ENIGMA OF OBESITY

571 LOWER ŒSOPHAGEAL SPHINCTER SIR,-Few surgeons, I imagine, will disagree with the views put forward by Dr Salter (March 2, p. 347) concerning the importance of the lower oesophageal sphincter as a major anti reflux mechanism or with his views on conservative measures aimed at preventing or reducing the reflux of gastric contents. Not all of us, of course, accept that the presence or absence of a sliding hiatus hernia is quite so unimportant as he or Cohen and Harris suggest. But what many will disagree with more particularly is Dr Salter’s statement in the summary of his paper that " surgery is unsatisfactory ". His remarks on surgical treatment in the body of his paper are rather more acceptable. He states, for example, that " the results of conventional surgical procedures " (presumably the standard anatomical type of repair) " are notoriously unpredictable ", and later that " presumably the benefits of surgery are the result of creating an additional anti reflux mechanism ". The plication operations that are increasingly replacing the anatomical type of repair do, in fact, create a new anti reflux mechanism-a valve mechanism. The good results of these operations are sometimes attributed to their maintaining the sphincter below the diaphragm and thus ensuring that it is supported in its function by surrounding intra-abdominal pressure. This overlooks the fact that these plication procedures prevent reflux equally as well when constructed above the diaphragm as when constructed below it. Whatever the effect these procedures may or may not have on sphincter function, it can be demonstrated clearly that they do create a valve mechanism. This is so whether the plication valve is constructed proximal to the sphincter or, as in the operation I favour, distal to the sphincter.1 The results of this procedure, far from being unpredictable or unsatisfactory, are extremely predictable and extremely satisfactory. When conservative measures such as those discussed by Dr Salter prove unsatisfactory, surgery can today virtually ensure relief from the symptoms and from the complications of gastric reflux. Royal Victoria Hospital, Belfast BT12 6BA.

J. A. W. BINGHAM.

myocardial infarction can be, in a few patients, extremely difficult, particularly in the first few days which are the time of highest mortality. Left bundle-branch block before the onset of acute pain can cause great problems in the differentiation of myocardial infarction from Serial enzyme acute pericarditis or dissecting aneurysm. values are also of practical help in patients with suspected second infarcts or dysrhythmias. " More of everything " is certainly not better, but standards of hospital practice require more of some things including (1) more financial investment in hospital service laboratories, which are for the most part grossly undercapitalised in relation to their high running cost for staff; and (2) more collaboration between clinicians and laboratory staff to ensure that appropriate tests are available at the acute

richt time.

King’s College Hospital Medical School, Denmark Hill, London SE5. 1. 2. 3. 4.

P.

J. N. HOWORTH.

Martin, N. H. J. clin. Path. 1973, 26, 886. Lancet, 1973, i, 977. Bold, A. M., Wilding, P. ibid. p. 1175. Boyle, C. M., Kapila, A. ibid. p. 538.

* ** Some cardiologists would disagree with Dr Howorth’s assertion of the value of urgent C.K. estimations. We are sure that he does himself and the Glaswegian physicians an injustice and that he would change his mind if faced with convincing evidence. We aimed, as Bold and Wilding said, " to encourage discussion of rational use of laboratory facilities ",3 and we hope that Dr Howorth’s letter may help to do this. He has not given evidence supporting his first conclusion. We too recommended more cooperation between clinicians and laboratory staff (and administrators): such teamwork helps to rationalise use and allocation of capital resources in all areas of medicine, in the interests of the patient.-ED. L. ENIGMA OF OBESITY

SIR,-Dr Fox (Dec. 29, p. 1487) has wrongly attributed his quotation nature seems to be intolerant of obesity in a ectomorphic types, which are rarely subject to obesity recognition of the constitutional individuality of the person may well give a greater understanding of the fact that some of us become obese and others do not under similar environmental circumstances ". This, and other illustrations, oblige him to believe that powerful mechaare of more significance nisms control our weight that than diet or physical activity ". The quotation is from Body Build and Obesity,l a study of 180 obese adolescent girls, the majority of whom were "

...

1.

Bingham, J. A. W. Proc.

R. Soc. Med. 1974,

67,

4.

IS MORE REALLY BETTER ?

SIR,-Prof. N. H. Martin, in his Dyke Memorial Lecturer when discussing laboratory automation, referred to your leading article 2 with evident approval, concluding with fine rhetoric but total inaccuracy3 " There has been no reply ". The failure of the leading article to provoke much correspondence was probably because some of its extravagant opinions led to it not being regarded seriously. Consider, for example, its comment on the determination of serum enzymes in myocardial infarction: " In myocardial infarction, too, routine measurement of enzymes seldom affects decisions on prognosis or diagnosis and even more rarely affects treatment ". The support for this claim, the only reference quoted in the entire leading article, referred to results of a gaming experiment in which 20 Glaswegian physicians guessed the probable extent of myocardial infarction and prognosis from summaries of clinical data, and were then invited to revise their prognostications after figures for serum-transaminases had been added to their data. Since few of the doctors were inclined to change their minds (how many of us do ?), it was concluded that enzyme values did not significantly affect prognostic or diagnostic decision making !1 In fact the urgent determination of serum-creatinephosphokinase is essential at times. Diagnosis of

"

attending a summer weight-control camp-Camp Seascape, Cape Cod. Dr Fox makes no reference to this paper. The paper to which Dr Fox attributes the quotation, Physical Activity of Obese and Non-obese Adolescent Girls Appraised by Motion Picture Sampling,2 is a study of 109 obese girls at Camp Seascape and 72 normal controls at a neighbouring camp (the same girls ?). Nothing in Dr Fox’s

is directly relevant to this paper, which different conclusion based on quite different observations: text

comes to a

"

The striking degree of inactivity of the obese girls, evident while participating in sports under optimum conditions, appears to be a significant factor. It would appear essential to attempt to teach these girls to enjoy more intensive exertion in sport or dance activities which are of social significance to them ". even

In their earlier paper, Seltzer and Mayer1 described anthropometric measurements of the obese girls, and, using Sheldon’s classification of somatotypes, concluded that ectomorphs are lean and endomorphs are obese. No

572 doubt the endomorphism of these obese, prosperous American girls describes a type of adolescent that is inclined to obesity, but surely reference should have been made to the parallel observation that the same girls were strikingly inactive. In fact, Seltzer and Mayer3 make no reference to the activity study of Bullen et awl.2 To say, " Endomorphy predisposes to the laying on of fat unless insufficient diet, excessive activity, disease, or voluntary weight control supervenes "1 is hyperbole and a misuse of English, for, unless the statement refers only to the treatment of established obesity, insufficient diet with excessive activity is what we call malnutrition. In their later paper,3 a happy printer’s error has altered that quotation to " sufficient diet " and so it should remain, with the further change of "adequate" in place of " excessive " activity. Department of Human Nutrition, London School of

Hygiene and Tropical Medicine,

T. P. EDDY.

London WC1. 1. 2.

Seltzer, C. C., Mayer, J. J. Am. med. Ass. 1964, 189, 677. Bullen, B. A., Reed, R. B., Mayer, J. Am. J. clin. Nutr. 1964, 14,

3.

Seltzer, C. C., Mayer, J. Ann.

211. N. Y. Acad. Sci.

1966, 134, 688.

age of 55 and, since the essence of our message is that vitamin-D deficiency is more widespread in the elderly population than has been generally suspected, it does not surprise us (indeed one might even expect it) that 4 of our 83 controls were definitely suffering from osteomalacia, and 2 possibly so. This of course raises the whole question of how one assesses abnormalities in old people. Should they be compared with young people or with other old people ? We decided to pool the data on young and old controls in the belief that the development of osteomalacia cannot be regarded as part of normal ageing. In so doing we ran into the problem of osteomalacia appearing in 6 elderly controls. Rather than extend our normal range to include them, we decided to accept them for what they appeared to beabnormal. The ultimate test must surely be the effect of specific therapy and we have already indicated that the abnormalities we have described in the femoral-neck fracture cases respond to vitamin-D treatment. This material will be published very shortly. As far as the biochemical data are concerned, they were not included in our histology paper for reasons of space, but we cannot accept Dr Hodkinson’s suggestion that the biochemical criterion of osteomalacia is more valid than the histological one. In the final analysis, osteomalacia terms.

OSTEOMALACIA AND FEMORAL FRACTURES

SIR,-Dr Hodkinson (March 9, p. 416) points

out

(quite correctly) that the control data on osteoid surfaces with which we have compared our femoral neck fracture biopsies are not distributed normally, claims that the distribution can be normalised by a logarithmic transformation, and alleges that if this is done the normal range extends from 2-5 to 37-7%, thus embracing a large proportion of the femoral-neck fracture cases which we regard as abnormal. In reply we wish to make three points. Firstly, we are aware of the skew distribution of the control data and therefore made no attempt to calculate a mean and standard deviation. We are of course not interested in the lower limit of these data but only in the upper limit, and the upper limit of 24% suggested by Bordier covers 77 of our 83 controls and appears to us to be a reasonable though arbitrary one to adopt. Secondly, a logarithmic transformation does not normalise the distribution but replaces a positive skewness by a negative skewness. Dr Hodkinson’s suggested upper limit of 37-7% is therefore invalid. A closer approximation to a normal distribution can be obtained by a square-root transformation, which yields an upper limit of 29%. Thirdly, these statistical manipulations depend on the assumption that all the control data are in fact " normal ". This is not necessarily the case. Dr Hodkinson knows as well as anybody how difficult it is to establish the normal range of any parameter in an ageing population, some of whom may be suffering from the very disease which is under study. In this situation, the definition of the " normal range " on strict statistical criteria becomes virtually and the only solution is to present all the impossible, " normal " and abnormal data so that the difference between them is apparent to any observer on simple inspection. This is what we thought we had done. Fig. 3 of our paper (Feb. 16, p. 229) shows the percent osteoid surfaces in all our controls and all our femoral-neck fracture cases, male and female. The line drawn at 24% on fig. 3 is intended as a guide and indicates what we and Bordier, after many years’ experience, regard as the upper normal limit. It is true that 2 of our " normal " females and 4 of our " normal" males are by this definition abnormal, but both the females and 2 of the males also have subnormal calcification fronts and must be regarded as osteomalacic. Moreover, all these 6 cases were over the

M.R.C. Mineral Metabolism

Unit, General Infirmary, Leeds LS1 3EX.

J. AARON J. C. G. GALLAGHER B. E. C. NORDIN.

BACTERÆMIC SHOCK

SIR,-Your editorial (Feb. 23, p. 296) states that most of the information on the pathogenesis of endotoxic shock is derived from work on normal animals receiving endotoxins. The main supporting reference for this statement is a review by R. P. Gilbert published in 1960. Of the clinical literature that has appeared in recent years your leader is chiefly concerned with a paper by Winslow et al. in 1973, which demonstrates the futility of conventional therapy for endotoxic shock, and makes no reference to many clinical as well as experimental studies that give promise for a more meaningful therapy. Much of this new information dates from 1967, with the introduction of the Limulus lysate test for endotoxin1 and shortly thereafter with the incidence of endotoxsemia in gram-negative sepsis in man.2 Another clinical paper (June, 1972)3 demonstrates the presence of circulating endotoxin in the absence as well as in the presence of sepsis, and in sepsis in the absence as well as in the presence of circulating bacteria. In a letter 4 to you in July, 1972, and in a later clinical paper 5 additional data are given to show that the endotoxin in sepsis is not wholly accounted for by the number of circulating bacteria, and that even when a septic focus is the source, some part of the circulating endotoxin is of intestinal origin, as is the case for all of it in non-septic disorders. Other clinical studies report endotoxsemia in non-septic as well as septic disorders, 6, and support the view that when a septic focus cannot account for a persisting endotoxsemia it is because the defence mechanisms, in particular the reticuloendothelial system in the liver, have lost their capacity to extract and detoxify endotoxin entering the circulation from the gut. In consequence of this development, the vascular collapse persists and accounts, in large part, for the high death-rate. It follows that an effective therapy must embrace methods to deal with the endotoxxmia. Recent experimental data indicate that: (1) suppression of gram-negative bacteria in the gut during the period of trauma 8; (2) a continuous infusion of drugs, including the corticosteroids, that counteract the vasoactive agents that increase intestinal

permeability

to

endotoxin 9and (3) peritoneal lavage

to