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Recent eLetters

Displaying 1-10 letters out of 312 published

  1. 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.

    References:

    1. Multiple Sclerosis International Federation. Number of People with MS Globally. Query Data for 2013 . 2014 [On line]. Available from: http://www.atlasofms.org/query.aspx

    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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  2. 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:

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  3. 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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  4. Low-fats and not low-carbs for better diabetes control in Indians

    This large study has clearly shown that Indians continue to consume more carbohydrates, but there was no association between this major source of calories and glucose levels in diabetics or non-diabetics. Since 1972, all national surveys in India have reported that there were no significant differences in dietary calories or carbohydrates, between normal populations and people with diabetes (newly ascertained or known).

    I have conducted population surveys between 1986-1990, among migrants of Indian origin (Southall, London), first-generation Malaysian Indians (Kelang), and second-generation Indo-Guyanese (Enterprise), as well as in rural Indian populations from 5 Indian States - Himachal Pradesh (Kalpa), Delhi (Palam), Gujarat (Khubadthal and Kuha), Orissa (Erasama), Kerala (Arivikkara Konam and Kottayam). Among these migrant and rural Indian populations, there were no differences in the total energy intake and, proportions of total or complex carbohydrates and free sugars. Complex carbohydrates constituted major source of carbohydrates even in those with abnormal glucose tolerance. It was not possible to identify any specific Indian dietary pattern to relate with diabetes. But, there was some evidence to suggest that total fats are more in Indian diets (1). Based on these findings, we have successfully conducted long-term (3-year) intervention studies with reduced-fat diets, and demonstrated better diabetes control in type-2 diabetes (2) and prevention of diabetes development among people with prediabetes (3).

    Current dietary advices for diabetes in India (and possibly in other Asian countries), are mostly based on Western literature and do not really apply to Indian context. It is not how much of 'sugar' one eats, but what matters is the amount and nature of the 'fat' in food. This warrants an urgent reconsideration of the conventional prescriptions of diabetic diets - "no rice, no sugar in coffee, no fruits or no potatoes" - just doesn't mean anything. Such practices inadvertently increase fat proportions in diets, and unknowingly diabetics are harmed. "No oils, no fats, no food fads" - should be the advice for diabetics in our country.

    References:

    1. Rao PV. Dietary patterns and glucose intolerance among rural Indian populations. J Indian Med Assoc. 2002;100:137-40.

    2. Neelima GR, Chandrakala G, Arpana G, Jain AK, Rao PV. Long-term (3 -year) effects of a reduced-fat diet in type 2 diabetes. Paper presented at: The 69th Scientific Sessions of the American Medical Association; 2009 June 5-9; New Orleans, USA. Available from: http://professional.diabetes.org/Abstracts_Display.aspx?TYP=1&CID=74437

    3. Chandrakala G, Arpana G, Rao PV. Long-term effects of a reduced fat diet intervention in pre-diabetes. Paper presented at: The 70th Scientific Sessions of the American Diabetes Association; 2010 June 25-29; Orlando, USA. Available from: http://professional.diabetes.org/Abstracts_Display.aspx?TYP=1&CID=81434

    Conflict of Interest:

    None declared

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  5. Request for correction to authors' affiliations

    Dear BMJ Open,

    We kindly request that the following amendments be made to the authors' affiliations in the Protocol:

    PROTOCOL FOR DEVELOPING THE EVIDENCE BASE FOR A NATIONAL SALT REDUCTION PROGRAM FOR INDIA

    Claire Johnson 1,2 Sailesh Mohan 3, Devarsetty Praveen 2,4, Mark Woodward 1,2, Pallab K Maulik 2,4, Roopa Shivashankar 3,6 , Ritvik Amarchand 7,Jacqui Webster 1, Elizabeth Dunford 1, Thout Sudhir Raj 4, Graham MacGregor 8, Feng He 8, K. Srinath Reddy 3, Anand Krishnan 7, Dorairaj Prabhakaran 3,6, Bruce Neal 1,9,10

    1 George Institute for Global Health, Australia,

    2 The University of Sydney

    3 Public Health Foundation of India, New Delhi, India

    4 George Institute for Global Health, India

    5 George Institute for Global Health, Oxford University

    6 Centre for Chronic Disease Control, India

    7 All India Institute of Medical Sciences, New Delhi, India

    8 Wolfson Institute of Preventative Medicine

    9 Royal Prince Alfred Hospital

    10 Imperial College London

    Conflict of Interest:

    None declared

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  6. Primal Lakeshore Diet

    Mosconi et al's (2014) fascinating study found a diet that is rich in produce and fish appears to be neuroprotective (1). This brought to mind some other literature.

    It has been asserted that our brains were shaped for a tropical lakeshore lifestyle (2, 3). The land/water interface would have provided docosahexaenoic acid (DHA), which is needed for brain development. Early man is believed to have had a DHA-rich diet featuring fish, shellfish, and shorebird nestlings and eggs. This supported the shaping of the human brain.

    It might also be argued that the tropical lakeshores likely would have been rich in plant life and thus produce. Milton (2000) points to physiological evidence indicating that our ancient ancestors ate a diet rich in tropical plant foods (4). There is some indication that phytochemicals play roles in brain health (5, 6). Produce would have also provided prebiotics (7). Gut microbiota are believed to influence brain health (8). A tropical lakeshore diet rich in prebiotics would have promoted a healthy gut ecosystem.

    Thus Mosconi et al's (2014) study is consistent with the idea that our brains were shaped by a tropical lakeshore lifestyle and modern health educators should take our primal diet into consideration when developing nutritional advice.

    About the author: www.CeliaMRoss.com

    (1) Mosconi L, Murray J, Davies M, et al. Nutrient intake and brain biomarkers of Alzheimer's disease in at-risk cognitively normal individuals: a cross-sectional neuroimaging pilot study. BMJ Open. 2014 Jun 24;4(6):e004850.

    (2) Crawford MA, Bloom M, Broadhurst CL, et al. Evidence for the unique function of docosahexaenoic acid during the evolution of the modern hominid brain. Lipids. 1999;34 Suppl:S39-47.

    (3) Broadhurst CL, Wang Y, Crawford MA, et al. Brain-specific lipids from marine, lacustrine, or terrestrial food resources: potential impact on early African Homo sapiens. Comp Biochem Physiol B Biochem Mol Biol. 2002 Apr;131(4):653-73.

    (4) Milton K. Hunter-gatherer diets-a different perspective. Am J Clin Nutr. 2000 Mar; 71(3):665-7.

    (5) Miller MG, Shukitt-Hale B. Berry fruit enhances beneficial signaling in the brain. J Agric Food Chem. 2012 Jun 13;60(23):5709-15.

    (6) Kesse-Guyot E, Andreeva VA, Ducros V, et al. Carotenoid-rich dietary patterns during midlife and subsequent cognitive function. Br J Nutr. 2014 Mar 14;111(5):915-23.

    (7) Blaut M. Relationship of prebiotics and food to intestinal microflora. Eur J Nutr. 2002 Nov;41 Suppl 1:I11-6.

    (8) Tillisch K. The effects of gut microbiota on CNS function in humans. Gut Microbes. 2014 May 16;5(3).

    Conflict of Interest:

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  7. Response to 'Supervised Learning Events: is rebranding enough?'

    Dear Editor

    We read with interest Mr Ali's response (Supervised Learning Events: is rebranding enough?) to our article (1) and we agree with the sentiments expressed in his letter.

    In terms of the issue of training raised by Mr Ali, although we did have a question on our discussion guide that asked trainees and trainers about their 'needs for SLE development in order to improve educational practice', we did not always specifically ask each participant 'what training have you had for SLEs?'. However, some participants did talk about this in response to our fourth research question (what are participants' suggestions for how SLEs should be developed?).

    While some trainers talked about receiving information from their Deaneries but perhaps not fully engaging with it, others talked about finding out about SLEs through courses attended, sometimes about WPBAs/SLEs or the tools used within them, but also through their attendance at courses meant to be about something else. Therefore, SLE training for trainers, who discussed this issue, seemed to be variable, serendipitous and lacking coordination.

    While some trainees mentioned receiving informal training about WPBAs/SLEs, formal training about SLEs was not particularly mentioned by our sample. Therefore, many of our study participants had not received training on SLEs.

    One of the key recommendations from our study is that we need to improve trainee and trainers' understandings of SLEs (1). Ultimately, we agree with Mr Ali that we cannot begin to improve trainee and trainer perceptions about SLEs and educational practices around them without trainees and trainers having a better understanding of what they are and how best to do them.

    References 1. Rees CE, Cleland JA, Dennis A, Kelly N, Mattick K, Monrouxe LV. Supervised learning events in the Foundation Programme: a UK-wide narrative interview study. BMJ Open. 2014 16;4(10).

    Conflict of Interest:

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  8. Risk factors for stroke

    Blomstrand et al's study on stroke incidence among women and associations with risk factors deserves comments.

    First, using arbitrary cut-points for risk factors is not appropriate when there is a continuous distribution of the values with no obvious modal values. Moreover, they risk factors were based on a single assessment at baseline and there are multiple dimensions including amount and duration as well as timing. Accordingly, the title is misleading, although the incidence study is prospective, the risk factors study is cross sectional. Breaches in such basic principles contrasts with the use of Cox proportional hazards regression models with complex adjustments and may explain why hazard ratios were low. The box "Strengths and limitations of this study" must be modified.

    Second hazard ratio is a relative measure, it tells us nothing about absolute risk and no gives us no information about how soon the stroke will occur.

    Third, Blomstrand et al should provide the population attributable fraction (PAF) which facilitates the true understanding of the contribution of a risk factor to disease burden: PAF is the proportional reduction in population disease or mortality that would occur if exposure to a risk factor were reduced to an alternative ideal exposure scenario.

    1 Blomstrand A, Blomstrand C, Ariai N, et al. Stroke incidence and association with risk factors in women: a 32-year followup of the Prospective Population Study of Women in Gothenburg. BMJ Open 2014;4:e005173.

    Conflict of Interest:

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  9. Fundamental concepts for male circumcision

    Surgery should not be performed unless a medical condition has developed. This is a fundamental concept in surgery [1, 2]. Unless a disease or medical condition is present the risk of surgery cannot be balanced against a risk of disease. If no disease is present no risk can be accepted [1]. This would make male circumcision in infants unacceptable, especially given the risk of death due to blood loss [3,4].

    Hidden motivations for circumcision can result from the trauma associated with the amputation of an area of the genitals [5]. People who have been circumcised, had people close to them circumcised or performed circumcision could encourage others to embrace circumcision, without fully considering the dangers, in order to deal with the trauma. This may occur consciously or subconsciously.

    Research into amputation would require consenting adults who would be fully informed about what will be amputated and the associated dangers. An alternative to this would be people having tissue removed to help solve a medical problem that has developed. The person's health after the procedure can then be monitored and studied. For many occurrences of male circumcision it appears the surgery has been carried out on children and now attempts are being made to explain why it was done. An example of this is the argument about circumcision to prevent sexually transmitted diseases (STDs) and the human immunodeficiency virus (HIV). A person who is circumcised can still contract HIV.

    Circumcision cannot be compared to vaccination as unlike vaccination it deprives the child of healthy tissue.

    Care must be taken to watch out for any bias in research (conscious or subconscious). This is relatively easy to notice in male circumcision research. For example the basic surgical concept (mentioned above) will often not be addressed or mentioned. Alternative arguments will not be addressed or discussed. There are three examples of this for male circumcision. Firstly, alternative factors, such as personal hygiene and exposure to carcinogens will not be discussed or considered. Secondly, lack of education amongst adults and medics means they often retract the foreskin with force causing damage to the gland, foreskin and opening the urethra further increasing the risk of infection especially during bathing. This concept of lack of education is often ignored and forgotten when a bias exists. Thirdly, less extreme methods (such as education and testing before sexual intercourse for HIV prevention and less invasive surgery for foreskin tightness [6]) will be ignored.

    REFERENCES 1. J M Hutson, Circumcision: a surgeon's perspective, J Med Ethics, 2004;30:238.

    2. American Academy of Pediatrics, Committee on Fetus and Newborn. Standards and recommendations for hospital care of newborn infants. [5th ed]. Evanston, IL: American Academy of Pediatrics, 1979

    3. Baker RL. Newborn male circumcision: needless and dangerous. Sexual Medicine Today. 1979;3(11):35-36.

    4. Bollinger, Dan. Lost Boys: An Estimate of U.S. Circumcision- Related Infant Deaths. Thymos: Journal of Boyhood Studies. 2010;4(1):78- 90.

    5. R Goldman, Circumcision: The Hidden Trauma, Boston, Vanguard Publishing, 1997

    6. P. M. Cuckow, G Rix, and P. D.E. Mouriquand Preputial Plasty: A Good Alternative to Circumcision Journal of Pediatric Surgery, Vol 29 (4): (April), 1994: pp 561-563

    Conflict of Interest:

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  10. Erratum

    Figure 3 reports yearly lung cancer incidence per 100 000 inhabitants and not percentage as stated in the main text (page 5, end of results).

    Conflict of Interest:

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