Re: The gap in life expectancy from preventable physical illness in psychiatric patients in Western Australia: retrospective analysis of population based registers. David Lawrence, Kirsten J Hancock, Stephen Kisely. 346:doi:10.1136/bmj.f2539

We commend Lawrence et al’s article on excess mortality in people with mental disorders, which is timely in view of the release of findings from the Global Burden of Disease 2010 Study (GBD 2010). Mental and substance use disorders are estimated to be the leading cause of burden in the UK amongst persons aged 5 to 49 years. The majority of burden is explained by time spent in ill-health; only 5% is attributed to premature mortality[1], which may lead to the mis-interpretation of summary findings that mental disorders have little impact on death.

Despite the enormous effort that went into GBD 2010, there are important limitations. In GBD calculations each death must be attributed to a single cause. Vital records, from where most data was drawn, identify the condition most directly related to loss of life. For example, in the UK, this is ischaemic heart disease (IHD), lung cancer and stroke. Deaths where other disorders, such as mental disorders, contribute are largely overlooked and the implication of this is that premature mortality in those with mental disorders was likely to have been underestimated in GBD 2010. As such, the low mortality estimates attributed to mental disorders in GBD 2010 cannot be interpreted as providing grounds to allocate a low policy priority to, not only the psychological health, but also the physical health of people with mental illness.

A person with a severe mental disorder can expect to live 10 to 20 years less than a person without a mental disorder and the life expectancy gap is increasing[2,3]. In the UK adults with a severe mental disorder are three times more likely than the general population to die of IHD and up to 80% more likely to die of stroke[4]. The relationship between mental disorders and increased deaths due to chronic disease is complex.

Major modifiable risk factors for chronic disease, such as smoking, poor diet and physical inactivity, are overrepresented, yet more tolerated, in people with mental disorders. This is despite the availability of programs to address modifiable risk factors, for instance smoking cessation[5]. In addition to unhealthy behaviours, mental disorders are in their own right considered an independent risk factor for diseases such as CHD[6,7].

Inequalities in access to and use of health services are well documented in people with mental disorders[8]. Physical health issues are overshadowed by the presence of mental disorders as health service providers may attribute symptoms of physical illness to the co-occurring mental disorder and associated medications. Evidence shows that those with mental disorders receive lower than average prescriptions for CVD[9] and are less likely to receive usual procedures[10]. In the same issue of the journal, the editor[3] points out that the continuing life expectancy gap in persons with mental disorders is a clear example of discrimination and lack of parity between this portion of the population and the community in general.

Whilst summary measures of disease burden have been important in recognising the impact of impaired health as well as premature death, the limitations of a single metric mean these alone cannot provide the information needed to develop effective health policies[11]. The Royal College of Psychiatrists[5] has, for example, provided comprehensive information making the case for parity between mental and physical disorders in policy, commissioning and service delivery, including in responding to premature mortality (see http://www.rcpsych.ac.uk/files/pdfversion/OP88xx.pdf).

There are effective interventions for CVD and other chronic disease which will improve outcomes in people with mental disorders[9,10]. Public health agencies and service providers need to take a decisive approach to integrating mental and physical health care. Beyond broad promises to ‘address’ the issue, health providers require integrated models of care to a) provide usual treatments for physical health problems in those with mental disorders, and b) ensure programs for risky behaviours such as smoking are in place that target the mentally ill and socially excluded. Our group is currently conducting a systematic review of interventions in people with mental disorders to prevent premature mortality. Although many effective interventions exist, their relative merits and effect sizes need to be investigated. Integrated treatment programs may be the best approach to reducing the life expectancy gap reported by Lawrence et al, and these deserve further investigation so that decision-makers can integrate best knowledge into policy and service planning.

References

1. Murray CJL, Richards MA, Newton JN, Fenton KA, Anderson HR, Atkinson C, et al. UK health performance: findings of the Global Burden of Disease Study 2010. The Lancet 2013;381(9871):997-1020.
2. Lawrence D, Hancock KJ, Kisely S. The gap in life expectancy from preventable physical illness in psychiatric patients in Western Australia: retrospective analysis of population based registers. Br. Med. J. 2013;346.
3. Thornicroft G. Premature death among people with mental illness: At best a failure to act on evidence; at worst a form of lethal discrimination. British Medicial Journal 2013;346.
4. Osborn DPJ, Nazareth I, King MB. Risk for coronary heart disease in people with severe mental illness: Cross-sectional comparative study in primary care. The British Journal of Psychiatry 2006;188(3):271-77.
5. Bailey S, Thorpe L, Smith G. Whole-person care: from rhetoric to reality. Achieving parity between mental and physical health. UK: Royal College of Psychiatrists, 2013.
6. Charlson FJ, Stapelberg NJC, Baxter AJ, Whiteford HA. Should global burden of disease estimates include depression as a risk factor for coronary heart disease? BMC Medicine 2011 3(9):47.
7. Baxter AJ, Charlson FJ, Somerville AJ, Whiteford HA. Mental disorders as risk factors: assessing the evidence for the Global Burden of Disease Study. BMC Medicine 2011;9:134.
8. Brugha TS, Wing JK, Smith BL. Physical health of the long-term mentally ill in the community. Is there unmet need? . Br. J. Psychiatry 1989;155:777-81.
9. Mitchell AJ, Lord O. Do deficits in cardiac care influence high mortality rates in schizophrenia? A systematic review and pooled analysis. J. Psychopharmacol. (Oxf). 2010;24:69-80.
10. Mitchell AJ, Lawrence D. Revascularisation and mortality rates following acute coronary syndromes in people with severe mental illness: comparative meta-analysis. The British Journal of Psychiatry 2011;198:434-41.
11. Watts C, Cairncross S. Should the GBD risk factor rankings be used to guide policy? The Lancet 2012;380(9859):2060-61.

Competing interests: None declared

Re: Poor uptake of hepatitis B vaccine in India has several causes, study finds. Cheryl Travasso. 346:doi:10.1136/bmj.f3596

As it is found in the study done by Lahariya et al, the coverage of Hepatitis B vaccination is poor in India. Additionally some basic issues related to HB vaccine need to be clarified before uptake improves.

Doctors and the public perceive that hepatitis B is not a major threat in India. Prevalence of Hepatitis B in Indian population varies from 2-4% in non-tribal and 15.9% in tribal populations (1). Meta-analysis of small studies in India estimates carrier rate at 1.7%. According to ORGI 1991, jaundice was associated with 1% of all cause deaths and deaths due to chronic liver cancer was 0.76% including death from both Hepatitis B & C. Therefore, Hepatitis B & C is a relatively low priority disease for mass vaccination.

The carrier rate in a country is not important in itself, because with some strains, there is a higher chance of becoming an asymptomatic carrier and the infected come to no harm. The vast majority of chronic carriers are completely asymptomatic all their lives (2). A detailed review on the different strains in different countries was done by Norder et al (3). Strains C and D have a greater chance than strain A and B for vertical transmission, increased duration of HBe positive status and increased progression to liver fibrosis and HCC. Modelling without reference to the local strain is an exercise in futility. The cost benefit assessment of Hepatitis B (4) uses the Hepatitis B disease progression rates from Taiwan and comes up with predictions that are not valid for India.

The draft National Policy on immunisation recommended a pragmatic HBV vaccination schedule starting at birth for institutional deliveries and at 6 weeks for the rest. Janani Suraksha Yojana under NRHM has led to a huge increase in institutional deliveries within just four years, the number of beneficiaries rising from 7.39 lakhs per year in 2005-06 to about 1 crore in 2009-10 (5). Yet the majority of births do not take place in institutions and hospitals where Hepatitis B vaccine is stored and given to newborns. Most children receive the vaccine starting only at 6 weeks.

In fact an extensive search of world literature has not shown even one study where immunization starting at 6 weeks in the community has brought down carrier rate of Hepatitis B (6). Also, one third of adult asymptomatic carriers are found to be due to vertical transmission (7). It is time to consider birth dose of Hepatitis B vaccination in UIP with more seriousness. Otherwise it appears we are giving the vaccine merely to comply with a WHO dictate to introduce the vaccine, not to reduce the problem of hepatitis B carrier state.

The question of selective immunization is not impractical (8). Universal testing of HBsAg status of pregnant primiparous mother any time during the 9 months of their pregnancy can be carried out and it can be ensured that babies of the 2% HBsAg carrier mothers get vaccinated at birth. Subsequent pregnancy needs no testing. Selective vaccination of high risk groups (medical, paramedical staff, blood donors, sex workers, soldiers) and selective vaccination of children born to Hepatitis B carrier mothers would be more cost effective. The first dose must be given at birth, as evidence shows that it is most effective in stopping Hepatitis B transmission from mother to child (2).

Thus we should first of all understand whether universal hepatitis B vaccination is really needed in India based on actual facts as mentioned above. If it is needed this data and science needs to be presented. Just providing managerial tips may not be enough to improve vaccine coverage.

Bibliography:
1. Batham A, Narula D, Toteja T, Sreenivas V, Puliyel JM. Sytematic review and meta-analysis of prevalence of hepatitis B in India. Indian Pediatr. 2007 Sep;44(9):663–74.
2. ICMR - Minutes Expert Group Hepatitis B and Hib vaccines. http://www.icmr.nic.in/minutes/Minutes%20Expert%20Group%20%20Hepatitis%2...
3. Norder H, Couroucé A-M, Coursaget P, Echevarria JM, Lee S-D, Mushahwar IK, et al. Genetic diversity of hepatitis B virus strains derived worldwide: genotypes, subgenotypes, and HBsAg subtypes. Intervirology. 2004;47(6):289–309.
4. Aggarwal R, Ghoshal UC, Naik SR. Assessment of cost-effectiveness of universal hepatitis B immunization in a low-income country with intermediate endemicity using a Markov model. J. Hepatol. 2003 Feb;38(2):215–22.
5. 9457038092AnnualReporthealth.pdf [Internet]. [cited 2013 Jun 9]. Available from: http://mohfw.nic.in/WriteReadData/l892s/9457038092AnnualReporthealth.pdf
6. Puliyel JM, Rastogi P, Mathew JL. Hepatitis B in India: Systematic review & report of the “IMA sub-committee on immunization.”Indian J. Med. Res. 2008 May;127(5):494–7
7. Nayak NC, Panda SK, Zuckerman AJ, Bhan MK, Guha DK. Dynamics and impact of perinatal transmission of hepatitis B virus in North India. J. Med. Virol. 1987 Feb;21(2):137–45.
8. Sahni M, Jindal K, Abraham N, Aruldas K, Puliyel JM. Hepatitis B immunization: cost calculation in a community-based study in India. Indian J Gastroenterol. 2004 Feb;23(1):16–8

Competing interests: None declared

Re: Consultants’ contracts: could do better. Des Spence. 346:doi:10.1136/bmj.f3701

I am using this portal not to knock our colleagues as those I speak to seem to be having a bad enough time without GP criticism.

However, Des Spence's articles used to be more focused on non-evidenced medicine.

Recently while doing postnatal maternal checks (? value of this) I noted that a baby was one of the epidemic we have in this area for having a tongue tie operation. On the day of the snip there were 10 other babies awaiting the proceedure. This is in a local small DGH where we have now a few enthusiasts for this as an aid to breast feeding and prevention of speech defects. Hard to find evidence for it, and until 3 years or so ago it was a once in a blue moon procedure. PCT, sorry CCG, seems to be happy paying as not on the LPP (low priority procedure) list. Am I out of date? Des, please help.

Competing interests: None declared

Re: Campaigners criticise report into Camelford water poisoning. Jacqui Wise. 346:doi:10.1136/bmj.f3376

In your recent News Report on the publication of the Final Report of the Committee on Toxicity of Chemicals (CoT) [1] you should be aware that criticism of this document is not confined to ‘campaigners’. Peter Smith and I served as Local Representatives on the Lowermoor Sub-Group (LSG) of CoT, appointed by Lord Tyler and Secretary of State Michael Meacher in 2001. We resigned in October last year, refusing to be associated with the proposed Final Report.

The original Draft, published for public consultation in 2005, was severely criticised by a large number of specialists in the field of aluminium toxicology. Much of that criticism has not been, and indeed can not now be addressed under the LSG’s Terms of Reference, nor by modification of the methodology adopted for the study. Since many of these defects persist unresolved in the LSG’s Final Report, most of that expert criticism remains valid. So the Report's misrepresentation of the extent of expert concern raises serious questions regarding its reliability.

The CoT’s web site provides direct electronic access to the latest documents [2]. However, the manner in which the contents of that Report are presented for access is highly misleading. Appendix 5 contains comments on the 2005 Draft, but the links to it on the web page direct readers only to four minor and anodyne letters. Appendix 6, the LSG’s response to comments on the Draft, consists of a mere three pages, in which almost all criticism is either summarily dismissed or else ignored.

This gives the impression that there was little adverse criticism of the Draft, and that even that has been fully resolved. The Final Report now appears to present a consensus on the health effects of the incident, whereas careful examination of the Main Report itself leads to a different conclusion.

In April 2005, Dr. (now Professor) Christopher Exley, at Keele University, a recognised world authority on aluminium ecotoxicology, submitted a devastating analysis of the in-built defects of the Draft, and BMJ published a similar statement by him, co-signed by 58 of his international colleagues [3]. This and feedback from others revealed considerable concern within the scientific and medical communities at the deflection of Meacher’s study into a politically unthreatening ‘risk assessment, when it should have been a far more incisive and pro-active field investigation of the incident.

Yet this crucial peer-reviewed commentary is now hidden from the public gaze. It occupies 95 unnumbered pages within the weighty Lowermoor Water Pollution Incident - Report. (pages 341 to 436 of the PDF file). In stark contrast to the prominent links on the web site to the relatively trivial Appendix 5 letters, and to the derisory Appendix 6 rebuff of criticism, there is no indication to the serious reader on the web page that a great deal more expert and decidedly adverse comment actually exists, It appears that a deliberate attempt has been made to conceal derision for the study amongst world experts in aluminium toxicology.

From the start, intense political opposition has been evident within the Department of Health (DoH) to any detailed investigation of the medical impacts of this incident, only 18 months before the planned privatisation of the water sector.The role of South West Water Authority (SWWA) has been fully established in the courts. In the inquest into my wife’s death in 2004, evidence by Profs. Exley and Esiri [4] raised very serious concerns over the DoH’s persistent denial that long-term effects were possible, yet this irrational conclusion reappears in the LSG Final Report, despite clear indications of the unreliability of that claim.

The sustained attempts by the DoH to prevent investigation of its own actions have resulted in serious miscarriages of justice, demanding a thorough and independent formal inquiry. By preventing the dispatch of an emergency Incident Control Team from the National Poisons Information Service at Guys Hospital during the incident [5] the DoH directly obstructed access to essential contemporary forensic evidence during subsequent legal proceedings

Then, in 2001 the DoH manipulated the study’s Terms of Reference to prevent the LSG examining its own role in the incident, and the absence of any member with recognised expertise in aluminium ecotoxicology has been remarked upon by a number of specialists in this field. Instead the study has been comfortably converted to the meaningless ‘risk assessment’ that has now been released by CoT.

So in response to your article on this Report, those most deeply concerned over the conclusions of this parody of incident investigation are not simply ‘campaigners’. We are professional scientists who are experienced in investigating environmental incidents and plans that have posed, or are likely to pose, serious harm to the public. We view with alarm and concern the travesty of scientific methodology that has been employed to compile this Report and present it to the public.

It does not, and it can not, replace a directly targeted forensic examination in which evidence is collected to a standard that is acceptable in legal proceedings. It is insulting to offer, after 25 years of apparent indifference, an irrelevant and highly flawed amateur risk assessment to the 20,000 people who were caught up in this terrifying incident. The Report depends on an inexpert assessment of mainly unvalidated anecdotal evidence and largely irrelevant published literature, instead of presenting the results of an active attempt to verify what the effects of this unique event really were. The DoH must be called to immediate account for its cynical and unethical mismanagement of the medical sector’s response to one of one of the greatest scandals in British public health history.

Douglas Cross, CSci. CBiol. FSB

References
1. Campaigners criticise report into Camelford water poisoning. BMJ 2013;346:f3376 23rd May 2013
Available at http://www.bmj.com/content/346/bmj.f3376
2. Available at http://cot.food.gov.uk/cotwg/lowermoorsub/draftlowermoorreport/
3. Exley et al. Inquiry questions long term effects on health of Camelford incident.
Available at http://www.bmj.com/rapid-response/2011/10/30/aluminium-and-camelford
4. Exley C, Esiri MM (2006).Severe cerebral congophilic angiopathy coincident with increased brain aluminium in a resident of Camelford, Cornwall, UK. J Neurol Neurosurg Psychiatry. 2006 Jul;77(7):877-9. Epub 2006 Apr 20. Available at http://www.ncbi.nlm.nih.gov/pubmed/16627535
5. Sigmund E. Inquiry questions long term effects on health of Camelford incident. Available at http://www.bmj.com/rapid-response/2011/10/30/handling-camelford-incident...

Competing interests: I was employed as Deputy Fisheries Officer by the Cornwall River Authority, a precursor to SWWA, between 1966 and 1968. I was a resident of Camelford, North Cornwall, from 1980 to 1989, and worked with local GP Dr. Richard Newman, and other professional scientists collecting data on the impacts of the incident. My wife developed a rapidly fatal early-onset undiagnosed form of dementia in late 2002, and died in February 2004. I arranged for post mortem brain samples to be provided to Profs. Exley and Esiri for detailed examination. I have assisted a number of other families to donate brain tissues from deceased members for analysis. I served as a Local Representative of the LSG from 2002 to 2012, until resigning in October last year.