Dear Editor

Does BJSM even use its review process? Being a runner and running trainer and scientist, I am embarrased about this article.[1] The news *running is unhealthy* quickly went the round. Here in Germany it already was in TV text, in several online newspapers (with headlines like 'Run into Osteoporosis'), and has reached internet discussion boards. It will supposedly appear in printed matter starting tomorrow.

The authors measured bone mineral density in female endurance runners. What, if there was no correlation between running and bone mineral density? No paper! There was no non-running group for comparison. What, if there was no correlation between running distance and bone mineral density? No paper!

Fortunately, there was a correlation.

The results of the regression analyses suggest that the bone mineral density of the lumbar spine and femoral neck are controlled by different parameters. They also suggest that aging alone increases the bone mineral density in the lumbar spine at ages from 18 to 28, whereas it decreases in the femoral neck from age 18. Does anybody believe this?

The suggested effects of running on bone mineral density are in the range of the standard deviations of the measurements. If they even existed, they would be overprinted by the much stronger effects of other parameters (according to the regression equations), i.e. age.

The regression equation regarding the bone mineral density of the femoral neck leads to manifold surprising results. For example, that the entire suggested effect of running would be compensated by a half Mg fizzy tablet per day.

This paper is a perfect example of pseudo-science. The Press turns its 'suggestions' into 'truths'. Thousands of female runners are made feeling insecure. It's embarrassing.

Reference

(1) M Burrows, A M Nevill, S Bird, and D Simpson. Physiological factors associated with low bone mineral density in female endurance runners. Br J Sports Med 2003;37:67-71.

Dear Editor

We cannot help but note the correlation between the results of this study of female athletes, and the study conducted on male long distance runners in Denmark [1]. We propose that sunshine might be the common factor driving the observed bone loss in these two, apparently disparate, sets of athletes.

The secosteroid hormone 1,25-dihydroxyvitamin-D (1,25-D) is a potent stimulator of osteoclast activity [2], and excessive levels of 1,25-D have a direct effect on BMD [3].

1,25-D is manufactured by skin keratinocytes upon exposure to sunlight [4]. Sunscreens have no measurable effect on the amount of 1,25-D produced by solar exposure [5].

Endurance runners are clearly exposed to unusual amounts of direct sunlight during both practice and competition, and we believe that excessive concentrations of 1,25-D could well have been an unconfounded variable in this study.

We would urge measurement of the level of this hormone during any future study of BMD in outdoor athletes.

References

(1) Hetland ML, Haarbo J, Christiansen C. Low bone mass and high bone turnover in male long distance runners. J Clin Endocrinol Metab 1993 Sep;77(3):770-5.
Pubmed Abstract

(2) Manolagas SC. Birth and Death of Bone Cells. Basic Regulatory Mechanisms and Implications for the Pathogenesis and Treatment of Osteoporosis. Endocr Rev 2000 Apr 01;21(2): 115-137.
 Publisher Full Text.

(3) Adams JS, Lee G. Gains in Bone Mineral Density with Resolution of Vitamin D Intoxication. Ann Intern Med 1997 Aug 1;127(3):203-6.
Publisher Full Text

(4) Marshall TG, Marshall FE. New Treatments Emerge as Sarcoidosis Yields Up its Secrets.Clinmed 2003 Jan 27;2003010001 Full Text

(5) Marks R, Foley PA, Jolley D, Knight KR, Harrison J, Thompson SC. The effect of regular sunscreen use on vitamin D levels in an Australian population. Results of a randomized controlled trial. Arch Dermatol 1995 Apr; 131(4): 415-21.
 PubMed Abstract

Dear Editor

With regard to the Leader by ADG Baxter-Jones and N Maffulli [1] we would like to extend our appreciation to the authors for their interest in this never ending “hot debate”.

The authors clearly point out difficulties and potential pitfalls of exercise testing, exercise prescription and the interpretation of acute responses and of the chronic adaptation to exercise training during growth and maturation.[1] We totally support the conclusion that appropriate endurance training in children and adolescents lowers blood lactate levels (BLC) at given workload and improves peak oxygen uptake and performance at anaerobic threshold (AT). However, we strongly feel that the comments on AT especially with respect to so called “lactate criteria” do not consider the current state of knowledge in this field of science.

There are a huge number of different concepts of AT that use BLC, ventilatory measures or the combination of both.[2] In theory the BLC based concepts of AT are supposed to identify the highest exercise intensity at which a steady state of BLC can be identified during a prolonged constant workload. The corresponding steady state BLC is defined as the maximal lactate steady state (MLSS).[3,4] Depending on the testing condition AT measurements determine a workload which correlates with the MLSS workload but which may not be identical to the latter.[3] Therefore behaviour of the BLC during prolonged constant workload exercise conditions has been systematically analysed for individuals aged between 9 and 32 years.[5-11] Differences in experimental methods have been analysed [5] and the procedures were validated against methods previously established and exclusively used in the adult population.[12] The results show that at given exercise intensities up to the level of the workload corresponding to the MLSS the BLC appears to be independent of age across the whole range of maturation from pre-puberty to adulthood.

We agree totally that the acute response and chronic adaptation to exercise of young athletes is not yet fully understood. However, based on the current state of knowledge there is no evidence for the statement:
“In general, BLC levels are lower in children and adolescents than in adults at any given exercise intensity”

and in fact experimental results support the opposing view point.

References

(1) Baxter-Jones ADG and Maffulli N. Endurance in young athletes: it can be trained. Br J Sports Med 2003; 37: 96-97.

(2) Loat CE, Rhodes EC. Relationship between the lactate and ventilatory thresholds during prolonged exercise. Sports Medicine 1993;15(2):104-115.

(3) Beneke R. Anaerobic threshold, individual anaerobic threshold, and maximal lactate steady state in rowing. Med Sci Sports Exerc 1995;27(6):863-867.

(4) Heck H, Mader A, Hess G, et al. Justification of the 4-mmol/l lactate threshold. Int J Sports Med 1985;6:117-130.

(5) Beneke R, Schwarz V, Leithäuser R et al. Maximal lactate steady state in children. Ped Exerc Sci 1996;8(4):328-336.

(6) Beneke R, Heck H, Schwarz V, et al. Maximal lactate steady state during the second decade of age. Med Sci Sports Exerc 1996;28(12):1474-1478.

(7) Beneke R, Leithäuser RM, Schwarz V, et al. Maximales Laktat-Steady- State bei Kindern und Erwachsenen. Dtsch Z Sportmed 2000;51:100-104.

(8) Heck H. Laktat in der Leistungsdiagnostik. Wissenschaftliche Schriftenreihe des deutschen Sportbundes. Schorndorf: Verlag Karl Hofmann, 1990.

(9) Mocellin R, Heusgen M, Korsten-Reck U. Maximal steady state blood lactate levels in 11-year-old-boys. Eur J Pediatr 1990;149: 771-773.

(10) Mocellin R, Heusgen M, Gildein HP. Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys. Eur J Appl Physiol 1991;62:56-60.

(11) Williams JR, Armstrong N. Relationship of maximal lactate steady state to performance at fixed blood lactate reference values in children. Ped Exer Sci 1991;3: 333-341.

(12) Beneke R. Methodological aspects of maximal lactate steady state – implications for performance testing. Eur J Appl Physiol 2003;89:95-99.

Dear Editor

We found the leader by Professor Ernst (Br J Sports Med 2003;37:195-196) to be rather disjointed, out of date and potentially misleading. This is particularly evident in the initial paragraph. The author begins by generally addressing sports medicine clinicians, including those who are trained in mobilisation and manipulation, namely osteopaths, physiotherapists and chiropractors and abruptly concludes, for no apparent reason, that chiropractic manipulation will be the focus of the remainder of the article. Our question is, "Why single out chiropractic manipulation when similar forms of manipulation are routinely practised by all of the other initially identified professions?".[1] This author has a long track record of reporting the potential adverse reactions specifically related to manipulation performed by chiropractors. Additionally, the author chooses a different forum for each "letter". The current leader appears to be simply rehashing old statements rather than adding new material to the discussion. Each new forum tends to confuse the issue further, as new groups of professionals are brought into the debate without all of the information required to make an informed decision. This type of approach requires the chiropractic profession to continually respond in a more defensive fashion. This undermines co-operative research efforts and thwarts any attempt at productive interprofessional debate.

Chiropractic manipulation is singled out, even though Assendelft et al,[2] concluded the minimum effectiveness of spinal manipulation irrespective of the provider was not superior to other treatments for back pain. Such results can also be interpreted as manipulation being at least equivalent to other available treatments. This would naturally increase the number of therapeutic options available for the management of a complex clinical condition. Under these circumstances, clinical utilisation and decision making should always take into account patient centred factors such as side effects and patient satisfaction. Professor Ernst clearly has reservations regarding the United Kingdom's current national clinical practice guideline and evidence review. This states that: "Within the first 6 weeks of acute or recurrent low back pain, manipulation provides better short-term improvement in pain and activity levels and higher patient satisfaction than the treatments to which it has been compared" and "the risks of manipulation for low back pain are very low, provided patients are selected and assessed properly and it is carried out by a trained therapist or practitioner [3] "; i.e., chiropractors, manipulating physiotherapists and osteopaths.

With respect to the forces applied during a manipulation, the paper quoted by Professor Ernst could appear misleading. The loads reported for manipulation by Triano and Schultz [4] do not take into account the surface area of contact and the dissipation of the forces by the local tissues. This would reduce and dissipate the forces over a wider area. Professor Ernst also misleads the reader by suggesting that these loads are inordinately high when in fact, as pointed out by Triano and Schultz [4] "estimates of the loads transmitted were consistent with those observed in common tasks requiring lifting and twisting movements". Furthermore, researchers in this area would freely admit that it has been poorly researched until more recently [5] with chiropractic manipulative forces being the most extensively studied of all the professions mentioned. Professor Ernst also appeared to be unaware of the recent publication by the UK BEAM group.[1] This group, while formulating their methodology concluded that chiropractic, osteopathic and physiotherapeutic manipulation had more similarities than differences: this would be expected to incorporate the potential risks as well as the potential benefits.

With respect to the statement that "dramatic complications have been noted with some degree of regularity" Professor Ernst abruptly switches the argument to cervical manipulation. This statement apparently refers to the potential yet unproven association made between stroke and cervical spine manipulation. Although this is out of direct context with the theme of the leader, namely osteoporosis and back pain, it would suggest there have been many incidences and that the manipulation was a causative factor in the production of vertebrobasilar artery accidents. There is experimental evidence which would argue to the contrary.[6] However, in the relative absence of direct evidence there exists an alternative, yet equally plausible hypothesis for this association: namely, that those people who already have problems with their vertebrobasilar artery (dissection or plaque) develop symptoms, which would lead them to seek out a chiropractor for treatment. This is made more evident in a society where chiropractic is more commonly available, such as Canada and USA. Such problems in diagnosing a patient in this situation are not unique to chiropractic. A recent case report in the Lancet [7] presented details of a patient with acute onset neck pain attending a hospital based emergency department. This patient was given analgesics and discharged. She returned (24 hours later) with more advanced symptoms suggestive of an acute anterior spinal artery syndrome. It is interesting to note that chiropractic manipulation had been ruled out, as had rapid head movement and head trauma, however, no mention of ruling out visits to other practitioners of manipulation was made. Although this is only one isolated report, it is probable that there are many such incidences that go unreported in all health care professions.

With respect to the osteoporotic patient, chiropractors are fully aware of the potential risks involved with the application of manual forces with respect to relative osseous fragility. As a result, osteoporosis has been on the British chiropractors list of relative contraindications for manipulation for years, hence it appears rather surprising that a Professor of complementary therapies would appear to be unaware of this fact. We disagree with the statement by Professor. Ernst, that there is no reliable diagnostic method available to chiropractors. Many chiropractors have alternative methods available to them for determining the potential presence of this condition. None more powerful than a comprehensive case history, which is a fundamental statutory competency. Furthermore, many chiropractors have alternatives to radiographs (DEXA, ultrasound) present in their offices or within a referral service, available for confirmatory objective quantification.

With respect to Professor Ernst's statement concerning information available to the patient; in Britain it is now necessary (indeed incorporated in the educational infrastructure) to inform all patient of the potential risks (benign and potentially serious) as well as expected therapeutic benefits. This is done under the umbrella term of "evidence based medicine" which has been the subject of both undergraduate and postgraduate education in UK chiropractic for at least 10 years. Patients are advised of all the treatment options, including referral to other practitioners. Furthermore they are informed about the use of Xrays and the limitations of plain film Xray to demonstrate the presence or absence of osteoporosis. They are also informed that osteoporosis is a relative contraindication to manual interventions and what that means to the patient in terms of overall case management.

So in conclusion the article by Professor Ernst does not appear to be well informed or well researched. It appears to target chiropractic because there is less information available about the other manipulating disciplines. The chiropractic profession has sought to engage Professor Ernst in constructive dialogue for at least 5 years. However, he still appears to have ignored the steps being taken by professions such as chiropractic whose clinical focus is guided by statutory regulation aimed at protecting the patient and raising standards of care and education.

References

1. Harvey E, Burton AK, Moffett JK, Breen A; UK BEAM trial team. Spinal manipulation for low-back pain: a treatment package agreed to by the UK chiropractic, osteopathy and physiotherapy professional associations. Man Ther. 2003; 8 (1):46-51.

2. Assendelft WJ, Morton SC, Yu EI, Suttorp MJ, Shekelle PG. Spinal manipulative therapy for low back pain. A meta-analysis of effectiveness relative to other therapies. Ann Intern Med. 2003; 138 (11):871-81.

3. Waddell G, Feder G, McIntosh A, Lewis M, Hutchinson A. Clinical guidelines for the management of acute low back pain: clinical guidelines and evidence review. London: Royal College of General Practitioners , 1996.

4. Triano J, Schultz AB. Loads transmitted during lumbosacral spinal manipulative therapy. Spine 1997;22:1955–64.

5. Herzog W. Clinical Biomechanics of spinal manipulation. Ed W Herzog. Pub Churchill Livingston, London, 2002

6. Symons BP, Leonard T, Herzog W. Internal forces sustained by the vertebral artery during spinal manipulative therapy. J Manipulative Physiol Ther. 2002; 25(8):504-10.

7. Latronico N, Fassini P, Antonini B, Gasparotti R. A pain in the neck. Lancet. 2002; 359 (9313):1206.