Mental health and incapacity benefit

Ben Goldacre has a show on Radio 4 about incapacity benefit, which has prompted me to write this loser length post (more of an essay really). Millions of adults receive incapacity benefits in the UK and over the last ten years mental ill health has grown to become one of the major reasons. This is now costing some billions of pounds in benefits yet we know that unemployment is generally harmful to mental health while return to employment can help improve mental health. While the Government has been noticeably successful in reducing levels of those on unemployment benefit it has had little effect on levels of incapacity benefit.

I'd like to discuss the reasons for the poor employment rate of those with mental illness, why mental ill-health now accounts for such a large proportion of incapacity benefit, what can be done to help those with mental illness back into work and what impact Labour's proposed reform of the incapacity benefit system is likely to have.



Introduction

There are around 2.7 million people receiving incapacity benefits in the UK (more than a trebling since 1979). These consist of ‘Incapacity Benefit’ proper (1.4 million), the main contributory benefit for those incapable of work because of illness or disability and with sufficient National Insurance contributions, and those receiving income support (1 million) or the legacy benefit ‘Severe Disablement Allowance’ (.3 million). Around half of IB claimants are over 50 (1.3 million) with equal proportions of men and women by age, except that women retire five years earlier at 60, so there is a greater overall number of men (although the retirement age for women will rise to 65 in the future), and they are more likely to be getting the contributory benefit. There is a view that IB claimant numbers will fall away through time as a cohort of older claimants reaches state pension age because a large part of this cohort is made up of older men who were made redundant during the wave of industrial job losses in the '80s. But projections suggest that there will be no fall over the next 10 years given existing stocks and flows.

The proportion of incapacity benefit claimants with mental ill-health as their main disability has increased steadily over the last ten years from a quarter of claimants in 1996 to over 40% of claimants in 2006, with a further 10% of claimants with mental illness as a secondary factor. This has also been accompanied by an increasing proportion of the working age population claiming incapacity benefits, rising from 2% in the 1970s to 7% today (figure top right - proportion of working age population in receipt of incapacity benefits from ref [2]), a continuation of a trend since the 1950s in sickness pay generally [8]. Although inflows onto incapacity benefits have fallen 40% over the last decade this has been offset by a 35% reduction in outflows, resulting in only a small net decline in claimants.

The Government has been noticeably successful in reducing levels of those on unemployment benefit since 1997, through a combination of welfare reform and a favourable economic climate. Incapacity claims, however, have continued to rise; now representing the largest group of working age benefit claimants without employment. There are currently more mentally ill people drawing incapacity benefit than there are unemployed people on Jobseeker’s Allowance, resulting in an overall cost to the Exchequer of £10 billion.

In the non-disabled population some 80% of people are employed and only 4% dependent on benefits. For people with a disability the employment rate is 50%, but those with mental illness have the lowest employment rate of any disabled group (with the exception of learning disabilities) at 20%. Therefore two-thirds of people with mental ill-health are dependent on state benefits, compared with one-third of disabled people in general. It has been estimated that the reduced employment rate of those with mental illness costs another £10 billion in lost productivity [6].

Apart from the direct financial costs of reduced employment there is evidence that unemployment is generally harmful to health, particularly mental health. Conversely, return to employment is associated with improved general and mental health. Paid employment offers financial, psychological and social benefits to people with mental health problems that can facilitate psychological recovery and symptom reduction.


Mental illness and employment

One way to think about incapacity benefit claimants with mental ill-health is as a subset of all people with mental illness. As mentioned above, people with mental illness have very low rates of employment, and, according to the Psychiatric Morbidity Survey, some 16% of adults of working age have a mental illness, of whom up to a half are seriously ill. Unemployment rates for those with serious mental health problems range from 60% to over 95%. Thus, it is not surprising that people with mental health problems make up a significant proportion of those claiming incapacity benefit. This high unemployment is at least partly due to social factors such as stigma in addition to the direct consequences of mental health problems on the ability to work.
There are potentially two approaches to the problem of low employment for those with mental illness. The first is to tackle mental illness directly, and the other is to improve the employment prospects of those with mental illness. The former is beyond the scope of this discussion but it is worth noting that the majority of NHS resources for mental illness go to the 1% of the population with psychotic illness. Only around half of depressed patients receive any treatment and less than 10% have seen a psychiatrist.

Given the evidence for the efficacy of pharmacological and cognitive behavioural therapy (CBT) in conditions such as depression and anxiety it has been argued that expanding the provision of therapy, particularly CBT where waiting times are currently very long, will result in substantial cost savings due to increased productivity as well as reduced suffering and morbidity [6]. Certainly GPs should consider initiating treatment in anyone that they are signing off work on mental health grounds. In studies of those with mental illness who manage to return to work from incapacity benefit almost all report that improvement in their mental health was a major factor, whether this be due to medication, therapy, or resolution of underlying stressors, and in those claiming incapacity benefit those with mental ill-health are the most likely to regard their condition as improving [9].

It has long been recognised that people with severe mental illness require help to re-enter the workforce. Pre-vocational training provides a period of preparation before entering into competitive employment. Work projects have long been utilised as a route into the labour market for people with mental health problems. Sheltered work creates part-time jobs, with low ‘therapeutic’ pay that doesn’t affect entitlement to benefits. This approach has a long history but is associated with relatively poor quality products and conditions and infrequent transition into paid employment.

Alternative models have attempted to formulate something of a halfway house between sheltered employment and the open market but supported employment programmes seek to facilitate the employment of people directly in the open workforce with market pay and conditions. This approach places people into jobs without extended preparation but provides support during employment such as for reasonable adjustments in the workplace. Studies from the US have shown supported employment to be more effective than pre-vocational training in helping people with severe mental illness to obtain employment in the open market at similar cost [5] and this result has been replicated in a European RCT [4]. This supports the use of supported employment programmes in facilitating the employment of those with severe mental illness and suggests consideration of this model for those with less severe forms of mental ill-health.


Incapacity benefit and mental ill-health

An alternative way to consider people on incapacity benefits with mental ill-health is as a subset of those claiming incapacity benefit overall.

Many reasons have been posited for the growth in incapacity benefit claimants over time. It has long been proposed that the impoverishment of old industrial areas is a causal factor. There are also suspicions that governments have used the higher payments of incapacity benefit as an incentive to reduce the headline numbers of those claiming unemployment benefit through transition to incapacity.

Along with this post-industrialisation the labour market has changed with an increasing predominance of low paid jobs with few prospects, many of which are part-time or temporary, resulting in poor employment stability and a tendency to enter and exit the labour market more frequently. For those claimants on benefits for a long time there is also now a mismatch between their perceptions of the workplace and the reality and they may need considerable help to prepare them to re-enter the workforce.

Evidence suggests that the state of the local labour market has a strong effect on the likelihood of disabled people working and it has been estimated that up to 40% of incapacity benefit claimants could be ‘hidden unemployed’ based on underlying rates of incapacitating ill health and the incapacity benefit claimant rates in areas of full employment. This would support the use of macroeconomic tools to improve the conditions in the labour market to encourage those with mental illness to re-enter employment. However, the creation of nearly two million new jobs between 1997 and 2005 was not associated with a fall in incapacity benefit claimants and other sources of labour filled the gap. Therefore, even if incapacity benefit claimant levels represent underlying economic trends, it may well require more than simply reversing these trends at a national level to tackle incapacity benefit levels.

The increasing proportion of incapacity benefit claimants with mental illness is due both to people with mental health problems leaving incapacity benefits more slowly than those with other disabilities as well as a relatively high proportion of new claimants with mental illness. The increasing contribution of mental illness to incapacity benefit claims is primarily in ‘depressive and neurotic’ conditions rather than psychoses which have remained fairly stable in incidence (and thus fallen as a proportion of claims) [8]. Consistent with the view that increasing incapacity benefit claims are the result of wider socioeconomic factors, rather than mental ill-health per se, the increase in claimants with mental ill-health has occurred despite no apparent increase in the prevalence of mental disorders (except for alcohol dependence) in the wider community. Similarly, the wide variations in numbers of incapacity benefit claims, where the North of England, Scotland and Wales have rates double that of the South of England is not reflected in the underlying prevalence of mental illness in those populations.

Ninety percent of people who start claiming incapacity benefit expect to return to work, and around 60% of people starting on incapacity benefit stop claiming within a year. However, once on incapacity benefit those that expect never to leave it trebles, and those that stay on benefits for more than two years are more likely to retire or die than get another job. This compares to less than 5 per cent of those on unemployment benefits who have been claiming for over five years. More adults with long-term mental health problems report that they wish to return to work than people with other disabilities, yet evidence from welfare to work programmes such as the New Deal for Disabled People and Pathways to Work suggests that people with mental health conditions have not been helped to the same extent as those with physical illness.

The bulk of incapacity benefit claimants are aged over 50yrs but the prevalence of mental health problems in claimants is highest among younger claimants. Of recent applicants for incapacity benefit those with mental ill-health are less likely to be currently working or to have a job to return to than other applicants. They are also more likely to say that they have low confidence about working, that they will need help, rehabilitation or other assistance before they could consider working, that they are unlikely to get a job due to their sickness record, and that they would be financially worse off if they got a job. Recent claimants with mental health problems were twice as likely as those with only physical conditions to report that they had problems with numeracy or literacy [9].

Even among those claming incapacity benefit for conditions other than mental health problems reported depression, stress, and anxiety are very high. In fact many of those claiming incapacity benefit with mental illness as their main condition also have a physical illness (although this could partly be due to the greater emphasis on physical conditions under the current capability assessment questionnaire) and those with comorbid physical and mental illness are more likely than those with physical or mental illness alone to fail to return to work. Studies have demonstrated a link between poverty and mental illness, with poverty causing mental ill-health as well as being a consequence, including through reduced standards of living causing depression and anxiety. Many people entering incapacity benefit do not come via employment but rather other benefits and it is conceivable that they have developed mental health problems at least in part due to the stresses of unemployment and poverty. The prevalence of mental ill-health is also especially high for people entering incapacity benefit who have been recently care-giving or looking after the home or children.

There is a strong interaction between physical and mental illness (such as the transition from acute to chronic back pain) and it is possible that poor management of physical illness could contribute to the emergence of depression and anxiety through loss of social roles, isolation, and poverty. Government trials of early access to psychological therapy have produced a 5% reduction in patients claiming sick pay through returning people to work [2].

There is evidence for an association between poor mental health and factors in the workplace such as long hours and workload and interventions use training and organisational approaches to increase support or participation in decision making can improve psychological health and levels of sickness absence [7]. Few people regard works stress as the sole trigger of their mental ill health but it is commonly cited as an exacerbating factor. Some people moving onto incapacity benefit with mental ill-health from work report having requested amelioration of work stress but none of these explicitly related these requests to mental health problems [9]. This highlights the reluctance of people to communicate their mental health problems to employers. When an employee develops a mental health problem they may initially exhibit reduced job performance which can cause loss of job satisfaction causing further decline in mental health.

Around two-thirds of those entering incapacity benefit with mental ill-health from employment regard the loss of their job as being due to their mental illness, while 20% say it was due to other unrelated factors (such as termination of contract) [9]. The period of sick leave before transition to incapacity benefit is likely to be a critical period and most people have not discussed their mental health problems with their employer at this point. It is therefore worth considering early intervention at this stage to try and prevent transition from sick leave onto incapacity benefit and to facilitate communication between health services, employee and employer.

A high proportion of incapacity benefit claimants with mental health problems report that their problems fluctuate over time, particularly in comparison to those with physical illness, and they are more likely to be younger and have characteristics that disadvantage them in gaining employment such as no recent employment, a poor work history, and minimal qualifications. Employers particularly discriminate against a history of long-term sick leave and are half as likely to say they would employ someone with a mental illness compared to someone with a physical illness.

Around a third of entrants onto incapacity benefit are not claiming for the first time, and a third have received unemployment benefit in the last two years. People with mental health problems are less likely to have moved onto incapacity benefit via work than other claimants, and this suggests that there is a considerable degree of movement into and out of incapacity benefit and employment and that this could be worse for those with mental illness due to their fluctuating course and adverse work history.

Fluctuating illness makes it difficult to return to work and difficult to reclaim benefits when leaving work again. The benefits system is not designed to cope with this other than in the short term and job retention may be facilitated by giving disabled people in employment a right to temporary leave to allow them time for rehabilitation support with a guaranteed return to work.

Problems with the incapacity benefits system include a failure to prevent people from moving onto incapacity benefits, benefits trapping people into dependency with financial disincentives to finding work or training, the likelihood of leaving benefits rapidly decreasing over time as people become disconnected from the workplace, financial incentives to stay on benefits for longer (incapacity benefit rates increase over time), and a lack of support for moving into employment.


Government reforms

The Government aims to reduce incapacity benefits claimants by one million from 2.7 million to 1.7 million over the 10 years from 2006 to 2015. It is using a combination of anti-discrimination legislation and reform of the benefit and employment systems to try and tackle incapacity benefit levels [1].

A new Employment and Support Allowance (ESA) replaced incapacity benefits for new claimants in October 2008 (being rolled out to existing claimants 2009-2013), with capability reports focusing on what people can do, rather than what they cannot and the ‘Pathways to Work’ scheme being rolled out across the country with compulsory work focused interviews, ‘Condition Management Programmes’, and financial bonuses for return to work. ESA rates will be comparable to jobseeker's allowance, rather than current IB levels, with the minority exempted from seeking work qualifying for an increased rate. Evidence from trials of Pathways suggests an eight percentage point increase in the incapacity benefit off-flow rates (figure bottom right - incapacity benefit 6-month off-flow rates from ref [3]) but unfortunately this benefit is not translated through to those with mental health problems. There is an additional concern that the destination of over half of those leaving IB is unknown, and the second largest group (25%) is those transferring to another benefit, only 4% return to work. There are substantial and rapid transfers between IB and job seeker's allowance, and, of those entering work from IB, some 14% return to IB within the year.

The reasons for the failure of Pathways to help those with mental health problems return to work is unclear. It is certainly the case that these claimants have an increase in those factors with have an adverse effect on gaining employment such as a poor work history. The recurrent pattern of mental illness may also make it difficult to stay in the workplace. Although GPs have not traditionally regarded as their role to be involved in detailed discussions about employment with their patients they could be encouraged to emphasis the importance of work for well being and self esteem.

In Pathways areas a formal 'In-Work Support' programme is available but this only lasts for six months. This has not been widely taken up but could be extended to form the basis for a supported employment model similar to that seen with severe mental illness to facilitate returning to and staying in work.

The Government’s published plans [1] do not currently contain any provisions to help people to remain in work during their initial period of ill-health. Carol Black has made a number of recommendations that go beyond the governments plans for helping those on incapacity benefit back to work [2] and, in particular, she proposes an early intervention service called ‘Fit for Work’ where a GP can refer patients to a multidisciplinary team with a case manager liaising with GP and employer. This might provide exercise and physical activity along with psychological therapies, physiotherapy and occupational therapy, social services help, and occupational health interventions such as workplace assessment and modification. Currently the Government has undertaken to trial this proposal.

GPs generally do not have easy access to mental health specialists from either occupational health or general psychiatry and the raft of new proposals appear to place considerable further burdens on GP time and expertise. Perhaps it is time to go further than ‘Fit for Work’ and consider the establishment of a specialised state occupational health service where capability assessors are controlled and trained by the government rather than contracted out (the current capability assessment contract is with Atos Origin until 2012). This could help address the widespread concern that under the existing system of capability assessment mental health problems are inadequately assessed, underemphasised and minimally explored and thus provide minimal benefit to advisers seeking to place claimants into work.

It seems likely that mental health problems will continue to represent a major proportion of those claiming incapacity benefits, although the reasons for this are far from clear (and likely multi-factorial), but, despite some limited success in reducing IB levels of those with physical illness in trial areas, it is not obvious that current proposals are likely to have much of an impact on helping people with mental health problems into work. The current disconnection between psychiatric, social, and employment services needs to be tackled before a comprehensive and succesful attempt can be made to reverse the long standing disengagement of people with mental health problems from the workforce. As things currently stand it looks like recent welfare reforms will result in a large increase in unemployment levels amongst the mentally ill, with a consequent cut in living standards.


[1] No one written off: reforming welfare to reward responsibility. Department for Work and Pensions, TSO, 2008.
[2] Black, C., Working for a healthier tomorrow. Health, Work and Well-being Programme, TSO, 2008.
[3] Blyth, B., Incapacity Benefit reforms - Pathways to Work Pilots performance and analysis. Working Paper No 26, Department for Work and Pensions, HMSO, 2006.
[4] Burns, T., Catty, J., Becker, T., Drake, R.E., Fioritti, A., Knapp, M., Lauber, C., Rossler, W., Tomov, T., van Busschbach, J., White, S. and Wiersma, D., The effectiveness of supported employment for people with severe mental illness: a randomised controlled trial, Lancet, 370 (2007) 1146-52.
[5] Crowther, R.E., Marshall, M., Bond, G.R. and Huxley, P., Helping people with severe mental illness to obtain work: systematic review, Bmj, 322 (2001) 204-8.
[6] Layard, R., Mental Health: Britain's Biggest Social Problem? No.10 Strategy Unit Seminar on Mental Health, 2005.
[7] Michie, S. and Williams, S., Reducing work related psychological ill health and sickness absence: a systematic literature review, Occup Environ Med, 60 (2003) 3-9.
[8] Moncrieff, J. and Pomerleau, J., Trends in sickness benefits in Great Britain and the contribution of mental disorders, J Public Health Med, 22 (2000) 59-67.
[9] Sainsbury, R., Irvine, A., Aston, J., Wilson, S., Williams, C. and Sinclair, A., Mental health and employment. Research Report No 513, Department for Work and Pensions, HMSO, 2008.

All advertisers are fuckwits

Reading this thread on the badscience forums I was introduced to the concept of 'Diagonal Thinking'. Apparently:

"At the ‘Creative Britain in Golden Square’ event held this week, Culture Secretary Andy Burnham launched a new, free online self-assessment tool that identifies if you have what it takes to succeed in the ad industry. This unique psychometric test, developed on behalf of the IPA by consultancy AgencyPeople, will tell you if you have ‘Diagonal Thinking’ ability. It is designed as a recruitment tool to encourage applicants from all backgrounds to consider a career in advertising. "

Here's the Diagonal Thinking Test:

"The Diagonal Thinking Self-assessment is an online tool, designed to aid recruitment into the advertising and communication industries. It tests the hypothesis that the most successful individuals working in the business are both Linear and Lateral Thinkers – they think ‘diagonally’. "

I started to have a go, and was presented with the linear thinking test:

"This part of the test assesses your ability to decide whether a conclusion logically follows from a statement or not. For example, in stating:

"Some chefs work very long hours. All people who work very long hours eventually suffer from stress."

you could logically conclude that some chefs will eventually suffer from stress. For the purpose of this test, you must consider all statements presented to you to be true. For each conclusion given, you must decide whether it logically follows from the statement. If so, click on the 'Yes' button. If you decide that the conclusion does not follow from the statement, click the 'No' button. If you believe the statement gives insufficient information to make a decision about a conclusion, click on the 'Don't know' button. Try not to let your general knowledge or opinions affect your judgements. Just stick to the given statement of facts when making your decision."

Here is a screenshot of one of the example questions (I didn't get as far as the actual test):



And here's another one:

It isn't entirely clear how we know that 'some scientists have very high levels of intellect' and 'all people with very high levels of intellect lack interpersonal skills' gives 'insufficient information to make a decision about a conclusion' over whether 'Some non-scientists are highly intellectual' yet we also know that 'all physicists have good interpersonal skills' 'does not follow from the statement'. One might be inclined to think that people in advertising know fuck all about logic and linear thinking, they certainly appear unable to figure out that despite physicists being a subset of scientists we can't tell whether any of them have high levels of intellect (and thus lack interpersonal skills) from these statements. Diagonal thinking my arse, smug self-congratulating tosspots more like.

Yet more antidepressants

Thanks to paul in the comments below here's a link to the Maudsley debate on antidepressant efficacy, 'This House Believes Antidepressants are no Better than Placebo', featuring Irving Kirsch, Joanna Moncrief (for), Guy Goodwin, and Lewis Wolpert (against).

Interestingly Kirsch turns the question around to argue that there is no evidence that antidepressants are clinically significantly better than placebo (as you may be aware, I've addressed the Kirsch et al PLoS paper before).

Both Kirsch and Moncrief make some good points, but I was struck by Moncrief's claim that because we don't know that antidepressants act specifically against 'the' biological cause of depression, and in fact may have rather more non-specific effects that help to ameliorate the symptoms of depression, we therefore should not use them.* She goes on to argue a completely contradictory point at the end of her speech to claim that because antidepressants are (according to her) no better than placebo they are therefore harmful because they are not inert. Yet her argument that antidepressants are not superior to placebo hinges on the claim that their apparent superority hinges on their active side effects in clinical trials.

Goodwin and Wolpert make some fairly pedestrian counterarguments, some fallacious, largely anecdotal in Wolpert's case. The comments from the floor included some 'service users' ranting and anti-psychiatry, which is quite common at psychiatric talks.


* I've long been drawn to the idea (can't remember who first proposed it) that serotonergic antidepressants flatten emotional responses and noradrenergic antidepressants are activating. But both these effects would seem to me to be very useful in helping to relieve symptoms of depression and facilitate true recovery. Comments from the floor point out that in the rest of medicine we don't abandon treatments proven to work in clinical trials because we don't know their mechanism of action. In fact, it is pretty hard to see what Moncrief would advocate to treat depression instead of antidepressants, surely we can't know that physical exercise or CBT are definitely treating the underlying physical abnormality?

Back from hols

EP debunking Friday - sniffing out the perfect partner

As people keep moaning about the length of these debunking posts, I'll keep this one short. Browsing Feminist Philosophers I was reminded of this story from a few days ago:

"They say that opposites attract. But it seems the Pill may be preventing women sniffing out men who are opposite enough...But researchers found that the Pill disrupts a woman's power to recognise the aroma of a suitable partner."

This story is based on this study, "MHC-correlated odour preferences in humans and the use of oral contraceptives" an epub in Proc. R. Soc. B. The reasoning behind the study is that the major histocompatibility complex (MHC) of our genome shows great variation and this is thought to be related to immune function, so it would be genetically better to have offspring with individuals with genetically dissimilar MHCs from you.

So what does the study do? It looks at a bunch of women, none of whom were on the pill, but some of whom were thinking about taking it. So they got these women to smell the shredded sweaty shirts of men with either genetically similar or dissimilar MHCs:

"Almost 100 women then sniffed the shirts and gave their opinions on the 'pleasantness' and ' desirability' of the odour twice over a three-month period. Many started taking the Pill during the experiment - and their opinions of the smell of the T-shirts changed...Researcher Craig Roberts said: 'The results showed that the preferences of women who began using the contraceptive Pill shifted towards men with genetically similar odours.'"

So this is supposed to be evidence that:

"Saddled with the wrong man - someone who in scientific terms has similar genes - she may find it hard to become pregnant and any children she does have may have a lower resistance to infection.

What is more, when she stops taking the Pill and her sense of smell returns to normal, she's more likely to fall out of love, the Liverpool and Newcastle universities research suggests."

So is this what the study actually shows? Of course not. Without even getting into the question of whether woman actually choose partners based on the smell of their sweat, in actual fact the study found that women didn't rate the pleasantness, desirability, or intensity of the odour of men with dissimilar MHCs as any higher than men with similar MHCs.

The only significant finding was an interaction on an ANOVA where women on the pill showed a reduction in the amount they favoured MHC dissimilar odours, but there was no statistically significant difference between women on the pill and women not on the pill in the degree to which they favoured genetically dissimilar men. The interesting finding is that women not yet on the pill, but who intended to go on the pill seemed to favour MHC dissimilar men more than other women (presumably this wasn't statistically significant) and this is what is driving the interaction (the preference for dissimilar men normalises back to being like other women after they are taking the pill (see the figure, average odour 'desirability' for MHC dissimilar men minus MHC similar men, white bar represents first rating {before women started the pill} and the grey bar the second rating {with women in the pill group having started the pill}).

So it is pretty unlikely that taking the pill will cause problems becoming pregnant or children with a lower resistance to infection, since women not on the pill don't seem to favour MHC dissimilar odours (and thus men?) anyway, and women taking the pill don't show any difference in their preference for MHC dissimilar men compared to women not on the pill anyway.

The Mail does carry a contrary opinion from Professor Bill Ledger (Sheffield University) who wonders whether the smell of sweat is likely to overide the 'intellectual and emotional feeling' of a relationship but curiously doesn't attack the methodology of the paper. I wonder whether this is another example of embargoed press releases where those commenting on the paper don't actually get to see it and point out the obvious flaws.

Ossetia

Oh shit, the South Ossetia situation looks bad, but I'm intrigued at some of the reactions (e.g. Crooked Timber here, and on Comment is Free). I've never understood the seeming willingness of people to back western proxies against Russia with some really specious and hypocritical arguments. It harks back to the sort of cold war rhetoric that saw leftists backing dictators against western imperialism, and western democratic governments destabilising democratic socialist regimes and propping up despots.

For my own part I think a 'Neither Washington or Moscow' approach is needed here (more like this article in the Guardian), although I'm fairly unimpressed by legalistic arguments about territorial integrity and sympathetic to calls for regional autonomy where this is backed by the population. I certainly won't be "stand[ing] in solidarity with Georgia" in their attempts to subjugate the population of South Ossetia.

More informed coverage from A Fistful of Euros and Lawyers, Guns and Money.

Shibboleth

Being an old fashioned kind of guy, I haven't really followed the withdrawal of funding by JISC from Athens in favour of the 'UK Access Management Federation' and 'Shibboleth' technology. But now that my institution has withdrawn Athens compliance, I can tell you that it is just like Athens only it works about 1/10th as well.

Currently I'm working outside the university network (you'd hope within a university network with relevant IP addresses anyone would be able to figure out how to organise access management) but under the new system instead of being able to sign in to Athens once and then access all journal articles via links in commonly used search engines like pubmed, or via links in journal articles, now I have to search the university database of subscribed journals, then enter the citation, then wait while it chugs along at about one mile per hour to finally serve up the paper. If I'm lucky the journal may have got around to adding the 'UK Access Management Federation' to its long list of alternative logins, and then if I find it, and select the relevant UK university from the long list, I may be able to get it to recognise that I've already signed in (saving me the time to type in my login and password, but little else).

So why change? Apparently 'federated access management' (where they ask your institution if you're signed in there, rather than having you sign in directly) is the bees knees, according to JISC:

"Users will have a single sign-on using an institutional ID and password for a wide range of resources, as well as the assurance that their personal data will not be disclosed to third parties.
Librarians will be free of the burden of user name and password administration, and will have new tools for managing licenses and service subscriptions.
IT managers will have more control of the access management process through enhancements to enterprise directories, although this will require additional institutional effort in the short term.
Institutions will have a single service to meet the requirements of e-learning, e-research and library-managed resources. Simplification of the authentication process has also proven to lead to increased use of subscribed services."

It is good to know that in order to allow a single sign-on username and password and to free up a little bit of time for librarians (the rest of that stuff is pie in the sky techno-wank) access to online journals has regressed ten years in terms of useability, speed of access. Am I missing something or is this another example of management idiots fucking it up again? The potential benefits seem minimal and the implmentation is woeful.

Atheists as bad as witches and paedophiles

Via strummer on the badscience forums, a lovely piece of managerial fuckwittery. Apparently Birmingham City Council has banned access to sites:

"to do with "witchcraft or Satanism" and "occult practices, atheistic views, voodoo rituals or any other form of mysticism".

But not mainstream religions like Christianity, noo, no 'mysticism' there! The national secular society is on the case as this is not only ridiculous but also illegal. It looks like this is an example of the council implementing some proprietrary net usage restriction sofware, presumably from the US (thanks to Szlater - Blue Coat WebFilter)- at least I hope so, the alternative is just too disturbing, but Szlater points out that "Alternative Spirituality/Occult" and "Religion" as seperate with atheism and Wicca presumably part of the former, and Christianity and Hinduism part of the latter (I note you can also ban "Abortion", "Education", "LGBT", "Political/Activist Groups", "Sex Education ", "Spyware Effects/Privacy Concerns") so Birmingham Council obviously have some choice in the matter.

UPDATE
More at Pharyngula, you can see how a site is categorised here, and the category descriptions here:

"22 - Alternative Spirituality/Occult

Sites that promote and provide information on religions such as Witchcraft or Satanism. Occult practices, atheistic views, voodoo rituals or any other form of mysticism are represented here. Includes sites that endorse or offer methods, means of instruction, or other resources to affect or influence real events through the use of spells, incantations, curses and magic powers. This category includes sites which discuss or deal with paranormal or unexplained events." [my emphasis]

Apparently RichardDawkins.net was listed as 'Religion' but is now 'Society/Daily Living'!

*Since I'm reusing old post titles, this one refers to previous posts pointing out that atheists are worse than terrorists and as bad as gays and Jews, apparently this Blue Coat software also blocks access to sites that "promote witchcraft, the paranormal, sexual deviancy and criminal activity."

I ate the baby Jesus too*

I haven't been following the crackergate story too closely, but PZ Myers seems to have fomented quite a little storm in a teacup (see Cosmic Variance).

Basically some student receives a Catholic communion wafer and instead of eating it he keeps it to show to his friend, some of the congregation get a bit upset about it and try to take it of him, he gets annoyed at this and takes it home, lots of Catholics are pissed off because he's taken the body of Jesus 'hostage' - nutjobs like Bill Donohue waded in to call for sanctions to be brought against the student and for extra security at a Republican convention to defend the delegates from the likes of PZ Myers. So far so dull - kid seems like he's being a bit silly, Catholics come across as over-reacting and their silly (and falsified) beliefs are highlighted.

So PZ writes about this taking the predictable line "Get some perspective, man. IT'S A CRACKER." He finishes by asking for someone to send him a consecrated wafer to desecrate. And when he gets one he sticks a nail through it also providing a delightful sample of the threats he's been sent in the meantime, e.g.:

"You fool, the vengeance for your sacrilege will not be . exhausted against you, but it will be carried out on your child. Wait and see."

It seems to have created quite a stir on teh internets, despite the fact that PZ has blogged about desecrating the quran and bible before without anywhere near such attention.

For what it's worth I think that deliberately winding up theists by threatening to violate their laughable taboos is a bit mean, but perfectly acceptable behaviour, particularly if it is funny (compare the Jyllands-Posten controversy to Jesus and Mo). D^2 lives up to his reputation as being vaguely amusing but a bit of a dick in this post at crooked timber:

"While I of course do not countenance the harassment of anyone by religious nuts, I also have something of a baleful view of the kind of self-conscious atheist who regards it as a good use of his time to spend the day winding up the god squad.
...
while I am perhaps the last person on earth who is well-placed to tell anyone else that winding people up for the sake of it is a really silly and childish thing to do … well, winding people up for the sake of it is a really silly and childish thing to do, and furthermore Dawkinsite militant atheists are as annoying as fundies in their own way and perhaps deserve a bit of winding up too.
...
And so it is that, at some point this weekend, I plan to tell a small, credulous child (about whom I will provide no other information) that a rainbow is a special sign from God that he promises never to flood the world again and that this proves that God exists."

It's summed up nicely by mpowell:

"I think Dsquared has outdone himself on this one.

Step one: Hypocritically look down on those who have a go at others for the sake of it.

Step two: Brazenly imitate this behavior.

It’s times like these that I realize that I can never really measure up in the area of being a pretentious, sarcastic wise-ass. It’s almost enough to make me give it all up, but I’m not sure my friends and family could bear the loss."

Some of the other comments are also priceless:

"The fact that you can generate such a reaction merely by claiming you plan to do something—which is, in the final analysis, totally harmless—says a lot about the New Atheism."

Obviously I don't think D^2 means it, nor particularly care if he does, but it is interesting to note the symmetry or lack of between his threat and PZ's threat - PZ is quite entitled to do what he wants to communion wafers, but it causes quite some stink. Theists are quite entitled to bring their children up with nonsensical stories about God and floods (or even other lies about Father Christmas) and this is so accepted in our society that no one would seek to prevent this - the only opposition from atheists and secularists is about willfully witholding information about alternatives and indoctrination at the state's expense.


*I appear to have used the pun in the title "I ate the baby Jesus" before, repeating myself already, oh dear.

Thrombolysis in stroke

In response to a post by Dr Crippen about thrombolysis in stroke I'm posting a nice graph showing how the outcome of thrombolysis is very dependent on speed of treatment.

I believe that thrombolysis was approved by the FDA in 1996 after a single positive RCT (National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group 1995, NEJM 333) although other trials showed no benefit. There has been much scepticism about the benefits and criticism of the original study (there was a baseline imbalance in stroke severity but reanalysis suggests this does not strongly affect the results – Ingall et al 2004, Stroke 35).

Uptake has been slow due to fears about intracranial bleeding and only around 3% of stroke patients are eligible (.

The figure above is from The ATLANTIS, ECASS, and NINDS rt-PA Study Group (2004) Lancet 363. They performed an individual patient meta-analysis of alteplase (2775 patients, 6 RCTs) and found:
•Logistic regression adjusted OR for 'favourable outcome' varied with time to treatment
•Substantial rate of intracerebral haemorrhage 6% vs 1%
•No significant difference in mortality

NICE Guidance (2007) is:
•Alteplase within 3 hours of symptom onset
•Exclude intracranial haemorrhage by imaging (i.e. CT)
•Administration by stroke specialists in a specialist centre
•Not indicated for under 18 yrs or over 80 yrs
•0.9 mg / kg (max 90 mg) infused i.v. in 60 mins, with 10% administered as an initial i.v. bolus
•Costs e.g. 75 kg patient, 67.5 mg alteplase at £480 (<£4000/QALY)

Post-marketing surveillance shows that thrombolysis is of similar efficacy and safety when used outside of clinical trials (Wahlgren et al 2007, Lancet 369 - SITS-MOST trial).

There's also been a Cochrane Review with similar results (Wardlaw et al 2003).

More on 'medical care practitioners'

Following on from my last post moaning about 'medical care practitioners' or 'physician assistants' being introduced to the NHS, I found this fascinating information from the Birmingham PA course about the difference between a PA and a doctor:

"After their internship, PAs can work in general practice, hospital medicine or A&E. Although they will be required to show that they continue postgraduate studies as all clinicians do in terms of keeping up to date, , they are not required to undertake further formal training. PAs who wish to work in other fields (e.g. paediatrics; intensive care) will have to undertake further training. Whether or not they specialise PAs will be assessed periodically to ensure that they retain broad general competence.

The clinical role of the PA is very similar to that of the doctor. Experienced PAs in A&E or general practice may see the same undifferentiated range of patients that the doctor would see; can request the same investigations and initiate management of the patient in the same way. The differences are twofold. Firstly, currently, PAs are not allowed to prescribe. All prescriptions they write must be signed by a doctor. This is expected to change along with registration of the profession. Secondly, throughout their careers, PAs will work as part of a medical team, under the supervision of a doctor and (whatever their previous experience) they cannot work outside the field of competence of their supervisor. Their supervising doctor will have a deeper / more highly developed knowledge base and the PA is able to refer cases to their own supervisor as well as to other specialists."[my emphasis]

Physician assistants

Apparently American style 'physician assistants' (PAs) are to be introduced to the NHS. This is a rather worrying prospect. A two year course (following a previous degree) and apparently they are ready to do the job of a house officer, senior house officer, or even a registrar (there's a minimum of four years training, for graduate entry to medicine, before becoming a house officer, it makes you wonder why they bother if PAs are so much better) in the primary care and emergency medicine setting (at a rather more generous salary of £39,500 in 2003 compared to an F1 house officer on £21k in 2008*) diagnosing, prescribing, and ordering investigations (although prescriptions or X-rays are supposed to be countersigned by a doctor in the UK at the moment, the experience seems to be that discussion with the doctor are perfunctory at best, and there is likely to be pressure to follow the US model and allow them to prescribe).

Somehow we're supposed to be reassured that a pilot study using US trained PAs (with an average of 11 years experience* as PAs and allied health professionals) found that they worked well. Presumably a study of consultant vascular surgeons would be good evidence for allowing new house officers to carry out AAA repairs unsupervised.

This is absolutely crazy, you cannot create a new paramedical profession de novo and then roll it out across the NHS on the basis of a single study of a highly selected cohort with extensive previous experience. They should at least have evaluated newly qualified US PAs (who, unlike doctors, don't have a probationary year).

Paramedics, nurses, and other allied health professionals jump through a million hoops just to be allowed to do a few extra procedures that doctors can do from day 1. Now we're handing over direct clinical diagnosis and management (and de facto prescribing) to people with minimal knowledge, experience or training. Whatever you think about nurse practitioners, at least they develop their clinical skills in line with their extra responsibilities. The US PAs in this study were a lot closer in experience to UK nurse practitioners than to the newly trained UK PAs that could soon be fucking up our healthcare. Newly qualified junior doctors are scary enough, this is terrifying.


* Hopefully the pay differential is due to the US PAs being highly experienced since otherwise I can see junior doctors going on strike, at this pay rate you could get yourself two newly qualified doctors, or even a single specialist registrar (similar level of training to a GP, likely to have higher qualifications such as membership of the Royal College of Physicians) for this price! According to the Wolverhampton course you can "earn a starting salary of £22,500 - £32,000 at current levels" [my emphasis], brilliant, why go to medical school just to end up earning less and taking legal responsibility for someone else's mistakes, while being told that these people are working at a higher level of competence than you after half the training?

Briffa demented loon: Official

In an apparent effort to ensure that no one is in doubt about his status as a complete nutjob following his comments on MMR and skin cancer, John 'SucroGuard' Briffa is accusing the charity Diabetes UK of deliberately trying to destabilise patients' blood sugar in order to increase the amount of medication they use in order to benefit BigPharma. You couldn't make this deranged shit up:

"Diabetes UK is the UK’s largest and most prominent diabetes charity...However, I’m doubtful that Diabetes UK is fulfilling its brief in this respect, seeing as it continues to suggest that diabetics should include starchy carbohydrates which every meal (see herefor more on this)...Yet, these starchy staples break down into sugar, and some of them can release their sugar quite quickly into the bloodstream too. And if we eat them in quantity, like we often do, that only adds to their disruptive effects. Now, what rationale is there for diabetics to include “at each meal” foods that are disruptive to blood sugar?...However, I reckon there’s another, far more relevant way of interpreting this sentence which goes something like: “The more starchy carbohydrate you eat, the more out-of-control your blood sugar level will be, the more ‘diabetic’ you will be, and the more likely you are to start to take medication for this or to need to increase your medication regime.” Remember the advice to eat generally sugar-disruptive starchy carbs with each meal comes from the UK’s largest diabetes charity which, it says, campaigns for “better standards of care for diabetics”.
What sort of care is it referring to, do you think? Because on the face of it, it doesn’t look like nutritional care is part of its remit. And if that’s the case, maybe what’s being referred to here is medical care including medication...I don’t want to come across unduly cynical, but is it right that a diabetes charity should have a less-than-transparent financial relationship with the drug industry. And is it right that this charity should be giving nutritional advice that, at the end of the day, looks likely to benefit the pharmaceutical industry. And after all of this, should it then go on to partner with that pharmaceutical industry in ‘research’ highlighting the need for people to take their diabetes medication. Or did I miss something?"

Briffa on skin cancer

John Briffa's latest post attempts to cast doubt on the association between skin cancer and sun exposure:

"I was therefore interested to read over the weekend an editorial in the British Medical Journal which highlights the importance of sunlight and vitamin D in health...

There are three main forms of skin cancer: what are known as ’squamus cell carcinoma’ and ‘basal cell carcinoma’, and ‘malignant melanoma’. The first two tend to develop on the most sun-exposed parts of the body (e.g. the top of the ear) and are generally very treatable. Malignant melanoma, on the other hand, is generally much less treatable, is quite often deadly, and is usually the major reason cited regarding why we should protect ourselves from the sun...

However, is the relationship between sunlight exposure and risk of malignant melanoma as clear-cut as we are generally led to believe it to be? Michael Holick’s editorial contains information that might cause us to question traditional wisdom on this. He writes: “Notably, non-melanoma skin cancers occur on the most sun exposed areas, such as the face and hands, whereas most melanomas occur on the areas least exposed to the sun [2]. Intermittent and occupational sun exposure has been found to reduce the risk of malignant melanoma [2–5].”

In short, Professor Holick appears to be asking: “If sunlight exposure causes malignant melanoma, how come it tends to develop on parts of the body that are not typically very sun-exposed, and how come there is evidence linking sun-exposure with reduced risk of this condition?” Professor Holick appears to cast considerable doubt on the notion that excessive exposure to sunlight is a major risk factor for malignant melanoma."

Apart from being a little concerned about his attitude to skin cancer (basal cell carcinoma is fairly benign but squamous cell carcinoma has a risk of around 4% of spreading, both need surgical excision, and this isn't always easy or complete) I wondered where he got this view from. The medical consensus is that sun burn (especially in early life) is associated with malignant melanoma (with chronic sun exposure, such as from outdoor jobs, associated with basal cell and squamous carcinoma). Here's what the NHS says:

"There is a definite link between sunbathing (including using a sunbed) and malignant melanoma. Probably the most dangerous type of sunbathing is a short, sharp period of intense exposure, either in a single day or over a short period such as a holiday. The larger the area of skin exposed, the greater the risk. Getting sunburnt increases the risk further. It is the ultraviolet (UV) part of sunlight that does the most damage.
Severe sunburn in childhood can significantly increase your chances of developing malignant melanoma in later life.
It is also possible that you have more chance of developing malignant melanoma if someone in your family has also had one. Family history is most likely to be the cause if you haven't had excessive exposure to the sun. About one in 10 people with a melanoma have family members who have also had at least one.
You may also be at a greater risk if you have a large number of non-cancerous(benign) birthmarks."

The BMJ does indeed contain an editorial by Michael Holick, which mentions in passing that melanomas occur on areas least exposed to the sun:

"Excessive exposure to sunlight causes an estimated annual loss of 1.6 million disability adjusted life years (DALYs)—0.1% of the total global disease burden in the year 2000. This compares with the loss of about 3.3 billion DALYs from bone disease caused by vitamin D deficiency as a result of too little exposure to sunlight.11 These figures do not take into account the other potential health benefits of sun exposure and vitamin D sufficiency in reducing other chronic diseases, which account for 9.4% of total global disease burden. Notably, non-melanoma skin cancers occur on the most sun exposed areas, such as the face and hands, whereas most melanomas occur on the areas least exposed to the sun.12 Intermittent and occupational sun exposure has been found to reduce the risk of malignant melanoma.1 4 5 12"

So does this observation support Briffa's rejection of the melanoma-sun exposure link? Well let's look at the papers Holick links to in his editorial.

Number 1:

"Children and young adults who are exposed to the most sunlight have a 40% reduced risk of non-Hodgkin's lymphoma65 and a reduced risk of death from malignant melanoma once it develops, as compared with those who have the least exposure to sunlight.66"

So, this tells us that once you have developed melanoma sunlight exposure improves prognosis, but has nothing to say on the question of sunlight and malignant melanoma incidence.

Number 4:

"An ecologic study was performed using age-adjusted annual mortality rates for Caucasian Americans for 1950-69 and 1970-94, along with state-averaged values for selected years for alcohol consumption, Hispanic heritage, lung cancer (as a proxy for smoking), poverty, degree of urbanization and UVB in multiple regression analyses. Results: Models were developed that explained much of the variance in cancer mortality rates, with stronger correlations for the earlier period. Fifteen types of cancer were inversely-associated with UVB. In the earlier period, most of the associations of cancer death rates with alcohol consumption (nine), Hispanic heritage (six), the proxy for smoking (ten), urban residence (seven) and poverty (inverse for eight) agreed well with the literature. Conclusion: These results provide additional support for the hypothesis that solar UVB, through photosynthesis of vitamin D, is inversely-associated with cancer mortality rates, and that various other cancer risk-modifying factors do not detract from this link. It is thought that sun avoidance practices after 1980, along with improved cancer treatment, led to reduced associations in the latter period."

Can't get the full text of this - I note it is evil epidemiology, Briffa's not keen on that as we have learned from his views on MMR - there are multiple potential confounds, but assuming that it found a robust correlation between sun exposure and reduced melanoma (can't tell from the abstract), this doesn't really add anything to what we already know, it doesn't separate chronic sun exposure and acute sun burn, and there have been more detailed studies going beyond epidemiology looking at this (see below).

Number 5:

"Because the mortality rates of CMM [cutaneous melanocytic melanoma] are much higher than those of nonmelanoma skin cancer (in some populations, more than a factor of 10 higher), this problem is the most important one to solve regarding the negative consequences of sun exposure. The solution is by no means certain yet. A number of investigators disagree, as we reviewed earlier (12, 13).
The main arguments against the concept that sun exposure causes CMM are that: (i) CMM is more common among persons with indoor work than among those people with outdoor work (14, 15); (ii) in younger generations, more CMMs arise per unit skin area on partly shielded areas (trunk and legs) than on face and neck (16); and(iii) CMMs sometimes arise on totally shielded areas (acral CMM and uveal melanomas). Although the connection between these melanoma types and sun exposure is controversial (17–19), their inclusion in the present discussion is justified because of the possible involvement of vitamin D.
However, in our opinion, a significant fraction of CMMs is related to sun exposure (16, 20). The main arguments for this relationship are: (i) the north–south gradients in CMM incidence between Scandinavia and Australia (16), (ii) before the advent of the "top-less" fashion, few women developed CMM on the breast area (13, 16), and (iii) in some animals (Sinclair swine, Monodelphis domestica, the fish Xiphophorus, white horses, angora goats, transgenic mice, etc.) UV exposure leads to CMM (16). The reason that CMM incidence rates decrease with decreasing latitude in Europe is likely because of differences in skin color from region to region."

So we have competing epidemiological observations, none of which is definitive (and I'd argue that their points ii and iii are irrelevant, including the idea that because melanoma more commonly arises on trunk or leg it can't be associated with sun exposure - since these are areas where acute sun burn is common - which could explain the male preponderance for melanoma on the back, and females on the legs).

Number 12:

"Acute and chronic sun exposure may exert different effects in the sequel from common melanocytic nevi, clinically atypical nevi to malignant melanoma (Elwood and Jopson, 1997;Gilchrest et al, 1999). Acute painful sunburns may promote the development of common melanocytic nevi, clinically atypical nevi, and thus, or possibly independently, the development of malignant melanoma. Although there are some contradictory findings regarding the association between chronic lifetime sun exposure and malignant melanoma, most studies found that chronic lifetime sun exposure was associated with a protective effect on the development of malignant melanoma.
This could be explained by the protective mechanisms, which are associated with heavy chronic sun exposure, such as tanning and skin thickening, but this may not be the total explanation (Elwood and Jopson, 1997;Gilchrest et al, 1999). Although it cannot be excluded that sun exposure during adult life promotes the disappearance of nevi, which could be an additional explanation of a decreased risk of malignant melanoma, in our study the disappearance of nevi was completely explained by increasing age of the individuals, and chronic sun exposure had no additional effect."

This case-control study confirmed the consensus that acute sun burn can increase the risk of malignant melanoma. It also supported the view that chronic sun exposure reduces the incidence.

So overall I'd say that this editorial in the BMJ, which really only tangentially mentions a couple of observations about melanoma incidence, far from "[casting] considerable doubt on the notion that excessive exposure to sunlight is a major risk factor for malignant melanoma" adds precisely nothing to what we already know about malignant melanoma and sun exposure, or at least, adds nothing to what well informed clinicians know about the link between malignant melanoma and sun exposure.

The Atheist Thirteen

Via nullifidian, one of those internet 'meme' things to "find out at least a little bit more about each other in the atheist blogging community...If you’d like to take part, copy these questions, and answer them in your own words on your own blog."

Q1. How would you define “atheism”?
The belief that the balance of evidence suggests that the existence of God, gods, or similar supernatural beings is improbable.

Q2. Was your upbringing religious? If so, what tradition?
Marginally. I was brought up in the Anglican tradition (non-evangelical low church), my mother and grandmother are low key believers as are other members of my extended family, and I went to a Catholic school for a few years, but religion was never a big part of my life, although I was more religious than my peers. I continued to be affiliated with the church, getting confirmed in my mid-teens. I increasingly adopted more heterodox positions (partly informed by an interest in church history and comparative religion), rejecting trinitarianism early on, so that I was probably more of a deist by the time I attended university. There I was confronted by the essentially contradictory nature of my continued belief in God (which was by now practically a metaphor for my conscience anyway) yet rejection of the other aspects of Christian belief on the basis of the paucity of evidence. I've self-identified as an atheist ever since.

Q3. How would you describe “Intelligent Design”, using only one word?
Delusion.

Q4. What scientific endeavour really excites you?
Neuroscience is my field of research, and the interface of neuroscience and medicine, particularly psychiatry, is where my interests lie. Fingers crossed we might actually find out something that is of some use to people soon.

Q5. If you could change one thing about the “atheist community”, what would it be and why?
I'd like there to be less smug sneering by certain aspects of the atheist 'community', who can combine a sense of superiority over those unsophisticated atheists who explicitly and unequivocally reject religion, with a patronising defence of the 'opium of the people'. There's a certain strand of studenty contrarianism that likes to say things like 'aah, but isn't science becoming the new religion', to which the answer is 'no, not aah!':



Q6. If your child came up to you and said “I’m joining the clergy”, what would be your first response?
"Shit, when the fuck did I have a child?" Actually, I'd like to think I'd already noticed that my child was religious so I wouldn't be inordinately surprised. I don't think I'd be too worried about my child becoming a protestant priest, in some ways it is a logical and worthy consequence of their beliefs, and many do good work in the community, but I'd be more concerned about them becoming a Catholic priest, because they are rejecting significant and rewarding parts of life. I like to think that if my child were to become religious they would have grown up in an environment where they were able to think about it for themselves, and were not directed one way or the other.

Q7. What’s your favourite theistic argument, and how do you usually refute it?
I'm quite fond of the ontological argument, and the argument from personal experience is always a good way to close down a conversation - but for raw rhetorical chutzpah the bait and switch of changing between a minimally specified deistic god to the God of orthodox Christianity is my favourite. The refutation is obvious.

Q8. What’s your most “controversial” (as far as general attitudes amongst other atheists goes) viewpoint?
I think islamophobia and the demonisation of Muslims is a real problem in the world today.

Q9. Of the “Four Horsemen” (Dawkins, Dennett, Hitchens and Harris) who is your favourite, and why?
I dislike Hitchens because his strand of offensive and arrogant contrarianism really winds me up (see Q5). I don't know much about Harris except that he is supposed to have said something rather Martin Amis-like about torture in the 'War on Terror TM'. I like Dennett as a philosopher, particularly regarding 'qualia', but I find his stuff about religion a bit dry. So Dawkins it is, populariser of evolutionary science, strident and often amusing, if not particularly original, and I think he shot himself in the foot a bit with that line about religion being child abuse.

Q10. If you could convince just one theistic person to abandon their beliefs, who would it be?
Hmm, not sure. Let's say Antony Flew for the moment, not because it would be a great intellectual struggle, but because his late conversion has been a rather sad spectacle.

Now name three other atheist blogs that you’d like to see take up the Atheist Thirteen gauntlet:
Journalology
jdc325
Jean Kazez

Briffa's devastating critique

According to John Briffa this is a devastating critique of the Honda et al study that showed there was no relationship between MMR rates and autism in Japan. Basically it claims that even though MMR rates don't correlate with autism rates this is because single measles jabs also cause autism! The data used is not the local single jabs rates for the area studied by Honda et al but the national Japanese rates. I don't know why Briffa thinks this argument supports the MMR-autism link, it looks like a simple post hoc rationalisation to me.

But let's look at this data (plotted top right), vaccination rates (national MMR + single measles, and local MMR) shifted by one year (the Japanese measles vaccines are given at 1-year according to Nakatani et al and Honda et al) plotted against autism rates (cumulative up to seven years) by year of birth - overall autism spectrum and autism with regression are plotted*. Here we can see that there is minimal relationship between overall rates of autism spectrum and combined vaccination rates, and essentially no relationship with autism with regression.

This can be better seen in the figure on the right where the regressions of total measles vaccination rate against autism incidence are plotted - with neither even approaching statistical significance (p>.3), and correlation coefficients .3 and -.2 for autism spectrum and autism with regression respectively. Note that the correlation between MMR vaccination and overall autism spectrum is -.7, so MMR protects against autism!**

*For those interested in these things, autism rates are from Honda et al, and measles vaccine rates are estimated from the figure in Nakatani et al.

**No, obviously I don't think this really.

UPDATE
Here's a bit of fun, let's try another national vaccination rates vs. local autism rate graph. California is apparently a popular target, so how does autism rate (as determined by autism case load - dodgy, but like I say, just a bit of fun) compare with US national vaccination rate (1-year time shift, WHO data)?

Well here it is top right, not very convincing (although r=.7, p<.01). It nicely demonstrates that correlations are fairly common in time series (because all you need for a correlation is a trend for both things to increase with time) but also shows that the relationship is far from a 'dose-response' (sic) since autism keeps climbing while vaccination rates plateau. It accords fairly well with the figure on the left from a study of MMR vaccination rates and autism in California from JAMA which also found little relationship, with a plateau in vaccination rates and a continuing rise in autism.

This is also an interesting figure (below) from a study in the BMJ based on the UK general practice research database. It found that there was no relationship between UK MMR coverage (which remained very high for cohorts from 1988 to 1993) while autism rates continued to climb and nicely reflects the US vaccination plateau.

Absolutes versus rates

This post on talking philosophy highlights another example of journalists willfully using absolute figures and using these to calculate meaningless headline statistics ('mobile phone thefts up one billion % since 1980!!!') even when the sensible rate figures have been provided and their significance explained. Do they not understand or just not care?

Creationism from the BBC Natural History Unit

On nullifidian:

"BBC (i.e. taxpayer) provided webcams at the creationist Noah’s Ark Zoo Farm near Bristol...Oddly enough, these webcams are still advertised within the “nature features” part of the BBC Bristol web site. I guess they haven’t got around to re-organising the web site since the supernatural became a part of everyday existence."

Birth rape

Interesting, if bad tempered, exchange going on between Dr Crippen and the F Word (and others) over this post there on 'birth rape' and 'medical rape':

"A woman who is raped while giving birth does not experience the assault in a way that fits neatly within the typical definitions we hold true in civilised society. A penis is usually nowhere to be found in the story and the perpetrator may not even possess one. But fingers, hands, suction cups, forceps, needles and scissors… these are the tools of birth rape and they are wielded with as much force and as little consent as if a stranger grabbed a passer-by off the street and tied her up before having his way with her. Women are slapped, told to shut up, stop making noise and a nuisance of themselves, that they deserve this, that they shouldn’t have opened their legs nine months ago if they didn’t want to open them now. They are threatened, intimidated and bullied into submitting to procedures they do not need and interventions they do not want. Some are physically restrained from moving, their legs held open or their stomachs pushed on."

I'm somewhat ambivalent as to where my sympathies lie in this argument. I've seen some callous behaviour in the delivery room (more often from midwives than doctors I have to say). Of course any medical procedure carried out without consent is assault, and a patient can withdraw that consent at any time. On the other hand, when carrying out examinations and procedures which are uncomfortable it is always sensible, when a patient wants you to stop because of discomfort, to engage in at least some discussion with them - this is because people are often just temporarily unhappy about the discomfort and will continue with a little encouragement, avoiding terminating the procedure and requiring the whole experience to be repeated. This applies as much to inserting a cannula as to intimate examinations. I don't think there is any easy answer as to where the line lies, which is why doctors are always walking something of a tightrope between best interest and violation of autonomy.

Mad Nad

Via Hawk/Handsaw, Nadine Dorries shares her unique perspective on the BMJ study of survival rates in preterm infants:

"No improvement in neo-natal care in twelve years? Really? So where has all the money that has been pumped into neo-natal services gone then? A baby born at 23 weeks today stands no better a chance of living than it did in 1996? This report is the most desperate piece of tosh produced by the pro-choice lobby and it smells of one thing, desperation."

You may remember Ms Dorries from the minority report on abortion from the Commons Science and Technology Committe.

Kirsch et al reply again

Huedo-Medina, Johnson, and Kirsch have submitted a further response on PLOS Medicine in reply to further comments by myself and others, after their last reply.*


Placebo response and severity

Interestingly, while I observed that they needed to:

"clarify their position on the claim that placebo response decreases with increasing baseline severity, since this appears to be an artefact"

Rather than address this observation they instead repeat the claim, saying that it is the 'unique' contribution of their article:

"without the within-group analyses it would not have been possible to conclude that placebo responses were lessening as initial severity of depression increased (whereas drug response remained constant; see our article’s Figures 2 and 3). This unique contribution of our article contradicts Wohlfarth’s conclusion that it contained “nothing new.”"

Flawed meta-analytic methods

Further, they defend their bizarre and biased analytical method:

"One of the main concerns in the new commentaries centred on one of our main analyses, which evaluated change for drug and placebo groups without taking a direct difference between them. Thus, effect sizes were calculated separately for each group for this analysis, though the analysis combined them. Leonard regarded this practice as “unorthodox” and Wohlfarth regarded it as “erroneous because the effect size in an RCT is defined as the difference between the effect of active compound and placebo.” First, these concerns ignore the fact that our article’s between-group analyses confirmed the major trends present in the analyses that considered within-group change. Specifically, both sets of analyses concluded that antidepressants’ efficacy was greater at higher initial severity, attaining clinical significance standards only for samples with extremely severe initial depression. Second, although the commentators may be correct that our within-group analyses are relatively innovative in this literature, it does not mean that they were wrong. To the contrary, these statistics are in conventional usage elsewhere (e.g., 3, 4, 5), as Waldman’s commentary implies...Finally, the analyses did incorporate a direct contrast between drug and placebo (see Table 2, and Model 2c, for example).

...

Although alternative weighting strategies may yield somewhat different results, the choices converge well both for the overall mean difference and for analyses of the trends across the literature. As an example, Leonard (04 March 2008) reported replicating our meta-regression patterns using alternative precision weights.

Importantly, as our article documented (Figures 2 & 3), the size of the difference between drug and placebo grows as the samples’ initial severity increases to extremely severe depression (but is very small at lower observed levels of initial severity). Because the overall differences between drug and placebo depended on initial severity, it is misleading to consider the overall difference in isolation."

But this does not address my objection that:

"This is not an acceptable analytic technique because it ignores that there is a relationship between the improvement in placebo and drug groups from the same study, but that the placebo and drug groups from any given study can have grossly different weightings when considered separately (e.g. there would be half as much weighting to the results from the fluoxetine trials in the drug analysis as the placebo analysis, the result of, for example, different sample sizes between the experimental arms)."

And as I say about the more conventional analysis they claim supports their 'unorthodox' analysis:

"I note that Figure 4 in the paper of Kirsch et al is actually more consistent with my finding of 'clinical significance' at a baseline of 26 (this threshold is found both by regression on the difference scores, or separate regressions for each group's change score) than their suggestion of 28 points..."

And Robert notes:

"The available unbiased estimate of the overall average benefit of NDA’s is equal to 2.65 HRSD units, which is considerably higher than Kirsch et al’s biased estimate [of 1.8]."

So while my and Robert's analyses confirm that the effect size of antidepressants increases with increasing baseline severity, they also show that their claim that placebo responses decrease with baseline severity of depression are false, and that Kirsch et al report effect sizes that are considerably biased downwards.

It is worth thinking about the references they give to support their analytical method (numbers 3,4, & 5, notice they are either in psychology or education journals), the most recent (and thus most easily available) is reference 5, Morris & DeShon (2002) 'Combining Effect Size Estimates in Meta-Analysis With Repeated Measures and Independent-Groups Designs' in Psychological Methods 7(1) 105-25. It is about combining the results from repeated measures designs and independent group designs, concentrating on training effectiveness, organizational development, and psychotherapy, and is not an article about medical meta-analysis:

"The issue of combining effect sizes across different research designs is particularly important when the primary research literature consists of a mixture of independent-groups and repeated measures designs. For example, consider two researchers attempting to determine whether the same training program results in improved outcomes (e.g., smoking cessation, job performance, academic achievement). One researcher may choose to use an independent-groups design, in which one group receives the training and the other group serves as a control. The difference between the groups on the outcome measure is used as an estimate of the treatment effect. The other researcher may choose to use a single-group pretest-posttest design, in which each individual is measured before and after treatment has occurred, allowing each individual to be used as his or her own control.1 In this design, the difference between the individuals’ scores before and after the treatment is used as an estimate of the treatment effect."

I hope you can already see why this situation is not comparable to a meta-analysis of double blind randomised placebo controlled drug trials because these repeated measures designs would not be appropriate (you can have within-subjects cross-over designs but that is not what is being discussed here) because we know placebo effects are very important in drug trials so we require the use of placebo control arms. Therefore the Kirsch et al meta-analysis only involved independent groups and there is no need to worry about combining repeated measures and independent groups, and, as Morris & DeShon say:

"When the research base consists entirely of independent-groups designs, the calculation of effect sizes is straightforward and has been described in virtually every treatment of meta-analysis"

That is there is no need to use this unusual method because perfectly good methods already exist for analysing this data.

So Morris & DeShon are concerned with what to do when you have no control group for some of your studies - which is not the case in double blind RCTs because a study without a control group is considered an invalid measure of drug effects. The other two references, number 4, Gibbons et al (1993), and number 3, Becker (1988), also emphasise this aspect of the method (I haven't read these studies):

"With this approach, data from studies using different designs may be compared directly and studies without control groups do not need to be omitted."

But we have no need to do this, so we have no need for the analytical method used by Kirsch et al, and we have no need for this method precisely because medical meta-analysis consider only double blind RCTs and explicitly rejects studies without control groups precisely because an estimate of placebo responses in each trial is considered essential.

So we have no reason to use the method of Kirsch et al, but what reasons do we have for not using these "innovative...statistics...in conventional usage elsewhere"? Well what do Morris & DeShon have to say? Well obviously they're concerned about when it is acceptable to combine studies with and without controls, and conclude that ideally, if you intend to do this, there oughtn't to be a change in the control group with time, i.e. there should be no placebo effect in the control group. But they do refer to Becker for a meta-analytic method proposed for use when there is a placebo effect:

"Becker (1988) described two methods that can be used to integrate results from single-group pretest-posttest designs with those from independent-groups pretest-posttest designs. In both cases, meta-analytic procedures are used to estimate the bias due to a time effect. The methods differ in whether the correction for the bias is performed on the aggregate results or separately for each individual effect size. The two methods are briefly outlined below, but interested readers should refer to Becker (1988) for a more thorough treatment of the issues.

An important assumption of this method is that the source of bias (i.e., the time effect) is constant across studies. This assumption should be tested as part of the initial meta-analysis used to estimate the pretest-posttest change in the control group. If effect sizes are heterogeneous, the investigator should explore potential moderators, and if found, separate time effects could be estimated for subsets of studies." [my emphasis]

That is, if you can't be sure that the placebo effect is constant across studies, you shouldn't combine studies using this method. And, of course, this is precisely the objection that I and others have raised to this method - because we already know that placebo responses can vary between trials - that is why we have placebo control arms in randomised controlled trials!

So Huedo-Medina, Johnson, and Kirsch are advocating the rejection of the usual meta-analytic techniques used in medical research where the highest standards are required and control groups considered very important, in favour of adopting a methods from psychology and education that is only used when two different designs, one of which is rejected in medical research, need to be combined, and where placebo effects are downplayed, a method that even its advocates recognise is unsuitable with heterogeneous placebo responses between studies.

This is quite some defence when you look at the scatter on the placebo responses in the Kirsch et al meta-analysis, that's about as heterogeneous as it gets, and it isn't explained by baseline severity of depression - so the assumptions underlying the meta-analytic method used by Kirsch et al are violated, even according to the citations they refer to in justifying their approach! Even the original study (with standardised mean differences rather than raw change scores) showed great heterogeneity in the placebo arm:

"The amounts of change for...placebo groups varied widely around their respective means, Q(34)s = ... 74.59, p-values [less than] 0.05, and I2s = ... 54.47"

Precision versus bias

Huedo-Medina et al also completely misunderstand the objections of Robert Waldmann and others by saying:

"Waldman argued that our estimates of the overall difference between drug and placebo was conservatively biased (i.e., too small) because of assumptions present in our estimates of precision for each effect size. It is of course not possible to be certain that one has completely removed error from any measurement, or for that matter, to do so in an analysis of measures from independent trials. As Young noted, there are uncontrolled measurement errors or artefacts that necessitate the use of a control group and the randomised controlled trial design.
...
The calculation of a weighted effect size by using the inverse of each within-subjects variance is more precise than a sample-size weighted average (9), contrary to the Waldman’s assertion."

When, of course, his assertion is that their estimates may be precise but are biased:

"In each case, Kirsch chose a method which, under strong assumptions, gives an efficient and unbiased estimate of the true overall average benefit. In each case there are alternative approaches which are less efficient under those assumptions but which are unbiased not only when the Kirsch et al estimates are unbiased, but also for many cases in which the Kirsch et al estimates are biased. That is they are less efficient under the null but more robust. In each case the null hypothesis that the Kirsch et al estimator is unbiased has been tested and overwhelmingly rejected. The available unbiased estimate of the overall average benefit of NDA’s is equal to 2.65 HRSD units, which is considerably higher than Kirsch et al’s biased estimate."

* UPDATE
PJ Leonard replies to Huedo-Medina et al on PLoS Medicine.