Recent eLetters

Displaying 11-20 letters out of 337 published

  1. Niall Dickson, Chief Executive of the General Medical Council

    Anyone who has been the subject of an investigation in any profession will testify to the stress and anxiety that it engenders. This was underlined in the study by Bourne et al in BMJ Open, which looked at the responses from nearly 8000 doctors who had been investigated by various organisations, the vast majority by local NHS bodies.

    Unsurprisingly the study found that among the 374 doctors who responded to the survey who had been referred to the GMC (1), levels of stress were higher - a referral to the national regulator is often more serious and, of course, carries with it the additional (albeit extremely small) risk that their livelihood could be taken away.

    Some distress is therefore inevitable, but the onus is on us to do whatever we can to reduce the fear and upset doctors experience, without in any way compromising our duty to investigate thoroughly in order to protect patient safety. This has become even more important in recent years as the number of doctors referred to the GMC has risen year after year - we saw a 64% rise between 2010 and 2013. (2) It is of course part of a wider trend which has seen big increases in complaints against health, and indeed other professionals, not just in this country but around the world. (3) But it does merit a response.

    Most of the complaints we receive are closed without a doctor ever facing action and only a small proportion lead to a sanction. (4) The increase in referrals though, makes it more important than ever that we resolve complaints as quickly as possible, sorting out those which are serious and which need our attention, explain our processes and decisions clearly and provide support for doctors during what will always be a very difficult time.

    That is why, over the last few years, we have committed ourselves to fundamental reform of our procedures with the aims of doing everything we can to demonstrate the system is fair, speed up the process at every stage and provide support in various ways for both doctors and patients who find themselves involved in our investigations.

    As a result, we established the autonomous Medical Practitioners Tribunal Service (MPTS) in 2012 under the leadership of a former deputy High Court judge which is now responsible for all the hearings and is separate from the GMC's investigation arm.(5)

    The new service has already cut the time lost to legal argument at this stage and, subject to parliamentary approval of changes of the Medical Act, will soon have more powers to prevent delays. (6) It has also begun to offer more support to unrepresented doctors. (7)

    Since 2012 the GMC itself has funded a confidential advice service run by the BMA which provides emotional support for any doctor who is being investigated by us. The response to the Doctors for Doctors service has been overwhelmingly positive and an independent evaluation which we will be publishing soon found that the service delivered real benefits to the doctors who used it. As one doctor noted:

    'It helped more than I could ever have imagined.'

    We have had a similar reaction to another key reform in this area. We have begun to pilot meetings with doctors towards the end of our investigations with the aim of seeing if we can we can agree a resolution that will protect the public and the reputation of the profession, but which could avoid the need for a hearing altogether. (8) This has the dual advantage of speeding up the process and reducing the stress for all involved. Under the current law we can only do this with some cases (the most serious must go to a hearing) but again the response has been extremely positive.

    Alongside these changes, we have been improving the tone of our communications with doctors - we need to make sure everything we send out is clear, straightforward and sensitive. We have been working with doctors who have been through our procedures and we are acting on this feedback (9) not least in updating doctors about the progress of our investigation.

    We have also revolutionised the way we engage at a local level, communicating with employers and doctors through face-to-face meetings and not just via correspondence. Our Employer Liaison Service (ELS) in particular has created strong links with employers and now supports Responsible Officers in managing concerns locally, helping to make sure that doctors are only referred to us when it is necessary.

    The Bourne study suggests that complaints may foster defensive medicine that is not in the interests of patients - clearly anyone who has been referred to the GMC may be more cautious while the issue is being investigated, but as the Chair of the GMC Professor Terence Stephenson indicated in his response to the Health Select Committee earlier this month, medicine has perhaps become more defensive and this is likely to have been caused more by fear of litigation, complaints to employers and being vilified, often unfairly, in the media, rather than fear of being referred to the GMC. (10)

    Most serious complaints that are upheld in our procedures are about conduct and health, rather than clinical decisions (11) and it is worth remembering that we will only take action when there have been serious or persistent breaches to our guidance - the vast majority of one off clinical mistakes are not matters we will pursue.

    So there is much we have done and there is much still for us still to do in this area - for example we have agreed to undertake a comprehensive review of how we handle vulnerable doctors following the report we commissioned into doctors who commit suicide in our procedures. (12)

    At the same time, creating a quick and simple complaints process that puts patients first, and is fair to those who are complained about, must be a matter for the health system as a whole. It is not something that professional regulation can achieve alone, indeed as the BMJ Open paper acknowledges, we are just one part of a much larger picture.


    1 Bourne T, Wynants L, Peters M, et al. The impact of complaints procedures on the welfare, health and clinical practise of 7926 doctors in the UK: a cross-sectional survey. BMJ Open 2014;4:e006687. doi:10.1136/bmjopen-2014-006687

    2 GMC: The State of Medical Education and Practice in the UK 2014 pp64

    3 GMC: The State of Medical Education and Practice in the UK 2013 pp44

    4 GMC: The State of Medical Education and Practice in the UK 2014 pp63

    5 The Medical Practitioners Tribunal Service (MPTS) website

    6 Department of Health Consultation Response report - January 2015.

    7 Medical Practitioners Tribunal Service (MPTS) information for unrepresented doctors:

    8 GMC Resolving complaints about doctors faster pilot leaflet

    9 GMC report: Exploring the experience of doctors and complainants who have been through the GMC's complaints and fitness to practise procedures

    10 GMC Annual Accountability Hearing, Health Select Committee, January 6, 2015

    11 GMC: The State of Medical Education and Practice in the UK 2014 pp 70

    12 Report commissioned by the GMC: Doctors who commit suicide while under GMC fitness to practise investigations, December 2014

    Conflict of Interest:

    None declared

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  2. GMC overinvestigation and poor handling of sick doctors

    Dear Authors, Congratulations for the great work. For a long time, doctors have been put in the dock for minor offences, including some non-offences, like illnesses mostly mental health and alcohol etc substance misuse related.

    The procedures applied by the GMC, after a complaint, Interim conditions or suspensions are placed by the panels, which convene upto six times in the first eighteen months period. At the end of this period, many doctors are being offered 'Voluntary Undertakings'(most doctors do not refuse for fear of referral to the Fitness To Practice). This pathways is highly questionable on moral and ethical grounds, as the doctor is persuaded to accept when there has been no findings of fact made against him.

    If and when the conditions and Undertakings make the doctor unemployable, the deskilled doctor cannot find support for retraining.

    Warnings by the GMC for minor dismeanours are affecting career and work prospects of doctors, which in some cases cause irreversible damage.

    The GMC has to use Occupational health procedures in sick doctors affairs instead of using the Fitness To Practice procedures, which are causing untold suffering and in some tragic cases, deaths.

    The deaths are only a tip of the iceberg, as most of the damage cannot be quantified, as it is manifested in loss of work of the doctors, emigration, burnout, early retirement.

    There needs steps taken by the Government to stem this unnecessary steady erosion of morale and the work force. I suggest

    1. A work force and planning body, independent of the NHS and the GMC 2. GMC to assess the impact of the procedures, more thoroughly, especially on the subgroups of Mentally/physically ill doctors and Ethnic and foreign gradute doctors 3. Use Occupational health supportive route in the sick/vulnerable doctors instead of the disciplinary route. 4. GMC to give 'advisory' letters instead of 'warnings'. 5. Government,NHS and the GMC to launch a fund for retraining of the deskilled doctors. 6. Fitness To Practice procedures to be used only in exceptional circumstances, unlike now. 7. Investigation into the lack of legal representation in upto half of the GMC hearings. 8. Making the GMC procedures accountable with compensation for the loss of earnings and careers of the doctors who are exonerated after prolonged, in some cases upto half a decade or more.

    Conflict of Interest:

    Been through the GMC procedures.

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  3. Re:CCBT for depression in adolescents

    We agree with Dr Dubicka and colleagues (2015) that the study of computerized CBT (cCBT) is to be welcomed especially to test treatments for those unable or reluctant to attend clinics or face to face therapies. Further research is also important to elucidate whether cCBT is a more cost effective alternative and explore its contribution at different points in the care pathway. We mistakenly described their study as randomising between 'medication and treatment as usual' and not 'medication and medication + CBT' and we apologise for this. As is often the case in studies of this nature clarity of treatment arms is often very difficult to achieve. For example, those in the medication arm of their study received psychosocial interventions including problem solving and psychoeducation (Goodyer et al, 2007) both of which can be part of broad based CBT packages. This issue is not specific to their study since in many studies, treatment as usual is a mix of approaches and may incorporate CBT techniques. They are right to point out that our protocol was written at a time when there was greater concern over the efficacy of anti-depressants in adolescents. Our cCBT study (Wright et al, 2014) is nearly at completion and we did not feel it appropriate to change the background narrative in the protocol at the point of publication since the protocol defines the rationale for the study being undertaken at that time.

    There are in fact two RCTs comparing antidepressants and CBT in adolescents (March et al, 2004; Melvin, 2006) and these are included in the Cochrane systematic review by Cox and colleagues (2012). This meta- analysis (Cox et al, 2012) shows mixed results with no statistically significant difference between antidepressants and CBT for the majority of outcomes. There is no difference between self-rated depression symptoms post intervention or at 6-9 months follow up between the two groups in the meta-analysis. At post-intervention there were significantly fewer participants with suicidal ideation in the CBT group than the antidepressant group and this was still the case at 6-9 months follow up. There is 'limited' evidence of improved remission in the antidepressant group but only in clinician rated remission ratings immediately post intervention. As further research is emerging this picture may change and clearly antidepressants have a place in the care pathway for adolescent depression and studies such as the ones under discussion support this (Goodyer et al, 2007; Byford et al, 2007).

    It is relevant to note that CBT (or indeed cCBT) is not the same treatment wherever it is delivered. CBT is a model of delivery that allows exploration of interactions between cognitions, emotions, behaviours and the environment. For depression packages may include a range of different elements that incorporate activity scheduling, social problems solving skill work, psychoeducation, coping strategy work, biofeedback, relaxation, behavioural experiments, work on automatic negative thinking (and other distortions of thinking) and so on. In this way SPARX (Merry et al, 2012) is a very different cCBT programme from Stressbusters (Abeles et al, 2009) and has different content, mode of delivery and number of standard sessions. Issues such as these make it difficult to generalize about CBT when comparing studies, or about the place of CBT or cCBT in the care pathway given the very limited number of RCTs in this age group.

    From a clinical perspective, we agree with Dubicka and colleagues that antidepressants have an important place in a stepped care approach. We welcomed Curry and colleagues' findings (2006) that suggest that there is no apparent benefit from adding CBT to fluoxetine for those adolescents with symptoms that are so severe that they cannot engage in CBT, and indeed this makes clinical common sense and maps onto local clinical practice. We agree with Cox and colleagues that 'there is very limited evidence upon which to base conclusions about the relative effectiveness of the psychological interventions, antidepressant medication and a combination of these interventions'. We strongly suggest, and would be hopeful that Dubicka and colleagues would agree, that further research in this area is important and we look forward to the results of ongoing CBT studies (Goodyer et al, 2011) and cCBT studies in London and Yorkshire (Wright et al, 2015).

    References Abeles P, Verduyn C, Robinson A, Smith P, Yule W, Proudfoot J. Computerized CBT for adolescent depression ("Stressbusters") and its initial evaluation through an extended case series. Behav Cog Psychotherapy 2009; 37: 151-165.

    Byford S, Barrett B, Roberts C, Wilkinson P, Dubicka B, Kelvin RG, White L, Ford C, Breen S, Goodyer I Cost-effectiveness of selective serotonin reuptake inhibitors and routine specialist care with or without cognitive behaviour therapy in adolescents with major depression. Brit J Psych 2007; 191: 521-527.

    Cox GR, Callahan P, Churchill R, Hunot V, Merry SN, Parker AG, Hetrick SE. Psychological therapies versus antidepressant medication, alone and in combination for depression in children and adolescents. Cochrane Database of Systematic Reviews 2014, Issue 11. DOI: 10.1002/14651858.CD008324.pub3.

    Curry J , Rohde P , Simons A , Silva S , Vitiello B , Kratochvil C , Reinecke M , Feeny N , Wells K , Pathak S , Weller E , Rosenberg D , Kennard B , Robins M , Ginsburg G , March J TADS Team : Predictors and moderators of acute outcome in the Treatment for Adolescents with Depression Study (TADS). J Am Acad Child Adolesc Psychiatry 2006; 45:1427- 1439

    Dubicka B, Wilkinson P, Kelvin R, Goodyer I (2015) cCBT for depression in adolescents. BMJ Open 4/10/e006488.full/reply

    Goodyer I, Dubicka B, Wilkinson P, Kelvin R, Roberts C, Byford S, Breen S, Ford C, barrett B, Leech A,Rothwell J, White L, Harrington R. Selective serotonin reuptake inhibitors (SSRIs) and routine specialist care with and without cognitive behaviour therapy in adolescents with major depression: randomised controlled trial. BMJ 2007; 335: 142.

    March J, Silva S, Petrycki S, et al. Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents with Depression Study (TADS) randomized controlled trial. JAMA 2004; 292: 807-20.

    Melvin G, Tonge BJ, King NJ, Heyne D, Gordon MS, Klimkeit E. A comparison of cognitive-behavioral therapy, sertraline, and their combination for adolescent depression. J Acad Child Adol Psych 2006; 45: 1151-1161.

    Merry SN, Stasiak K, Shepherd M, Frampton C, Fleming T, Lucassen MF. The effectiveness of SPARX, a computerised self help intervention for adolescents seeking help for depression: randomised controlled non- inferiority trial. BMJ 2012; 344:e2598.

    Wright, B., Tindall L., et al (2014) Computerised cognitive behaviour therapy for depression in adolescents: study protocol for a feasibility randomised controlled trial. BMJ Open 4 (10).

    Barry Wright, Lucy Tindall

    Conflict of Interest:

    None declared

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  4. CCBT for depression in adolescents

    We wish to highlight a number of inaccuracies noted in the protocol for a proposed feasibility study of computerised cognitive behavioural therapy (CCBT) in depressed adolescents (Wright et al, 2014). We believe that the introduction to the study overplays concerns about the use of antidepressants and the effectiveness of CBT in adolescents. The authors fail to differentiate the level of severity of depression with respect to the use of antidepressants, and only very briefly refer to the TADS data (March et al, 2004). This remains the only trial in adolescents which compares antidepressants and CBT, and demonstrated a lack of effect of CBT over placebo at 12 weeks, but a substantial effect size of fluoxetine over both placebo and CBT. In addition, fluoxetine has been demonstrated to be superior to placebo in the treatment of acute depression (Emslie et al, 1997;2002), and has been shown to prevent relapse (Emslie et al, 2004). We do think that our UK ADAPT trial has been misrepresented here. While our Brief Initial Intervention did lead to improvement in a minority of adolescents, we did move to antidepressants after 1-4 sessions for those who did not respond; and those with severe depression would have been offered antidepressants sooner. Also, ADAPT did not randomise between medication and treatment as usual: all received medication and psychosocial treatment as usual and half were randomly allocated to CBT. The most important outcome of the ADAPT trial was that there was no additional benefit in adding CBT to an antidepressant and routine care, a finding that was replicated in the most impaired adolescents in TADS (Curry et al, 2006). Based on the TADS data we would challenge the statement that antidepressants show poor efficacy, particularly when compared to CBT. Although the authors quote older studies in support of CBT, more recent evidence challenges the extent of the effectiveness of CBT both in adolescent and adult depression, particularly when studies with sub-standard methodology are excluded (e.g. Weisz et al, 2006; Cuijpers et al, 2013; Klein et al, 2007). While some small studies suggested that CBT prevents depression, larger, more robust studies have demonstrated no effect, and one of these demonstrated that CBT was actually less effective at preventing depressive symptoms than standard PHSE sessions from teachers (Challen et al, 2014; Sawyer et al, 2010; Stallard et al, 2012). A Cochrane review of psychological treatment and antidepressants (Cox et al, 2012) failed to come to any definitive conclusions regarding the relative benefit of treatments, but did find some superiority of antidepressants over CBT. Thus the assumption that antidepressants are ineffective and CBT is more effective is not supported by the research evidence. In addition, the authors describe the addictive potential of antidepressants, however to our knowledge there is no definitive evidence for this from any clinical trial in young people or from clinical practice.

    We do welcome this proposed study. Computerised CBT may be an effective treatment for adolescents, and could be particularly helpful for those who do not want to/are unable to attend clinics. It is also likely to be cheaper than conventional CBT. We were surprised that the authors have not referred to the large published trial of CCBT by Merry et al (2012), which indicated that CCBT had similar effectiveness as routine care in depressed adolescents. This is indeed a promising finding which deserves replication in the UK. However, we believe the evidence is clear in advocating the use of antidepressants within a stepped care approach and await the results of IMPACT (Goodyer et al, 2011) which may provide further information regarding the place of CBT in the treatment pathway.

    References Challen, A. R., S. J. Machin, et al. (2014). The UK Resilience Programme: A school-based universal nonrandomized pragmatic controlled trial. Journal of Consulting and Clinical Psychology 82(1): 75-89. Cox, G. R., P. Callahan, et al. (2012). Psychological therapies versus antidepressant medication, alone and in combination for depression in children and adolescents. Cochrane Database of Systematic Reviews. 11. Cuijpers, P., M. Berking, et al. (2013). A meta-analysis of cognitive- behavioural therapy for adult depression, alone and in comparison with other treatments. The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie 58(7): 376-385. Curry, J., Rodhe, P., Simons, A., Silva, S., Vitiello, B., Kratochvil, C., et al. (2006) Predictors and Moderators of Acute Outcome in the Treatment for Adolescents With Depression Study (TADS). Journal American Academy Child Adolescent Psychiatry, 45(12), 1427-1438. Dimidjian, S. and S. D. Hollon (2010). How would we know if psychotherapy were harmful? American Psychologist Vol.65(1): 21-33. Emslie, G. J., A. J. Rush, et al. (1997). A double-blind, randomised, placebo-controlled trial of fluoxetine in children and adolescents with depression. Archives General Psychiatry 54: 1031-1037. Emslie, G. J., J. H. Heiligenstein, et al. (2002). Fluoxetine for acute treatment of depression in children and adolescents: a placebo-controlled, randomized clinical trial. Journal of the American Academy of Child and Adolescent Psychiatry 41(10): 1205-1215. Emslie, G. J., J. H. Heiligenstein, et al. (2004). Fluoxetine treatment for prevention of relapse of depression in children and adolescents: a double-blind, placebo-controlled study. Journal American Academy Child Adolescent Psychiatry 43(11): 1397-1405. Goodyer, I., Tsancheva, S., et al. (2011). Improving mood with psychoanalytic and cognitive therapies (IMPACT): a pragmatic effectiveness superiority trial to investigate whether specialised psychological treatment reduces the risk for relapse in adolescents with moderate to severe unipolar depression: study protocol for a randomised controlled trial. Trials 12:175. Klein, J. B., R. H. Jacobs, et al. (2007). Cognitive-Behavioural Therapy for Adolescent Depression: A meta-analytic investigation of changes in effect-size estimates. Journal American Academy Child Adolescent Psychiatry 46(11): 1403-1413. March, J., Silva, S., et al. (2004). Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial. JAMA, 292, 807 - 820. Merry, S., K. Stasiak, et al. (2012). The effectiveness of SPARX, a computerised self help intervention for adolescents seeking help for depression: Randomised controlled non-inferiority trial. BMJ: British Medical Journal 344(7857): 1-16. Sawyer, M. G., T. F. Harchak, et al. (2010). School-based prevention of depression: A 2-year follow-up of a randomized controlled trial of the beyondblue schools research initiative. Journal of Adolescent Health 47(3): 297-304. So, M., S. Yamaguchi, et al. (2013). Is computerised CBT really helpful for adult depression?-A meta-analytic re-evaluation of CCBT for adult depression in terms of clinical implementation and methodological validity. BMC Psychiatry 13(ArtID 113). Stallard, P., K. Sayal, et al. (2012). Classroom based cognitive behavioural therapy in reducing symptoms of depression in high risk adolescents: pragmatic cluster randomised controlled trial. BMJ 345. Weisz, J. R., C. A. McCarty, et al. (2006). Effects of Psychotherapy for Depression in Children and Adolescents: A Meta-Analysis. Psychological Bulletin 132(1): 132-149. Wright, B., L. Tindall, et al. (2014). Computerised cognitive behaviour therapy for depression in adolescents: study protocol for a feasibility randomised controlled trial. BMJ Open 4 (10).

    Conflict of Interest:

    PW, RK, IG have acted as consultants to Lundbeck. PW is an interpersonal psychotherapy supervisor BD, RK, IG are investigators on the HTA funded IMPACT study of psychological treatments in adolescent depression

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  5. It's not all negative!!

    I read the article by Marston et al ( with keen interest as my role in the crisis team involves assessment and management of a majority of patients included in the cohort. However, I would urge cautions on the author's interpretations on the following grounds.

    1. I would like to point out the definition of Severe Mental Illness has specifically excluded depression as a severe mental illness, despite its devastating effects on an individual and family. This might be due to a variety of factors, including recent negative publications (of wide spread antidepressant prescriptions/ineffective antidepressants) and potentially due to stigma. 2. A variety of antipsychotics mentioned have licenses for non-smi related illness. Olanzapine has a license in the USA for treatment resistant depression ( and Quetiapine for Major depressive disorder (licensed as add on in the UK but has a license overseas as monotherapy for MDD), along with NICE (in generalised anxiety disorder) advising "Moderate evidence suggests that quetiapine monotherapy at most doses statistically significantly improved rates of GAD response or remission compared with placebo (4 RCTs lasting 8-9 weeks) but not compared with escitalopram or paroxetine (2 RCTs lasting 8 weeks)." 3. These drugs could have easily be commenced in secondary care (e.g. while under the care of the crisis team) and continued in primary care hence not being initiated there at all. 4. My thoughts on use of antipsychotic medication in the elderly have been explored here ( Even though I do not condone wide spread use of antipsychotic medication in this population, it could clearly be initiated by a specialist and dispensed in primary care, keeping all relevant national guidance in mind and having a discussion with patient's family. 5. The authors quote Speilmans et al metaanalysis on atypical antipsychotic use in major depressive disorder to suggest lack of functional improvement in those patients ( However, despite including only 14 short term (4-12 weeks) trials, all four drugs had statistically significant effects (effects unlikely to have happened by chance) on remission (a much higher threshold), which was most commonly defined as a score of less than eight at the study end point on the Montgomery-Asberg Depression Rating Scale. The NNT was 9 for Quetiapine, Risperidone and Aripiprazole. Arguably, the trials were too short to effectively address functional recovery. It is however posited with remission being the outcome measure; the functional recovery would follow in time. 6. Ethically, "do no harm" seemingly applies to patients treated by antipsychotics, including risks of sudden death and of deep vein thrombosis, not mentioned by the authors. However, if a partially treated/untreated patient with major depressive disorder chooses to end their life, I would suggest that is a bigger harm. My comment on the recent annual report by the National Confidential Enquiry into Suicide and Homicide by People with Mental Illness, which was publicized for highlighting that 72% of those who died by suicide between 2001 and 2011, were not in contact with mental health services for the full year before their death is available here ( Hence to conclude, there are several ways to interpret the data and I would urge readers to consider alternatives and not just draw similar conclusions mentioned by the authors.

    Conflict of Interest:

    None declared

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  6. Comparing the incomparable may be erroneous .

    Dear Editor: We peruse with interest the interesting study by Meng Lee et al (1). We would like to share the followings:

    1.One of the strengths of any retrospective data analysis is the acceptance/compliance with therapy in the real-life situation ( whatever the compliance rate may be).The exclusion of 1632 patients ( 42% of the total) because of medication possession ratio <80% has limited the external validity of the study.

    2.Excluding 355 patients (9% of the total) further because of Atrial fibrillation, valvular heart diseases or coagulopathy may not be justified ( if they were put either on aspirin or clopidogrel ,they should have been included).

    3.During the follow-up period, statin and diuretics were used more frequently ( statistically significant) in the clopidogrel group. It is well known that statin and diuretics reduce ischemic strokes (2,3).Thus tilting the balance in favor of clopidogrel.

    4.Much less patients were put on clopidogrel (384 patients) versus aspirin (1500 patients),even the best statistical model may not be able to completely nullify the bias as the disparity is substantial.

    As the above mentioned limitations are influential, the results of the study may be biased and should be interpreted with caution.


    1.Meng Lee, Yi-Ling Wu, Jeffrey L Saver, Hsuei-Chen Lee, Jiann-Der Lee,Ku-Chou Chang, Chih-Ying Wu, Tsong-Hai Lee, Hui-Hsuan Wang, Neal M Rao, and Bruce Ovbiagele.Is clopidogrel better than aspirin following breakthrough strokes while on aspirin? A retrospective cohort study. BMJ Open 2014 4:e006672; doi:10.1136/bmjopen-2014-006672

    2.Pierre Amarenco, Julien Labreuche.Lipid management in prevention of stroke:review and updated meta-analysis od statin for stroke prevention.The Lancet Neurology. 2009;8(5):453-463.doi:1016/s1474-4422(09) 70058-4

    3.PROGRESS Collaborative group. Randomised trial of a perindopril- based blood pressure-lowering regimen among 6105 individuals with previous stroke or transient ischemic attack.The Lancet. 2001;358:9287,1033-1041. doi:10.1016/s014-6736(01)06178-5

    Conflict of Interest:

    None declared

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  7. RE: Low-fats and not low-carbs for better diabetes control in Indians

    Dear Editor

    I wish to address the eLetter responding to our recently published article in BMJ Open (Joshi SR, et al. Results from a dietary survey in an Indian T2DM population: a STARCH study. BMJ Open. 2014 Oct 31;4(10):e005138.) Firstly, thank you to Prof.Vishnupriya R Paturi for taking the time to read our article and providing feedback. We believe that the impact and relative importance that the type or source of carbohydrate has on postprandial glucose level has continued to be an area of debate. However, many studies highlights that the dietary carbohydrate determines the postprandial blood glucose response. Garg A & Parillo M reported that dietary carbohydrate increases blood glucose concentrations, particularly in the postprandial period. Therefore, in diabetic patients, particularly those treated with insulin or who have more severe forms of type 2 diabetes, a carbohydrate-rich diet can have detrimental effects on glycemic control, which plays a major role in the development of coronary artery disease and other macrovascular and microvascular complications (1,2). In parallel with the plasma glucose rise, plasma insulin and triacylglycerol concentrations also tend to increase with a high- carbohydrate diet, along with other cardiovascular disease risk factors(3). Although, it is known that not all carbohydrate-rich foods are equally hyperglycemic: differences in the postprandial blood glucose response to various carbohydrate-containing foods have been shown in both healthy subjects and diabetic patients, even when consumed in portion sizes containing identical amounts of carbohydrate. It was observed that carbohydrate-rich foods represent a heterogeneous category and, therefore, may have a variable effect on energy and substrate metabolism in humans. (4-6). The American Diabetes Association reviewed the available scientific data regarding the effect of the type or source of carbohydrate on the prevention and management of diabetes and suggested the following statements: [7] * The component of the diet that has the greatest influence on blood glucose is carbohydrate. However, other macronutrients in the diet, i.e., fat and protein, can influence the postprandial blood glucose level. * Regulation of blood glucose to achieve near-normal levels is a primary goal in the management of diabetes, and, thus, dietary techniques that limit hyperglycemia following a meal are likely important in limiting the complications of diabetes. * Low-carbohydrate diets are not recommended in the management of diabetes. Although dietary carbohydrate is the major contributor to postprandial glucose concentration, it is an important source of energy, water-soluble vitamins and minerals, and fiber. * Both the amount (grams) of carbohydrate as well as the type of carbohydrate in a food influence blood glucose level. * The maintenance of a healthy body weight is strongly recommended as a means of preventing this disease, because much of the risk of developing type 2 diabetes is attributable to obesity,

    Also most experts agree that the total carbohydrate intake from a meal or snack is a relatively reliable predictor of postprandial blood glucose. Thus in addition to advice fat proportions in diets, monitoring total grams of carbohydrate, whether by use of exchanges or carbohydrate counting, remains a key strategy in achieving glycemic control.In our study, we suggested the need to investigate further the benefit of various therapeutic interventions in high carbohydrate-consuming Indian type-2 diabetes mellitus participants in a prospective randomised controlled study.

    References: 1.Garg A, Bonanome A, Grundy SM, et al. Comparison of a high carbohydrate diet with a high-monounsaturated-fat diet in patients with noninsulin- dependent diabetes mellitus. N Engl J Med 1988;319:829 -34. 2.Parillo M, Giacco R, Ciardullo AV, et al. Does a high carbohydrate diet have different effects in NIDDM patients treated with diet alone or hypoglycemic drugs? Diabetes Care 1996;19:498 -500. 3.Rivellese A, Giacco R, Genovese S, et al. Effects of changing amount of carbohydrate in diet on plasma lipoproteins and apolipoproteins in type II diabetic patients. Diabetes Care 1990;13:446-8. 4.Coulston AM, Hoolenbeck CB. Swislocki AML, et al. Deleterious metabolic effects of high carbohydrate, sucrose containing diets in patients with NIDDM. Am J Med 1987;82:213-20. 5.O'Dea K, Nestel R, Autonoff L. Physical factors influencing postprandial glucose and insulin responses to starch. Am J Clin Nutr 1980;33:760-5. 6.Liljeberg H, Granfeldt Y, Bjorck I. Metabolic responses to starch in bread containing intact kernels versus milled flour. Eur J Clin Nutr 1992;46:561-5. 7.Nancy F. Sheard, et al. Dietary Carbohydrate (Amount and Type) in the Prevention and Management of Diabetes. Diabetes Care 2004; 27(9):2266- 2271

    Conflict of Interest:

    Competing interests SRJ: Author: Bayer Zydus Pharma; Speaker: Sanofi, Abbott, USV, Franco Indian, Ranbaxy, PHFI, MSD, Novartis, J & J, Roche Diagnostics, Novo Nordisk, Marico, Emcure; Consultant, Investigator: Bayer Zydus Pharma; Research Support: Bayer Zydus Pharma; AB: Research Grant: Bayer Zydus Pharma

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  8. NCCAM

    CAM includes both complementary and alternative practices. Alternative practices, by definition, either have not been proven to work, or have been proven not to work. Complementary practices have always been mainstream and many are evidence-based. There is no sound scientific or medical justification for analysing the two together. Alternative practitioners may prefer them to be considered together, as this may provide a halo effect of legitimacy from being considered alongside obviously valid concepts such as diet and exercise, but in analysing the cost-effectiveness of these interventions it seems to me rather important to unpick the two.

    For example, any judgment of the validity of medical training in nutrition cannot possibly shed light on the validity of training in a refuted dogma such as homeopathy or reiki.

    It is plausible that autohypnosis may be able to materially benefit patients with anxiety disorders. It is wholly implausible that homeopathy would deliver any objectively provable benefit at all. To consider the two jointly, is to needlessly muddy the waters.

    The authors reference the US National Center for Complementary and Alternative Medicine (NCCAM), a body set up at the instigation of a pro- CAM legislator to investigate and produce evidence around CAM interventions.

    Dr. David Gorski has been looking closely at NCCAM for some years, along with several colleagues. They have noted that NCCAM has spent in excess of one billion dollars since its inception in 1993. To date, they have failed to validate a single alternative intervention. They have produced supportive evidence for massage therapy (which is scarcely controversial), but not for any of the alternative therapies tested - many of which are by now considered refuted though still doggedly promoted by believers.

    I would suggest the authors do their best in future to unpick the effects of legitimate and medically plausible complementary therapies, from those of alternative therapies. This will reduce the risk of their research being abused by advocates as support for therapies which, of themselves, have little or no provable validity.

    In the light of surveys showing that large numbers of doctors knowingly prescribe placebos, it would also be valuable to understand how many of the doctors using CAM therapies consider them to be valid interventions and administer them on that basis.

    Conflict of Interest:

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  9. Prevention of Risk Factors: Eat and Have Physical Activity What Our Grandparents Used to Have.

    "Let food be thy medicine and medicine be thy food." Hippocrates

    We read with interest the study by T.Sekhri,R.S.Kanwar et al(1).The authors needs to be congratulated for such a meticulous and unique study involving subjects from all over India.The study is first of its kind in India and an eye-opener. However,the following issues we shall like to share:

    1.As it was a non-interventional and free-of-cost to the participating subjects study.Why only 14,500 subjects( 55%) gave the informed consent out of approximately 26,000.It may be worth mentioning some important reasons of this rather less acceptance for the study.This low level of participation compromises the external validity of the study.

    2.The subjects with known coronary artery disease (CAD) were excluded.It would have been interesting to know how many subjects with newly discovered CAD were detected,including silent old MI pattern in ECG.

    3.As mentioned in the introduction of the study(1),over 60% of CAD in native Indians remain unexplained by conventional risk factors,why only conventional risk factors were considered in the study.

    4.Gainfully,in the protocol,disease history is included,it would have been relevant to know about the other diseases and if any correlation with the risk factors could have been made. Like patients with depression/psychiatric morbidity (common diseases these-days)and obstructive sleep apnea have much worse risk factor profile and are increasing recognized as novel risk factors per se. Interestingly in women( obstetric history was ascertained),any correlation with adverse obstetric history and risk factor profile was observed?.The data is rapidly accumulating between adverse obstetric history and development of cardiovascular disease in future(2).

    5.In the present study interestingly only 27% of hypertensives were aware about their condition ( 73% were newly discovered).A rather lower percentage particularly for civilian government employee,having free access to the medical services.

    6.78.6% of the subjects had two or more risk factors is a disturbing fact.In Prabhakaran's study(3) in 2005 amongst industrial workers of north India 47% subjects had atleast two risk factors.Is it a temporal trend or the difference is due to the location of the subjects in the study,needs to be explained.

    The study emphasized the disturbing trend in the health status in India and serious thoughts and actions are needed to contain this unabated epidemic.What will be the peak of the epidemic is anybody's guess. However, we have the following suggestions to offer:

    1.When the epidemic reaches this gigantic proportion,secondary and tertiary prevention have very limited impact at a community level.

    2.The primordial and primary prevention assume huge importance. As they are much more cost-effective and result yielding.

    3.For Primordial prevention and primary prevention ,in a nutshell the message is : to eat and try to assume the level of physical activity and lifestyle ( may not be possible for everyone) similar to what our grandparents used to have.

    4.To counteract the adverse health consequences of modern life .We advocate three levels of prevention: health education, health education and health education of the entire world ( in particular developing world), with emphasis upon educating health policy - makers.


    1.T Sekhri, R S Kanwar, R Wilfred, P Chugh, M Chhillar, R Aggarwal, Y K Sharma, J Sethi, J Sundriyal, K Bhadra, S Singh, N Rautela, Tek Chand, M Singh, and S K Singh.Prevalence of risk factors for coronary artery disease in an urban Indian population. BMJ Open 2014 4:e005346; doi:10.1136/bmjopen-2014-005346

    2.Bellamy L,Casas JP,Hingorani AD,Williams DJ.Pre-eclampsia and risk of cardiovascular disease and cancer in later life:Systematic review and meta-analysis.BMJ.2007;335:974

    3.Prabhakaran D, Shah P, Chaturvedi V, et al. Cardiovascular risk factor prevalence among men in a large industry of northern India. Natl Med J India 2005;18:59-65.

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  10. Cause of the nodding syndrome

    Landis et al. describe a temporal association between wartime conflict, internal displacement, and Nodding syndrome (NS)(1). They raise infectious, nutritional and neuropsychiatric elements as possible causal factors. The authors, however, do not mention a key factor that may have played a major role during the NS epidemic in northern Uganda: a lack of ivermectin treatment in onchocerciasis endemic areas.

    Mass-distribution of ivermectin is routinely used to interrupt onchocerciasis transmission in endemic foci, and an association between NS and onchocerciasis has repeatedly been reported (2). NS only occurs in onchocerciasis hyperendemic areas, and other forms of epilepsy are also thought to be highly prevalent in many of these regions(3).

    During the civil war in northern Uganda (1986-2006/2008), there was no access to ivermectin in districts affected by NS, and it was only after the war that ivermectin treatment programmes were established. Ivermectin has been distributed annually in NS-affected districts since 2008, and biannually since 2012 (2). This has coincided with a dramatic drop in the number of new NS cases, and no new cases were officially reported in 2013 (4). The ivermectin distribution programme in northern Uganda was supplemented by control measures targeting blackflies (Simuliidae), the vectors of onchocerciasis, in late-2012. The Achwa and Pager rivers were initially treated with larvicides applied from boats and light aircraft, and larval breeding sites are now being treated with the organophosphate, temephos, at predefined points along the rivers (2). We believe that this integrated approach, targeting both the vectors of onchocerciasis and the parasite in the human population, has contributed to the reduction of NS cases in northern Uganda.

    The link between NS and onchocerciasis appears to be further reinforced by a recent study which suggests that an antibody-mediated autoimmune response to leiomodin-1 may be involved in the etiology of NS. Johnson et al. have demonstrated that antibodies against leiomodin-1 are more likely to be present in NS cases than in controls (5). These antibodies are also present in the cerebrospinal fluid of certain patients with NS, are neurotoxic in vitro, and cross-react with Onchocerca volvulus -specific proteins.

    We do not believe that NS can be explained by events only related to war. In the Mahenge NS-focus in Tanzania, there is no recent history of conflict or household internment. Hypotheses regarding NS etiology should be based on information from all affected regions.

    Further research is needed to explore whether NS is caused by an auto -immune reaction in response to Onchocerca volvulus infection; whether the species or strain of Onchocerca is unique in NS-affected areas, or whether NS is caused by a currently unidentified agent transmitted by blackflies (6).

    R. Colebunders, K. Coudere, N. Van der Moeren, A Hendy

    Reference List

    (1) Landis JL, Palmer VS, Spencer PS. Nodding syndrome in Kitgum District, Uganda: association with conflict and internal displacement. BMJ Open 2014;4(11):e006195.

    (2) Colebunders R, Post R, O'Neill S, Haesaert G, Opar B, Lakwo T et al. Nodding syndrome since 2012: recent progress, challenges and recommendations for future research. Trop Med Int Health 2014 October 28.

    (3) Pion SD, Kaiser C, Boutros-Toni F, Cournil A, Taylor MM, Meredith SE et al. Epilepsy in onchocerciasis endemic areas: systematic review and meta-analysis of population-based surveys. PLoS Negl Trop Dis 2009;3(6):e461. (4) Ministry of Health, Uganda. Weekly epidemiological bulletin. 2014.

    (5) Johnson T, Tyagi R, Lee PR, Leea M-h, Johnson KR, Kowalak J, Medynets M, Hategan A, Nutman TB, Sejvar J, Makumbi I, Aceng JR, Dowell SF, Nath A. Detection of auto-antibodies to leiomodin-1 in patients with nodding syndrome. j.jneuroim , 103. 2014.

    (6) Colebunders R, Hendy A, Nanyunja M, Wamala JF, van OM. Nodding syndrome-a new hypothesis and new direction for research. Int J Infect Dis 2014 August 23;27C:74-7.

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    None declared

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