Recent eLetters

Displaying 11-20 letters out of 329 published

  1. 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.

    Conflict of Interest:

    None declared

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  2. 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.

    Conflict of Interest:

    None declared

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  3. Reply to Ole Olsen (2)

    Thanks to statistician Ole Olsen who again expresses his concern about the validity of the data in the National Birth Registry, and the inconsistent reporting of these data on the official on-line sites. This time Ole Olsen, however, goes one step further. Now he demands the editors of BMJ open to ensure "documentation of the validity of all variables for all years in the study period".

    To validate all recorded birth related diagnosis and procedural codes over a time span of 13 years, during which more 829,000 women have delivered, would require providing the clinical notes of a representative sample of these deliveries to see first, if all the relevant codes were recorded appropriately, and secondly, if any non-relevant codes had been recorded. Fortunately such validation studies have been made, demonstrating a general high validity of the recorded obstetrical diagnosis and procedural codes in the National Health Registry, which feeds the Danish Birth Registry (1).

    The main variables used for our study were calendar years, the gestational age of delivering women, and the codes assessing stillbirth. As reported, the gestational age was recorded in 99.4 % of all deliveries, and has been found to have a high validity (1). The same applies to the codes for stillbirths, which is generally considered as a "hard" end point. We have previously indicated how we assessed stillbirths (2).

    So the remaining question is whether other circumstances than the earlier induction practice could explain the encouraging substantial decline in stillbirths - not whether such a decrease actually occurred. Considering the dramatic increase in risk of stillbirth with increasing gestational age, it is not surprising that moving deliveries from high- risk post-term weeks to earlier weeks with substantial lower risk of intrauterine death would decrease the overall stillbirth rate from 37 gestational weeks. This is possibly not a very welcome message for people like Ole Olsen, who for many years has argued for home deliveries, but it does not make the scientific evidence less valid. Ole Olsen indicates specifically, that the recording of induction of labour may have had a lower validity than ideal. However this variable was used only for descriptive purposes in our study, to demonstrate the increasing proportion of inductions of deliveries from 12.4% to 25.2% during the study period. If some of the codes used to assess labour induction have been prone to variation between departments, which is not unlikely, these circumstance would not change anything in our analysis or in our conclusion.

    As Ole Olsen also demonstrates, there have been several attempts to ensure the validity and standardisation of obstetrical coding in Denmark. This has been done through national guidelines elaborated by the Danish Society of Obstetrics and Gynaecology (DSOG)(3), and by annual meetings where these registration rules are discussed and posted solid. These attempts are expected generally to have improved the registration practice in Denmark by time.

    The experiences Ole Olsen and his midwife collaborators Rydahl and Clausen have had by getting access to data in the Danish Birth Registry, and the inconsistencies in the official online statistics are - again - not our responsibility and should be addressed to the relevant bodies.

    About data sharing, one of the strengths about Danish registry research is that these registry data are available for all scientists, including Ole Olsen, who want to investigate any obstetrical question.

    Based on the high validity of the diagnosis codes used in our study, we are still confident with our analyses, and with the conclusions drawn.

    1) Langhoff-Roos J, Rasmussen S. [Validation of the National Health Registry concerning obstetrical research and quality assurance][In Danish]. National Health Board 2003. Page 1-193.

    2) Lidegaard O. Reply to Rydahl and Clausen. BMJ open 2014, October 13, 2014.

    3) Accessed December 4, 2014.

    Conflict of Interest:

    See original article

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  4. Re:Response to the A population-based observational study of diabetes during pregnancy in Victoria, Australia article

    Dear Editor

    I wish to address the eLetter responding to our recently published article in BMJ Open (Abouzeid M, Versace VL, Janus ED, et al. A population -based observational study of diabetes during pregnancy in Victoria, Australia, 1999-2008). Firstly, thank you to Wigdan Farah for taking the time to read our article and providing positive feedback. Specifically they suggest that we add the variable 'socio-economic status' (SES) to our analysis. They cite the paper by Nomura Y, Marks DJ, Grossman B, et al. (2012) in Archives of Pediatrics & Adolescent Medicine as an example of the influence of SES on health outcomes. We are pleased to advise that we have just had an article accepted by PLoS One entitled 'Socio-cultural disparities in GDM burden differ by maternal age at first delivery' (accepted December 2nd, 2014, Abouzeid M, Versace V, Janus E, et al.). We encourage Wigdan Farah to access this article once it appears online in the near future.

    Kind regards

    Abouzeid M, Versace VL, Janus ED, M-A Davey M-A, Philpot B, Oats J, and Dunbar JA

    Articles cited

    1. Abouzeid M, Versace VL, Janus ED, et al. A population-based observational study of diabetes during pregnancy in Victoria, Australia, 1999-2008. BMJ Open. 2014;4(11):e005394.

    2. Nomura Y, Marks DJ, Grossman B, et al. Exposure to gestational diabetes mellitus and low socioeconomic status: effects on neurocognitive development and risk of attention-deficit/hyperactivity disorder in offspring. Arch Pediatr Adolesc Med. Apr 2012;166(4):337-343.

    3. Abouzeid M, Versace VL, Janus ED, et al. Socio-cultural disparities in GDM burden differ by maternal age at first delivery.(Accepted December 2nd, 2014). PLoS One.

    Conflict of Interest:

    None declared

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  5. Re:Is self-identification as 'obese' really a public health solution?

    Dr Ian Brown rightly highlights the potential dangers of an atmosphere of stigma around weight, and suggests that rejection of the term 'obese' may be protective of body self-esteem (1). This is an important point, as the term 'obese' is clearly perceived as stigmatising by many, and perceived stigma has been associated with poorer weight outcomes as well as psychological distress (2). However, our perspective is that the specific terminology used to discuss body weight may be less important than there being a common language shared between health professionals, the research community, media and the public. At present, clinically descriptive approaches to weight classification are severely out of kilter with the way in which the public perceives body weight, which must impede individuals' ability to access information and make informed decisions about their own health and lifestyle.

    Meanwhile, a valuable asset in tackling weight stigma could be a far greater public understanding that there is no level playing field when it comes to body weight. It is well recognised in the research community that there are strong genetically-mediated predispositions that mean that some individuals are more susceptible to weight gain, and make the challenge of weight management in an obesogenic environment far greater for them. This fact does not seem widely understood by the public or discussed in the media (3, 4), and greater awareness of this could contribute to less judgemental (and self-blaming) attitudes towards difficulties with weight control (5).

    Ultimately the best solution to the problem of high levels of population obesity lies in reversing the trajectory of the food environment, but progress toward this is minimal at present. In the meantime, the lack of effective channels of communication about weight must be a formidable obstacle to fostering the knowledge and skills required to manage the difficulties of living in an obesogenic society.

    1. Brown, I. Is self-identification as 'obese' really a public health solution? BMJ Open. 2014 Letter (Response to Johnson F, et al. BMJ Open 2014; 4(11):e005561. doi: 10.1136/bmjopen-2014-005561) 2. Jackson SE, Beeken RJ, Wardle J. Perceived weight discrimination and changes in weight, waist circumference, and weight status. Obesity (Silver Spring). 2014 Dec;22(12):2485-8. 3. Beeken RJ, Wardle J. Public beliefs about the causes of obesity and attitudes towards policy initiatives in Great Britain. Public Health Nutr. 2013 Dec;16(12):2132-7. 4. Sikorski C, Luppa M, Kaiser M, Glaesmer H, Schomerus G, K?nig HH, Riedel-Heller SG. The stigma of obesity in the general public and its implications for public health - a systematic review. BMC Public Health. 2011 Aug 23;11:661. doi: 10.1186/1471-2458-11-661. 5. Meisel SF, Wardle J. 'Battling my biology': psychological effects of genetic testing for risk of weight gain. J Genet Couns. 2014 Apr;23(2):179 -86.

    Conflict of Interest:

    Authors of the original research article

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  6. Still need for validation of the data

    I am still concerned about the validity of the data used in the paper "Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention" (1). The paper covers the time period 2000-2012. Lack of validity of the used registry data was documented in 2003 (2) and serious concern about the validity of the data in the registries still exist.

    For the year 2001 the validity of the data in the registers was thoroughly investigated for all Danish births during one specific week by comparing register data with data extracted from patient records by two senior obstetricians (2). In a 192 page report in Danish the authors conclude that "you cannot use the registered interventions to calculate the rates of induction of birth [my translation]" (2) and they note that "the use of the codes in the register is different from one hospital to the other" (2). The work in the report had been initiated because "Since the medical birth registration [...] was transferred to electronic reporting to the National Patient Register (LPR), there has been uncertainty about the quality of the reported data and a growing need for a current validation and a prospective quality improvement of registration practice" (2). Particularly "the lack of feedback from the Board of Health gave uncertainty about the validity of the data reported among health professionals, who entered data, and clinical researchers who used the data" (2). I would appreciate if the authors of the paper (1) could explain how they have overcome this problem for the early years of their study period.

    For the more recent years in the study period I have previously documented several large inconsistencies in annual stillbirth rates between the paper published in this journal (1) and the official published national statistics (comment published 10th September 2014) and Rydahl and Clausen have brought attention to unexplained and dramatic retrospective changes in the online electronic register that supplied data to the paper (7th October). In a joint newspaper commentary leading Danish obstetricians and midwives state "access to the data has been difficult, costly and time consuming" (3), and they add that "[u]nfortunately, we are no longer able to use the data to navigate in everyday clinical practice. Data not used regularly lose their immediate value - proper registration requires motivation and ongoing feedback" (3). The latter concern is identical to the concern issued ten years earlier (2). I would appreciate if the authors of the paper (1) could explain in sufficiently transparent detail how they have overcome the inconsistencies, variability and motivational problems for the middle and late years of their observation period and ensured validity of their data.

    Editors are responsible for everything published in their journals and should ensure the quality of the material they publish (4). I thus ask the editors of BMJ Open to ensure transparent documentation of the validity of all variables for all years in the study period. I also propose that the authors publish and share data and documentation with other researchers on the web as it is encouraged by The BMJ (5).

    1. Hedegaard M, Lidegaard O, Skovlund CW, M?rch LS, Hedegaard M. Reduction in stillbirths at term after new birth induction paradigm: results of a national intervention. BMJ Open. 2014 Aug 14;4(8)

    2. Sundhedsstyrelsen, Center for Evaluering og Medicinsk Teknologivurdering. Validering af Landspatientregistret (LPR) med henblik p? obstetrisk forskning og kvalitetssikring - et kvalitetsudviklingsprojekt [Validation of the National Patient Register (LPR) in relation to obstetric research and quality - a quality development project]. Sundhedsstyrelsen, Copenhagen 2003.

    3. Krebs L, Langhof-Roos J, Petersen KR, Bondo L. Sundhedsstyrelsen gemmer vigtig viden om f?dsler [National Board of Health hides important information on births]. Politiken, 14. okt. 2013 [at -vigtig-viden-om-foedsler/; accessed 25. Nov 2014].

    4. Kleinert S & Wager E (2011) Responsible research publication: international standards for editors. A position statement developed at the 2nd World Conference on Research Integrity, Singapore, July 22-24, 2010. Chapter 51 in: Mayer T & Steneck N (eds) Promoting Research Integrity in a Global Environment. Imperial College Press / World Scientific Publishing, Singapore (pp 317-28). (ISBN 978-981-4340-97-7)

    5. The BMJ. Data sharing [at authors/article-types/research; accessed 25. Nov 2014].

    Conflict of Interest:

    None declared

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  7. Responce to the A population-based observational study of diabetes during pregnancy in Victoria, Australia article

    Dear Editor,

    I am writing to support the author in their outcomes and to add one point to their article "A population-based observational study of diabetes during pregnancy in Victoria, Australia 'from the British Medical Journal on November 14th, 2014 1

    It is an interesting article specially with the significant side effect of diabetes during pregnancy and I suggest the author to add the socioeconomic status as one of the study variable, depending on the Exposure to Gestational Diabetes Mellitus and Low Socioeconomic Status Effects on Neurocognitive Development and Risk of Attention-Deficit Hyperactivity Disorder in Offspring study 2,which showed that maternal gestational diabetes and low socioeconomic status were associated with an approximately 2-fold increased risk for ADHD at age 6 years, impaired neurobehavioral functioning, including lower IQ, poorer language, and impoverished behavioral and emotional functioning.

    Sincerely, Wigdan Farah Research Trainee Preventive Medicine Department Mayo Clinic Rochester, MN

    References: 1. Abouzeid M, Versace VL, Janus ED, et al. A population-based observational study of diabetes during pregnancy in Victoria, Australia, 1999-2008. BMJ Open. 2014;4(11):e005394.

    2. Nomura Y, Marks DJ, Grossman B, et al. Exposure to gestational diabetes mellitus and low socioeconomic status: effects on neurocognitive development and risk of attention-deficit/hyperactivity disorder in offspring. Arch Pediatr Adolesc Med. Apr 2012;166(4):337-343.

    Conflict of Interest:

    None declared

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  8. Almond as a potential nutritional supplement in patients with multiple sclerosis-associated fatigue

    The result of the study presented by Dr. MC Pantzaris and colleagues showed the efficacy of a formulations containing omga-3, omega-6 and vitamin A and -E in relapsing-remitting multiple sclerosis (RR-MS). We want to discuss here on potential benefits of almond as a natural source of these nutritional elements, and other previously shown beneficial nutritional elements in patients with MS and fatigue. Multiple Sclerosis (MS) is one of the most frequent causes of permanent disability in young adults. Its incidence and prevalence vary geographically, ranging from 0-60 per 100,000 in low frequency areas such as India or Brazil to 240-300 per 100,000 in high frequency areas like Canada and Sweden [1]. MS is a heterogeneous disorder with different pathologic features including Inflammation, demyelination, and axonal degeneration [2,3]. The cause of MS is unknown, however it is widely accepted that MS is an inflammatory autoimmune disorder resulting in chronic neurodegeneration [2]. Fatigue is a one of the most prevalent co-morbid conditions in patients with MS, with reported prevalence up to 90 percent [4]. It has important disrupting effect on patient's daily activities and quality of life. The patients fatigue typically exacerbate as the day goes on. It is also a known association between fatigue and sleep disturbance in MS patients [5]. It is suggested that axonal dysfunction and following increased recruitment of cortical areas and pathways in response to brain injury can be considered as pathologic mechanism of fatigue in patients with MS [6]. A number of medications such as amantadine, methylphenidate, selective serotonin reuptake inhibitors, aspirin and modafinil are used in treating fatigue related to MS [7]. Traditionally nutritional supplements are widely recommended and used in multiple sclerosis patients with fatigue [8,9]. Among different nutritional recommendations different preparations of Almond are very popular [10,11]. It is an excellent source of unsaturated fats (9 g per oz) and magnesium (76 mg per oz) which have shown their benefits in both conditions in different investigations.

    Studies have shown an association between low levels of unsaturated fat consumption and an increased risk of MS [12]. In vitro and animal studies also have demonstrated inhibiting the autoimmune pathways with the supplementation with poly unsaturated fatty acids (PUFA) [13]. Some clinical trials also have confirmed beneficial potentials of PUFA supplementation in patients with MS [14].

    Unsaturated fatty acids also have shown their benefits in clinical studies of fatigue patients with different causes [15]. The bypass of impaired ability of the body to biosynthesize n-3 and n-6 long-chain polyunsaturated fatty acids by inhibiting the ?-6 desaturation of the precursor essential fatty acids is considered as the PUFA mechanism of action in patients with fatigue [16].

    Magnesium, as another active ingredient of almond, has previously shown to be decreased in nervous tissue of patients with multiple sclerosis [17]. Some clinical reports also have supported the role of magnesium supplementation in patients with multiple sclerosis [18]. The important known role of magnesium in development, structure and stability of myelin is considered as possible mechanism of the mentioned effects. Magnesium has also shown its positive effects in patients with fatigue in multiple clinical studies [19]. Supplementation of magnesium appears to improve subjective and objective measures of insomnia in elderly people and may become a useful instrument in managing sleep disorders as one of the etiological factors in development of fatigue [20,21]. According to the mentioned information almond along with its traditional use in patient with MS like symptoms [22], as a rich source of unsaturated fat and magnesium, can be considered hypothetically as a potential nutritional supplement in patients with MS. Upcoming clinical studies are required to evaluate its efficacy.

    Acknowledgment: This letter is contributed to the thesis entitled: ''Clinical Trial of the Effect of Traditional Medicine Nutritional Recommendations on Multiple Sclerosis-related Fatigue level''; which was supported by a grant from Tehran University of Medical Sciences (grant number: 92/d/130/1485). The authors would like to thank Dr Sahraian M.,Dr Azimi A. and Dr Naser Moghadasi A. The authors declare that there is no other conflict of interests.


    1. Multiple Sclerosis International Federation. Number of People with MS Globally. Query Data for 2013 . 2014 [On line]. Available from:

    2. Weiner HL. Multiple sclerosis is an inflammatory T-cell-mediated autoimmune disease. Arch Neurol 2004; 61:1613.

    3. Compston A, Coles A. Multiple sclerosis. Lancet 2008; 372:1502.

    4. Nagaraj K, Taly A.B, Gupta A, Prasad Ch, Christopher R. Prevalence of fatigue in patients with multiple sclerosis and its effect on the quality of life. J Neurosci Rural Pract. 2013 Jul-Sep; 4(3): 278- 282. doi: 10.4103/0976-3147.118774

    5. Veauthier C, Radbruch H, Gaede G, Pfueller CF, D?rr J, Bellmann- Strobl J, Wernecke KD, Zipp F, Paul F, Sieb JP. Fatigue in multiple sclerosis is closely related to sleep disorders: a polysomnographic cross- sectional study. Mult Scler. 2011 May;17(5):613-22. doi: 10.1177/1352458510393772..

    6. Tartaglia MC, Narayanan S, Francis SJ, et al. The relationship between diffuse axonal damage and fatigue in multiple sclerosis. Arch Neurol 2004; 61:201.

    7. Branas P, Jordan R, Fry-Smith A, Burls A, Hyde C. Treatments for fatigue in multiple sclerosis: a rapid and systematic review. Health Technol Assess. 2000;4(27):1-61. Review. PubMed PMID: 11074395.

    8. Parviz, M., Sahraian, M. A., & Rezaeizadeh, H. (2013). Historical Issues of Optic neuritis and Sensory Disorder in Persian Traditional Medicine. Iranian J Publ Health, 42(6), 644-5.

    9. Kannappan, R., Gupta, S. C., Kim, J. H., Reuter, S., & Aggarwal, B. B. (2011). Neuroprotection by spice-derived nutraceuticals: you are what you eat!.Molecular neurobiology, 44(2), 142-159.

    10. Yi, Muqing, Jinde Fu, Lili Zhou, Hong Gao, Chenguang Fan, Jing Shao, Baohua Xu et al. "The effect of almond consumption on elements of endurance exercise performance in trained athletes." Journal of the International Society of Sports Nutrition 11, no. 1 (2014): 18.

    11. Farinotti, M., Simi, S., Di Pietrantonj, C., McDowell, N., Brait, L., Lupo, D., & Filippini, G. (2007). Dietary interventions for multiple sclerosis. Cochrane Database Syst Rev, 1.

    12. Esparza ML, Sasaki S, Kesteloot H. Nutrition, latitude, and multiple sclerosis mortality: an ecologic study. Am J Epidemiol. 1995 Oct 1;142(7):733-7.

    13. Gil A. Polyunsaturated fatty acids and inflammatory diseases. Biomed Pharmacother. 2002 Oct;56(8):388-96.

    14. Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet. 1990 Jul 7;336(8706):37-9.

    15. Behan PO, Behan WM, Horrobin D. Effect of high doses of essential fatty acids on the postviral fatigue syndrome. Acta Neurol Scand. 1990 Sep;82(3):209-16.

    16. Puri BK. Long-chain polyunsaturated fatty acids and the pathophysiology of myalgic encephalomyelitis (chronic fatigue syndrome). J Clin Pathol. 2007 Feb;60(2):122-4.

    17. Yasui M, Yase Y, Ando K, Adachi K, Mukoyama M, Ohsugi K. Magnesium concentration in brains from multiple sclerosis patients. Acta Neurol Scand. 1990 Mar;81(3):197-200.

    18. Rossier P, van Erven S, Wade DT. The effect of magnesium oral therapy on spasticity in a patient with multiple sclerosis. Eur J Neurol. 2000 Nov;7(6):741-4.

    19. Baars EW, Gans S, Ellis EL. The effect of hepar magnesium on seasonal fatigue symptoms: a pilot study. J Altern Complement Med. 2008 May;14(4):395-402.

    20. Abbasi B, Kimiagar M, Sadeghniiat Kh, et al. The effect of magnesium supplementation on primary insomnia in elderly: A double-blind placebo-controlled clinical trial. J Res Med Sci. Dec 2012; 17(12): 1161- 1169.

    21. Barun B. Pathophysiological background and clinical characteristics of sleep disorders in multiple sclerosis. Clin Neurol Neurosurg. 2013 Dec;115 Suppl 1:S82-5. doi: 10.1016/j.clineuro.2013.09.028.

    22. IbneSina H. Al-Qanoon fi al-Tibb (The Canon of Medicine). Beirut: Dare Ehia Attorath Al Arabi; 2005.

    Conflict of Interest:

    None declared

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  9. Is self-identification as 'obese' really a public health solution?

    Johnson et al. [1] provide a benchmark figure for the low (and lowering) levels of identification with the term 'obese' in Great Britain. The stance of the article, not unreasonably, is that low self- identification is a problem for public health. An alternative conclusion might be that respondents have increasingly sophisticated appreciation of social desirability and demonstrate a valuable resistance to the negative stereotypes and stigma of obesity. Is there clear evidence that self- identification as 'obese' is actually good for you? The 'benefits' identified are more about responding to healthcare diagnosis and healthcare advice. Accepting advice from a health professional, albeit dressed up in medical categories, is different from self-identifying as obese in a social survey. In the meantime the evidence is mounting that amplifying the stigma of obesity puts people at risk of chronic stress with negative implications for weight management and long term health [2- 3]. So, it is a serious and pressing question: is beating your self up, identity-wise, about obesity really a public health solution? It seems to have been a gently downward path for society to collectively gain weight. The obvious response for public health is to retrace the steps rather than point out a stigmatised self-identification route for individuals to take up a cliff face. (Metaphorically of course!) Finding the political leadership to tackle the interests vested in an obesogenic path may be the real problem for public health.

    1. Johnson F, et al. BMJ Open 2014; 4(11):e005561. doi: 10.1136/bmjopen-2014-005561

    2. Puhl R, Peterson R, Luedicke J. (2012) Motivating or stigmatizing? Public perceptions of weight-related language used by health care providers. Int J Obesity. doi: 10.1038/ijo.2012.110

    3. Major B, Hunger J, Bunyan D, Miller C (2014) The ironic effects of weight stigma. Journal of Experimental Social Psychology 51, 74-80

    Conflict of Interest:

    None declared

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  10. Re:"Stroke incidence and association with risk factors in women: a 32-year follow- up of The Prospective Population Study on Women in Gothenburg.

    Answer to Comment by prof Alain Braillon

    Thank you for commenting on our paper "Stroke incidence and association with risk factors in women: a 32-year follow- up of the Prospective Population Study of Women in Gothenburg". We appreciate your proposals for extension of the paper, and in this reply, we have clarified the study design and added the inquired information.

    1. We used continuous variables in the analysis of baseline data except for categorical data as the ordinal data for leisure time physical inactivity, self-perceived mental stress, education where a dichotomization was used in accord with given references and data in Methods and Supporting file with references. Smoking was assessed in three categories as described. Blood pressure, blood lipids were assessed and analyzed as continuous variables. The measures were repeated as described in the original papers with references given in the "supporting file". In addition to the baseline blood pressure values analyzed as continuous variables we also used baseline diagnosis of hypertension yes/ no according to present criteria at that time. The criteria are given in Methods. To add facts in the ongoing clinical discussion about low grade hypertension we studied three levels of hypertension 1-3 at baseline in accordance to modern guidelines. We further made a model-predicted risk plot for systolic and diastolic blood pressures. Risk factors as atrial fibrillation, myocardial infarction and diabetes during follow-up were analyzed through survival curves based on Cox regression analysis. We do not agree that the title is misleading; Studying associations between baseline risk factor levels in cohort studies (e.g. Framingham, Nurse's Health Study) is an accepted epidemiological method. However, as we have the advantage of access to 4 follow-up examinations in the Prospective Population Study of Women in Gothenburg (PPSWG) during the 32 year observation period (performed 1974,1980, 1992 and 2000), we could regard it as a limitation that we have not taken full advantage of the possibility to take into account also individual changes in risk factor levels during the 32 years. However, this was not within in the aim of this study which focused on associations between baseline risk factors and stroke during follow-up.

    2. You are quite right that hazard ratio is a relative measure and gives no information about how soon stroke will occur. We have calculated median time to stroke for the women with systolic blood pressure <140 and >= 140, respectively, during the 32 years (n=105 and n=81), which was 27 (95% CI 24.17 - 26.44) and 24 (95% CI 20.50- 24.14) years (significant difference); and with diastolic blood pressure <90 and >= 90 (n=111 and n=75), which was 26 (95% CI 23.84-26.12) and 24 (95% CI 20.65-24.47) years(non-significant difference). '

    3. We have calculated population attributable fraction (PAF) for hypertension as follows:

    PAF% =100 x (NO-NE)/NT where NE= numbers expected in the exposed group if the (age standardized) risk is the same as in the control group; NO= numbers observed in the exposed group; NT= total number of cases. PAF% for SBP >140=10.91% PAF% for DBP >90=15.89%

    Thank you once again for showing interest in our paper! Ann Blomstrand, Christian Blomstrand, Nashmil Ariai, Cecilia Bjorkelund

    Conflict of Interest:

    None declared

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