Reluctance to think: unable or unwilling?

Point of View
Reluctance to think: unable or unwilling?

Simon Brown
School of Human Life Sciences, University of Tasmania,
Locked Bag 1320, Launceston, Tasmania 7250, Australia
Correspondence to Dr Simon Brown at: Simon dot Brown at utas dot edu dot au

Submitted 2 Jul 2011; first decision 15 Jul 2011; revision received 21 Jul 2011;
accepted and published 21 Jul 2011

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Students have started to tell me that they do not want or need to think about science. Those concerned were undergraduate and graduate students pursuing degrees in various biomedical sciences. The thinking expected was entirely normal for science, involving the synthesis of information, problem analysis, calculation, the solution and analysis of practical problems and question development, for example. I have not solicited expressions of reluctance, but I have attempted to elicit more information from those students volunteering them.

While this explicit reluctance to think is new to me, there are reports of similar observations [1-3]. Of course, we are all reluctant to think sometimes, but the new willingness of students to express it implies a more profound problem. If education is intended in part to train students how to learn and think for themselves [4], the reluctance of students to practise this compromises the value of education. For those students intending to practise medicine, work as scientists, formulate health policy, teach or engage in any of the many other occupations that might suit biomedical scientists, an ability to think effectively and efficiently is essential [5]. Students must be helped to prevent a reluctance to think becoming a habit.

Effective thinking relies on both the ability and the willingness to think [4]. Moreover, the ability to think necessarily implies a recognition of the possibility of error [6], which is relatively uncommon among students. There is a considerable difference between the thought patterns of practising scientists and clinicians and those of students. It takes time for thought and practice to develop the questioning, analysis, pattern matching, deduction and educated guesswork that contribute to thinking [7-9]. This is reinforced by a Xhosa speaking South African student of speech and hearing therapy who wrote “… I fail because I have to learn more than the words of your teaching — I have to give back to you the way you think. This is what you are really testing, this is how you assess my ‘intelligence’. You test to see whether I have learnt to think like you yet” [10]. Even if students are willing to think, they may not be as capable as we might hope because they may not have had enough time to develop the necessary thinking skills.

The reluctance of students to think prompts at least four questions. These relate to the significance of the reluctance, the reasons for refusing, the consequences of refusing and how we might encourage students to be more willing to think better. I consider each of these in turn.

What does the reluctance signify?
The reluctance to think could have at least four different interpretations. First, students may believe that they are not required to think or, if it is expected, that it will be done by someone else, such as the teacher [1, 3]. While this may seem unlikely, such a view must have been fostered in class (although it may not have been ours) and it may be that the explicit expectations of the students are insufficient [11]. Second, the student may not really understand what is expected. This may mean that teacher and student do not communicate or that the student does not have a clear understanding of what thinking might be required. Third, the student might understand or have some idea what is expected, but does not know how to go about it. Finally, the student might simply be overwhelmed by work, assessment, personal issues, the demands of holding down a job while studying, for example. This is very common: most of us have had the experience of a student struggling in class simply through lack of sleep resulting from working into the early hours to earn a living.

Why are students reluctant?
The explanations given to me fell into two broad categories: some just wanted ‘the’ answer, and others claimed to be able to think, but did not want to and did not ‘like’ being pushed to do so. Assuming that a student demanding ‘the’ answer is temporarily unable to think, these explanations correspond to deficiencies in Siegel’s [4] two requirements for effective thinking.

The first explanation implies that the student considers that there is only one correct ‘answer’ that is known to the teacher and that all other responses are wrong. Such a view neglects the possibility that there might be several ways of considering a problem [12], that more than one of these might be helpful and that a consideration of an issue from several perspectives might be what the teacher actually wants to elicit. Moreover, it incorrectly presupposes that a ‘wrong’ answer might not provide an indication as to the nature of a better one or to other questions that might be asked [13: 211]. Of course it may be that no definitive answer is known or it may be that there are several partial ‘answers’, which is the nature of science.

This explanation reflects the dualistic thinking that is common [6]. This sort of thinking is reinforced by the formulaic nature of most journal articles, of which Richard Feynman [14] said at the start of his Nobel Prize lecture “[w]e have a habit in writing articles published in scientific journals to make the work as finished as possible, to cover all the tracks, to not worry about the blind alleys or to describe how you had the wrong idea first, and so on. So there isn’t any place to publish, in a dignified manner, what you actually did in order to get to do the work …”. Experienced scientists appreciate how science actually works, but the impression of omniscience conveyed by so much science communication reinforces the dualistic thinking of students.

The predominance of dualistic thinking prompts one to ask what might have happened to students in their previous education that might explain it. Young children ask many questions and clearly do not believe that there is only one answer [15]. By the time a student enters university those skills are largely lost, so questioning may be educated out of young people [16]. There is some evidence that science teachers tend to misrepresent the nature of science to their students [17] which may contribute to the development of the dualistic thinking that can take many years to reverse [6]. Some forms of assessment may also reinforce dualistic thinking because of the implication that there is only one ‘right’ way of considering any problem [18]. Certainly, some students concentrate on what it is necessary to know in order to pass the examination. Consequently, it may be unreasonable to expect students to think like a scientist [19] because most students can only think dualistically [6]. Of course, an important aim of teaching is to foster the development of the ability to think in a more sophisticated manner.

The second explanation is a lack of a desire to think. This represents a greater problem because it may reflect an underlying intellectual laziness that can become a dangerous habit for a biomedical scientist [5]. Of course, it is demanding to think and we all have moments when it is beyond us or subjects about which we are reluctant to think on occasion. If the unwillingness is due to a lack of interest, exhaustion or being over worked it can be difficult to assist. However, more can be done to help if the lack of a desire to think arises from a fear of failure.

Some consequences of not thinking
It is important to have a body of knowledge on which to rely, but the ability to manipulate the information and consider a problem in various ways is essential. The volume and complexity of technical material that students have to come to terms with is enormous and represents a considerable burden. Despite this, students often attempt to memorise almost everything [19]. If they were willing and able to think well, so that they could identify patterns and work things out from a few important pieces of information, students would be empowered, their burden would be reduced and unnecessary stress alleviated. Gagné [20] distinguishes between concepts and principles. A concept can often be encapsulated in a name, whereas a principle involves combinations of or actions on concepts [20]. For example, the concept ‘three’ enables one to identify a group of three objects and distinguish it from groups of different sizes. However, the higher order principles that 2 + 1 = 3, 5 – 2 = 3 or 6/2 = 3 imply a deeper understanding of ‘threeness’. Obviously, an attempt to memorise every instance involving ‘three’ would be futile and misses the point that the principles are transferrable (to ‘four’, for example).

What can be done to encourage a willingness to think?
Several simple techniques can encourage a willingness to think, but their success depends on the establishment of a supportive environment in the classroom. First, demonstrate the appropriate thinking skills, perhaps by including the reasoning in lectures not just detail, even if this must be at the expense of content. Second, admit your own ignorance, because the first step in learning is to learn to identify an absence of knowledge and because it provides an opportunity to involve students in an exploration of the problem. Third, explicitly require that every student think and provide regular opportunities for each of them to practise. Fourth, encourage students to discuss problems with each other in person rather than just electronically. Fifth, assess thinking, having warned your students that you will do so, and accept that this may require recognition of more than one ‘right’ answer.

Conclusions
Some students are reluctant to think, either because of a lack of ability or unwillingness. Irrespective of the reason, students must be persuaded that the ability to think is at least as important as the body of knowledge on which they usually focus. While we may expect too much of some students, it is necessary to help all of them to develop the necessary skills. Thinking strategies should be demonstrated and practised in class and students should be expected to show that they are able to think at an appropriate level.

Funding – none; Conflict of Interests – none declared.

References:

[1] Friedman AM and Heafner TL. “You think for me, so I don’t have to.” The effect of a technology-enhanced, inquiry learning environment on student learning in 11th-grade United States history. Contemporary Issues in Technology and Teacher Education. 2007, 7: 199-216; http://www.citejournal.org/vol7/iss3/socialstudies/article1.cfm

[2] Birkhead T. We’ve bred a generation unable to think. Times Educational Supplement. 6 February 2009, 2009; http://www.tes.co.uk/article.aspx?storycode=6008340

[3] Beachboard MR and Beachboard JC. Critical-thinking pedagogy and student perceptions of university contributions to their academic department. Informing Science. 2010, 13: 53-71; http://inform.nu/Articles/Vol13/ISJv13p053-071Beachboard548.pdf

[4] Siegel H. The rationality of science, critical thinking, and science education. Synthese. 1989, 80: 9-41; http://www.jstor.org/pss/20116665

[5] Kopelman LM. Philosophy and medical education. Academic Medicine. 1995, 70: 795-805; http://www.ncbi.nlm.nih.gov/pubmed/7669156

[6] Brown S. “On the other side of the barrier is thinking”. Acta Didactica Napocensia. 2009, 2: 1-8; http://dppd.ubbcluj.ro/adn/article_2_3_1.pdf

[7] Inhelder B and Piaget J. The growth of logical thinking from childhood to adolescence. New York: Basic Books, Inc.; 1958.

[8] Vygotsky LS. Thought and language. Cambridge: MIT Press; 1962.

[9] Perry WG, Jr. Forms of intellectual and ethical development in the college years: a scheme. New York: Holt, Rinehart and Winston; 1970.

[10] Mpumlwana N. The monster of professional power. Teaching in Higher Education. 2000, 5: 535-540; http://www.tandfonline.com/doi/abs/10.1080/713699169

[11] Rowe WG and O’Brian J. The role of Golem, Pygmalion, and Galatea effects on opportunistic behavior in the classroom. Journal of Management Education. 2002, 26: 612-628; http://jme.sagepub.com/content/26/6/612.abstract

[12] Brown S and Salter S. Analogy in science and science teaching. Advances in Physiology Education. 2010, 34: 167-169; http://advan.physiology.org/content/34/4/167.abstract

[13] Viennot L. Reasoning in physics. The part of common sense. New York: Kluwer Academic Publishers; 2001.

[14] Feynman RP. The development of the space-time view of quantum electrodynamics. Science. 1966, 153: 699-708; http://www.sciencemag.org/content/153/3737/699

[15] Stead EA, Jr and Starmer CF. Restoring the joy in learning. Medical Physiology Online. 16 January 2008; https://medicalphysiologyonline.wordpress.com/2008/01/16/restoring-the-joy-in-learning/

[16] Kuhn D. Children and adults as intuitive scientists. Psychological Review. 1989, 96: 674-689; http://psycnet.apa.org/journals/rev/96/4/674

[17] Benson GD. The misrepresentation of science by philosophers and teachers of science. Synthese. 1989, 80: 107-119; http://www.jstor.org/pss/20116669

[18] Rogers EM. Examinations: powerful agents for good or ill teaching. American Journal of Physics. 1969, 37: 954-962; http://dx.doi.org/10.1119/1.1975217

[19] Copes L. Can college students reason? Spring Meeting of the Seaway Section, Mathematical Association of America, 1975; Toronto; http://www.larrycopes.com/papers/piaget.pdf

[20] Gagné RM. The learning of concepts. School Review. 1965, 73: 187-196; http://www.jstor.org/pss/1083668

Hyperlinks in this manuscript were last accessed 21 Jul 2011. Please cite this article as: Brown S. Reluctance to think: unable or unwilling? Medical Physiology Online 2011; available from https://medicalphysiologyonline.wordpress.com

Reviewers: The original submitted version was reviewed by Dr Frank Starmer, Duke-NUS Graduate Medical School, Singapore; Dr Balint Kacsoh, Mercer University School of Medicine, USA, and the editor E.S.Prakash. The reviewers and the editor have no conflict of interests related to this submission.

Prepublication Record: The Prepublication record containing the original version of the manuscript, reviewers comments, editor’s comments, the authors’ response can be accessed at https://medicalphysiologyonline.wordpress.com/home/archive/

License: This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work, is properly cited.

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Freeing didactic lectures from monotony with a brief mid-lecture presentation on innovations in biomedical technology unrelated to the original lecture

Point of View

Freeing didactic lectures from monotony with a brief mid-lecture presentation on innovations in biomedical technology unrelated to the original lecture

Rajashekar Rao Barkur*, Ullas Kamath*, and K.G.Mohandas Rao

Departments of Biochemistry*, and Anatomy, Melaka Manipal Medical College (Manipal Campus), International Center for Health Sciences, Manipal, Karnataka 576104, India.

Correspondence to Dr Mohandas Rao at mohandaskg at gmail dot com

Submitted 18 Mar 2010; first decision 13 Apr 2010; first revision received 19 Apr 2010;

Second revision accepted 25 Apr 2010; published 27 Apr 2010

This article does not have an abstract.

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Funding – none

Conflict of Interests – none

Please cite this article as: R.R.Barkur, U Kamath and K G Mohandas Rao. Freeing didactic lectures from monotony with a mid-lecture presentation unrelated to the original lecture. Medical Physiology Online 2010; published 27 April 2010 available from http://www.medicalphysiologyonline.org

Reviewer: Dr William H Cliff, Niagara University, USA, reviewed the first version of this manuscript. His comments for the authors are available in the Prepublication Record. The reviewer reports no conflict of interests related to this review.

The revised version of the manuscript was reviewed, further revision requested and the second revision accepted by Editor E.S.Prakash. The accepted version was further edited for brevity, clarity and style by the editor and approved by the authors. The editor has no conflict of interests related to this submission.

Prepublication Record: The prepublication record containing the original version of the manuscript, reviewers comments, editor’s comments, the authors’ response, and the revised versions of the manuscript can be accessed at https://medicalphysiologyonline.wordpress.com/home/archive/

License: This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work, is properly cited.

Can we use will power to negate effect of general anesthetics?

ASK A QUESTION

Can we use will power to negate effect of general anesthetics?

Is it possible for an individual to consciously alter or negate the effect of a drug? For example, can an individual use his will power to remain conscious after being administered a general anaesthetic? Can an individual retain motor function using his will even after being administered skeletal muscular relaxants, eg succinyl choline?. Just out of curiosity..

Janarthan Rama Murti
Second Year Medical Student, AIMST University, Malaysia

E-mail: scientist768 at gmail dot com

Letter regarding the article ‘Cold-activated brown adipose tissue in healthy men’ by Lichtenbelt et al.

LETTER TO THE EDITOR

Using integrated ¹⁸F-fluorodeoxyglucose positron emission tomography and computed tomography, Lichtenbelt et al [1] have demonstrated cold induced brown adipose tissue activity in lean and overweight healthy men. The authors also find a significant negative correlation between body mass index and brown adipose tissue activity.

In this study, body mass index (BMI) was used to classify subjects as lean (BMI < 25 kg/m²) or overweight/obese (BMI ³ 25 kg/m²). However, the percentage of body fat in overweight/obese subjects varied from 16.9 – 41.8%, the lower limit of this being much lower than that in ‘lean’ subjects, indicating that at least some of the subjects who were classified as obese were not ‘excessively fat’. Indeed, for body fat percentage values between 10 and 20% (n = 10 in this study), the authors also found a steep inverse relationship between body fat percentage and brown adipose tissue activity (Figure 3B in Ref. 1). Although what is a healthy body fat percentage remains to be established from prospective studies [2] and obesity is not currently defined on the basis of body fat percentage or fat mass index (i.e., fat mass in kg divided by square of the height expressed in meters; Ref. 3), we are interested in knowing how the volume of brown adipose tissue and resting metabolic rate compared if subjects in this study were dichotomized on the basis of an arbitrary body fat percentage (say 20%) or fat mass index rather than BMI.

Secondly, since waist circumference, an estimate of abdominal adiposity, has been demonstrated to independently predict mortality, [4] we wonder if this was measured in this study and if so how it correlated with brown adipose tissue activity.

Conflict of interests: none

E.S.Prakash and K.R.Sethuraman,

Faculty of Medicine, AIMST University, 08100 Semeling, Kedah, Malaysia

E-mail: dresprakash at gmail dot com

Acknowledgment:

E.S.Prakash is the Editor and Dr K.R.Sethuraman is a member of the Senior Advisory Board of Medical Physiology Online.

Editor for this Submission: This letter was reviewed and accepted for publication by Dr Roger Evans, Department of Physiology, Monash University, Melbourne, Australia. e-mail: roger dot evans at med dot monash dot edu dot au. Dr Evans is a member of the Senior Advisory Board for Medical Physiology Online.

Submitted 15 June 2009, revised 16 Jun 2009, accepted and published 17 Jun 2009.

References:

[1] van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, et al. Cold-activated brown adipose tissue in healthy men. New England Journal of Medicine 2009; 360:1500-8 [Abstract]

[2] Gallagher D, Heymsfield SB, Heo M, Jebb SA, Murgatroyd PR, and Sakamoto Y. Healthy percentage body fat ranges: an approach for developing guidelines based on body mass index. American Journal of Clinical Nutrition 2000; 72: 694–701. [Full text]

[3] Schutz Y, Kyle UUG and Pichard C. Fat-free mass index and fat mass index percentiles in Caucasians aged 18 – 98 y. International Journal of Obesity 2002; 26: 953–960. [Abstract]

[4] Pischon T, Boeing H, Hoffmann K, et al. General and abdominal adiposity and risk of death in Europe. New England Journal of Medicine 2008; 359: 2105-2120. [Full text]

Please cite this letter as E.S.Prakash and K.R.Sethuraman. Letter regarding the article ‘Cold-activated brown adipose tissue in healthy men’ by Lichtenbelt et al. Medical Physiology Online 2009; available from http://www.medicalphysiologyonline.org

Some rights reserved © E.S.Prakash and K.R.Sethuraman, 2009. This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by-nc-sa/3.0/

Cardiac inter-beat interval complexity is influenced by physical activity

RESEARCH COMMUNICATION

Benjamin J. Wilson¹, Gus L. W. Hart², and Allen C. Parcell³

¹Department of Recreation Management and Youth Leadership, Brigham Young University, Provo, Utah; ²Department of Physics and Astronomy, Brigham Young University, Provo, Utah; ³Human Performance Research Center, Department of Exercise Sciences, Brigham Young University, Provo, Utah.

Correspondence to: Benjamin J. Wilson, 3838 S 1860 E, Salt Lake City, UT 84106, USA.

E-mail: benjaminjameswilson at gmail dot com

Submitted 25 Oct 2008; time to first decision 25 days; revision accepted and published 1 Jan 2009.

Abstract:

The complexity of physiological signals may be a more sensitive indicator of health than standard or average measurements. We examined cardiac inter-beat intervals of healthy subjects who are either physically active or sedentary to determine whether measures of complexity are more sensitive to subtle cardiac changes than standard measures. Subjects were pre-screened by self-report, and qualifying subjects were placed in either the active group (n = 10) or sedentary group (n = 10). Cardiac inter-beat intervals were recorded and subsequently analyzed using standard time and frequency domain heart rate variability measurements as well as multiscale entropy and the detrended fluctuation analysis, both measures of complexity. Of the measurements, the detrended fluctuation analysis was the only tool that significantly (P = 0.04) differentiated between the active and sedentary groups. This suggests that the complexity of physiologic signals is a more sensitive indicator of cardiac health than standard measures.

 

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Please cite this article as: Wilson BJ, Hart GLW, Parcell AC. Cardiac inter-beat interval complexity is influenced by physical activity. Medical Physiology Online, 1 Jan 2009, available from http://www.medicalphysiologyonline.org

Brief Review: Premature skeletal muscle fatigue in multiple sclerosis and its implications for exercise therapy

Elizabeth Harper

Department of Health Studies, Program in Therapeutic Recreation,

New York University, NY, 10003, USA;

E-mail: eh403 at nyu dot edu

Submitted 19 March 2008; first decision 9 April 2008; revised 21 May 2008; revision accepted 19 Jun 2008; published 4 Jul 2008

Abstract:

This paper reviews work on skeletal muscle fatigue as it relates to multiple sclerosis. Accumulation of products of metabolism contribute significantly to the onset of fatigue in normal healthy muscles whereas the primary cause of muscle fatigue in multiple sclerosis is due to impairment of central nervous system activation of motor units followed by changes in muscle metabolism due to progressive disuse. As performing repetitive gross motor activity of the limbs becomes increasingly difficult, the MS individual becomes vulnerable to a host of secondary health concerns including weak respiratory muscles. Pranayam is a type of yogic exercise that focuses one’s attention on regulation of the breath. Many of the benefits of practicing pranayam are similar to the physiological and psychological benefits attributed to performing repetitive gross motor exercises of the limbs. Pranayam should be explored as a potential adjunctive therapeutic exercise modality in individuals with multiple sclerosis.

Content outline:

1. Introduction

1.1 Noninvasive muscle testing techniques

1.1A Electromyography

1.1B Magnetic resonance spectroscopy

2. Fatigue in healthy muscle

3. Fatigue in multiple sclerosis

3.1 Origin of fatigue in MS

3.2 Central motor drive in MS

3.3 Deconditioning in MS

3.4 Skeletal muscle fatigue vs. perceived fatigue

3.5 Exercise in the management of multiple sclerosis

3.6 Potential role of pranayam as adjunctive therapy

3.7 Summary and Research Directions

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Please cite this article as Harper E. Premature skeletal muscle fatigue in multiple sclerosis and its implications for exercise therapy. Medical Physiology Online, 4 Jul 2008, available from http://www.medicalphysiologyonline.org

Some rights reserved (C) 2008, E. Harper. This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by-nc-sa/3.0/

What is the link between psychologic stress, caffeine, sympathetic activity and ventricular ectopics?

ASK A QUESTION

Karthik Viswanathan, Coronary Artery Disease Clinical Research Network Group, Leeds Institute for Genetic, Health & Therapeutics, Leeds, United Kingdom. E-mail: drkarthikv at gmail dot com

I see a lot of patients referred to us in the cardiology department with palpitations due to ventricular ectopics, and if there is no evidence of structural heart disease or coronary artery disease, we usually reassure and discharge these patients. Some of them have unifocal ventricular ectopics, some have multifocal ventricular ectopics, others have bigeminy or trigeminy. Few have pauses with compensatory tachycardia thereafter. Very often we get asked: Is there anything we can do to stop these symptoms? We usually say that reducing caffeine, alcohol, stress may help but I don’t really know if there is any physiological basis for this recommendation. Is there any evidence that physiological ventricular ectopics are driven by increased sympathetic activity or by increased levels of stress, caffeine in susceptible people?

Conflict of interests: none declared

When we measure extracellular fluid volume, is transcellular fluid volume also measured?

When we measure extracellular fluid volume, is transcellular fluid volume also measured? How is the total volume of transcellular fluid determined?

Dineash Kumar, Year 1 Medical Student, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah, Malaysia; e-mail: dineashkumar at yahoo dot com

Is 5% dextrose solution an effective osmole?

Ravivarma Rao Panirselvam, Year 1 Medical Student, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah, Malaysia; e-mail: unicorn063 at hotmail dot com

On the real cause of pyloric stenosis of infancy

POINT OF VIEW: 

ON THE REAL CAUSE OF PYLORIC STENOSIS OF INFANCY

An interview with Ian Munro Rogers, School of Medicine, Asian Institute of Medicine, Science & Technology, 08100 Bedong, Kedah Darul Aman, Malaysia. 

Correspondence: irogers2000 at hotmail dot com

Interviewed by E.S.Prakash, Editor, Medical Physiology Online

Interviewed 4 Feb 2008; manuscript received 6 Feb 2008; accepted and published 11 Feb 2008.

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Abbreviations: PS – pyloric stenosis; ESP – E.S.Prakash; IMR – Ian Munro Rogers 

Background: Dr.I.M.Rogers has put forth the hypothesis that the inheritance of a higher than normal parietal cell mass and the ensuing hyperacidity is the primary cause of pyloric stenosis (PS) of infancy. See ref. [1] Rogers IM. The true cause of pyloric stenosis is hyperacidity. Acta Paediatrica 2006; 95: 132–136 available at http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1651-2227.2006.tb02197.x. In this interview, Dr. Rogers answers some questions that come in the wake of this hypothesis.

1. ESP: If the hypothesis that hyperacidity is the ultimate cause of PS of infancy is correct, then, patients with pronounced hyperacidity (example, patients with Zollinger-Ellison syndrome) should also develop this complication. Your comments on this.

IMR: Patients with Zollinger-Ellison syndrome usually have acid-induced peptic ulcers – normally duodenal ulcers which perforate and bleed. Some of them will have PS or rather duodenal stenosis. I think newborns with hyperacidity are a different kettle of fish in the sense that the pyloric canal is very narrow, and even a small further reduction due to acid-induced pyloric sphincter hypertrophy would be enough to precipitate functional stenosis. At this point, other factors which further increase acidity begin to operate and a self-perpetuating process begins, culminating in PS. In a sense, this condition occurs because the rate of pyloric narrowing due to acid exceeds the rate at which age related widening of the pyloric canal occurs. This may be the reason why this condition presents within 3-4 weeks (a narrow interval indeed) of birth. Further, hypergastrinaemia, a phenomenon known to occur at this time (as alluded to my in my review [1]), is also likely to facilitate hypertrophy of the sphincter.

2. ESP: You have mentioned in your review [1] that in babies with PS, the negative feedback relationship between fasting gastrin and acid secretion is not evident until the third week of life. Is this also true for normal babies? If so, what does this indicate?

IMR: Yes, it is true for normal babies. In papers from Dr. MacGuigan’s laboratory, Florida, USA [2, 3], normal babies were found to have hypergastrinaemia without postprandial elevation in gastrin up to 2 months of age. Between 3-4 months, fasting gastrin levels had fallen and postprandial gastrin responses became evident. The implication is that from birth to 2 months of age, gastrin is maximally stimulated and hence can not become higher when exposed to constitutional hyperacidity or after ingestion of a protein containing formula [2].

3. ESP: Are there any studies of plasma levels of secretin (the major humoral mediator regulating meal stimulated secretion of bicarbonate rich secretions from the gastrointestinal tract) in neonates with PS? The question comes as defects in neutralizing the effects of gastric acid might also predispose to the hyperacidity that you consider the prime pathogenetic mechanism in PS.

IMR: In 1975, we published a study [4] in which we evaluated the secretion of secretin in neonates. Curiously, the rise between day 1 and 4 was similar to that observed with gastrin. I know of no more investigations of secretin levels in neonates

4. ESP: Is hyperacidity a consistent feature of PS of infancy?

IMR: Strangely, there have been very few studies of gastric acid secretion in PS. In 1979, we first reported basal hyperacidity in babies with PS compared to normal babies [5]. Heine et al [6] reported higher histamine induced gastric acid secretion in babies with pyloric stenosis before and 1 week after pyloromyotomy.

5. ESP: Is there evidence that a high parietal cell mass is inherited?

IMR: Babies with PS do secrete more acid than normal babies, and this persists after pyloromyotomy [6]. Supporting evidence for primary acidity is the observation that babies who are vomiting and are alkalotic at this age invariably have PS. The condition is strongly familial; it is much more common in males compared to females (4: 1) as duodenal ulcers are in adults. Long term studies have documented problems with hyperacidity long after pyloromyotomy. Preterm normal male babies have been shown to secrete more acid than maturity matched female babies [7]. Thus, while there is no direct evidence of supernormal parietal cell mass, available evidence is indeed consistent with this theory.

6. ESP: Given your hypothesis, it is indeed surprising to me that the tumor does not disappear following gastroenterostomy; i.e., if hyperacidity were the primary cause of the growth of the pyloric sphincter, gastroenterostomy which allows drainage of acid should lead to a perceptible reduction in the size of the pyloric sphincter.

IMR: The extraordinary thing is that the pyloric tumour disappears within days of pyloromyotomy [8] and within weeks of successful medical treatment [9]. Regarding the failure of the tumor to regress following gastroenterostomy [1], it simply may be that unless the hypertrophied pyloric sphincter is divided, it can not relax or dilate with the passage of food. Further, a posterior gastroenterostomy may not drain the antrum well. A poorly drained alkaline antrum is a classical way of increasing gastrin levels – especially after vagotomy, and thus the continuing presence of trophic factors such as gastrin may in addition explain the persistence of the pyloric tumor following gastroenterostomy.  

7. ESP: Alternate causes for pyloric stenosis have been proposed; for example, a relative deficiency of neuronal nitric oxide synthase at the sphincter [10] may be primary to the condition – something like in achalasia. Your comments on this:

IMR: Deficiency of nitric oxide explains the pylorospasm. It does not explain the predominance of this condition in males; neither does it explain spontaneous self-cure after a certain age. The failure of this condition to recur after simply dividing the sphincter and the very good response to adequate medical therapy is also not explained. How does it explain the persistence and complications of high acidity after pyloromyotomy?

8. ESP: The observation that rats with an artificially narrowed pylorus secrete more acid and gastrin in response to a meal and the fact that gastrin producing antral cells become hyperplastic [11] in this model is interesting but in this instance hypergastrinaemia and hyperacidity are secondary to pyloric stenosis not the cause of it. What is your opinion?

IMR: First, the hypothesis that primary hyperacidity is the cause of PS is based on the premise that all babies are potentially at risk of acid induced pylorospasm at around 3-4 weeks; however, babies who develop PS are most vulnerable because the burden of constitutional hyperacidity proves too great. Secondly, in my review [1], I cited the study by Omura et al [11] to suggest that once PS is established, there are mechanisms that maintain hyperacidity. The authors [11] demonstrated hypergastrinaemia secondary to PS. Furthermore, there is evidence for a gastrin independent pyloro-oxyntic local neural reflex [12] that can induce acid secretion. Indeed, Talbot [13] has reported improvement in symptoms in patients with peptic ulcer induced gastric outlet obstruction treated with proton pump inhibitors.

9. ESP: Please tell us what you believe would be the most important research questions that need to be investigated in the management of infantile hypertrophic PS?

IMR: To evaluate the benefit of intravenous proton pump inhibitors after making a diagnosis of PS and while awaiting surgery. Indicators of improvement would be reduced acid and volume loss from the nasogastric aspirate and a reduction in metabolic alkalosis. A period of 2 days is not unusual between diagnosis and surgery; this should allow an adequate appraisal. Retrospective data on patients undergoing surgery for PS on whom 2 acid base studies (preoperatively and intraoperatively) are usual would allow a comparison to be made with the acid base changes as a result of treatment with proton pump inhibitors. In adults who have high acidity and who vomit; i.e., adult pyloric stenosis, preoperative administration of proton pump inhibitors is standard therapy to reduce loss of fluids as well as acid. Indeed, in some instances, the alleged pyloric stenosis is functionally improved or cured by this treatment alone – so the question is why babies in whom acid base and volume homeostasis is less secure should be denied this treatment. I believe that the baby diagnosed early enough to have PS but without access to safe surgery would be advantaged by the sole temporary use of proton pump inhibitors while awaiting the enhanced possibility of spontaneous cure. That is my opinion.

ESP: Thank you very much Dr. Rogers for sharing your thoughts with us.

 

Conflict of interests: none declared.

References:

1. Rogers IM. The true cause of pyloric stenosis is hyperacidity. Acta Paediatrica 2006; 95: 132–136. Free full text at http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1651-2227.2006.tb02197.x
2. Rodgers BM, Dix PM, Talbert JL, McGuigan JE. Fasting and postprandial serum gastrin in normal human neonates. Journal of Pediatric Surgery 1978; 13: 13–16; abstract at http://www.ncbi.nlm.nih.gov/pubmed/633050
3. Moazam F, Kirby WJ, Rodgers BM, McGuigan JE. Physiology of serum gastrin production in neonates and infants. Annals of Surgery 1984; 199: 389–392. Free full text  http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=6712312
4. Rogers IM, Davidson DC, Lawrence J, Buchanan KD. Neonatal secretion of secretin. Archives of Disease in Childhood 1975; 50: 120–122. Abstract at http://adc.bmj.com/cgi/content/abstract/50/2/120
5. Rogers IM, Drainer IK, Dougal AJ, Black J, Logan R. Serum cholecystokinin, basal acid secretion and infantile hypertrophic pyloric stenosis. Archives of Disease in Childhood 1979; 54: 773–775. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/507900
6. Heine W, Grager B, Litzenberger M, Drescher U. Results of Lambling gastric juice analysis in infants with spastic hypertrophic pyloric stenosis. Pädiatrie und Pädologie 1986; 21: 119–125 [Article in German] abstract at http://www.ncbi.nlm.nih.gov/pubmed/3737214
7. Yamataka A, Tsukada K, Laws YY, Murata M, Lane GJ, Osawa M,  Fujimoto T, Miyano T. Pyloromyotomy versus atropine sulphate for infantile hypertrophic pyloric stenosis. Journal of Pediatric Surgery 2000; 35: 338–341. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/10693692
8. Yamamoto A, Kuno M, Sasaki T, Kobayashi Y. Ultrasonographic follow-up of the healing process of medically treated hypertrophy pyloric stenosis. Pediatric Radiology 1998; 28: 177–178. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/9561540
9. Vanderwinden JM, Mailleux P, Schiffmann SN, Vanderhaeghen JJ, De Laet MH. Nitric oxide synthase activity in infantile hypertrophic pyloric stenosis. New England Journal of Medicine 1992; 327: 511–515. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/1378938
10. Omura N, Kashiwagi H, Aoki T. Changes in gastric hormones associated with gastric outlet obstruction. An experimental study in rats. Scandinavian Journal of Gastroenterology 1993; 28: 59–62. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/8103237
11. Proof of a pyloro-oxyntic reflex for stimulation of acid secretion. Gastroenterology 1974; 66: 526–532. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/8103237
12. Talbot D. Treatment of adult pyloric stenosis: a pharmacological alternative? British Journal of Clinical Practice 1993; 47: 220–221. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/8260347

Copyright © IM Rogers, 2008. This is an open access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by-nc-sa/3.0

Editor’s note (conflict of interest): I invited this manuscript from Dr. Rogers, reviewed and edited it. Both Dr. Rogers and I work in the School of Medicine, Asian Institute of Medicine, Science & Technology, Malaysia, but that wouldn’t affect my review and disposition of this manuscript. – E.S.Prakash, Editor, Medical Physiology Online.

Please cite this article as Rogers IM. On the real cause of pyloric stenosis of infancy. Medical Physiology Online, 11 Feb 2008, available from http://www.medicalphysiologyonline.org