Recent eLetters

Displaying 1-10 letters out of 268 published

  1. Stand up for better research - avoiding cherry picking when reporting results

    With great interest we read Sj?gren et al.'s contribution that analyzed changes in telomere length in association to the time spent exercising and the time spent sitting in a 6-month randomized controlled trial in 49 older sedentary and overweight men and women. Sj?gren et al. concluded that reduced sitting time was significantly associated with telomere lengthening. These findings are of great potential interest, as highlighted in the accompanying press release. However, several questions remained for us after carefully reading this contribution: 1. In Figure 1 the associations for change in exercise time and change in telomere lengths for control and intervention group are given. When looking only at those participants with no or positive changes in exercise time, there seems to be a zero or even slightly positive association between change in exercise time and change in telomere length. With regard to the main hypothesis as laid down by the authors, we wonder why participants with reduced exercise time over the course of the study show highest values of lengthening. These are participants who exercised up to 500 minutes per week less at the end of the study than they did at baseline. It would be interesting to see an ANCOVA analysis of both groups combined including baseline telomere length values and baseline exercise time values. This would account for differences in baseline values of each subject and additionally for a possible curvilinear relationship between the change in exercise time and the change in telomere length. 2. Sj?gren et al. stated that they did not find significant associations between changes in steps per day and changes in telomere lengths. It would be helpful to see some descriptive statistics and the test results for that statement. Thus, the reader may get a more comprehensive picture of the study result; e. g., non-significance may just be due to small sample size. 3. The main result of the study is provided in figure 2: associations of change in sitting time and change in telomere length by group. Interestingly Sj?gren et al. only refer to the (significant) result in the intervention group which compiles data from 12 individuals. There is almost no association to be seen in the control group. This raises additional questions: How would the authors explain the differential results for the control and the intervention group? Was change in sitting time related to changes in steps per day or to changes in exercise time? 4. To gain a more comprehensive picture of the associations of interest, additional information as outlined above would be helpful. Furthermore, the role of confounders should be more thoroughly discussed, and results from the entire trial included in the discussion. Generally, it should be avoided to focus only on the subgroup with significant test results (Dwan et al. 2008).

    Getting the information to the points above would shine more light on the association between time spent for sitting, exercising and telomere lengths.

    Reference: Dwan K, Altman DG, Arnaiz JA, Bloom J, Chan AW, Cronin E, Decullier E, Easterbrook PJ, Von Elm E, Gamble C, Ghersi D, Ioannidis JP, Simes J, Williamson PR. (2008). Systematic review of the empirical evidence of study publication bias and outcome reporting bias. PloS one, 3(8), e3081.

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  2. Thoracic outlet and pectoralis minor syndromes in sports

    The article by Dr. Twaij and associates nicely covers the range of thoracic outlet syndromes (TOS) seen in athletes. However, several important points have been overlooked. The chief diagnostic tool for neurogenic TOS is physical examination that includes four provocative maneuvers: Upper limb tension test (ULTT}, elevated arm stress test (EAST), neck rotation, and head tilt. 1(Sanders2007) We agree with the authors that pulse deficits by the Adson maneuver are too unreliable to use.

    The most important objective test is measurement of latency and amplitute of the medial antebrachial sensory cutaneous nerve (MAC) on EMG. 2 (Machanic2008) For neurogenic TOS, the only imaging study of value is the plain X-ray of the chest to reveal cervical or anomalous first ribs. MRI is helpful for recognizing associated or differential diagnoses, such as cervical spine or shoulder disease, but MRA to reveal arterial stenosis is not helpful in diagnosing neurogenic TOS because it is relying on a vascular sign to diagnose a neurologic condition. There are too many false negatives and positives.

    The underlying pathology in NTOS, is scarred muscle, not muscle hypertrophy. This comes from the healing of torn muscle fibers from neck trauma, which can be from a single acute accident or repetitive stress injury. 3 (Sanders 1990).

    The second observation in the article is failure to mention another group of closely related diagnoses in athletes that have similar symptoms, but lie below the clavicle in the subpectoral area--namely neurogenic pectoralis minor syndrome (NPMS), as well as arterial pectoralis minor syndrome (APMS) and venous pectoralis minor syndrome (VPMS). It is important to recognize the subpectoral conditions, as when they are present they can be treated by minimal risk surgical procedures, performed as outpatients and have recovery times of only one or two weeks.

    NPMS is a condition seen in athletes who use their arms above shoulder level to throw or pull, such as swimming, baseball, volleyball, gymnastics, and weight lifting. The pectoralis minor muscle (PMM) attaches to the coracoid process of the scapula. As such, repetitive actions of the shoulder that pull back the scapula stress the PMM. In time, the PMM scars, tightens, and can put pressure on any of the three structures in the axillary neurovascular bundle, but most often on the cords and branches of the brachial plexus.

    Symptoms of NPMS are the same as NTOS, pain, numbness, tingling, and weakness in the upper extremity, pain over the trapezius, and a lesser degree of neck pain and occipital headache. It is quite common for NPMS to accompany NTOS.

    Physical examination may reveal the same positive findings as NTOS, but in addition, there are two findings specific for NPMS: Tenderness over the PMM, just below the clavicle, and tenderness in the axilla. These two findings are not from NTOS, but indicate NPMS.

    A very helpful diagnostic test is a PMM muscle block with local anesthetic. After this is performed, the physical examination is repeated and the tenderness in those areas should temporarily disappear or be greatly reduced; provocative maneuvers show improvement. 4 (Sanders 2010)

    Arterial PMS is a condition seen almost exclusively in athletes who use there arms for vigorous overhead throwing. Baseball pitchers and volleyball players are the ones most often affected but it also can occur in mechanics and laborers who work with their arms above their heads. The pathology is either in the axillary artery or one of its branches, most often the posterior circumflex humeral artery(PCHA). This artery traverses the quadralateral space and wraps around the humeral head increasing resistance within the artery and causing aneurysm formation at the axillary-PGHA junction. These aneurysms tend to thrombose. When thrombus breaks off, it enters the axillary artery and embolizes distally.

    Arterial PMS elicits the same symptoms as Arterial TOS: Coldness, palor, arm claudication, and ischemic fingers. Diagnosis is by arteriograms revealing arterial occlusion by emboli in the forearm or hand. It also reveals a normal subclavian artery and may or may not reveal a normal axillary artery. Other mechanisms of APMS are compression of the axillary artery between the PMM and head of the humerus. This can result in axillary artery stenosis or even occlusion. 5 (Atema 2012 )

    Finally, venous PMS is rarely seen and caused by PMM compression of the axillary vein. It is the result of repetitive overhead activities with the upper extremities. Its symptoms are similar to venous TOS, intermittent swelling and cyanosis of the upper extremity. To date, all reported cases have been axillary vein obstruction without thrombosis.6 (Sanders 2007)

    Treatment for neurogenic PMS initially is physical therapy which is mainly stretching exercises of the PMM. If this fails, surgical treatment is minimum risk, outpatient pectoralis minor tenotomy (PMT) with a short recovery time. Treatment for venous TOS is also PMT.

    Arterial PMS is a surgical problem. Physical therapy is not an option. If the problem is stenosis of the axillary artery, PMT may be all that is required. If the axillary artery is aneurysmal or too badly scarred, repair by patch or replacement graft is required.7 (Duwayri 2011)

    Above all, the most important point is to recognize whether the pathology lies above the clavicle in the thoracic outlet area, or below the clavicle in the pectoralis minor area.


    1. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for pectoralis minor syndrome alone or accompanied by neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.

    2. Machanic BI, Sanders RJ. Medial antebrachial cutaneous nerve measurements to diagnose neurogenic thoracic outlet syndrome. Ann Vasc Surg 2008; 22:248-254.

    3. Sanders RJ, Jackson CGR, Banchero N, Pearce WH: Scalene muscle abnormalities in traumatic thoracic outlet syndrome. Am J Surg. 1990; 159:231-6.

    4. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for pectoralis minor syndrome alone or accompanied by neurogenic thoracic outlet syndrome. Ann Vasc Surg 2010 24:701-708.

    5. Atema JJ, Unlu C, Reekers JA, Idu MM. Posterior circumflex humeral artery (PCHA) injury with distal embolizaion in professional volleyball players: Discussion of three cases. Eur J Vasc endovascular Surg 2012;44:195-198.

    6. Sanders RJ, Rao NM. Pectoralis minor obstruction of the axillary vein: Report of six patients. J Vasc Surg 2007; 45:1206-1211.

    7. Duwayri YM, Emery VB, Driskill MR, Earley JA, Wright RW, Paletta GAJr, Thompson RS. Position compression of the axillary artery causing upper extremity thrombosis and embolism in the elite overhead throwing athlete. J Vasc Surg 2011;53:1329-1340.

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  3. Role of intermittent hypoxic expression of Hypoxia Inducible Factors and NFKB in endurance exercise

    We have read the respective article and we agreed with all great findings. Nevertheless, we wish to emphasize the need to address the role of some molecular and physiological markers that may elaborate and possibly support the findings of the study. Intermittent hypoxia exposure can enhance the generation of red blood cells, which may consequentially increase hemoglobin concentration and hematocrit depending on the model of IHE exposure and its effect on serum hypoxia inducible factors (HIF-1 alpha, HIF-2alpha and HIF-3 alpha), erythropointin (EPO) levels and some signaling pathways (such as those mediated by the nuclear factor-kappa light chain B: NF-kB for stress and inflammation examinations) [1]. Hypoxia-inducible factors (HIF-1 alpha, HIF-2alpha and HIF-3alpha) are transcriptional regulatory factors that orchestrate cellular responses to hypoxia and regulates oxygen homeostasis[2]. However hypoxic induction of HIF-1alpha and HIF-2alpha leads to the transcriptional activation of HIF- 3alpha expression as a target gene, which in turn is involved in the reverse negative regulation of other HIFs activities [3]. Less intramuscular hypoxic shifts of metabolic parameters (lactate and pyruvate concentration, lactate/pyruvate and NAD/NADH ratios) after IHT [4] are accompanied by marked decrease of HIF-3alpha expression and increase in the resistance to physical exercise (with up to 70% increase endurance and 25% oxygen pressure in muscle). This indicates the importance of establishing the changes in HIFs system included in this study. Successive normobaric hypoxia-reoxygenation cycles in intermittent hypoxia exposure is associated with generation of cytosolic reactive oxygen species (ROS) which aid in transduction of cellular signals by stabilizing the HIF alpha subunits and promoting its translocation to nucleus and subsequent dimeruization with its alpha subunit to form complexes that binds to hypoxia response element (HRE) to express certain genes (e.g EPO, VEGF, NOS/HO-1 etc) that mediate cellular oxygen adaptation mechanism that will in the long run reflect on exercise performance and endurance[5]. Erythropoiesis is a classic physiologic response to hypoxia that is mediated by the HIFs through inducing cell-type specific gene expression changes that result in increased erythropoietin (EPO) production in kidney, liver and facilitates erythroid progenitor maturation and proliferation. HIF-2 is the main transcription factor that regulates EPO synthesis in the kidney and liver and plays a critical role in the regulation of intestinal iron uptake [6]. Although the heart rate during graded swim test was found to be the same before and after IHE, cardiac responses to hypoxia are quite dependent on carotid body function, which is deeply affected by its oxygen sensing capability. Tissue specificity of HIF-1 homolog (HIF-2alpha) may play an important role in the stable heart rate observed because irrespective of the wide expression of HIF-1 in many cells, including the carotid body glomus cells, hypoxia elicits different responses in different cell types [7]. Additionally, endurance training and intermittent hypoxia are effective preventive strategies against stress induced cardiac and mitochondrial dysfunction. There is need to support the findings of normal heart rate with further studies on signaling pathways, consequent metabolic and redox remodeling associated with a cardioprotective phenotype. This could be achieved by analyzing the myocardial heat shock proteins, cyclooxygenase-2 activity, endoplasmic reticulum stress proteins, nitric oxide production, myocardial antioxidant capacity, sarcolemmal and mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels [8]. In order to obtain a viable result, the inclusion and exclusion criteria must address previous exposure ti intermittent hypobaric hypoxia as it has been reported to decreases myocardial infarction size, reduces the number of ventricular arrhythmias, and improves the recovery of cardiac contractile function against acute ischemia-reperfusion (I/R) injury [9]. The crucial role of mitochondria in cellular energetics, metabolism and intracellular signaling processes regulating cell death and survival [10] has made it important to assess the role of mitochondria in the 4.8% and 1.6% performance declines observed in middle-distance (MD) and long-distance (LD) subjects as reported by the study.

    References: [1]. Zhang, C. Y., Zhang, J. X., L?, X. T., & Li, B. Y. (2009). Effects of intermittent hypoxic exposure on the parameter of erythrocyte and serum hypoxia inducible factor-1 alpha and erythropoietin levels. Xi bao yu fen zi mian yi xue za zhi= Chinese journal of cellular and molecular immunology, 25(10), 932. [2]. Semenza, G. (2009). Regulation of oxygen homeostasis by hypoxia- inducible factor 1. Physiology, 24:97-106. [3]. Hara, S., Hamada, J., Kobayashi, C., Kondo, Y., Imura, N. (2001). Expression and characterization of hypoxia-inducible factor (HIF)-3? in human kidney: suppression of HIF-mediated gene expression by HIF-3?. Biochemical and Biophysical Research Communications, 287:808-813. [4]. Semenza, G.L. (2001). HIF-1 O2 and the 3 PHDs: how animal cells signal hypoxia to the nucleus. Cell 107, 1-3. [5]. Mankovskaya, I., Drevitskaya, T., Dosenko, V., Gavenauskas, B., Moiseenko E. (2006). Expression of transcriptional factor HIF subunits in rat tissues under acute and intermittent hypoxia. Hypoxia Medical Journal, 35:1-2. [6]. Haase, V. H. (2013). Regulation of erythropoiesis by hypoxia- inducible factors. Blood reviews, 27(1), 41-53. [7]. Lahiri, S., Di Giulio, C., & Roy, A. (2002). Lessons from chronic intermittent and sustained hypoxia at high altitudes. Respiratory physiology & neurobiology, 130(3), 223-233. [8]. Kavazis, A.N. (2009). Exercise preconditioning of themyocardium. Sports Med, 11:923-35 [9]. Ostadal, B. and Kolar, F. (2007). Cardiac adaptation to chronic high- altitude hypoxia: beneficial and adverse effects. Respir Physiol Neurobiol. 2(3):224-36. [10]. Ascensao A, Magalhaes J, Soares JM, et al. Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis. Am J Physiol Heart Circ Physiol 2005;2:H722-31.

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  4. Angiogenesis towards Adipogenesis: Role of vascular endothelial growth factor

    We have read the respective article and we agreed with all great findings. But just need to emphasized on some thing very important and crucial. We are working with adipocytes and adipose tissue is capable of expanding many-fold during adulthood, therefore requiring the formation of new vasculature to supply growing and proliferating adipocytes. The expansion of the vasculature in adipose tissue occurs through angiogenesis, where new blood vessels develop from those pre-existing within the tissue (Corvera et al., 2013). Previous studies indicated that adipogenesis may be regulated by factors that drive angiogenesis. Fundamental aspects of angiogenesis, including basement membrane breakdown, vasculogenesis, angiogenic remodeling, vessel stabilization, and vascular permeability. Critical angiogenic factors include vascular endothelial growth factor (VEGF), VEGF receptors, angiopoietins (Ang), ephrins, matrix metalloproteinases, and the plasminogen enzymatic system. Vascular endothelial growth factor is the most critical factor because it initiates the formation of immature vessels and disruption of a single VEGF allele leads to embryonic lethality in mice. Expression of VEGF is influenced by hypoxia, insulin, growth factors, and several cytokines (Hausman et al., 2004). The VEGF has been reported to be modulated by leptin and hCG (Islami et al., 2003) and more recently the expression of angiogenic regulators, VGEF and leptin has been reported to be regulated by the EGF/PI3K/STAT3 pathway (Cascio et al., 2009). These vital findings reflects a regulation of secondary diseases related to obesity to be the result of complex molecular events and adipose tissue vasculature as a source of new targets for metabolic disease therapies. This gene is located on chromosome 11q13 (7 exons). VEGFB has been reported to have a role in endothelial targeting of lipids to peripheral tissues. Dietary lipids present in circulation must be transported through the vascular endothelium to be metabolized by tissue cells. Bioinformatic analysis showed that VEGFB was tightly coexpressed with nuclear-encoded mitochondrial genes across a large variety of physiologic conditions in mice, pointing to a role for VEGFB in metabolism. VEGF specifically controlled endothelial uptake of fatty acids via transcriptional regulation of vascular fatty acid transport proteins. As a consequence, Vegfb-/- mice showed less uptake and accumulation of lipids in muscle, heart, and brown adipose tissue, and instead shunted lipids to white adipose tissue. The co-expression of VEGFB and mitochondrial proteins introduces a novel regulatory mechanism, whereby endothelial lipid uptake and mitochondrial lipid use are tightly coordinated (Hagberg et al., 2012). In our study, we are also looking in to identify the mutation(s) in the VEGF-B gene in Malayisan Obese attributes towards CHD risk. We hypothesized, if there is a mutation in VGEF-B, then the obese subject will be predicted to have hypertension and if there will be no mutation then signs of metabolic syndrome and diabetes type II will be predicted in obese attribute in future. Most important the role of VEGF as major autocrine mediator of FGF-2-induced angiogenesis and proliferation (Naim et al 2005) should be considered by respective researchers in future.


    Cascio S, Ferla R, D'Andrea A, Gerbino A, Bazan V, Surmacz E, Russo A. Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells. J Cell Physiol. 2009 Oct;221(1):189-94. doi: 10.1002/jcp.21843.

    Corvera S, Gealekman O. Adipose tissue angiogenesis: Impact on obesity and type-2 diabetes. Biochim Biophys Acta. 2013 Jun 12. doi:pii: S0925-4439(13)00211-1. 10.1016/j.bbadis.2013.06.003.

    Hagberg CE, Mehlem A, Falkevall A, Muhl L, Fam BC, Orts?ter H, Scotney P, Nyqvist D, Sam?n E, Lu L, Stone-Elander S, Proietto J, Andrikopoulos S, Sj?holm A, Nash A, Eriksson U. Targeting VEGF-B as a novel treatment for insulin resistance and type 2 diabetes. Nature. 2012 Oct 18;490(7420)

    Islami D, Bischof P, Chardonnens D. Modulation of placental vascular endothelial growth factor by leptin and hCG. Mol Hum Reprod. 2003 Jul;9(7):395-8.

    Naim R, Chang RC, Sadick H, Bayerl C, Bran G, Hormann K. Effect of vascular endothelial growth factor on fibroblasts from external auditory canal cholesteatoma. Arch Med Res. 2005 Sep-Oct;36(5):518-23. PubMed PMID: 16099332.

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  5. Fundamentally important information

    Having taught medical students about the benefits of PA for the past 20 years and lived through WHO's 2002 World health day on PA, I had the belief that PA was now integrated and implemented in everyday practice. This nice little piece of research reminds us how difficult it is to change "routine" and how uncomfortable some of us feel when encouraging people to change their behaviour. Back to the drawing board...

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  6. Endurane Running and nutrition

    The article suggests that using fat as an energy source is how to fuel endurance events.

    Why is it that top marathons runners and the SKY/GB team don't do this but have a good balance of mainly carbohydrate and protein?

    Because using fat requires 3% more oxygen for the same amount of energy. Thus energy release is slower and it is why top athletes train specifically to perform glycogen depleted. If you understand the physiology it is so wrong. Why do cyclists consume carbohydrate during long stages

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  7. Can evolution explain the jumper's knee paradox?

    Dear Editor

    I read the excellent study by Halland et al with great interest (1). This study adds further support to the link between higher jumping performance and the development of patellar tendinopathy, as the authors note in the discussion (2). The reasons for this link are unclear but it is worth considering evolutionary theory in any explanation. The 'pleiotropy' theory for the evolution of ageing proposes that there are genetically determined 'trade-offs' between benefits to younger organisms and their viability at older ages (3, 4). In this way the advantage conferred by better jumping performance at a young age may be part of the same genetic package that results in the disadvantage of an increased susceptibility to tendinopathy at an older age.

    1. Helland C, Bojsen-Moller J, Raastad T, Seynnes OR, Moltubakk MM, Jakobsen V, et al. Mechanical properties of the patellar tendon in elite volleyball players with and without patellar tendinopathy. British journal of sports medicine. 2013. Epub 2013/07/09. 2. Visnes H, Aandahl HA, Bahr R. Jumper's knee paradox--jumping ability is a risk factor for developing jumper's knee: a 5-year prospective study. British journal of sports medicine. 2013;47(8):503-7. Epub 2012/10/13. 3. Kirkwood TB. Evolution of ageing. Mechanisms of ageing and development. 2002;123(7):737-45. Epub 2002/03/01. 4. Partridge L, Gems D. Mechanisms of ageing: public or private? Nature reviews Genetics. 2002;3(3):165-75. Epub 2002/04/25.

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  8. "Role of Micronutrients, Antioxidants, Vitamin D and Virgin Olive Oil in Promoting Oral Health"


    Dear Sir, We have read the nice article "Oral health and impact on performance of athletes participating in the London 2012 Olympic Games: a cross-sectional study" by Dr. Needleman and colleagues in your journal (Br J Sports Med2013;47: 1054-1058)(1). In developing countries, the prevalence of dental and periodontal diseases is very high as people have lack of knowledge and are ignorant about oral health(2). Even though the athletes are having physical fitness they might not have given importance for oral health. Food and liquids should be kept in the mouth for a very brief period (3). Food particles continue to remain in the mouth after food and liquid intake because sensory adaptation of the mouth for these particles is very rapid. Lack of antioxidants and micronutrients increases the incidence of dental and periodontal diseases. During high stress periods, intake of micronutrients and antioxidants results in decreased inflammatory processes. High stress exposure is one of the possible factors for exerting an unfavorable influence on periodontal health such as plaque accumulation, local gingivitis and a change in salivary composition (4). In developing countries, the prevalence of vitamin D deficiency ranges between 30-90% (5). Vitamin D acts as an anti- inflammatory agent and stimulates the production of anti-microbial peptides in the saliva (6). Use of 1-2 ml of virgin olive oil (rich in Oleic acid and Phenolic antioxidants)after brushing in the morning and at night before going to sleep will be of help in removing residual food particles and decreasing bacterial growth and adhesion in oral cavity (7, 8).


    1. Needleman I, Ashley P, Petrie A, Fortune F et al. Oral health and impact on performance of athletes participating in the London 2012 Olympic Games: a cross-sectional study Br J Sports Med 2013;47:1054-1058

    2. Petersen PE, Bourgeois D, Ogawa H, Estupinan-Day S, Ndiaye C. The global burden of oral diseases and risks to oral health. Bull World Health Organ. 2005; 83(9):661-9.

    3. Dawes C Salivary flow patterns and the health of hard and soft oral tissues. JADA 2008; 139(5 supp); 18S-24S. 4. Willershausen B, Ross A, F?rsch M, Willershausen I, Mohaupt P, Callaway A. The influence of micronutrients on oral and general health Eur J Med Res. 2011; 16(11): 514-518 5. Arabi A, El Rassi R, El-Hajj Fuleihan G. Hypovitaminosis D in developing countries-prevalence, risk factors and outcomes. Nat Rev Endocrinol. 2010;6(10):550-61

    6. Stein SH, Tipton DA; Vitamin D and its impact on oral health--an update. [Journal Article, Review]; J Tenn Dent Assoc 2011; 91(2):30-33.

    7. Pretty IA, Gallagher MJ, Martin MV, Edgar WM, Higham SMA study to assess the effects of a new detergent-free, olive oil formulation dentifrice in vitro and in vivo. Dent. 2003 Jul;31(5):327-32

    8. Math M.V. Olive Oil and Water - Role in Oral Care. International Journal of Medical and Clinical Research 2013; 4 (1); 258-260.

    From .

    Dr Mahantayya V Math Dr Yashoda R kattimani Dr Rita M khadkikar MGM Medical College Kamothe, Navi Mumbai Maharashtra state, India

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  9. Combined exercise and mobilisation techniques beneficial in treating lateral epicondylalgia

    As a topic worthy of updating, it is disappointing to note fundamental issues with both the methodology of this review as well as errors in reporting of studies, leading to a limited perspective of the role of exercise therapy and mobilisation techniques in treatment of epicondylalgia. There are two major issues that readers ought to be made aware of regarding this review.

    Issue 1: A major issue is the lack of a comprehensive search strategy, with a simple pubmed search identifying several studies (Smidt et al., 2002; Bisset et al., 2006; Croisier et al., 2007 ; Luginbuhl et al., 2008; Nagrale et al., 2009) and at least two other systematic reviews (Bisset et al., 2005; Herd et al., 2008) published within the author specified census period. Stark omissions are two randomised trials, which followed 185 (Smidt et al., 2002) and 198 (Bisset et al., 2006) participants over one year. At least nine additional studies (Park et al., 2010; Slater et al., 2010; Tyler et al., 2010; Peterson et al., 2011; Wen et al., 2011; Fernandez-Carnero et al., 2012; Soderberg et al., 2012; Viswas et al., 2012; Coombes et al., 2013) and a systematic review (Raman et al., 2012) could be found beyond the census period, indicating that an update is already timely.

    The most noticeable gap in the literature presented by Hoogvliet, is that in which exercise and manipulative treatments are included as a part of a multimodal therapy program. Amongst missing evidence in this review, is that which favours, in terms of speeding up resolution, the use of a multimodal program including elbow mobilisation and concentric and eccentric exercise compared to wait and see (Bisset et al., 2006) or placebo intervention (Coombes et al., 2013). Given that combining exercise and manual therapy reflects much of what occurs in clinical practice, its absence is concerning.

    Issue 2: There are errors in presentation of data from individual studies. Readers might be better advised to refer to individual papers, however, this in itself may be problematic given some studies were not correctly referenced to the intended trials (e.g., #30(Cleland et al., 2005), #11(Fernandez-Carnero et al., 2008)). That is, the study by Cleland should refer to the pilot study of 10 participants (Cleland et al., 2005), not the retrospective analysis of 112. There is misrepresentation of studies, for example patient numbers, study design and results are ether incorrect, incomplete or missing for #24 (Vicenzino et al., 1996) variably so in Appendix 1 and text.


    Bisset, L., Beller, E., Jull, G., Brooks, P., Darnell, R. & Vicenzino, B. (2006) Mobilisation with movement and exercise, corticosteroid injection, or wait and see for tennis elbow: randomised trial. BMJ 333, 939.

    Bisset, L., Paungmali, A., Vicenzino, B. & Beller, E. (2005) A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia. Br J Sports Med 39, 411-422; discussion 411-422.

    Cleland, J., Flynn, T.W. & Palmer, J.A. (2005) Incorporation of manual therapy directed at the cerviothoracic spine in patients with lateral epicondylalgia. A pilot clinical trial. J Man Manip Ther 13, 143- 151.

    Coombes, B.K., Bisset, L., Brooks, P., Khan, A. & Vicenzino, B. (2013) Effect of corticosteroid injection, physiotherapy or both on clinical outcomes in patients with unilateral lateral epicondylalgia. A randomized controlled trial. JAMA 309, 461-469.

    Croisier, J.L., Foidart-Dessalle, M., Tinant, F., Crielaard, J.M. & Forthomme, B. (2007) An isokinetic eccentric programme for the management of chronic lateral epicondylar tendinopathy. Br J Sports Med 41, 269-275.

    Fernandez-Carnero, J., Cleland, J.A. & Arbizu, R.L. (2012) Examination of motor and hypoalgesic effects of cervical vs thoracic spine manipulation in patients with lateral epicondylalgia: a clinical trial. J Manipulative Physiol Ther 34, 432-440.

    Fernandez-Carnero, J., Fernandez-de-las-Penas, C. & Cleland, J.A. (2008) Immediate hypoalgesic and motor effects after a single cervical spine manipulation in subjects with lateral epicondylalgia. J Manipulative Physiol Ther 31, 675-681.

    Herd, C.R. & Meserve, B.B. (2008) A systematic review of the effectiveness of manipulative therapy in treating lateral epicondylalgia. J Man Manip Ther 16, 225-237.

    Luginbuhl, R., Brunner, F. & Schneeberger, A.G. (2008) No effect of forearm band and extensor strengthening exercises for the treatment of tennis elbow: a prospective randomised study. La Chirurgia degli organi di movimento 91, 35-40.

    Nagrale, A.V., Herd, C.R., Ganvir, S. & Ramteke, G. (2009) Cyriax physiotherapy versus phonophoresis with supervised exercise in subjects with lateral epicondylalgia: a randomized clinical trial. J Man Manip Ther 17, 171-178.

    Park, J.Y., Park, H.K., Choi, J.H., Moon, E.S., Kim, B.S., Kim, W.S. & Oh, K.S. (2010) Prospective evaluation of the effectiveness of a home-based program of isometric strengthening exercises: 12-month follow- up. Clinics in orthopedic surgery 2, 173-178.

    Peterson, M., Butler, S., Eriksson, M. & Svardsudd, K. (2011) A randomized controlled trial of exercise versus wait-list in chronic tennis elbow (lateral epicondylosis). Upsala journal of medical sciences 116, 269 -279.

    Raman, J., Macdermid, J.C. & Grewal, R. (2012) Effectiveness of different methods of resistane exercses in lateral epicondylosis - a systematic review. J Hand Ther 25, 5-25.

    Slater, H., Theriault, E., Ronningen, B.O., Clark, R. & Nosaka, K. (2010) Exercise-induced mechanical hypoalgesia in musculotendinous tissues of the lateral elbow. Man Ther 15, 66-73.

    Smidt, N., van der Windt, D.A., Assendelft, W.J., Deville, W.L., Korthals-de Bos, I.B. & Bouter, L.M. (2002) Corticosteroid injections, physiotherapy, or a wait-and-see policy for lateral epicondylitis: a randomised controlled trial. Lancet 359, 657-662.

    Soderberg, J., Grooten, W.J. & Ang, B.O. (2012) Effects of eccentric training on hand strength in subjects with lateral epicondylalgia: a randomized-controlled trial. Scand J Med Sci Sports 22, 797-803.

    Tyler, T.F., Thomas, G.C., Nicholas, S.J. & McHugh, M.P. (2010) Addition of isolated wrist extensor eccentric exercise to standard treatment for chronic lateral epicondylosis: a prospective randomized trial. J Shoulder Elbow Surg 19, 917-922.

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  10. Judo, the way of mutual welfare and benefits

    I would like to congratulate Dr. Nikos Malliaropoulos for the initiative to organize a Judo and Martial Arts issue in this prestigious journal1, a topic with increased number of publications in the last decades.2 However, despite the broad range of topics suggested in the initial call for papers1, only four papers (including the editorial) about judo/martial arts were published, which can be an indicative that the high -level quality required by the British Journal of Sporst Medicine is still to be achieved by researchers working on this topic, although no information was provided in the editorial concerning the number of papers submitted and the proportion of articles approved. Other aspects in this editorial also deserve attention: (a) despite the fact that the Kodokan Judo Institute 3 and the International Judo Federation4 present the date of judo creation as 1882, the authors presented 1888 as the year judo was invented, but no reference was given for this fact; (b) the affirmation that "very little has changed since judo was invented.."(p.1137)5 is greatly different from what researchers in judo history6 and sport sociology7 have presented, especially about what has been called judo Westernization or reflexive judo institutional modernization7,8 and women participation, mainly in Japan9; (c) it is well known that Dr. Jigoro Kano (the founder of judo) proposed this modality to achieve different groups and to contribute to physical, moral and intelectual development6 and that there is a tendency to believe that martial arts can contribute to children development especifically 10, but the use of the International Judo Federation4 as reference to describe the benefits of judo lacks scientific background. Prudent skepticism was recommended11 and a lack of evidence was presented12 concerning the real effects of martial arts programs on children development. Furthermore, many recent cases of catastrophic head and neck injuries13, and of female Japanese athletes being physically punished by their coaches, among other problems, have been reported recently in judo.14 Thus, a more balanced and critical view would be preferred in this editorial; (d) although a traditional judo especialization course has been promoted by the International Budo University (Japan) for many years15, and a specialization for judo coaches has been offered by Leipzig University since 199116, the authors of the editorial opted to describe only a course in which one of them is the coordinator and another is a former student, while no competing interests were reported; (e) finally, there is no such institution called "International Judo Federation Union" as presented in the end of the editorial. I hope this letter helps to improve the information provided by the authors and contribute to discussions concerning judo and martial arts research for mutual welfare and benefits as proposed by the founder of judo, Dr. Jigoro Kano. Emerson Franchini Martial Arts and Combat Sports Research Group, School of Physical Education and Sport, University of S?o Paulo, Brazil The author of this letter declare no competing interests.

    References 1. Khan, K. Call for papers - the ECOSEP BJSM judo and martial arts issue 2013. -judo-and-martial-arts-issue-2013/ (accessed 19 Nov 2013) 2. Peset F, Ferrer-Sapena A, Villam?n M et al. Scientific literature analysis of judo in Web of Science ?. Arch Budo 2013;9:81-91. 3. History of Kodokan Judo. Kodokan Judo Institute. (accessed 19 Nov 2013) 4. What is judo? International Judo Federation. (accessed 20 Nov 2013) 5. Malliaropoulos, N, Callan M, Puim B. Judo, the gentle way. Br J Sports Med 2013;47:1137. 6. Carr KG. Making way: war, philosophy and sport in Japanese judo. J Sport Hist 1993;20:167-88. 7. Villam?n M, Brown D, Espartero J, Guti?rrez C. Reflexive modernization and the disembedding of judo from 1946 to the 2000 Sydney Olympics. Int Review Sociol Sport 2004;39:139-56. 8. Saeki T. Organizational reformation of the All Japan Judo Federation organization: a sociological study of issues surrounding the conflict between tradition and modernization in a sport. Int Review Sociol Sport 1994;29:301-15. 9. Miarka B, Marques JB, Franchini E. Reinterpreting the history of women's judo in Japan. Int J Hist Sport 2011;28:1016-29. 10. Diamond A, Lee K. Interventions shown to aid executive function development in children 4 to 12 years old. Science 2011;333:959-64. 11. Strayhorn JM, Strayhorn JC. Martial arts research: prudente skepticism. Science 2011;334:310. 12. Mercer J. Martial arts research: weak evidence. 2011;334:310-1. 13. Kamitani T, Nimura Y, Nagahiro S, et al. Catastrophic head and neck injuries in judo players in Japan from 2003 to 2010. Am J Sports Med 2013;41:1915-21. 14. Judo coach's physical assault off emale athletes is a warning to entire Japanese sporting world. http://www.japan- (accessed 20 Nov 2013). 15. International Budo University Special Course - Budo Specialization Program. (accessed 20 Nov 2013). 16. International Coaching Course. http://www.uni- (accessed 20 Nov 2013).

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