Short Term Disability: Fill & Download for Free

I would not be able to comment on schemes per se due to regulation restrictions unless i have a client sign-up with complete financial details, risk profile, etc.Among the schemes you are trying to choose, it’s like asking ‘i am not feeling well…which medicine should i take?’ - Aspirin, Paracetamol, Ibuprofen or any antacid …. It ranges from Large cap to Multicap (but skewed towards large-cap growth stocks) and one is small cap-blend stocks and the other is small cap- Growth stocks.You may think you are an Aggressive investor, but makes more sense when you undergo a Risk profile questionnaire that will give clarity. Depending on your investment horizon and risk profile - ability to digest volatilities, you may choose the fund accordingly. A help from a professional would be better way to go forward.But before investments you need to make sure that you have made provisions for other important requirements like Emergency fund, Health insurance, Accident and Disability insurance, Life insurance (if you have any financial dependents or any liability), any other financial obligations in short, medium or long term horizon.

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.

Common Mental Health Disorders: Identification and Pathways to Care.2COMMON MENTAL HEALTH DISORDERS2.1. INTRODUCTIONThis guideline is concerned with the care and treatment of people with a common mental health disorder, including depression, generalised anxiety disorder (GAD), panic disorder, phobias, social anxiety disorder, obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD). It makes recommendations about the delivery of effective identification, assessment and referral for treatment in primary care. The guideline will also be applicable to secondary care, and relevant (but does not make specific recommendations) for the prison service and non-NHS services such as social services, and the voluntary and independent sectors. A particular purpose of this guideline is to integrate existing NICE guidance on the identification and assessment of common mental health disorders and to provide recommendations to support the development of local care pathways for these disorders.The purpose of this introductory chapter is to provide an overview of the epidemiology and treatment of the common mental health disorders, and to highlight important issues related to identification and assessment of the disorders and the relevant local care pathways within the NHS.This guideline does not cover interventions to treat the disorders and should be used in conjunction with other relevant NICE guidelines, which give evidence of the effectiveness of interventions for the specific disorders, including drug treatments and psychological therapies:Self-harm: the Short-term Physical and Psychological Management and Secondary Prevention of Self-harm in Primary and Secondary Care (NICE, 2004c; NCCMH, 2004b).Obsessive-compulsive Disorder (NICE, 2005a; NCCMH, 2006).Post-traumatic Stress Disorder (PTSD) (NICE, 2005b; NCCMH, 2005).Antenatal and Postnatal Mental Health (NICE, 2007a; NCCMH, 2007).Depression (NICE, 2009a; NCCMH, 2010b).Depression in Adults with a Chronic Physical Health Problem (NICE, 2009b; NCCMH, 2010a).Generalised Anxiety Disorder and Panic Disorder (with or without Agoraphobia) in Adults(NICE, 2011a; NCCMH, 2011a).Self-harm: Longer-Term Management (NICE, 2011c; NCCMH, forthcoming). A NICE guideline on social anxiety disorder is expected in 2013.Go to:2.2. THE DISORDERSThis guideline covers the following common mental health disorders in adults (18 years and older):depression (including subthreshold disorders)anxiety disorders (including GAD, panic disorder, phobias, social anxiety disorder, OCD and PTSD).The guideline will also cover, where relevant, issues relating to comorbidity; however, as no separate NICE guideline addresses comorbid presentations of common mental health disorders, this will not be a key topic of the guideline. Groups not covered include adults with subthreshold mixed anxiety and depression, adults with psychotic and related disorders (including schizophrenia and bipolar disorder), people for whom drug and alcohol misuse are the primary problem, people with eating disorders, and children and people younger than 18 years old.2.2.1. Symptoms and presentationDepressionDepression refers to a wide range of mental health problems characterised by the absence of a positive affect (a loss of interest and enjoyment in ordinary things and experiences), low mood and a range of associated emotional, cognitive, physical and behavioural symptoms. Distinguishing the mood changes between clinically significant degrees of depression (for example, major depression) and those occurring ‘normally’ remains problematic and it is best to consider the symptoms of depression as occurring on a continuum of severity (Lewinsohn et al., 2000).Commonly, mood and affect in a major depressive illness are unreactive to circumstance remaining low throughout the course of each day, although for some people mood varies diurnally, with gradual improvement throughout the day only to return to a low mood on waking. In other cases a person's mood may be reactive to positive experiences and events, although these elevations in mood are not sustained with depressive feelings often quickly re-emerging (Andrews & Jenkins, 1999).Behavioural and physical symptoms typically include tearfulness, irritability, social withdrawal, an exacerbation of pre-existing pains, and pains secondary to increased muscle tension (Gerber et al., 1992). A lack of libido, fatigue and diminished activity are also common, although agitation and marked anxiety can frequently occur. Typically there is reduced sleep and lowered appetite (sometimes leading to significant weight loss), but some people sleep more than usual and have an increase in appetite. A loss of interest and enjoyment in everyday life, and feelings of guilt, worthlessness and deserved punishment are common, as are lowered self-esteem, loss of confidence, feelings of helplessness, suicidal ideation and attempts at self-harm or suicide. Cognitive changes include poor concentration and reduced attention, pessimistic and recurrently negative thoughts about oneself, one's past and the future, mental slowing and rumination (Cassano & Fava, 2002).Generalised anxiety disorderThe essential feature of GAD is excessive anxiety and worry (apprehensive expectation), occurring on more days than not for a period of at least 6 months, about a number of events or activities. The person with GAD finds it difficult to control the anxiety and worry, which is often accompanied by restlessness, being easily fatigued, having difficulty concentrating, irritability, muscle tension and disturbed sleep (Brownet al., 2001).The focus of the anxiety and worry in GAD is not confined to features of another disorder, for example having panic attacks (as in panic disorder) or being embarrassed in public (as in social anxiety disorder). Some people with GAD may become excessively apprehensive about the outcome of routine activities, in particular those associated with the health of or separation from loved ones. Some people often anticipate a catastrophic outcome from a mild physical symptom or a side effect of medication. Demoralisation is said to be a common consequence, with many individuals becoming discouraged, ashamed and unhappy about the difficulties of carrying out their normal routines. GAD is often comorbid with depression and this can make accurate diagnosis problematic (Wittchen et al., 2002).Panic disorderPeople with panic disorder report intermittent apprehension, and panic attacks (attacks of sudden short-lived anxiety) in relation to particular situations or spontaneous panic attacks, with no apparent cause. They often take action to avoid being in particular situations in order to prevent those feelings, which may develop into agoraphobia (Breier et al., 1986).The frequency and severity of panic attacks varies widely. Situational triggers for panic attacks can be external (for example, a phobic object or situation) or internal (physiological arousal). A panic attack may be unexpected (spontaneous or uncued), that is, one that an individual does not immediately associate with a situational trigger.The essential feature of agoraphobia is anxiety about being in places or situations from which escape might be difficult, embarrassing or in which help may not be available in the event of having a panic attack. This anxiety is said to typically lead to a pervasive avoidance of a variety of situations that may include: being alone outside the home or being home alone; being in a crowd of people; travelling by car or bus; being in a particular place, such as on a bridge or in a lift.Obsessive-compulsive disorderOCD is characterised by the presence of either obsessions or compulsions, but commonly both. An obsession is defined as an unwanted intrusive thought, image or urge that repeatedly enters the person's mind. Obsessions are distressing, but are acknowledged as originating in the person's mind and not imposed by an external agency. They are usually regarded by the individual as unreasonable or excessive. Common obsessions in OCD include contamination from dirt, germs, viruses, body fluids and so on, fear of harm (for example, that door locks are not safe), excessive concern with order or symmetry, obsessions with the body or physical symptoms, religious, sacrilegious or blasphemous thoughts, sexual thoughts (for example, of being a paedophile or a homosexual), an urge to hoard useless or worn out possessions, or thoughts of violence or aggression (for example, stabbing one's baby) (Lochner & Stein, 2003).Compulsions are repetitive behaviours or mental acts that the person feels driven to perform. A compulsion can either be overt and observable by others, or a covert mental act that cannot be observed. Covert compulsions are generally more difficult to resist or monitor than overt ones because they can be performed anywhere without others knowing and are easier to perform. Common compulsions include checking (for example, gas taps), cleaning, washing, repeating acts, mental compulsions (for example, repeating special words or prayers in a set manner), ordering, symmetry or exactness, hoarding/collecting and counting (Foa et al., 1995). The most frequent presentations are checking and cleaning, and these are the most easily recognised because they are on a continuum with everyday behaviour. A compulsion is not in itself pleasurable, which differentiates it from impulsive acts such as shopping or gambling, which are associated with immediate gratification.Post-traumatic stress disorderPTSD often develops in response to one or more traumatic events such as deliberate acts of interpersonal violence, severe accidents, disasters or military action. Those at risk of PTSD include survivors of war and torture, of accidents and disasters, and of violent crime (for example, physical and sexual assaults, sexual abuse, bombings and riots), refugees, women who have experienced traumatic childbirth, people diagnosed with a life-threatening illness, and members of the armed forces, police and other emergency personnel (Foa et al., 2008).The most characteristic symptoms of PTSD are re-experiencing symptoms. People with PTSD involuntarily re-experience aspects of the traumatic event in a vivid and distressing way. Symptoms include flashbacks in which the person acts or feels as if the event is recurring; nightmares; and repetitive and distressing intrusive images or other sensory impressions from the event. Reminders of the traumatic event arouse intense distress and/or physiological reactions. As a result, hypervigilance for threat, exaggerated startle responses, irritability, difficulty in concentrating, sleep problems and avoidance of trauma reminders are other core symptoms. However, people with PTSD also describe symptoms of emotional numbing. These include inability to have any feelings, feeling detached from other people, giving up previously significant activities and amnesia for significant parts of the event.Two further common mental health disorders, social anxiety disorder and specific phobias, are briefly described below. However, because no NICE guidelines currently exist for these disorders they will not be discussed in detail in the remainder of this chapter.Social anxiety disorderSocial anxiety disorder, also referred to as social phobia, is characterised by an intense fear in social situations that results in considerable distress and in turn impacts on a person's ability to function effectively in aspects of their daily life. Central to the disorder is a fear of being judged by others and of being embarrassed or humiliated. This leads to the avoidance of a number of social situations and often impacts significantly on educational and vocational performance. The fears can be triggered by the actual or imagined scrutiny from others. The disorder often begins in early adolescence, and although an individual may recognise the problem as outside of normal experience, many do not seek help (Liebowitz et al., 1985).Social anxiety disorder is characterised by a range of physical symptoms including excessive blushing, sweating, trembling, palpitations and nausea. Panic attacks are common, as is the development of depressive symptoms as the problem becomes chronic. Alcohol or drug misuse can develop because people use these substances in an attempt to cope with the disturbing and disabling symptoms. It is also often comorbid with other disorders such as depression (Kessler et al., 1999).Specific phobiasA specific phobia is an unwarranted, extreme and persistent fear of a specific object or situation that is out of proportion to the actual danger or threat (Humphris et al., 1995). The fear and anxiety occur immediately upon encountering the feared object or situation and tend to lead to avoidance or extreme discomfort. The person with a specific phobia recognises that the fear is excessive, unwarranted or out of proportion to the actual risk. Specific phobias result in significant interference with the activities of daily life; they are usually grouped under a number of subtypes including animal, natural environment, blood-injection-injury and situational.2.2.2. Incidence and prevalenceEstimates of the prevalence of common mental health disorders vary considerably depending on where and when surveys are carried out, and the period over which prevalence is measured.The 2007 Office for National Statistics (ONS) household survey of adult psychiatric morbidity in England found that 16.2% of adults aged 16 to 64 years met the diagnostic criteria for at least one disorder in the week prior to interview (McManus et al., 2009). In the three ONS surveys carried out so far, the proportion of adults meeting the criteria for at least one disorder increased between 1993 and 2000 but did not change between 2000 and 2007 (15.5% in 1993, 17.5% in 2000 and 17.6% in 2007). The largest increase in the rate of disorders found between 1993 and 2007 was in women aged 45 to 64 years, among whom the rate went up by about one fifth (McManus et al., 2009).More than half of the adults identified with a common mental health disorder in the ONS survey presented with a mixed anxiety and depressive disorder (9% in the past week). The 1-week prevalence for the other common mental health disorders were 4.4% for GAD, 2.3% for a depressive episode, 1.4% for phobia, 1.1% for OCD and 1.1% for panic disorder (McManus et al., 2009).In the US, Kessler and colleagues conducted the National Comorbidity Survey, a representative household interview survey of 9,282 adults aged 18 years and over, to estimate the lifetime (Kessler et al., 2005a) and 12-month (Kessler et al., 2005b) prevalence rates of mental disorders classified using theDiagnostic and Statistical Manual of Mental Disorders (4th text-revision version; DSM-IV-TR) of the American Psychiatric Association (APA, 2000). A summary of their findings can be seen in Table 1. Of the 12-month cases in the US National Comorbidity Survey, 22.3% were classified as serious, 37.3% as moderate and 40.4% as mild. Fifty-five per cent carried only a single diagnosis, 22% two diagnoses and 23% three or more diagnoses. Latent class analysis identified three highly comorbid classes representing 7% of the population, and the authors concluded that, although mental disorders are widespread, serious cases are concentrated among a relatively small proportion of people with high comorbidity (Kessler et al., 2005b).Table 1Summary of prevalence rates for common mental health disorders.In summary, at any given time common mental health disorders can be found in around one in six people in the community, and around half of these have significant symptoms that would warrant intervention from healthcare professionals. Most have non-specific mixed anxiety and depressive symptoms, but a proportion have more specific depressive disorder or anxiety disorders including panic disorder, phobias, OCD or PTSD.The location, time and duration of the survey are not the only factors to influence prevalence rates. A number of demographic and socioeconomic factors are associated with a higher risk of disorders, including gender, age, marital status, ethnicity and socioeconomic deprivation. These will be discussed below.GenderDepression and anxiety disorders tend to have a higher prevalence in women. Prevalence rates of depression have consistently been found to be between 1.5 and 2.5 times higher in women than men (Waraich et al., 2004). In the ONS survey (McManus et al., 2009) women were more likely than men to have a disorder (19.7 and 12.5%, respectively), with rates significantly higher for women across all categories of disorder except for panic disorder and OCD. The greatest difference between genders was among South Asian adults where the age-standardised rate among women (34.3% of South Asian women) was three times that of men (10.3% of South Asian men). Reasons cited in the 2007 ONS survey (McManus et al., 2009) include the impact of having children (Bebbington et al., 1991), exposure to domestic or sexual violence (Patel et al., 2006), adverse experiences in childhood and women's relative poverty (Patel et al., 1999; Piccinelli & Wilkinson, 2000).AgeIn the 2007 ONS survey (McManus et al., 2009) rates varied by age, with those aged 75 years and over least likely to have a disorder (6.3% of men and 12.2% of women). In women, the rate peaked among 45- to 54-year-olds of whom 25% met the criteria for at least one disorder. Among men, the rate was highest in 25- to 54-year-olds (14.6% of 25- to 34-year-olds, 15.0% of 35- to 44-year-olds and 14.5% of 45- to 54-year-olds).Marital statusWomen across all marital-status categories were more likely than their male counterparts to have disorders in the 2007 ONS survey (McManus et al., 2009), except for divorced people in whom the prevalence for men and women was very similar (26.6% for women and 27.7% for men). Among men, those currently divorced had the greatest likelihood of having a disorder, but variation by other marital status categories was less pronounced. For women the rate of disorder was high for divorced women, but even higher for separated women (33.0%). Men and women who were married or widowed had the lowest observed rates of disorder (10.1% of married men and 16.3% of married women; 10.4% widowed men and 17.4% widowed women).EthnicityIn the 2007 ONS survey (McManus et al., 2009), after age-standardisation of the data, there was little variation between white, black and South Asian men in the rates of any disorder. However, among women rates of all disorders (except phobias) were higher in the South Asian group. The number of South Asian women in the sample was small, so while the differences were pronounced they were only significant for disorders as a whole for GAD and panic disorder.Socioeconomic factorsIn the 2007 ONS survey (McManus et al., 2009), people living in households with the lowest levels of income were more likely to have a disorder than those living in the highest income households. A number of socioeconomic factors significantly affected prevalence rates in the 2000 ONS survey (Singleton et al., 2001): those with a depressive episode were more likely than those without a disorder to be unemployed, to belong to social classes 4 and below, to have no formal educational qualifications, to live in Local Authority or Housing Association accommodation, to have moved three or more times in the last 2 years and to live in an urban environment.An illustration of the social origins of depression can be found in a general practice survey in which 7.2% (ranging 2.4 to 13.7%, depending upon the practice) of consecutive attendees had a depressive disorder. Neighbourhood social deprivation accounted for 48.3% of the variance among practices. Other variables were the proportion of the population having no or only one car and neighbourhood unemployment (Ostleret al., 2001). The evidence therefore overwhelmingly supports the view that the prevalence of common mental health disorders, however it is defined, varies according to gender and social and economic factors.Learning disabilitiesThe rates of common mental health disorders in adults with learning disabilities are generally considered to be higher, but limited data and methodological problems (Smiley, 2005) mean that precise estimates are often not available and so uncertainty remains. In contrast, there is clearer evidence that other mental disorders such as problem behaviour have a higher rate of learning disabilities (Cooper et al., 2007). Rates of mental disorders may vary with the severity of the learning disability, being higher in more severe disability (Whitaker & Read, 2006), and challenges in assessment and diagnosis are considerable especially for those with more severe learning disabilities (Smiley, 2005; Whitaker & Read, 2006). However, some indication of the possible differential incidence of common mental health disorders can be obtained from the following studies. Richards and colleagues (2001) report a four-fold increase in the rates of affective disorders for people with mild learning disability. Rates of problems may also vary with the disorder; for example, Collacott (1999) reports a higher rate of depression in adults with Down's syndrome than in adults with other causes of learning disability. With regard to anxiety disorders, Cooper (1997) reports a rate of 2.5% for OCD in adults with a learning disability, which is higher than in the general adult population.2.2.3. AetiologyThe aetiology of common mental health disorders is multi-factorial and involves psychological, social and biological factors. Many of the common mental health disorders have similar aetiologies. For example,King and colleagues (2008) identified five immutable risk factors for depression. These were younger age, female gender, lower educational achievement, previous history of depression and family history of depression. Brewin and colleagues (2000) and Ozer and colleagues (2003) identified similar risk factors for PTSD, including a previous personal or family history of anxiety disorders or affective disorders, neuroticism, lower intelligence, female gender and a history of previous trauma. The ONS survey (McManus et al., 2009) identified factors that may be associated with increased duration of an episode of depression or anxiety. These can be broadly defined as biological factors, social stresses and life events. These risk factors will now be discussed in general. For information regarding factors for specific disorders, please refer to the relevant NICE guideline (see Section 2.1).There is good evidence for biological factors in the development of many psychological disorders. Biological factors can be biochemical, endocrine and neurophysiological (Goodwin, 2000; Malhi et al., 2005) or genetic (Kendler & Prescott, 1999), and can interact with early trauma ultimately leading to psychological distress (Heim & Nemeroff, 2001).Support for this claim often comes from family-history studies (Angst et al., 2003). A family history of depressive illness has been linked with an increased chance of developing depression (Kendler et al., 2001). Similarly, the risk of GAD in first-degree relatives of patients with GAD was five times that of controls (Noyes et al., 1987). Although specific genes conferring vulnerability to GAD have not yet been reliably identified, the genes involved in the transmission of GAD appear to increase susceptibility to other anxiety disorders such as panic disorder and agoraphobia as well as major depression (Hettema et al., 2001 and 2005; Kendler, 1996). There is some evidence to suggest that personality traits such as neuroticism may have a role in the development of common mental health disorders. Personality traits such as neuroticism have been identified as risk factors for both depression (Fava & Kendler, 2000) and GAD (Hettema et al., 2004). However, the specific role of neurotransmitters and other chemical mediators in the aetiology of common mental health disorders is currently unclear.According to a stress-vulnerability model (Nuechterlein & Dawson, 1984), it is not only biological factors that can trigger the development of a common mental health disorder. Social triggers may also play an important role (Harris, 2000). The ONS survey (McManus et al., 2009) identified perceived financial strain (Weich & Lewis, 1998a), work stress (Stansfeld et al., 1999), poor housing (Weich & Lewis, 1998b) and social isolation (Bruce & Hoff, 1994) as key factors that can influence the development of common mental health disorders. In the UK, an influential study found that social vulnerability factors for depression in women in Camberwell, south-east London, included: having three or more children under the age of 14 years living at home; having no paid employment outside the home; and not having a confiding relationship with another person (Brown & Harris, 1978). The importance of a confiding relationship has been further reiterated by Patten (1991) who found that a lack of such a relationship was a strong risk factor for depression.Negative life events, particularly those relating to health, can also impact on the development of depression and anxiety, although vulnerabilities will vary between individuals (Harris, 2000). The ONS survey identified poor physical health and problems with alcohol use as predictors of anxiety and depression (Salokangas & Poutanen, 1998), while King and colleagues (2008) found that current poorer physical and mental health functional status, based on the 12-Item Short Form Health Survey (SF-12) questionnaire, was linked to the development of depression. However, it is also important to note that depression may lead to secondary disability that compounds, and is difficult to distinguish from, the depression itself.Early life experiences as well as current social stressors must also be considered. A poor parent–child relationship, marital discord and divorce, neglect, and physical and sexual abuse almost certainly increase a person's vulnerability to depression in later life (Fava & Kendler, 2000) and can play a vital role in the development of GAD. Barlow (2000) reported that good parenting experiences are important in providing children with a secure base from which to explore the world. Problems in child–parent attachment have been linked to feelings of diminished personal control of potentially threatening events (Barlow, 2000), which can in turn increase susceptibility to psychological illness.However, when considering the importance of life events it is important to remember that events may not have a causal impact on the development of symptoms. Instead, they may act as a trigger among people who are biologically or psychologically predisposed to a disorder, for example OCD (Gothelf et al., 2004; Khanna et al., 1988). The authors of the ONS survey make the point that although these risk factors are associated with disorders and tend to increase the duration of episodes it is not clear whether or not they cause the onset of an episode.2.2.4. Development, course and prognosisFor many people the onset of common mental health disorders occurs in adolescence or early adult life, but the disorders can affect people at any point. Earlier onset is generally associated with poorer outcomes. Kessler and colleagues (2005a) reported an estimated median age of onset for anxiety disorders of 11 years and for mood disorders of 30 years in their US National Comorbidity sample. Half of all lifetime cases had started by 14 years and three quarters by 24 years. Many anxiety disorders also have a chronic course. This chronic course may be associated with a considerable delay in presenting to services, with consequent significant personal and social impairment. Therefore, Kessler and colleagues (2005a) concluded that interventions aimed at prevention or early treatment needed to focus on young people.DepressionThe average age of the first episode of major depression is the mid-20s and although the first episode may occur at any time, from early childhood through to old age, a substantial proportion of people have their first depressive episode in childhood or adolescence (Fava & Kendler, 2000).Although depression has been understood to be a time-limited disorder lasting on average 4 to 6 months with complete recovery afterwards, it is now clear that incomplete recovery and relapse are common. The World Health Organization (WHO) study of mental disorders in 14 centres across the world found that 50% still had a diagnosis of depression 1 year later (Simon et al., 2002) and at least 10% of patients have persistent or chronic depression (Kessler et al., 2003). At least 50% of people following their first episode of major depression will go on to have at least one more episode (Kupfer, 1991), and after the second and third episodes the risk of further relapse rises to 70 and 90%, respectively (Kupfer, 1991). Early-onset depression (at or before 20 years of age) and depression occurring in old age have a significantly increased vulnerability to relapse (Giles et al., 1989; Mitchell & Subramaniam, 2005). Thus while the outlook for a first episode is good, the outlook for recurrent episodes over the long term can be poor with many patients experiencing symptoms of depression over many years (Akiskal, 1986).Generalised anxiety disorderMost clinical studies suggest that GAD is typically a chronic condition with low rates of remission over the short and medium term. Evaluation of prognosis is complicated by the frequent comorbidity with other anxiety disorders and depression, which worsen the long-term outcome and accompanying burden of disability (Tyrer & Baldwin, 2006). In the Harvard-Brown Anxiety Research Program, which recruited patients from Boston hospitals, the mean age of onset of GAD was 21 years, although many patients had been unwell since their teens. The average duration of illness in this group was about 20 years and despite treatment the outcome over the next 3 years was relatively poor, with only one in four patients showing symptomatic remission from GAD (Yonkers et al., 1996). The proportion of patients who became free from all psychiatric symptomatology was even smaller, at about one in six. In patients who remitted from GAD, the risk of relapse over the next year was about 15% increasing to about 30% in those who achieved only partial symptomatic remission (Yonkers et al., 1996).The participants in the above study were recruited from hospital services and may not be representative of GAD in general. In a naturalistic study in the UK, Tyrer and colleagues (2004) followed up patients with anxiety and depression identified in psychiatric clinics in primary care and found that 12 years later 40% of those initially diagnosed with GAD had recovered, in the sense of no longer meeting criteria for any DSM-III psychiatric disorder. The remaining participants remained symptomatic, but only 3% still had GAD as the principal diagnosis; in the vast majority of patients, conditions such as dysthymia, major depression and agoraphobia were now more prominent. This study confirms the chronic and fluctuating symptomatic course of GAD in clinically-identified patients. It should be noted, however, that the majority of people with GAD in the community do not seek medical help for their symptoms (Wittchen & Jacobi, 2005) and the course of the illness in these circumstances is not established.Panic disorderPanic disorder comprises two main subtypes; panic disorder without agoraphobia and panic disorder with agoraphobia, with different presentations and often different courses. Panic disorder with agoraphobia (about one third of all presentations of panic disorder) is characterised by an avoidance of situations from which escape may not be possible or help not available in the event of a panic attack. Panic disorder with agoraphobia is also more common in women by a factor of approximately two to one. In contrast, panic disorder without agoraphobia is not situation-specific and symptoms may develop with no obvious or apparent cause (Weissman & Merikangas, 1986).The most common age of onset is from the mid-teens to the mid-20s; however, onset may occur at any time. Panic disorder often begins with occasional panic attacks that increase in frequency and which in time lead to a pattern of a generalised avoidance. The course of this disorder often follows a chronic pathway for many people with panic disorder, with agoraphobia likely to have an even more chronic course (Francis et al., 2007).Panic attacks commonly occur in many other disorders including specific phobias and social anxiety disorder, but they can also occur in GAD, drug or alcohol misuse, personality disorders and a number of physical disorders.Obsessive-compulsive disorderThe mean age of onset of OCD is in late adolescence for men and early 20s for women, although age of onset covers a wide range of ages. However, it may take individuals between 10 and 15 years or longer to seek professional help. There is often comorbidity with a range of disorders, especially depression (for example, Abramowitz, 2004; Abramowitz et al., 2003; Apter et al., 2003), and other anxiety disorders (for example, Biederman et al., 2004; LaSalle et al., 2004; Nestadt et al., 2003; Welkowitz et al., 2000).OCD may follow an acute, episodic or chronic course. In one of the largest follow-up studies, Skoog and Skoog (1999) conducted a 40-year prospective study and reported that approximately 60% of people with OCD displayed signs of general improvement within 10 years of illness, increasing to 80% by the end of the study. However, only 20% achieved full remission even after almost 50 years of illness; 60% continue to experience significant symptoms; 10% displayed no improvement; and 10% had deteriorated. A fifth of those who had displayed an early sustained improvement subsequently relapsed, even after 20 years without symptoms. This suggests that early recovery does not eliminate the possibility of very late relapse. Intermittent, episodic disorder was more common during the early stage of illness and predicted a more favourable outcome, whereas chronic illness predominated in later years. Worse outcome was predicted by early age of onset (particularly in males), experiencing obsessions and compulsions or magical thinking, poor social adjustment and early chronic course.Post-traumatic stress disorderThe onset of symptoms in PTSD is usually in the first month after the traumatic event, but in a minority (less than 15%; McNally, 2003) there may be a delay of months or years before symptoms start to appear. PTSD also shows substantial natural recovery in the initial months and years after a traumatic event. Whereas a high proportion of trauma survivors will initially develop symptoms of PTSD, a substantial proportion of these individuals recover without treatment in the following years, with a steep decline in PTSD rates occurring in the first year (for example, Breslau et al., 1991; Kessler et al., 1995). On the other hand, at least one third of people who initially develop PTSD remain symptomatic for 3 years or longer and are at risk of secondary problems such as substance misuse (for example, Kessler et al., 1995). In the 2007 ONS (McManus et al., 2009) survey, screening positive for current PTSD declined with age, from 4.7% of 16- to 24-year-olds to 0.6% of adults aged 75 years or over.2.2.5. Impairment, disability, secondary problemsDepressionApart from the subjective suffering experienced by people who are depressed, the impact on social and occupational functioning, physical health and mortality is substantial. In fact, depressive illness causes a greater decrement in health state than major chronic physical illnesses such as angina, arthritis, asthma and diabetes (Moussavi et al., 2007).Depression is a major cause of disability across the world. In 1990 it was the fourth most common cause of loss of disability-adjusted life years (DALYs) in the world and by 2020 it is projected to become the second most common cause (World Bank, 1993). In 1994 it was estimated that about 1.5 million DALYs were lost each year in the West as a result of depression (Murray et al., 1994). Depressive disorders account for 4.4% of the global disease burden or the equivalent of 65 million DALYs (Murray & Lopez, 1997; WHO, 2002).Emotional, motivational and cognitive effects substantially reduce a person's ability to work effectively, with losses in personal and family income as well as lost contribution to society in tax revenues and employment skills. Wider social effects include: greater dependence upon welfare and benefits with loss of self-esteem and self-confidence; social impairments, including reduced ability to communicate and sustain relationships during the illness with knock-on effects after an episode; and longer-term impairment in social functioning, especially for those who have chronic or recurrent disorders. Some of the features of depression (such as lethargy) may impede access to appropriate healthcare.Depression can also exacerbate the pain, distress and disability associated with physical health problems, and can adversely affect outcomes. Depression combined with chronic physical health problems incrementally worsens health compared with a physical health problem alone or even combinations of physical health problems (Moussavi et al., 2007). In addition, for a range of physical health problems findings suggest an increased risk of death when comorbid depression is present (Cassano & Fava, 2002). In coronary heart disease, for example, depressive disorders are associated with an 80% increased risk both for its development and of subsequent mortality in people with established disease, at least partly because of common contributory factors (Nicholson et al., 2006).Suicide accounts for nearly 1% of all deaths and nearly two thirds are people with depression (Sartorius, 2001); putting it in another way, having depression leads to over a four-times higher risk of suicide compared with the general population, which rises to nearly 20 times in the most severely ill (Bostwick & Pankratz, 2000). Sometimes depression may also lead to acts of violence against others, and may even include homicide. Marital and family relationships are frequently negatively affected, and parental depression may lead to neglect of children and significant disturbances in children (Ramachandani & Stein, 2003).Generalised anxiety disorderLike major depression GAD is associated with a substantial burden of disability, equivalent to that of other chronic physical health problems such as arthritis and diabetes (Wittchen et al., 2002). There is evidence that comorbid depression and anxiety has a worse prognosis and more persistent symptoms than either depression or anxiety disorders alone (Kroenke et al., 2007). There is also evidence that, in the community, anxiety disorders are independently associated with several physical health problems and that this comorbidity is significantly associated with poor quality of life and disability (Sareen et al., 2006), and high associated health and social costs (Simon et al., 1995).Studies have shown that the presence of GAD is also associated with significant impairments in occupational and social functioning. For example, over 30% of patients with GAD showed an annual reduction of work productivity of 10% or more compared with 8% of people with major depression. The figure for people with comorbid GAD and depression was over 45% (Wittchen et al., 2000). A large part of the economic cost of anxiety disorders is attributable to the costs of non-medical psychiatric treatment. Patients with GAD have increased numbers of visits not only to primary care doctors but also to hospital specialists, particularly gastroenterologists (Kennedy & Schwab, 1997; Wittchen et al., 2002). This may be a consequence of the distressing somatic symptoms that many people with GAD experience.GAD also carries a considerable cost in personal suffering and difficulties. In the Harvard-Brown Program, one third of patients had never married and unemployment was higher than average (Yonkers et al., 1996). Suicidal ideation and suicide attempts are significantly increased in GAD, particularly in women, and this increase is still greater in the presence of comorbid major depression (Cougle et al., 2009).Panic disorderPanic disorder has considerable impact on the NHS, such as general practitioners (GPs), society as a whole (in terms of sickness and absence from work, labour turnover and reduced productivity), and individuals and families (Sherbourne et al., 1996). The impact in any of these spheres is difficult to measure accurately and there may be an underestimation of the impact, but it is still substantial. A person with panic disorder may experience severe and enduring physical sensations, which may lead them to think that they have a physical illness; it can be difficult for healthcare professionals to provide adequate reassurance that this is not the case, which may lead to multiple consultations. Their economic wellbeing may also be affected (Edlund & Swann, 1987).Obsessive-compulsive disorderOCD is ranked by the WHO in the top ten of the most disabling illnesses by lost income and decreased quality of life (Bobes et al., 2001). The severity of OCD differs markedly from one person to another. While some people may be able to hide their OCD from their own family, the disorder may have a major negative impact on social relationships leading to frequent family and marital discord or dissatisfaction, separation or divorce (Koran, 2000). It also interferes with leisure activities (Antony et al., 1998) and with a person's ability to study or work, leading to diminished educational and/or occupational attainment and unemployment (Koran, 2000; Leon et al., 1995). The social cost (that is the person's inability to fully function in society) has been estimated as US$5.9 billion in 1990, or 70.4% of the total economic cost of OCD (DuPont et al., 1995).Post-traumatic stress disorderSymptoms of PTSD cause considerable distress and can significantly interfere with social, educational and occupational functioning. It is not uncommon for people with PTSD to lose their jobs either because re-experiencing symptoms, as well as sleep and concentration problems, make regular work difficult or because they are unable to cope with reminders of the traumatic event they encounter while at work (Zatzick et al., 1997). The resulting financial problems are a common source of additional stress and may be a contributory factor leading to extreme hardship, such as home-lessness. The disorder has adverse effects on the person's social relationships, leading to social withdrawal. Problems in the family and break-up of significant relationships are not uncommon.People with PTSD may also develop further, secondary psychological disorders as complications of the disorder. The most common complications are:the use of alcohol, drugs, caffeine or nicotine to cope with their symptoms, which may eventually lead to dependencedepression, including the risk of suicideother anxiety disorders, such as panic disorder, which may lead to additional restrictions in their life (for example, inability to use public transport).Other possible complications of PTSD include somatisation, chronic pain and poor health (Schnurr & Green, 2003). People with PTSD are at greater risk of physical health problems, including circulatory and musculoskeletal disorders, and have a greater number of medical conditions than those without PTSD (Ouimette et al., 2004).The course and prognosis of all common mental disorders are affected by a range of social factors, a number of which have been already discussed above. However, a range of factors related to social exclusion have a specific effect on access to services. This means that a number of groups may have particular problems accessing services including: those involved with the criminal justice system; homeless or precariously housed people; travelling communities; some groups of younger people (including those who have been in care as children and adolescence); people who misuse drugs and alcohol; and those of uncertain immigration status.2.2.6. Economic costsThe ONS report (McManus et al., 2009) makes the point that although common mental health disorders are usually less disabling than major psychiatric disorders such as psychosis, their greater prevalence means that the cumulative cost to society is vast. Mixed anxiety and depression has been estimated to cause one fifth of days lost from work in Britain (Das-Munshi et al., 2008). Even before the recent expansion of the European Union, it was estimated that work-related stress affected at least 40 million workers in its then 15 member states and that it cost at least €20 billion annually. In the UK, it has been suggested that over 40 million working days are lost each year due to stress-related disorders (European Agency for Safety and Health at Work, 2000).Costs of depressionDepression is associated with high prevalence and treatment costs, and as stated above is considered one of the most important risk factors for suicide (Knapp & Illson, 2002). Furthermore, depression has a large impact on workplace productivity. As a result, depression places an enormous burden on both the healthcare system and the broader society.Depression has a major financial impact on health and social services and the wider economy. A review was conducted by the King's Fund in 2006 to estimate mental health expenditure including depression in England for the next 20 years, to 2026 (McCrone et al., 2008). The study estimated the total cost of services for depression in England in 2007 to be £1.7 billion, while lost employment increased this total to £7.5 billion. Based on the estimate that 1.45 million people would have depression in 2026, the authors estimated that the total service cost would be £12.2 billion when accounting for prescribed drugs, inpatient care, other NHS services, supported accommodation, social services and lost employment in terms of workplace absenteeism.One of the key findings from the cost-of-illness literature is that the indirect costs of depression far outweigh the health service costs. A study by Thomas and Morris (2003) suggested that the effect on lost employment and productivity was 23 times larger than the costs falling to the health service. Other studies have also supported these findings. Based on UK labour-market survey data, Almond and Healey (2003)estimated that respondents with self-reported depression/anxiety were three times more likely to be absent from work (equivalent to 15 days per year) than workers without depression/anxiety. Furthermore, a US-based study suggests that depression is a major cause of reduced productivity at work, in terms of ‘work cut-back days’ (Kessler et al., 2001). This reduced workplace productivity is unlikely to be adequately measured by absenteeism rates and further emphasises the ‘hidden costs’ of depression (Knapp, 2003). A recent study conducted by the the Centre for Economic Performance's Mental Health Policy Group estimated that the total loss of output (in terms of lost productivity, absenteeism from work or benefits received) due to depression and chronic anxiety is some £12 billion per year (Layard, 2006).Other intangible costs of illness include the impact on the quality of life of people with depression and their families and carers. Certainly, the cost-of-illness calculations presented here and in Table 2 show that depression imposes a significant burden on individuals and their families and carers, the healthcare system and the broader economy through lost productivity and workplace absenteeism. Furthermore, it is anticipated that these costs will continue to rise significantly in future years. Therefore, it is important that the efficient use of available healthcare resources is used to maximise health benefits for people with depression.Table 2Summary of cost of illness data for depression and anxiety.Costs of anxiety disordersAnxiety disorders place a significant burden on individuals as well as on the healthcare system. Although direct comparisons between studies are difficult to make due to variations in country, health services and year of interest, economic cost has been estimated at over US$40 billion (Andlin-Sobocki et al., 2005; see Table 2 for further information). Estimated costs are incurred by healthcare resource utilisation such as mental health services, medication, hospitalisation, nursing homes and outpatient visits, productivity losses and, to a lesser extent, by provision of other services such as criminal justice services, social welfare administration and incarceration, as well as family care-giving (0.8%) (Andlin-Sobocki et al., 2005).Total healthcare cost is not the only important outcome to consider when investigating cost. Marciniak and colleagues (2005) found that the total medical cost per person with any anxiety disorder was estimated at US$6,475 in 1999. More specifically, when looking at GAD alone, the figure increased to US$2,138 when controlling for demographics and other disease states. This increased cost may be due to factors such as increased outpatient mental health service use or medical specialist service use. Furthermore, people with anxiety tend to miss more days of work or have a short-term disability than controls (Marciniak et al., 2004).Anxiety disorders are associated with a wide range of comorbidities, which result in a substantial increase in the total healthcare costs. Souêtre and colleagues (1994) estimated the total direct and indirect costs incurred by people with GAD with and without comorbidities using data on 999 people participating in a French cross-sectional study. Controlling for confounding variables, the prevalence of healthcare utilisation in terms of hospitalisation, laboratory tests and medications, and the respective medical costs were found to be significantly higher in people with GAD and other comorbidities than those without comorbidities. Moreover, comorbidities were associated with increased absenteeism from work. In particular, comorbid depression (Marciniak et al., 2005; Wetherell et al., 2007; Zhu et al., 2009) and physical pain (Olfson & Gameroff, 2007; Zhu et al., 2009) have been found to have a significant impact on treatment costs incurred by people with GAD.Costs of post-traumatic stress disorderIn 2003 to 2004, social and welfare costs of claims for incapacitation and severe disablement from severe stress and PTSD amounted to £103 million, which is £55 million more than was claimed 5 years previously (Hansard, 2004). Therefore, PTSD presents an enormous economic burden on families, the national health services and society as a whole.Go to:2.3. TREATMENTA number of treatments exist for common mental health disorders. However, because this guideline is predominantly interested in the identification and assessment of these conditions, the treatments will only be discussed briefly. For more information, please see the relevant guideline (see Section 2.1).2.3.1. Pharmacological treatmentsDepressionThere is a wide range of antidepressant drugs available for people with depression. These can be grouped into tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors and a range of other chemically unrelated antidepressants (British National Formulary [BNF] 59; British Medical Association & the Royal Pharmaceutical Society of Great Britain, 2010).Generalised anxiety disorderPlacebo-controlled trials indicate that a wide range of drugs with differing pharmacological properties can be effective in the treatment of GAD (Baldwin et al., 2005). In recent years, antidepressant medications such as SSRIs have been increasingly used to treat GAD (Baldwin et al., 2005).Conventional antipsychotic drugs and the newer ‘atypical’ antipsychotic agents have also been used in the treatment in GAD, both as a sole therapy and as an ‘addon’ to SSRI therapy when the latter has proved ineffective (Pies, 2009). However, the greater side-effect burden of antipsychotic drugs means that presently their use is restricted to people with refractory conditions, with prescribing being guided by secondary care physicians.Panic disorderThere is evidence to support the use of pharmacological intervention in the treatment of panic disorder, in particular with SSRIs. When a person has not responded to an SSRI, other related antidepressants may be of benefit. There is little good evidence to support the use of benzodiazepines. In contrast to a number of other depressive and anxiety disorders, there is little evidence to support the use of pharmacological and psychological interventions in combination.Obsessive-compulsive disorderPharmacological investigations have demonstrated effectiveness in OCD, in particular with SSRIs and related antidepressants (Montgomery et al., 2001; Zohar & Judge, 1996) for moderate to severe presentations, especially if the problem has a chronic course; this may be in combination with psychological interventions.Post-traumatic stress disorderAt present there is no conclusive evidence that any drug treatment helps as an early intervention for the treatment of PTSD-specific symptoms (NCCMH, 2005). However, for people who are acutely distressed and may be experiencing severe sleep problems, consideration may be given to the use of medication. Drug treatments for PTSD should not be used as a routine first-line treatment for adults (in general use or by specialist mental health professionals) in preference to a trauma-focused psychological therapy. Drug treatments should be considered for the treatment of PTSD in adults when a person with the disorder expresses a preference not to engage in a trauma-focused psychological treatment. The SSRI paroxetine is the only drug with a current UK product licence for PTSD.2.3.2. Psychological treatmentsDepressionEffective psychological treatments for depression identified in the NICE Depression guideline (NICE, 2009a) include: cognitive behavioural therapy (CBT), behavioural activation, interpersonal therapy (IPT),behavioural couples therapy and mindfulness-based cognitive therapy. For moderate to severe disorders these are often provided in conjunction with antidepressants. For subthreshold and milder disorders, structured group physical activity programmes, facilitated self-help and CCBT are effective interventions.Generalised anxiety disorderCognitive and behavioural approaches are the treatments of choice for GAD. People who have moderate to severe disorder, particularly if the problem is long-standing, should be offered CBT or applied relaxation. For those with milder and more recent onset disorders, two options are available: facilitated ornon-facilitated self-help based on CBT principles and psychoeducational groups also based on CBT principles.Panic disorderCognitive and behavioural approaches are again the treatments of choice for panic disorder. People who have a moderate to severe GAD, particularly if it is longstanding, should receive between 7 and 14 hours of therapist-provided treatment over a 4-month period. For those with milder and more recent onset GAD, facilitated or non-facilitated self-help based on CBT principle are efficacious treatments.Obsessive-compulsive disorderCBT is the most widely used psychological treatment for OCD in adults (Roth & Fonagy, 2004). The main CBT interventions that have been used in the treatment of OCD are exposure and response prevention (ERP) (for example, Foa & Kozak, 1996; Marks, 1997), different variants of cognitive therapy (Clark, 2004; Freeston et al., 1996; Frost & Steketee, 1999; Krochmalik et al., 2001;Rachman, 1998, 2002 and 2004; Salkovskis et al., 1999; van Oppen & Arntz, 1994; Wells, 2000), and a combination of ERP and cognitive therapy (see Kobak et al., 1998; Roth & Fonagy, 2004). ERP and cognitive therapy have different theoretical underpinnings, but may be used together in a coherent package.Post-traumatic stress disorderGeneral practical and social support and guidance about the immediate distress and likely course of symptoms should be given to anyone following a traumatic incident. Trauma-focused psychological treatments are effective for the treatment of PTSD, either trauma-focused CBT or eye movement desensitisation and reprocessing (EMDR). These treatments are normally provided on an individual outpatient basis and are effective even when considerable time has elapsed since the traumatic event(s).2.3.3. Current levels of treatment of common mental health disordersIt is concerning that, according to the 2007 ONS survey (McManus et al., 2009), only one quarter (24%) of people with a disorder were receiving any treatment for it in the week prior to interview. Treatment received by that 24% was mostly in the form of medication: 14% were taking psychoactive medication only, 5% were in receipt of counselling or therapy and 5% were receiving both medication and counselling/therapy.Use of healthcare servicesOf the people reporting a common mental health disorder in the ONS survey (McManus et al., 2009), 39% had used some type of healthcare service for a mental or emotional problem within the last year, compared with 6% of men and women without a disorder.Primary care servicesGeneral practice services were the most common healthcare service used in the ONS survey. A total of 38% of people with a common mental health disorder contacted their GP for help. Depression and phobias were associated with the highest use of healthcare services for a mental or emotional problem (both 67%), and mixed anxiety and depression was associated with the lowest use (30%) (McManus et al., 2009).Community care servicesAll respondents in the ONS survey (McManus et al., 2009), were asked about community and day care services used in the past year. Community and day care services were used less than healthcare services. Those with phobias made most use of community or day care services (49%), while mixed anxiety and depressive disorder was associated with the lowest rate of community or day care service use (12%).SummaryIn summary, common mental health disorders are associated with a range of symptoms that can lead to significant impairment and disability, and high costs both for the individual with the disorder and for society as a whole.Effective treatments are available that differ depending on the disorder. As a result, early detection, assessment and intervention are key priorities for any healthcare system. This guideline, which is focused on primary care, will provide recommendations on how to best identify and assess common mental health disorders and the key indicators for treatment in order to help improve and facilitate access to care, and the route through care.Go to:2.4. IDENTIFICATION, ASSESSMENT AND PATHWAYS TO CAREGoldberg and Huxley (1992) described a useful model within which to consider issues relating to the identification, assessment and pathway to psychiatric care for people with a common mental health disorder (see Figure 1). They identified five levels of care, with ‘filters’ between them relating to the behaviour of those with the disorders and the behaviours of the healthcare practitioners with whom they came into contact, emphasising that only a small proportion of people with a mental disorder receive specialist psychiatric care.Figure 1Levels and filters model of the pathway to psychiatric care (adapted from Goldberg & Huxley, 1992).The prevalence rates given above are taken from the original model and relate to proportions found in epidemiological surveys conducted before 1980. The Level 1 figures refer to all psychiatric disorders in the population, including psychotic and organic disorders, so the prevalence rates are somewhat higher than those given for the common mental health disorders in Section 2.2.2 above.For Filter 1 (the decision to consult a primary care physician), the key individual is the patient themselves. Level 2 refers to all psychiatric disorders in general practice, even if the GP has not diagnosed the disorder. Filter 2 refers to the detection and diagnosis of psychiatric disorder; Level 3 is ‘conspicuous’ or diagnosed psychiatric disorder within primary care. The third filter is the process of referral to secondary care, and Level 4 and Level 5 refer to the small proportion of patients with illnesses severe enough to need specialist secondary care.2.4.1. Increasing access to careThere are significant concerns about a number of barriers to access to care. These may include stigma (both cultural and self, and stigmatisation), misinformation or cultural beliefs about the nature of mental disorder, social policy or other approaches that limit access to services.Presentation of people with a common mental health disorder to primary careOf the 130 cases of depression (including mild cases) per 1000 population, only 80 will consult their GP. The stigma associated with mental health problems generally (Sartorius, 2002), and the public view that others might view a person with depression as unbalanced, neurotic and irritating (Priest et al., 1996), may partly account for the reluctance of depressed people to seek help (Bridges & Goldberg, 1987). The most common reasons given for reluctance to contact the family doctor include: did not think anyone could help (28%); a problem one should be able to cope with (28%); did not think it was necessary to contact a doctor (17%); thought problem would get better by itself (15%); too embarrassed to discuss it with anyone (13%); and afraid of the consequences (for example treatment, tests, hospitalisation or being sectioned under the Mental Health Act; 10%) (Meltzer et al., 2000).Most anxiety disorders are found more frequently in primary care than in the community except for social anxiety disorder and agoraphobia, both of which involve avoidance of public places such as doctors' surgeries (Bushnell et al., 2005; Oakley Browne et al., 2006; see Table 3). However, even when people with anxiety and depression do consult their GP, their disorder often goes unrecognised, partly because many do not present their psychological symptoms overtly.Table 3Twelve-month prevalence of anxiety disorders in New Zealand (Oakley Browne et al., 2006).Dowrick and colleagues (2010) carried out systematic reviews to identify groups for whom there are particular problems accessing mental health services, and to identify systems for promoting access. Poorer access to care has been found to be associated with lower social class, geographical location, ethnic minority groups, the presence of sensory or other impairments, the presence of learning difficulties, and particular demographic factors including age and gender (for example, older people or younger men).This guideline seeks to identify service developments or changes that may be specifically designed to promote access, both for the general population and for specific outreach groups (see Chapter 4). Particular areas include: community outreach; providing education and information concerning the nature of mental disorder; and new and adapted models of service delivery, which focus on the needs of black and minority ethnic (BME) groups and older people.2.4.2. IdentificationRecognition of depressionOf the 80 people with depression per 1000 population who do consult their GP, 49 are not recognised as depressed, mainly because most such patients are consulting for a somatic symptom and do not consider themselves mentally unwell despite the presence of symptoms of depression (Kisely et al., 1995). People who present with somatic symptoms are especially unlikely to be recognised (Kisely et al., 1995). GPs tend to be better at recognising more severe forms of the disorder (Goldberg et al., 1998; Thompson et al., 2001). With 50% of people with depression never consulting a doctor, 95% never entering secondary mental health services, and many more having their depression going unrecognised and untreated, this is clearly a problem for primary care.Recognition of anxiety disordersAnxiety symptoms are also often not recognised by primary healthcare professionals because, once again, patients may not complain of them overtly (Tylee & Walters, 2007). Cases of anxiety are especially likely to be missed when people frequently attend with multiple symptoms, despite reassurance. Instead, these symptoms are often characterised as possible symptoms of cardiovascular, respiratory, gastrointestinal, neurological or musculoskeletal disease (Blashki et al., 2007).For many people with a common mental health disorder, stigma and avoidance may contribute to under-recognition of their condition. Pessimism about possible treatment outcomes may further contribute to this. However, GPs themselves can contribute to the under-recognition of these conditions.Consultation skillsGPs are immensely variable in their ability to recognise depressive illnesses, with some recognising virtually all of the patients found to be depressed at independent research interview, and others recognising very few (Goldberg & Huxley, 1992; Üstün & Sartorius, 1995).The communication skills of the GP make a vital contribution to determining their ability to detect emotional distress, and those with superior skills allow their patients to show more evidence of distress during their interviews thus facilitating detection (Goldberg & Bridges, 1988; Goldberg et al., 1993).According to Goldberg and colleagues (1980a and 1980b), ten behaviours are associated with greater detection. These include factors such as making eye contact, having good interview skills, asking well-formulated questions and focusing on more than just a symptom count. Attempts to improve GP behaviour have been successful (Ostler et al., 2001; Tiemens et al., 1999), although results are mixed (Kendrick et al., 2001; Thompson et al., 2000) and interventions sometimes fail to impact on patient outcomes despite changes in clinician behaviour (Gask et al., 2004).Case identificationThe fact that common mental health disorders often go undiagnosed among primary care attenders has led to suggestions that clinicians should systematically screen for hidden disorders. However, general screening is not without its problems and is currently not recommended in most countries, including the UK. Instead, targeted case identification, which involves screening a smaller group of people known to be at higher risk based on the presence of particular risk factors, may be a more useful method of improving recognition of psychological disorders in primary care.Whooley and colleagues (1997) found that two questions were particularly sensitive in identifying depression:During the last month, have you often been bothered by feeling down, depressed or hopeless?During the last month, have you often been bothered by having little interest or pleasure in doing things?The current NICE Depression guideline (NICE, 2009a) recommends that GPs be alert to possible depression in at-risk patients and consider asking the above Whooley questions when depression is suspected. If the person screens positive, further follow-up assessments should then be considered. Currently, no equivalent Whooley questions have been recommended for anxiety.The view of the GDG for this guideline was that the development of separate case identification questions for each type of anxiety disorder would very likely be impractical and have no utility for routine use in primary care. The preference was to explore the possibility of a small number of case identification questions with general applicability for a range of anxiety disorders. A potentially positive response would then prompt a further assessment. This is dealt with in Chapter 5.2.4.3. AssessmentSince April 2006, the UK general practice contract Quality and Outcomes Framework Guidance for GMS Contract (QOF) has incentivised GPs for measuring the severity of depression at the outset of treatment in all diagnosed cases, using validated questionnaires (British Medical Association & NHS Employers, 2008). The aim is to improve the targeting of treatment of diagnosed cases, particularly antidepressant prescribing, to those with moderate to severe depression, in line with the NICE guidelines.A number of assessment tools have been identified as potentially useful for the assessment. The NICEDepression guideline (NICE, 2009a), for example, recommends the use of the nine-item Patient Health Questionnaire (PHQ-9) (Spitzer et al., 1999), the depression scale of the Hospital Anxiety and Depression Scale (HADS) (Zigmond & Snaith, 1983) and the Beck Depression Inventory, 2nd edition (BDI-II) (Beck, 1996; Arnau et al., 2001). The rationale for using such instruments is that doctors' global assessments of severity do not agree well with valid and reliable self-report measures of severity in terms of cut-off levels for case identification (Dowrick, 1995; Kendrick et al., 2005; Lowe et al., 2004;Williams et al., 2002), which can result in over-treatment of mild cases and under-treatment of moderate to severe cases (Kendrick et al., 2001 and 2005).However, the QOF guidance, again in line with NICE guidance, also recommends that clinicians consider the degree of associated disability, previous history and patient preference when assessing the need for treatment rather than relying completely on the questionnaire score (British Medical Association & NHS Employers, 2006). This is especially important given that people with mental illness vary in the pattern of symptoms they experience, their family history, personalities, pre-morbid difficulties (for example, sexual abuse), physical illness, psychological mindedness, current relational and social problems and comorbidities – all of which may affect the outcomes of any intervention (for example, Cassano & Fava, 2002; Ramachandani & Stein, 2003).Currently, evidence exists that points practitioners in the direction of well-validated tools. As a result, this guideline will not attempt to recommend specific tools because preferences vary between practices. Instead, this guideline will focus on ways to improve the assessment process, specifically, how to assess the nature and severity of a common mental health disorder, factors that may influence referral for treatment, routine outcome monitoring (ROM) and risk assessment.2.4.4. Pathways to careGiven the complexity of healthcare organisations and the variation in the way care is delivered (inpatient, outpatient, day hospital, community teams and so on), choosing the right service configuration for the delivery of care to specific groups of people has gained increasing interest with regard to both policy (for example, see Department of Health, 1999) and research (for example, evaluating day hospital treatment [Marshall et al., 2001]). Research using randomised controlled trial (RCT) designs has a number of difficulties; for example, using comparators such as ‘standard care’ in the US makes the results difficult to generalise or apply to countries with very different types of ‘standard care’.Stepped careCurrently, much of the UK mental health system is organised around the principles of stepped care. Stepped care (Scogin et al., 2003) is a framework that is increasingly being used in the UK to provide a structure for best-practice clinical pathways to care. It is designed to increase the efficiency of service provision with an overall benefit to patient populations. The basic principle is that patients presenting with a common mental health disorder will ‘step through’ progressive levels of treatment as necessary, with the expectation that many of these patients will recover during the less intensive phases. High-intensity treatments are reserved for patients who do not benefit from low-intensity treatments, or for those who can be accurately predicted not to benefit from such treatments. Thus, stepped care has the potential for deriving the greatest benefit from available therapeutic resources (Bower & Gilbody, 2005) and has been recommended in a number of NICE guidelines including Depression (NICE, 2009a) and Generalised Anxiety Disorder and Panic Disorder (With or Without Agoraphobia) in Adults (NICE, 2011a).A potential disadvantage of a stepped-care approach is that patients who do not benefit from low-intensity treatments may still have to undergo such treatments before a successful outcome is achieved. To maximise the efficiency of care delivery, patients who can be predicted as unlikely to respond to less intensive treatments ideally should be referred straight to higher levels; that is, care should be ‘stratified’ to an extent (Bower et al., 2006). However, prognostic evidence to support such decisions is currently lacking.Improving Access to Psychological Therapies programmeIn 2004 the economist Richard Layard made the case for a major expansion in the availability of psychological treatments, which he suggested could bring a significant reduction in the welfare benefits bill and increased tax contributions of those helped back to work. In 2006 the government established the Improving Access to Psychological Therapies (IAPT) programme, based heavily on the stepped-care approach. Clark and colleagues (2009) reported on the initial success of two demonstration sites in Newham and Doncaster, and the IAPT programme proposes a phased national roll-out by 2013 (to date, over 50% of Primary Care Trusts have an IAPT service). Self-referral to IAPT services is also actively encouraged, with emerging evidence to suggest that it increases access for vulnerable groups, such as BME groups to psychological interventions (Clark et al., 2009). In addition, an analysis of the first full year of operation of the first wave of roll-out sites (October 2008 to September 2009) has recently been published (Glover et al., 2010). Anonymous patient-level data were collected from 32 sites with the aim of evaluating whether the ‘commitments relating to accessibility, the provision of NICE-approved therapies and detailed outcome monitoring were progressing appropriately’. The authors concluded that the large amount of outcome data collected is a remarkable achievement, although there are some limitations and shortcomings that need to be addressed. For example, the analysis suggests that the diagnostic coding frame needs to be extended to include panic disorder and more research needs to be conducted to establish how reliable diagnoses can be obtained. Furthermore, in terms of equality of access, the authors state that ‘older people and men appeared under-represented in relation to expectation based on the patterns of morbidity shown by the psychiatric morbidity survey. The position for people with disabilities is not recorded at all in most sites, making it difficult to see how commissioners and providers can discharge their responsibilities to promote access to services for disabled people under disability discrimination legislation.’ Also, ‘after allowing for all other relevant factors for which data were available, Black people were significantly less likely to receive any treatment or to recover on either the two-scale or the three-scale makers, Asians were less likely to receive high intensity treatment (CBT or counselling), and both were significantly less likely to receive CBT’. More generally, with regard to treatment received, there was evidence to suggest that more needs to be done to ensure that the treatment given for specific diagnoses is aligned to that recommended in NICE guidelines.