, but it is unlikely that they have been the only ones.1. Untrue assertion that “Chronic mercury poisoning is highly unlikely to present in a psychiatric setting”.2. Use of proven useless urine tests for supposed (dis-) diagnosis of chronic mercury poisoning.3. Use of proven useless blood tests for supposed (dis-) diagnosis of chronic mercury poisoning.4. Chief Dental Officer’s untrue assertion that “no mercury vapor” emits from amalgams, or alternatively “not measureably”.5. Chief Dental Officer’s untrue denial that amalgams are the main source of mercury in the body.6. NHS Chief Executive’s re-insistence on the untruth that dentists have capability for mercury diagnosis whereas doctors do not.The existence of these untruths is authenticated via my Freedom of Information requests as documented partly in an Appendix hereto and more fully via dental mercury falsehoodsDates of introduction and usageNon-gamma-2 amalgams are very much more durable than the previous types. Consequently, declining rates of amalgam install-ation would conceal an increase of prevalence of the amalgams in patients’ mouths. And it is here expected that the key variable would be that rising prevalence rather than the declining rate of installations and replacements.A number of US patents for non-gamma-2 were granted in the mid-1970s. The famous US dentist Hal Huggins states that the changeover to “high copper”, i.e. non-gamma-2, occurred in 1976. In 1986 the ISO standard was changed retrospectively to incorporate them. The non-gamma-2 amalgams took over in the period 1975-79 in Denmark (Hansen et al., 1993). In Germany the use of the earlier types was banned in 1992, making the non-gamma-2 the only option. And according to the manufacturer’s product sheet, Dispersalloy is the most widely used amalgam with over 25 years of proven performance, i.e., since before 1979, but perhaps after their 1974 patent no. 3841860.I have been unable to obtain any numerical data on usage or total prevalence of non-gamma-2 in people’s mouths. The DH have told me they have no such records. And NHS dental records have not recorded the types of amalgam used. It is unlikely that any better information is available in other countries. But we can very reasonably assume that the overall prevalence of non-gamma-2 will have gradually, progressively increased in the decades following its introduction.My epidemiological investigationsHaving become aware of the changeover to non-gamma-2 amalgams, I decided to look to see if there might be epidemiological evidence of any consequences. It appears that no-one has ever done this before.In respect of the following accounts it is important to understand that I have not cherry-picked selected data to prove any point, but instead have used all the best data readily available to me.To avoid undue length here, the reader is referred to consult prior reviews of substantial important other data pointing to similar conclusions as those here, including Hanson (2004), Mutter (2011), Geier et al. (2010), Homme et al. (2014), and others not specifically cited.Is mercury involved in causation of autism?Before presenting the epidemiological findings it will be useful to first show the context of existing evidence from clinical studies on this question.A number of reviews have suggested there is persuasive evidence that mercury is importantly involved in causing of autism (Geier et al., 2010; Bernard et al., 2001; DeSoto and Hitlan, 2010; Kern et al., 2012). And yet the evidence can be shown to be far more decisive than any of these suggest, and indeed beyond all reasonable doubt.In any combinatory review of studies it is necessary firstly to rule out those which lack a sound rationale. A number of studies have used blood mercury or urine mercury as criterion measures, and yet it has been known for decades that these lack merit as indicators of chronic mercury toxicity. Indeed, the most prominent such study, Hertz-Picciotto et al. (2010), stated in its second-last sentence that: “This report did not address the role of prenatal or early-life Hg exposure in the etiology of autism” [i.e., the study could not provide any evidence against causation by mercury].Another danger in meta-reviewing of studies is the merging together of data which should be kept separate. In respect of mercury in autistics’ hair, the most enlightening study is that of Majewska et al. (2010). They found that in younger children autism was associated with markedly decreased hair mercury (p<0.01), whereas in older children autism was associated with markedly increased hair mercury (p<0.01). If they had just lumped all their results together they would have got an entirely unwarranted “no difference” non-result instead. Viewed in the light of Majewska et al, all or most of the other hair mercury studies fall into a coherent pattern. There are several which have smudged together the different ages and therefrom invalidly declared non-results. Meanwhile others strongly reinforce the notion that there are real effects.Holmes et al. (2003) obtained an eightfold difference of mercury in hair, with significance level of 1 in 250,000 (p<0.000004). Some commenters dismiss that study on a basis that it was done by opponents of mercury, and “therefore” their results may have been biased or fraudulent. But one would have expected any bias or fraud to result in a finding that hair mercury was increased in autistics, as that would have been in accordance with the standard rationale for diagnosing toxin exposure from increased hair measurements. They found instead 8‑fold reduced levels, which strongly suggests that they were instead acting competently and honestly. Their rational-ising notion of paradoxical reductions of measurements in mercury toxic subjects has since been supported by much other evidence that mercury sometimes impairs its own excretion.A study in India (Lakhshmi Priya and Geetha, 2010) found 8-fold increased hair mercury (p<0.001). Another in Kuwait (Fido and Al-Saad, 2005) found 15-fold increased hair mercury (p<0.001).Bradstreet et al. (2003) found that a challenge test with the chelating agent DMSA caused a release of mercury 3.15 times greater in autistic cases than in controls (p<0.0002). That is a 1 in 5000 probability that that excess mercury was just a fluke.The probability of just these results listed above being all due to mere chance is 1/5000 x 1/250000 x 1/100 x 1/100 x 1/1000 x 1/1000, that is one in 12,500,000,000,000,000,000, vastly beyond the standard of proof ever required in any criminal prosecution.And far more than one negative result is required to call into question one significantly positive result. There are far more ways of making a “negative” car that does not move than of making a “positive” one that does. I and thousands of others have lived in the UK for many years and never seen the Queen in all that time, and yet that does not constitute significant grounds for dismissing the testimony of those who claim she has existed. If there were in reality no mercury-autism connection there should be a huge pile of “no-difference-found” results among which these high-significance results would be a small minority. But there is no such pile of null results to speak against the mercury-autism connection.One could seek to interpret all those results with a notion that there could be an unknown factor which both causes autism and also harmlessly causes mercury to vary in hair and other tissues. But that notion is brought into question by the extensive commonalities between autism and mercury toxification (Kern et al., 2012). And it is completely demolished by the observations of the Autism Research Institute which has for decades been surveying the effectiveness of many potential treatments for autism. Of more than 80 treatments tested, the ARI has found that one of the most effective has been removal of mercury by careful chelation. And Blaucok-Busch et al. (2012) obtained highly-significant behavioral improvements even with the rather poor Hg chelator DMSA (p<0.001; p<0.001; p<0.001).Meanwhile, three studies have been promoted as supposedly disproving any mercury-autism thesis. The study by Ip et al. (2004) was shown to be riddled with arithmetical errors, and in reality indicated that there was indeed a mercury connection (DeSoto and Hitlan, 2010). Likewise Soden et al. (2007) actually proved the opposite (DeSoto and Hitlan, 2010). And Hertz-Picciotto et al. (2010) stated in their own second-last sentence that their study did not address causation of autism by prenatal or early-life mercury exposure. Such falsely proclaimed studies are all that stands in supposed defiance of that astronomically large number calculated above. There is even more evidence that merits mention here but it would be superfluous. We can resolutely conclude that mercury is now a major cause of autism. [Updates: Autism association with prenatal SSRI use (Harrington et al., 2014) = amalgam causes both depression of mother and autism of baby. Widespread reports of seizures in 1/3 of autistics = perinatal mercury causes both autism and seizures (Szasz et al., 2002; Klinghardt, 1998).]Increased autism?In academic papers and elsewhere, certain myths about autism are constantly portrayed as self-evident truths, so they must be addressed here. Firstly, the human race does not divide into those “with” autism and those “without” it, or those “on the spectrum” and those “not on the spectrum”. Rather, there is a continuum of variation in the extent to which individuals are more or less autistic (in varying ways). Secondly, there is no scientific basis for a distinction between autism and Asperger’s. It was merely a historical accident that Kanner and Asperger made simultaneous rediscoveries of the syndrome described by JL Down in 1887. Thirdly, there is no scientific basis for the routine references to autism as a “disorder”. Autism can be severely disabling, is often terribly distressing, and may often be a consequence of a disorder (such as maternal infection), but rather than a disorder it is properly considered to be just atypicality (as is genius). [This is now more fully discussed in Chapter 2.]Some researchers with decades of direct experience, such as Bernard Rimland and Lisa Blakemore-Brown, have been of the view that there has been a substantial increase of autistic behaviors, and not just increase of diagnoses.[Update for this book: Significant further discussion of the increase “controversy” is contained in Chapter 2 in the section “The autism increase controversy” (page 68), just before the appendix to that chapter, and also majorly in Chapter 12 and pages 188-189.]The NHS has published a report claiming to show that there has not been any increase, by supposedly showing the prevalence of autism among older adults to be the same as in children (Brugha, 2011). The report detailed the elaborate measures taken to ensure reliability of the autism assessments. And yet it gave no details at all of any measures taken to ensure the validity, that is the (infinitely more important) comparability of the diagnostic procedures as applied to adults relative to applied to children. The reason there were no such details is because there was no way of establishing such validity. And in absence thereof, such a study proves nothing about changing prevalence of autism. I myself have direct knowledge of two older persons given baseless diagnoses of autism by this same NHS that proclaims as expertise the untruths listed on a preceding page here.The Autism Research Institute has a uniquely extensive historical database of cases. Figure 1 [here 3.1] is my re-plot of a graph published by the Autism Research Institute of its own records. Figure 2 shows my extraction from Figure 1 of the time-series of case ratios between late and early onset. Before 1980, onset at birth was twice as frequent as onset in the second year (i.e. regressive autism), whereas after 1990 the later onset rose to become five times more frequent than the onset at birth. The switch-over began at the end of the 1970s and was well under way by 1990. It closely related with the apparent increase of autism illustrated in Figure 3 and elsewhere. Figure 3 shows the data from the California DDS 2003 report (2003), with the earlier 1999 report (1999) (1998 data) re-calculated to the same basis. [Note added to book chapter version: Figure 3 also shows what mathematicians call an exponential increase curve; basically it gets increasingly steeper exactly in proportion to the higher it gets.](Figure legends are below the figures, as is customary.)Fig. 3.1. “U.S. Cases: Autistic children who behaved normally before 18 months vs. those with no normal period.” From Rimland (2000) (replotted)Fig. 3.2. Data from Figure 1 here used to show the changing ratio of cases in respect of age-of-onset. A further datum is from Mrozek-Budzyn et al. (2009) p.109.Fig. 3.3. Autism enrolment in California.Fig. 3.4. Concurrence of California data of Figure 3.3 with total autism implied in Figure 3.2 if onset at birth is assumed to have constant incidence of one unit.In Figure 4 I have added together the two series of Figure 2 such as to give a nominal “total autism” curve based on an assumption that onset at birth has had constant prevalence during those years, and that early onset cases plus late onset cases equals total autism. Figure 4 shows that the increase curves of Figure 3 peculiarly coincided in time with the ratio-change curve of Figure 2. This enables substantial confidence that the conceptually independent Figures 2 and 3 are tracking exactly the same causal phenomenon.The late-onset, regressive autism is much more difficult to overlook than the at-birth autism, as parents are baffled by the regression of their children. Any under-awareness would not have been concentrated on those late-onset cases. And yet it is those which have increased about tenfold, not the more overlookable early-onset. So this data argues against interpretation in terms of mere changing of awareness or diagnostic thresholds. And it cannot be dismissed as due to demise of the diagnosis of “childhood schizophrenia”, because ARI’s survey questionnaire asked about age of onset rather than presumed about it, and indeed the ARI was neutrally called the “Institute for Child Behavior Research” until 1991.These curves strongly suggest that the autism increase was caused by something that started having an effect on children around the end of the 1970s and also caused a tenfold change of ratio of late-onset cases relative to early onset.An overview of autism trends in the US and UK found essent-ially the same trends of increase in both areas and in respect of both autism and “autism spectrum disorders” (Blaxill, 2004). Information about other capitalist countries has been less systematic, but generally similar trends appear to prevail. In respect of Sweden, Gillberg’s three prevalence studies in Gothenburg (Stehr-Green et al., 2003) could have been plotted into Figure 3, but they would have collided impressively with the California data. The data of Denmark is rich in potential for confusion but the careful analysis by Goldman and Yazbak (2004) shows an increase from at least about 1987 onwards. Likewise, the general observation in the other countries is that there has been an increase in recent decades. And the age-of-onset data in Figure 2 follows the same pattern too. (The notion of Bernard (2003) that autism decreased in Denmark after removal of mercury from vaccines is misfounded for various reasons partly explained by Hviid (2004).)So there is here a simple thing to be explained, seemingly beginning around the end of the 1970s.Some years ago there was published “A theory of general impairment of gene-expression manifesting as autism” (the antiinnatia theory). It remains unchallenged in reasoning and evidence, and unrivalled as the only comprehensive fully satisfact-ory explanation of the supposed mystery of autism. Martha Herbert has recently been arguing that autism is not a brain/behavior condition but rather “whole body”, and also not essentially genetic or developmental and fixed. But the antiinnatia theory already embodied all those notions decades ago.The theory also specified circumstances in which autism would change from a mainly genetic condition to a mainly environmental one. Autism has now indeed markedly changed to a mainly environmental causation (Hallmayer et al., 2011).That antiinnatia theory paper made no mention of mercury or an increase of autism (which was only vaguely becoming apparent at the time of writing it). But it did explicitly explain why molecules which randomly, dose-dependently bind to DNA and thereby reduce gene-expression would thereby cause autism. Mercury is now known to do exactly that binding and reducing at levels far below those producing other toxic effects (Ariza et al., 1994; Goyer, 1991; Rodgers et al., 2001; Walter and Luck, 1977).A preceding section here has shown the decisive recent evid-ence of major involvement of mercury in many autistic cases. And thimerosal in vaccines cannot have been a main source of that mercury, for reasons explained in [Chapter 6]. So the question arises of:where else is the source of the mercury that is now so strongly associated with most autism.An update review of the antiinnatia theory was subsequently written, and showed confirmation of various peculiar predictions [Update: including Clarke (2015)], and explained the amalgam-autism causation more fully. But almost all medical researchers have a false presumption about theories, whereby “skepticism” (in reality a prejudice against new ideas) is supposedly a characteristic of intellectual superiority (Eysenck, 1995). And “peer review” systems block from effective publication any ideas that are more than routinely original (Eysenck and Eysenck, 1992).Because readers are deprived of that update review I will outline here just a few of its important points. (1) Many mothers keep their infants close by at all times, and many people keep their homes very unventilated, even installing draught-proofing. The new prediction that autism would be associated with lack of ventilation (of the mercury vapor breathed out by parents or carers then inhaled by infants) has already found significant accidental confirmation (Waldman et al., 2008). (2) The antiinnatia theory points to causation not so much like an overdose “hammer-blow” but rather more like a sustained suppression of genetic data, and thus the every-day inhalation of mercury would be much more impactful than occasional large injections. (3) The tenfold change to predominantly later onset is explained by gradual accumulation when infants regularly inhale the vapor. (4) Any persons who dismiss the antiinnatia theory must logically be supporting one of a handful of utterly absurd alternatives, and this author requests that such “skeptics” kindly state which ones they find so credible: (i) “anti-innatia factors don’t tend to produce biological advantageousness”; (ii) “they don’t exist anyway despite their experimental demon-stration” (genuine flat-earthers will prefer that one); (iii) “they would not tend to become excessive”; (iv) “excess would not manifest as autism”.Some studies have found positive associations between maternal dental amalgams and autism (Holmes et al., 2003; Geier et al., 2009). There have also been some seemingly conflicting findings, such as Adams et al. (2008) compared to Holmes et al. (2003). But rather than concluding from these that the whole mercury or amalgam theories are unsound, or that there has been falsification or error, we may better understand them as reflecting a fact that autism is far from being simply “a novel form of mercury poisoning”, and instead other factors impact in ways not yet known. Even the causation of autism by amalgam vapor alone would be complicated by variables of ventilation, parental habits, galvanic contacts in the mouth, genetics and epigenetics, intake of protective selenium, and other intakes and exposures. That complexity could explain why small cross-sectional studies have given inconsistent results. And meanwhile the time-series data shown in the charts here reflects varying levels of non-gamma-2 applied to whole populations, such that all those confounding variables are evened out, which explains why they show a clear association with the growing prevalence of the non-gamma-2 in adults’ mouths.Increased adult disability?In 2010 I heard on BBC Radio a claim by a government minister that “There certainly hasn’t been a threefold increase of disability”. This suggested to me that perhaps there had indeed been an increase of adult disabilities, threefold or even greater.On investigating this possibility, the most extensive data I could obtain was a chart on page 9 of pathways-presentation.pdf, (DWP, no date a) and online data timeseries (DWP, no date b) from the DWP’s website.I then took the Figure 4 chart from my (long-obstructed) autism theory update review draft, and removed my data-series derived from age-of-onset ratio-change, leaving only the two data-series of autism enrolment in California. I then added in the data of granted invalidity benefits from the DWP’s chart. I used only zero-baselines, so as to not to misuse the statistics to create artificial alignments. All I did was set the righthand scale such that the first datum of the invalidity benefits data was level with the autism data at that same year, 1979.This showed a close relationship of timing between the two, as shown in Figure 5 here.Figure 3.5. Autism enrolments (DDS) in California compared with UK adult invalidity benefits claims granted (excluding short-term lower-rate cases and excluding claims denied for policy reasons of “caseload growth now controlled”)Figure 3.6. Autism enrolments under theIndividuals with Disabilities Education Act (IDEA)At this point it will be useful to show you a second chart of the autism increase, this time a different administrative database (IDEA rather than DDS) and covering the whole US, namely Figure 6. This is a more complex graph, with each data-series representing a different age at recording of the cases.With the increasing of age, fewer children from any particular birth-year cohort remain undiagnosed. So in respect of each year on Figure 6, the highest datum is the most accurate estimate to date of the real underlying level. And the falling off at the top of the latest years is due to diagnoses not yet being made.The first important thing that this chart of IDEA data shows is that the increase has been a remarkably uniform exponential sort of curve, with just a moderate decrease of slope after 1992. The other curves, from the California DDS data, can be understood as showing what would be a similarly uniform exponential, but distorted by noticeable “noise” due to smaller samples or mislaid records.Another important thing to understand about all these curves is that we are not here counting clear distinct things like apples or oranges. The number of people granted invalidity benefits in a particular year is a precisely-known integer, but the underlying number of people who were more or less “disabled” is necessarily a debatable, fuzzy one. Likewise with the autism numbers, and this goes some way to explaining why these two autism databases (DDS and IDEA) show significant discrepancies, most obviously in the starting levels before the increase. So we must understand that none of these curves document validly exact measurements of the underlying pathologies in their vertical scales. And therefore we should not be looking for particularly close alignments in the vertical scales; and if we do find such precision it should be considered largely a fluke. Also there is a lack of numerical data on usage or total prevalence of non-gamma-2 in people’s mouths.But these charts nevertheless do give an accurate document-ation on the horizontal scale, of the timing of the increases and of the form of the increases (i.e. not one big jump over a couple of years). And the four series (DDS, IDEA, onset ratio, and invalidity claims) show closely similar timing, of an increase that was gently starting off just before 1980, and then accelerating rapidly through the 1980s and well into the 1990s.Meanwhile, there is also a weight of other facts attesting to the reality of an increase of invalidity.The symptoms of chronic mercury vapor poisoning have been known for centuries, and include most especially all manner of mental and neurological disturbances, but also a variety of other symptoms. The wide variability of the presentation is easily under-stood in terms of the effects of mercury as a general anti-anti-oxidant, and as an antagonist to zinc thereby disrupting hundreds of enzymes, and also binding to the body’s own proteins thereby causing the immune system to identify them as alien and thereby producing auto-immune reactions.Page 14 of pathways-presentation.pdf gives an analysis of diagnoses of the claimants. It shows that 83% of cases are accounted for by those categories especially readily attributable to amalgam illness:Mental disorder 35%Nervous system 10%Musculo-skeletal* 22%Others** 16%(* Which could be mostly fibromyalgia, a modern “mystery” illness commonly sharing features of typical amalgam illness and often cured by amalgam removal.)(** An all-too-likely official label for cases of the amalgam illness which officially does not exist.)[Book update: In David Brownstein’s book Overcoming thyroid disorders, he quotes Dr Derry saying: “Chronic fatigue and fibro-myalgia were non-existent before 1980. So where did these two new diseases come from?” Errm.... no idea, please tell me, folks.]Further evidence supports the reality of the increase. I web-searched for the minister’s words “been a three-fold increase in disability” and found instead that in Finland 1987-1994 there was a threefold increase of disability pensions granted in respect of affective disorders (mainly depression) (Salminen et al., 1997), which is one of the most common effects of amalgam illness.And the disability claimants are now being regularly character-ised by ministers and propagandists as “workshy”, “bogus”, or merely making a “lifestyle choice” of fraudulent leisure.In 2010, the government minister Mark Harper declared on BBC Any Questions that “There are definitely some people in this country—and everyone in every community knows who they are—who are perfectly able to work, and don’t.” and then reiterated with “Everybody knows them, able-bodied people with no barriers to work who choose not to.”Another government minister, George Osborne, asserted that there were a sizeable number for whom claiming disability was a “lifestyle choice”.Meanwhile we are also being told that immigrants are subst-antially more hardworking than the natives of the UK, who appear by contrast to be “workshy”. And indeed employers confirm such a difference.In the real world of disability, the effects of adult mercury vapor poisoning can be far from obvious to “everyone in every community”. As stated in the book Amalgam Illness by Andrew Hall Cutler, at page 78, “Extremely poisoned patients do not look as sick as they are …. they make adequate adrenaline during the stressful time and perform. Then they collapse for a long time while nobody is around.” And at page 13, “One very important note: the patient looks a lot healthier than he is…..It is important to keep in mind that the patient may look well during appointments and yet be unable to conduct day-to-day activities, as well as be experiencing great discomfort on an ongoing basis.”And note also the following 1926 account by the famous chemist Alfred Stock of his own mercury vapor poisoning. Note how easily it could be “known” to be “workshy” were it not that the author was a notable professor.“Mental weariness and exhaustion, lack of inclination and ability to perform any, particularly mental, work, and increased need for sleep. …. My memory, which had previously been excellent, left more and more to be desired and became worse and worse until, two years ago, I suffered from nearly complete memory loss….. I forgot the content of the book or theater play I had just read or seen as well as my own work, which had been published. ….. Obstacles, which formerly I would have overlooked smilingly (and am overlooking again today), seemed insurmountable. Scientific work caused great effort. I forced myself to go to the laboratory without being able to get anything useful accomplished in spite of all efforts. Thought came laboriously and pedantically. I had to deny myself working on solutions to questions beyond the nearest tasks at hand. The lecture that used to be a pleasure became a torture. The preparations for a lecture, the writing of a dissertation, or merely a simple letter caused unending effort in styling the material and wrestling with the language.” (translated by Birgit Calhoun)(Stock, 1926)You can see from all the above that the characteristics ascribed to the allegedly bogus claimants are characteristics of mercury poisoning. With this understanding we can even account for the peculiar observations that workers from Eastern Europe and from more distant countries are found to be more “hardworking” than the native British, who by contrast are accused of being “workshy”. In fact a whole peculiar myth about normal human nature has been deployed here. Any normal healthy person, yourself for instance, would positively want to go out and do things rather than just lie in bed or slump in front of the tv all day every day. The normal healthy person would experience the latter prospect as more like a form of imprisonment than as an agreeable “lifestyle choice”.[[ Update for this book: Here are the words of Frank Field MP speaking on BBC Any Questions (Field, 2012):“London’s got the second highest youth unemployment, and yet it is the mecca for immigrants to come in and work. Now why is it that our schools produce people who cannot work or don’t work, as opposed to other people who at the very same time have work as part of their dna and the best thing in the world they want to do is to actually work? (loud applause).” [He then answers in terms of lazy racist white people, presumably with inferior dna, before continuing....]“It doesn’t take much money to get the kids to school on time, washed, clothed, breakfasted, and to school on time, and it is worrying that something is happening here...” [Indeed, and my own inability to get to the grammar school on time had nothing to do with my family’s shortage of money either.]And here are words about chronic fatigue syndrome from the book Plague (Heckenlively & Mikovits, 2014):“If this had been going on in the fifties and sixties, even if we had discarded it as psychiatric, it would have been written about, and [yet] it’s not in the literature.” ..... “How could we have possibly missed this disease for all these years?”. ....“....by the mid-1980s, distressed doctors and desperate patients had turned the disease into the top category of inquiry at both the CDC and public health departments ....”“Aided by a passive lay press, government scientists have sought to dismiss the disease by labeling sufferers with all manner of deficiencies and malevolent motives. That list has included malingering and cheating welfare systems, .... or people who [had] read about the disease and “wanted to have it”.“By 2009.... patients were denied not merely medical care, payouts on disability claims, and the emotional support that might have been forthcoming from family and friends had they suffered from a “real” disease,..... If they were children, they were denied educations ....” [like don’t I know myself, and see Chapter 8 here] ]]And furthermore, in reality almost all people are desperate to avoid becoming categorised as disabled, going to near-psychotic lengths of denial in the opposite direction. Few people would be pleased to be in any social context, with no better answer to a common question than: “I’ve been chronically disabled for the past five years (mentally rather than physically of course).” Virtually no-one in any society treats mentally disabled people as even near to being social or intellectual equals of themselves (in terms of marriage or educational opportunities for instance) (notwithstanding their pretentions to otherwise).An even greater catastrophe?Notably in line with the UK data, recipients of disability benefits in the US (SSI/SSDI) also increased more than twofold between 1987 and 2007.Here are some further facts. Figure 5 indicates a levelling off at 2.5 million claimants from 1995 onwards. But this must be put in the context of the words of the DWP document those figures came from. It was an internal discussion document about the “Personal Capability Assessment”, and its page 11 was headed “Caseload growth now controlled”. Translating those words from Officialese, they mean that there has been political resistance to the growth of disability claims, and that many thousands of persons genuinely disabled by DH recklessness have been denied the disability benefits they needed for survival, and that if the graph had reflected the real increase of disability it would not have levelled off, but instead would probably have surpassed more like 4 million by 2000 (which is about 10% of the UK’s working-age population). [Update August 2015: “Statistics [reluctantly] released by the DWP on Thursday revealed that 2,380 people died between December 2011 and February 2014 within 14 days of being taken off Employment and Support Allowance because a Work Capability Assessment had con-cluded they were able to work.” (Butler, 2015).][Update November 2015: 590 additional suicides linked to WCA reassessments (Barr et al., 2015; Benefits and Work, 2015).]And yet more. Four of the most characteristic symptoms of chronic mercury vapor poisoning are fatigue, depression, sleep disturbances, and poor memory. And surveys in recent years have found that now a gigantic proportion of the NON-claimant pop-ulation have these very symptoms, as follows.Depression:A survey of 2000 women and girls in England and Wales found 63% had been affected by mental health problems, having “a devastating impact on their lives”, and “48% experiencing mental health problems had stayed in bed or not left the house for a long period as a result” (Platform 51, 2011). Meanwhile, Colin Walker of Mind said his organisation’s research showed men and women experienced mental health problems such as depression and anxiety in roughly equal numbers (Hill, 2011).Insomnia:A report from the Mental Health Foundation (2011) states: “Only 38% of survey respondents (2522 people) were classified as ‘good sleepers’, whilst 36% were classified as possibly having chronic insomnia (2414 people). …. Other estimates of insomnia have put the total figure at around 30% of adults, …. although rates depend upon the criteria used to define it. Of the people reporting insomnia in the survey, over 30% have had insomnia for 2–5 years, and over 25% for over 11 years (figure 4).”The figure 4 in question then shows a distinctly bimodal distribution, in which the larger, longer-term, mode can be reasonably attributed to the effects of the dental amalgam toxicity.Fatigue:In a survey by Pharmaton (2010) in the UK, 24% said they are mentally or physically exhausted every day, 45% say they miss socialising due to tiredness, and 60% of the young are too tired to socialise, compared to 40% in 2002. And that is in line with the widespread experience that immigrants from less-developed countr-ies are substantially more “hardworking” than those who have grown up in the UK, who are conversely “workshy” as discussed on a preceding page here.Memory:Almost everyone nowadays wishes they had “better” memory, by which they mean more remembering rather than less. And yet contrary to the common assumption, memory is not something which natural selection would always be pressuring for more of (such as health or beauty). On the contrary, some persons (e.g. Solomon Shereschevsky) have had more memory than was actually useful for them. And history attests to the powerful memorising abilities of our ancestors.(This chapter continues on the next page.)Update 1All the preceding evidence here was suggesting to me an obvious further question, namely whether the original introduction of amalgams in the 19th century had caused an earlier increase of mental disabilities to the baselines shown here. Subsequent to my writing all the preceding, I learnt of the detailed historical review by Torrey & Miller (2002) of what was then called “insanity”, and the time-series graphs therein (at pages 94, 152, 188, 271, and frontispiece). In Figure 7 here I have re-plotted their data along with dates relating to the introduction of amalgam. Their book makes no mention of amalgam, or dentistry, nor of mercury as a possible cause of that increased morbidity. And yet their graphs show that rates of mental disability steadily increased from the original introduction of amalgams till a century later, by fourteenfold in Ireland and Canada, elevenfold in the US, and fivefold in the UK. These increases occurred in the context of vociferous contemporary condemnations of the use of amalgam due to its causing of mercury toxicity disabilities. The ASDS disbanded and the ADA replaced it because too many dentists preferred making quick profits from poisoning their patients with fillings deceitfully referred to as “silver”.Two curious observations on Figure 7. Firstly, the starting level being much higher in England/Wales, which could be because England was the first industrialised country, and with the main fuel both in houses and factories being mercury-emitting coal, besides which mercury was used for other purposes (such as hat-making). And indeed there is much reference in Torrey & Miller to insanity having been considered “the English disease”.Secondly, the ending level being much higher in Ireland, which could be because Ireland gets high rainfall from the Gulf Stream and consequently people are much more indoors and hence breathing in the amalgam mercury (as per my citation of Waldman et al earlier here). These two reality-harmonious observations suggest that these statistics reflect real increases rather than what some might construe as just some speculated mysterious spontaneous increase of awareness of what was then called insanity.And the Preface of their book states: “It has now been almost thirty years since one of us—E. Fuller Torrey—submitted a paper for publication suggesting that epidemic insanity was a recent phenomenon. .... The paper was summarily rejected by all journals .... and it was never published.... “.And then even my own copy of their extraordinary book had come from being dismissed from a library in Illinois.[Update 2 (added to this book chapter, August 2015)[See Experts Catatrophe book at Amazon.]Conclusions and PredictionsIt is important to bear in mind here the further supporting data reviewed by Mutter (2011), Hanson (2004), Geier et al (2010), Homme et al (2014), and others.There are roughly two alternative viewpoints which may be reached from the data presented here. On the one hand there is a notion which entails that:(1) The heavy involvement of mercury in modern autism has nothing to do with the largest source of mercury input but instead is due to some other mysterious source or process.(2) And these graphs and other observations are mere coincid-ences in time.(3a) And either some mysterious unknown substance caused all these disabilities just so as to resemble the mercury symptoms that Mutter, Hanson, Geier, etc., have long been predicting anyway on entirely different evidence, and just happened to coincide at the right time to neatly confuse the author.(3b) Or there has been either a huge moral degeneration into “workshy” or else millions of people have enthusiastically embraced a “lifestyle choice” of living like a prisoner combined with the social leper dis-status of being mentally disabled, and furthermore these shirkers by some fluke just happened to be getting diagnosed with mercury symptoms even though they knew nothing about mercury toxicity, and by further impressive fluke so closely coincided with the increases of autism diagnoses and non-gamma-2 prevalence. And these “workshy” millions are somehow descendants of the people who hand-built the huge medieval cathedrals in a cold wet small island ­and then went on to create the largest empire (of hardworking foreigners) in history.(4) And a many-fold increase of mercury burden has not had any harmful effects on the millions thus burdened.(5) And the change of autism from life-long genetic to environmental and recoverable is just another of these mysteries.(6) And those gross untruths from the NHS just happened by fluke to all relate to preventing people getting diagnosed with mercury poisoning (two evidence-defying pseudo-tests, the “birds are highly unlikely to have wings” nonsense, the “see a dentist instead” - “see a doctor instead” nonsense, the review of my non-dental problems complaint exclusively by a dental panel with no toxicological or neurological expertise, the NHS’s own pseudo-study to pretend away the autism increase, and the Chief Dental Officer’s evidence-defying insistence that no mercury vapor comes off anyway).(7) And merely by yet another fluke Torrey’s graphs confirmed my suspicion that there would have been a previous increase of mental disabilities following the original introduction of amalgam 150 years earlier.(8) And merely by yet another fluke there is that observation that most mental disorders start in the 12-25 age-range.Alternatively there is a notion that non-gamma-2 amalgam has been the main cause of a tenfoldish increase of autism and a fourfoldish increase of adult disability including so-called “workshy”. It is the view of this author that this latter interpretation of the data strains credibility very much less than the former. It is hardly a surprising discovery given what Mutter, Hanson, and others have previously predicted on entirely different evidence already.And likewise the data of an increase in the 19th century cannot be lightly dismissed as “merely” coincidence. Some such increase was to be suspected by inference from the later non-gamma-2 data; it is scientifically explainable in terms of known mercury toxicity; and indeed it was very much pre-warned of already by ASDS members 170 years ago. And the ADA then adopted the propaganda language of “silver amalgams” by way of the ongoing cover-up. And I obtained that data from a very detailed review book which did not even mention dental or amalgam, so can hardly be dismissed as some sort of cherry-picking.Editors of putatively scientific medical journals have a duty to ensure that the public is not being kept unaware of evidence of possible serious harm from standard medical practices. It is a serious breach of ethics for such evidence as contained here to be refused publication other than for rigorously justified reasons. If there really are any serious faults in the case presented here, they should be openly published in the scientific literature rather than used as mere excuses to prevent the evidence being raised in the first place.It is here predicted that these increases will tend to correlate together in comparisons between different nations, due to the common causality. It is predicted that these epidemics will only be reversed by reduction of prevalence of non-gamma-2 in victims’ mouths. And meanwhile the risk of autistic disability can be reduced by ensuring adequate ventilation (in practice with a through draught at breathing-level).[[Update 3 (added to this book chapter, August 2015)[See Experts Catastrophe book]Appendix: Four Freedom of Information requests(more fully documented via Additional File 1.htm) or http://tinyurl.com/dentmercWhy “Chronic mercury poisoning is highly unlik­­ely to present in a psychiatric setting.”?Mr Clarke made this Freedom of Information request to Birmingham and Solihull Mental Health NHS Foundation TrustRESPONSE TO THIS REQUEST IS LONG OVERDUE6 September 2011Dear Birmingham and Solihull Mental Health NHS Foundation Trust,1. Given that it has been well-known for years, decades, and even centuries, that among the most characteristic symptoms of chronic mercury poisoning are nervousness, shyness, depression, agitation, fatigue, impaired memory, lack of concentration, and indecision (as per abundant documentation indicated below):Why did the BSMHFT (Birmingham and Solihull Mental Health Foundation Trust) state this year in a FOI reply that “Chronic mercury poisoning is highly unlikely to present in a psychiatric setting.”?2. What scientific or evidential basis existed to justify such a statement?3. Who in the BSMHFT gave that answer, and from where did they derive that conclusion? Where did the notion originate?Yours faithfully,Mr ClarkeDOCUMENTATION:[See Experts Catastrophe book, links in my profile here.]