This page lists correspondence with the National Institute for Health and Clinical Excellence. On 3 December 2012 BMJ editor in chief Dr Fiona Godlee wrote to NICE's chair, Professor Sir Michael Rawlins. In her letter she says: "Now that serious doubts have been raised about the evidence behind claims for oseltamivir’s effectiveness and safety, I am asking you to withdraw approval for oseltamivir until NICE has received and reviewed the full clinical trial data and those anonymised data are available for independent scrutiny."
All rapid responses
Reducing what should be a sensitive discussion about death to a ‘tick-box exercise’ is wrong; in this case, in a survey as part of the unplanned admissions enhanced service, which intends to save the NHS money by decreasing hospital admissions. However, discussions about death are crucial in ensuring we give the best care to patients. As underwritten in GMC guidance, where CPR will not be successful “making and recording an advance decision not to attempt CPR will help to ensure that the patient dies in a dignified and peaceful manner”. In the Telegraph article, Peter Carter justly states that such sensitive questions should be asked by those who have already developed a trusting relationship with patients. However, in the modern healthcare system this is not always possible.
On medical admissions wards it is often necessary to discuss and make DNACRP decisions, despite not having a pre-existing relationship with the patient. It is therefore particularly tempting to brush the subject under the carpet due to fear of the reaction from patients and relatives (something not helped by the aforementioned article). However in my (though limited) experience as a junior doctor, when approached sensitively, the majority of patients and relatives greatly appreciate being involved in this decision, regardless of whether they have met you before. This is far better for patient care than side-stepping the issue until it is too late.
In summary: it is not feasible to expect that this subject will always be broached by a healthcare professional who already knows the patient, but ultimately with good communication skills, sensitivity and the best interests of the patient at the centre of the decision, it is still a good thing to talk about death.
As a consequence of the increasing number and urbanisation of the world’s population it is estimated that the number of people affected by natural disasters will rise from the current 250 million people per year to 375 million by the year 2015 . Individuals most affected tend to be from poor communities in developing countries, with poverty being the single most important factor in determining vulnerability . Upon this back drop of increasing need there are very few organisations that can assist individuals who feel that they would like to offer their help. Many of the well-known charitable relief organisations require a lengthy time commitment and most consultants working for the NHS are unable to offer this.
I have launched a charity ‘FaceFacts’ (Scottish Charity number SC 042622), one of the aims of which is to help individuals donate short periods of time to working abroad in the developing world. The voluntary work may be as part of a team mobilised for disaster relief or may be more formally arranged educational/operating visits.
The charity also aims to share knowledge and skills with oral and maxillofacial surgeons across the world. As well as organising overseas visits the charity would also encourage foreign surgeons to come on funded observerships to units within the UK.
All volunteers would provide their time gratis and trips would usually last only one or two weeks at a time. If there are any maxillofacial colleagues who would like to donate either time or money to help or register for emergency disaster relief then please contact me at email@example.com.
2. Redmond AD. Natural disasters. BMJ 2005 May 28; 330:1259–61
We appreciate the comments from Drs Panei and Paola, hereafter referred to as PP, on our study published in BMJ.1 Our study (which was not sponsored by pharmaceutical industry) aimed to explore suicidal behavior as a potential adverse effect of ADHD medication. The main conclusion of our study was that no evidence was found for an increased rate of suicide-related events (suicide attempt/completed suicide) associated with the use of ADHD medication. We also observed a protective effect of psycho-stimulants on suicidal behavior. Issues concerning drug efficacy and other adverse effects of pharmacotherapy, though critical, are beyond the scope of our research question. We now take this opportunity to clarify some major points misunderstood by PP.
PP express strong suspicions against our observational (i.e. non-randomized) study design and statistical analysis. They state that “What we need are results from well-designed systematic reviews based on good quality clinical trials addressing the multiple social and familial factors responsible for ADHD”. We agree that randomized clinical trials are ideal for examining treatment efficacy and for establishing causality. However, clinical trials are often not practical for investigating such association for the following reasons. First, although it is possible to examine treatment-emergent suicidal ideation in clinical trials, any study participants with notable suicidal ideation should be provided acute intervention or be excluded from the trial due to ethical concerns. Accordingly, suicide attempt and completed suicide are unlikely to be observed thereafter. Second, since clinical trials are limited in sample size, duration of follow-up and patient compliance, they are not feasible for studying rare events as suicidal behavior. Thus, we find PP’s suggestion to discard observational studies unreasonably rigid.
PP state that “Second, the study by Chen et al. has major statistical limitations. … they used a complex Cox regression model splitting the population into thousands of groups using each patient as their own control”. PP gives three arguments as to why our “within-analysis” would be problematic. First, they argue that we are “presumably dangerously limiting [our] fragmented analysis to patients who will never attempt suicide…” This is mathematically, wrong. Rather, it is the other way around; the within-analysis is limited to those patients who attempt suicide at least once during follow-up. This is intuitively reasonable; we cannot compare the rate of suicide attempt during medicated and non-medicated periods in those patients who never make suicide attempts. Also, this is not a limitation, since those who never make suicide attempts (even if medicated) do obviously not need to worry about the elevated risk during medication. Second, PP argue that “In real life, because children differ in construct skills their decisions could reflect unpredictable cognitive and emotional patterns, determining complex interrelated variables that are difficult to analyze within each patient.” We interpret this as sentence as expressing a worry for unmeasured time-varying confounding. We agree with PP in this aspect, but note that the potential for unmeasured time-varying confounding can not be ruled out by any statistical method that we are aware of. We also note that we mentioned the potential for unmeasured time-varying confounding in the Discussion of our paper. Third, PP state that our design/analysis “fails to give readers the simple statistical measures, such as odds ratios (proportions), number needed to treat and number needed to harm”. We don’t agree that an odds ratio is a simpler or more transparent measure of association than a hazard ratio. But we do agree that number need to treat/harm is a more clinically useful measure than both hazard ratios and odds ratios. However, these measures cannot (as for as we know) be obtained from a within-analysis. They can be obtained from a more standard “between-analysis”, but such analysis would not automatically adjust for all (measured and unmeasured) time-stationary confounders, as the within-analysis does. Therefore, since we share PP’s concern about confounding, we chose to “sacrifice” the number needed to treat/harm, to be able to make an extensive confounding adjustment.
PP claim that there is a “the known association between medications prescribed for patients with ADHD and risk of concomitant suicidal behavior”. However, the references that PP give to support this claim 2 3 focused only on a positive relationship between use of atomoxetine and treatment-emergent suicidal ideation. The author of the meta-analysis did not draw any conclusion on suicidal behavior because only one suicide attempt and no completed suicide was observed in the clinical placebo-controlled trials which the meta-analysis was based on. Moreover, a recent update of this meta-analysis demonstrated no significant association between the use of atomoxetine and suicidal ideation, and still no more than 1 case of suicidal behavior was documented after 9 years of the FDA warning.4 Therefore, the “known association” for suicidal behavior referred to by PP was actually unknown, and even the associations for suicidal ideation varied from time to time. This is a good example of why clinical trials are not practical for examining potential treatment-emergent suicidal behavior.
PP also mentioned the negative attitude of parents of children with ADHD towards non-pharmacological interventions of ADHD in Italy. This might reflect inadequate instruction and counseling of parents on the management of the disorder. In addition, better evidence is needed for the efficacy of non-pharmacological interventions.5
We did observe a protective effect of psycho-stimulant on suicidal behavior, which makes a harmful effect of psycho-stimulants on suicidal behavior seem even less likely. A protective effect of psycho-stimulant is possible because dysfunction of impulse control resulted from imbalance of serotonergic system has been involved in the pathophysiology of both ADHD and suicidal behavior.6-8 Medications improving symptoms of impulse control might be beneficial for patients with ADHD who are also at increased risk of suicidal behavior, which is worthy of future investigation.
Finally, we agree with PP that well-designed research is needed to fully understand the benefits and risks associated with treatment for ADHD among both children and adults. Recommendations and guidelines for both pharmacological and non-pharmacological interventions should be evidence based.
1. Chen Q, Sjolander A, Runeson B, D'Onofrio BM, Lichtenstein P, Larsson H. Drug treatment for attention-deficit/hyperactivity disorder and suicidal behaviour: register based study. Bmj 2014;348:g3769.
2. Food and Drug Administration. Public health advisory: suicidal thinking in children and adolescents being treated with Strattera (atomoxetine), 2005.
3. Bangs ME, Tauscher-Wisniewski S, Polzer J, Zhang S, Acharya N, Desaiah D, et al. Meta-analysis of suicide-related behavior events in patients treated with atomoxetine. Journal of the American Academy of Child and Adolescent Psychiatry 2008;47:209-18.
4. Bangs ME, Wietecha LA, Wang S, Buchanan AS, Kelsey DK. Meta-Analysis of Suicide-Related Behavior or Ideation in Child, Adolescent, and Adult Patients Treated with Atomoxetine. Journal of child and adolescent psychopharmacology 2014.
5. Sonuga-Barke EJ, Brandeis D, Cortese S, Daley D, Ferrin M, Holtmann M, et al. Nonpharmacological interventions for ADHD: systematic review and meta-analyses of randomized controlled trials of dietary and psychological treatments. The American journal of psychiatry 2013;170:275-89.
6. Asberg M, Traskman L, Thoren P. 5-HIAA in the cerebrospinal fluid. A biochemical suicide predictor? Archives of general psychiatry 1976;33:1193-7.
7. Banaschewski T, Becker K, Scherag S, Franke B, Coghill D. Molecular genetics of attention-deficit/hyperactivity disorder: an overview. European child & adolescent psychiatry 2010;19:237-57.
8. Nordstrom P, Samuelsson M, Asberg M, Traskman-Bendz L, Aberg-Wistedt A, Nordin C, et al. CSF 5-HIAA predicts suicide risk after attempted suicide. Suicide & life-threatening behavior 1994;24:1-9.
Re: Commentary: Evidence versus influence in the WHO procedure for approving essential medicines: misoprostol for maternal health
Nowhere in our commentary do we refer to ‘corporate pharma lurking’, nor do we imply that pharma has put corporate pressure on researchers over misoprostol. On the contrary, Searle acted most responsibly in issuing safety warnings in 2000 about its use in pregnant women (1). These safety warnings were borne out in an independent review of the evidence which highlighted the risks and lack of evidence for misoprostol especially with respect to PPH published by the NEJM in 2001 (2,3,4). Weeks implies an ulterior motive or underlying reason for our opposition. This is not the case. Our opposition to the use of misoprostol for prevention of PPH is quite simply the absence of good evidence.
In 2011 we conducted a review of the evidence on misoprostol use in low resource settings of developing countries (5). Weeks' summary of this review is misleading. We identified weaknesses in all six studies reviewed including the four (6,7,8,9) which formed the basis of the decision by the WHO EML committee (10). We note that behind the facade of GDG’s ‘moderate’ quality grading of the evidence for the use of misoprostol by community or lay health workers are six studies graded as very-low quality (6, 7, 9, 11, 12, 13) and one RCT evaluated as moderate (8). The GDG itself noted (14) that the moderate-quality study “reported too few events related to the impact of misoprostol in severe health outcomes, including severe PPH” and therefore “firm conclusions cannot be drawn from this evidence.” (p.14) In addition, misoprostol was administered and deliveries attended by auxiliary nurse-midwives and the results might not be transferable to settings where skilled birth attendants are not available.
Our review concerned six of these studies (excluding a non-randomized cluster trial by Hashima) and our conclusions about the weaknesses of the evidence are in accord with the very-low quality grading by GDG (although we dispute the overall recommendation by GDG based on this evidence).The conclusion of our review prompted us to write to the WHO EML committee to ask for misoprostol to be deleted (10). Our analysis is new evidence, though not in the sense that Weeks means i.e. new clinical trials. The WHO EML committee had a responsibility to review it and to act consistently with their criteria for evidence.
Misoprostol came off patent in 2000, and despite the fact that there are now more than 20 pharmaceutical companies worldwide who are producing generic forms of the drug (15) we could find no evidence that this was driving the growing interest in its use for PPH, and this in combination with the lack of scientific evidence, drove us to try to understand what other influences, including research and programme funding, might be motivating its dissemination and distribution.
The social network analysis shows the considerable influence that charities, NGOs and researchers have exerted, despite the lack of good evidence; the progressive development of this network can be clearly seen in the chart in our commentary. The fact that more than 60,000 women have been recruited to numerous studies up until 2012 highlights how much money is going into the promotion of this drug and also how weak the evidence still is. This is not a good sign.
Philanthropic organisations such as Gates have played a major role in programmes which seek to reduce maternal mortality and targets for MDGs. But messianic zeal is no substitute for evidence and can be counter productive. We should not forget that those conducting and evaluating misoprostol research in low resource settings are subject to funders’ influences and in turn funders have their own programme targets to satisfy.
In summary, contrary to Weeks’ claims, there is not considerable evidence that in settings where oxytocin is unavailable, misoprostol is a safe and effective agent for reducing postpartum blood loss, rather the evidence is limited and of poor quality. Questions concerning the risks for women have not been resolved and the money spent on rolling out misoprostol might be better spent on the underlying causes such as malnutrition and anaemia, trained birth attendants and efforts to make oxytocin available. We continue to call upon the WHO EML committee to review the evidence we have put to them.
1. Chong. Y, Su. L, Arulkumaran. S, Misoprostol: a Quarter Century of Use, Abuse, and Creative Misuse. Obstetrical & Gynecological Survey. 2004: 59 (2): 128–40.
2. Goldberg. A B, Greenberg. M B, Darney. P D, Misoprostol and pregnancy. N Engl J Med 2001;344:38-47.
3. Hale. R W, Zinberg. S, Use of misoprostol in pregnancy. N Engl J Med 2001;344:59-60.
4. Friedman. M A, Manufacturer’s Warning Regarding Unapproved Uses of Misoprostol. N Engl J Med 2001; 344:61.
5. Chu CS, Brhlikova P, Pollock AM. Rethinking WHO guidance: review of evidence for misoprostol use in the prevention of postpartum haemorrhage. J R Soc Med 2012;105:336-47.
6. Walraven G, Blum J, Dampha Y, Sowe M, Morrison L, Winikoff B, et al. Misoprostol in the management of third stage labour in the home delivery setting in rural Gambia: a randomised controlled trial. Br J Obstet Gynaecol 2005;112:1277-83.
7. Høj L, Cardso P, Nielsen BB, Hvidman L, Nielsen J, Aaby P. Effect of sublingual misoprostol on severe postpartum hemorrhage in a primary health centre in Guinea-Bissau: a randomized double blind clinical trial. BMJ 2005;331:723.
8. Derman RJ, Kodkany BS, Goudar SS, Geller SE, Nail VA, Bellad MB et al. Oral misoprostol in preventing postpartum haemorrhage in resource-poor communities: a randomised controlled trial. Lancet 2006;368:1248-53.
9. Mobeen N, Durocher J, Zuberi NF, Jahan N, Blum J, Wasim S, et al. Administration of misoprostol by trained traditional birth attendants to prevent postpartum haemorrhage in homebirths in Pakistan: a randomised placebo-controlled trial. BJOG 2011;353-61.
10. WHO. Essential medicines selection. www.who.int/selection_medicines/committees/en/.
11. Chandhiok. N, Dhillon. B S, Datey. S, Mathur. A, Saxena. N C. Oral misoprostol for prevention of postpartum hemorrhage by paramedical workers in India. Int J Gynaecol Obstet. 2006 Feb. 92(2):170-5.
12. Prata N, Gessessew A, Abraha AK, Holston M, Potts M. Prevention of postpartum hemorrhage: options for home births in rural Ethiopia. Afr J Reprod Health. 2009 Jun;13(2):87-95.
13. Hashima EN, Nahar S, Al Mamun M, Afsana K, Byass P. Oral misoprostol for preventing postpartum haemorrhage in home births in rural Bangladesh: how effective is it? Glob Health Action. 2011, 4.
14 WHO recommendations for the prevention and treatment of postpartum haemorrhage. World Health Organization 2012 WHO/RHR/12.29
15. Fernandez MM, Coeytaux F, Gomez Ponce de León R, Harrison DL. Assessing the global availability of misoprostol. International Journal of Gynecology & Obstetrics. 2009;105(2):180–6.
I agree, evidence based medicine is a movement in crisis, and indeed EBM needs to be more usable for clinicians and patients as well.
In order to serve this goal, a more comprehensive approach to EBM is needed.
Therefore I should like to point out, that in the area of occupational therapy, physiotherapy and speech and language therapy a new model for establishing the value of evidence from multiple research approaches in a systematic review was prosposed.
By separating the evidence-level criteria of internal and external validity, by incorporating explicitly the evidence provided by qualitative studies, and by retaining the critical notion of rigor, a pyramidal evidence model emerges. This model, the Research Pyramid, aligns itself with the basic modes of clinical reasoning.
The Research Pyramid should yield a superior portrayal of evidence by providing quantitative-abstract and qualitative-dense and complex information about both efficacy and effectiveness of clinical interventions.
More information about the model ist presented in the attached figure and in the following publications:
 Tomlin, G., & Borgetto, B. (2011). Research Pyramid: A new evidence-based practice model for occupational therapy.
American Journal of Occupational Therapy, 65, 189–196. doi: 10.5014/ajot.2011.000828
 Pfingsten A, Trickes C, Max S, Borgetto B. Die Forschungspyramide: Ein Modell zur Bewertung der Evidenz durch Zusammenführung verschiedener Forschungsansätze in einem systematischen Review. pt_Zeitschrift für Physiotherapeuten 2011; 63:16-8.
In their discussion, Bech et al (1) state that the lack of association of antiepileptic drug use [during pregnancy] with spontaneous abortion "does not entirely exclude the possibility of a harmful effect of antiepileptic drugs on spontaneous abortion because antiepileptic drugs may decrease the risk of seizures in pregnant women with epilepsy, and seizures might be a stronger risk factor for spontaneous abortion than use of antiepileptic drugs".
This statement does not hold water because prevention of seizures will not lower the spontaneous abortion rate below that of the unexposed comparison group, whereas if antiepileptic drugs do increase the abortion risk, the rate will rise above that of the comparison group. In other words, regardless of their protective effect against seizures, if antiepileptic drugs truly increase the spontaneous abortion rate, this will not be masked (in an adequately powered study) by a reduction in the abortion rate mediated by better seizure protection.
1. Bech BH, Kjaersgaard MI, Pedersen HS, Howards PP, Sorensen MJ, Olsen J et al. Use of antiepileptic drugs during pregnancy and risk of spontaneous abortion and stillbirth: population based cohort study. BMJ 2014; 349: g5159.
Chittaranjan Andrade, M.D.
Professor and Head, Department of Psychopharmacology
National Institute of Mental Health and Neurosciences
Bangalore 560 029, India
Audit of three, independent, UK units delivering over 4000 women per annum in the past twelve months shows increases in postpartum haemorrhage rates (>1000 mls) of over 500% in the past decade (2003-2013). In 2003, such a unit might experience a massive PPH (>2000 mls) twice per year though is now having one of these events once a fortnight. Not only have PPH rates increased dramatically but they appear to be less predictable and unrelated to traditional risk factors.
Injured uteri, inexperienced clinical staff, and, increasing rates of induction of labour may all contribute to this increasing incidence of serious morbidity and mortality (1). Injuries to uterine nerves result from prolonged straining during defaecation (endemic in Western countries) and excessive traction to the cervix and uterosacral ligaments during surgical evacuation of the uterus in the second trimester (endemic in some developing countries). Whether “injured” uteri respond appropriately to ergometrine, oxytocin and prostaglandins is not known.
It is unlikely that these dramatic increases in the incidence of PPH in the UK result from genetic factors. Clustering of cases in Swedish families may result from similar diets and bowel habits though Oberg et al. do not report similar changes in incidence in Sweden (2) ? Whatever the reasons, obstetricians and haematologists need to be aware of any such changes in their clinical services and respond appropriately.
(1) Quinn MJ.
Postpartum hemorrhage and “injured” uteri.
AJOG 2014 Jun; 210(6):588.
(2) Oberg AS, Hernandéz-Diaź S, Frisell T, Greene MF, Almqvist C, Bateman BT,
Genetic contribution to postpartum haemorrhage in Swedish population: cohort study of 466 686 births.
Re: HPV vaccination. 1. True statistics? 2. Just needling? Where have all the health educators gone?
In response to Prue's article and Gupta (Indian Council of Medical Research, New Delhi), I asked in a rapid response, on 2 August:
1. Would Dr Gupta please give us figures in support of her claims of "universal" HPV vaccination?
2. Would Public Health England please tell us whether the GPs contracted to give HPV vaccine to children could also be required as part of the contract, to tell the children before vaccination, that anal sex is best avoided at least in their teens?
No answer from either party I addressed.
Dr Gupta may be on holidays. Could the ICMR please tell us if Dr Gupta is correct?
Public Health England, funded by the British tax-payers, please tell us your response to my question. Or, should I assume we assume that your contract writers forgot something? Or, should we assume that Health Education is unnecessary, the needle is the answer?
It was probably in my late thirties that I first noticed pain in one of my ears.
I assumed that it was probably one of those symptoms which would subside within a few days without treatment, but it persisted, and became gradually worse until it was intolerable.
I also considered the possibility that if I didn’t do something about it that it may lead to ear damage and deafness, so I consulted a doctor.
He examined my ear with an otoscope and said that he could see that a lump of ear wax was blocking the ear canal and that he would try to remove it.
He then placed a towel on my shoulder and filled a small kidney bowl with warm water and placed it close to my neck and under my ear.
He then filled an ear syringe with some of the water and put it’s tip into the opening of my ear and then began pushing the plunger to gently force the water into the outer auditory canal, and then withdrew the plunger to suck the water out again.
As he did that repeatedly I could hear the swishing and swirling sound of the water gushing in and out very clearly but it didn’t relieve the pain.
However he was able to extract some small pieces of ear wax which he emptied into the kidney bowl.
He then filled the syringe with clean water and repeated the process about six times.
During that procedure he told me that if he couldn’t remove the wax blockage he would give me some ear drops to use to gradually dissolve the wax and that I could return to have it removed later.
He was about to give up and provide me with the ear drops when he tried one more time and a few moments later I felt an immediate relief of the pain.
He said that the wax lump had came out into the syringe and had been ejected into the kidney bowl, and then he showed it to me.
It was an uneven shape perhaps three or more millimetres in total circumference.
He then syringed my ear again several times to clear out any other loose wax debris until the water was clear.
I asked him what caused the problem and he said he didn’t know.
I suppose another ten years went by when I began to feel a sense of pressure in one of my ears, and as the weeks went by it became more and more noticeable, and somewhat uncomfortable and annoying, so I began to drag on my ear lobe in an attempt to open my ear canal wider and clear it, and it was sometimes effective.
However I eventually experienced a reduction in my hearing from that ear, and I noticed that if someone was talking to me from one side I could hear them clearly, but if they were on the other side my hearing was muffled.
That problem persisted and was no longer responding to my attempts to clear the ear canal, so I consulted a doctor again.
He inspected my ear with an otoscope and said that the outer ear canal was blocked, so he arranged for a nurse to remove it by the same method which had been used a decade earlier.
The same process of gently plunging warm water into and out of my ear canal was applied and reapplied until I noticed an immediate ability to hear clearly again, and the nurse said that she had just ejected a lump of wax into the kidney bowl to show me.
She also re-syringed the ear several times to clear any remaining debris, and applied the same method to the other ear, but only small amounts of wax were found.
When I asked her if she knew the cause she said she didn’t, so I became curious about why it should affect me and not other individuals, and whether or not it would happen again.
I was told that it was a common problem of unknown cause.
Several more years went by when I had the same problem of discomfort and muffled hearing, and went through the process of having the wax extracted again, so, although it wasn’t a serious problem, I became even more curious about the cause for the purpose of developing a way of preventing a recurrence.
One day I had just had a shower, and a few minutes later felt some mild discomfort in my ear so I placed my small finger tip against the outer indentation of the ear canal and noticed that it was occupied by a quantity of water of perhaps two or three drops, and because of it’s location I could hear the squishing sound as I gently pressed on it.
I then considered the possibility that the soap or hair shampoo which I had been using previously while showering may have been getting into my ear, and staying there, instead of running outwards, and that the soap was dissolving very small amounts of wax each time, so that it drained through the ear canal to became deposited as an accumulating lump.
I then compared it to the way in which small amounts of water drain from the top of lime stone caves to gradually form stalactites or stalagmites over a period of years, decades, or centuries.
By comparison, the amount of wax being dissolved by three drops of soapy water during two showers a day, or 730 times a year, for several years, may be what causes the gradual build up of a wax lump in the ear until it was large enough to cause the blockage.
I don’t know if it will make any difference, but I now minimise the exposure of my ears to soapy water when having a shower, and check them after each shower, and if there is any moisture present I gently remove it by softly touching the area with a towel to absorb it.
I consider it to be worth trying because it is easy, and won’t do any harm, and might solve the problem.
No one has spoken out for the scandalous waste of resources by the government. The Czar should remember the fate of the Czar of All Russia.
The silence of the RCGP, the RCPsych, the BMA is testimony to the unwillingness of the medical profession to speak out against Authority. It wasn't ever thus.