obesity in childhood

1
1353 work. As to crowns, the fee allowed is not regarded as an economic one by most dentists, and they say that they cannot afford to undertake this type of work. The likely outcome in the end is extraction of the damaged teeth and the fitting of a denture. One of the arguments advanced in the report against the designation of dental erosion as an industrial disease is the difficulty of disposing of doubtful claims for dental services. But if the disability were assessed on the life expectancy of the dentition as a whole, the finding of a neglected mouth would rule out conservation. Such a patient would have to have full dentures early, regardless of the erosion. The subcommittee was not unanimous in its opinion, so we hope that the subject may be reconsidered. ALCOHOL AND THE PANCREAS THERE is a definite association between alcoholism and chronic pancreatitis, but the mechanism of this link is obscure. Certainly, one or two whiskies are unlikely to impair pancreatic secretion; in fact, intravenous alcohol in dogs stimulates secretion.’ I Alcohol encourages the production of hydrochloric acid by the stomach, and that in turn releases secretin from the duodenum, followed by increased pancreatic secretion, and after total gastrec- tomy, alcohol given by mouth or intravenously has no effect on the volume of pancreatic juice.2 One suggestion was that pressure in the pancreatic duct may rise high enough to produce pancreatitis if there is coincidental obstruction by oedema of the papilla or spasm of the sphincter of Oddi, such as may accompany the gastro- duodenitis often produced by alcohol. 3 Davis et al .4 have now shown that alcohol given intravenously to healthy people greatly reduced the volume of duodenal aspirate evoked by secretin under strictly controlled conditions; but amylase and bicarbonate concentrations in the aspirate were normal or raised. The effects of intraduodenal alcohol were less striking, but the blood-alcohol levels reached under these conditions were much less than after an intravenous dose. The association of reduced volume with normal or raised enzyme and bicarbonate levels suggests obstruction of the pancreatic duct. 5 Oral or intraduodenal alcohol might cause duodenitis and duct obstruction," but intravenous administration would be unlikely to do so. Davis et al. also stimulated pancreatic secretion by a constant infusion of secretin, and they found that intravenous alcohol caused a fall in the volume of duodenal aspirate from 9 ml. to 2 ml. in 5 minutes. Sublingual glyceryl trinitrate then raised the volume to 6 ml. in 5 minutes, suggesting that a readily reversible spasm of the outflow tract may have been responsible. These results suggest that the effects of acute administra- tion of alcohol are due to obstruction of the pancreatic duct, and that this action is more closely related to blood-alcohol level than to the route of administration. 1. Walton, B. E., Schapiro, H., Woodward, E. R. Am. Surg. 1962, 28, 443. 2. Preston, F. W., Kukral, J. C. Surg. Clin. N. Am. 1962, 42, 203. 3. Cecil and Loeb’s Textbook of Medicine (edited by P. B. and W. McDermott). Philadelphia, 1963. 4. Davis, A. E., Pirola, R. C., Blagonravoff, L. Med. J Aust. 1966, ii, 757. 5 Dreiling, D. A., Janowitz, H. D Ciba Foundation Symposium on the Exocrine Pancreas (edited by A. V. S. de Reuck and M. P. Cameron). London, 1962 6. Dreiling, D. A., Richman, A., Fradkin, N. T. Gastroenterology, 1952, 20, 636. The relevance of these findings to chronic pancreatitis is unknown. One difficulty is that chronic alcoholism is often associated with chronic gastritis and achlorhydria, which would abolish the acid-secretin secretory reflex in the pancreas. Moreover, though a long-continued increase in pancreatic-duct pressure sounds a likely cause of chronic pancreatitis, many workers disagree about this. While it can be shown that continued pancreatic secretion against an obstructed duct leads to a rise in serum-amylase levels this does not necessarily imply acinar necrosis, for the blood levels of amylase are determined by the sum of the processes of production and elimination; and if the elimination is restricted, the blood level rises. McCutcheon, summarising the evidence against the obstruction hypothesis, pointed to the fact that obstruc- tion of the major pancreatic duct in cats, dogs, and rabbits causes atrophy of acini with preservation of the islets of Langerhans, but not pancreatitis 8; and, according to Thal et al.,9 experiments in which maximum secretory activity was provoked in the presence of complete duct obstruction failed to produce pancreatic necrosis. Nevertheless, these observations have been concerned largely with the production of acute pancreatitis, and their relevance to the chronic state is questionable. Chemical as well as mechanical factors may operate. For example, an excess of ethyl radicals may compete with methyl groups in a metabolic pathway analogous to that followed when the administration of ethionine to experimental animals is associated with severe pancreatic necrosis.3 10 OBESITY IN CHILDHOOD COMMENTING 11 on the treatmemt of obesity in childhood, we remarked that most obese children grow into even more obese adults. But some do not, and in a survey Grant 12 has tried to distinguish between obesity in children which was likely to be temporary and that which would persist into adult life. Growth records of about 1000 English children showed that somatic types were remarkably constant over the whole period from below 8 to over 14 years of age. There was an average gain of 10% in weight with every 2 inches gained in height, and this was observed in children varying from l5O/., underweight to 15’% overweight. Progressive obesity resulted when a gain in weight of more than 10%, was maintained for eight or more years. A few children had transient obesity which was different from progressive obesity in its abrupt onset, high initial rate of gain, and rapid slowing down with a gradual return to the previous physique. The constancy of the individual growth-rates over long periods suggests that internal constitutional factors rather than environment play the biggest part in their pro- duction. It also suggests that short-term treatment with drugs or psychotherapy is unlikely to be of permanent value. The best chance of prophylactic success in preventing progressive obesity may be found in detecting growth-rates in excess of 10%, at the earliest oppor- tunity, and regulating dietary intake from this stage to maintain them at or below this critical level. 7. McCutcheon, A. D. Lancet, 1962, i, 710. 8. Wang, C., Strauss, L., Adlersberg, D. Gastroenterology, 1958, 35, 465. 9. Thai, A., Perry, J. F., Egner, W. Surgery Gynec. Obstet. 1957, 105, 191. 10. Meister, A. Biochemistry of the Ammo-acids. New York, 1965. 11. Lancet, Aug. 6, 1966, p 327. 12. Grant, M W. Med. Offr 1966, 115, 331

Upload: ngodieu

Post on 30-Dec-2016

216 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: OBESITY IN CHILDHOOD

1353

work. As to crowns, the fee allowed is not regarded as aneconomic one by most dentists, and they say that theycannot afford to undertake this type of work. The likelyoutcome in the end is extraction of the damaged teeth andthe fitting of a denture.One of the arguments advanced in the report against the

designation of dental erosion as an industrial disease isthe difficulty of disposing of doubtful claims for dentalservices. But if the disability were assessed on the life

expectancy of the dentition as a whole, the finding of aneglected mouth would rule out conservation. Such a

patient would have to have full dentures early, regardlessof the erosion. The subcommittee was not unanimousin its opinion, so we hope that the subject may bereconsidered.

ALCOHOL AND THE PANCREAS

THERE is a definite association between alcoholism andchronic pancreatitis, but the mechanism of this link isobscure. Certainly, one or two whiskies are unlikely toimpair pancreatic secretion; in fact, intravenous alcoholin dogs stimulates secretion.’ I Alcohol encourages the

production of hydrochloric acid by the stomach, andthat in turn releases secretin from the duodenum, followedby increased pancreatic secretion, and after total gastrec-tomy, alcohol given by mouth or intravenously has noeffect on the volume of pancreatic juice.2 One suggestionwas that pressure in the pancreatic duct may rise highenough to produce pancreatitis if there is coincidentalobstruction by oedema of the papilla or spasm of thesphincter of Oddi, such as may accompany the gastro-duodenitis often produced by alcohol. 3Davis et al .4 have now shown that alcohol given

intravenously to healthy people greatly reduced thevolume of duodenal aspirate evoked by secretin understrictly controlled conditions; but amylase and bicarbonateconcentrations in the aspirate were normal or raised.The effects of intraduodenal alcohol were less striking,but the blood-alcohol levels reached under these conditionswere much less than after an intravenous dose. Theassociation of reduced volume with normal or raised

enzyme and bicarbonate levels suggests obstruction of the

pancreatic duct. 5 Oral or intraduodenal alcohol mightcause duodenitis and duct obstruction," but intravenousadministration would be unlikely to do so. Davis et al.also stimulated pancreatic secretion by a constant infusionof secretin, and they found that intravenous alcoholcaused a fall in the volume of duodenal aspirate from9 ml. to 2 ml. in 5 minutes. Sublingual glyceryl trinitratethen raised the volume to 6 ml. in 5 minutes, suggestingthat a readily reversible spasm of the outflow tract mayhave been responsible.These results suggest that the effects of acute administra-

tion of alcohol are due to obstruction of the pancreaticduct, and that this action is more closely related to

blood-alcohol level than to the route of administration.1. Walton, B. E., Schapiro, H., Woodward, E. R. Am. Surg. 1962, 28, 443.2. Preston, F. W., Kukral, J. C. Surg. Clin. N. Am. 1962, 42, 203.3. Cecil and Loeb’s Textbook of Medicine (edited by P. B. and W.

McDermott). Philadelphia, 1963.4. Davis, A. E., Pirola, R. C., Blagonravoff, L. Med. J Aust. 1966, ii, 757.5 Dreiling, D. A., Janowitz, H. D Ciba Foundation Symposium on the

Exocrine Pancreas (edited by A. V. S. de Reuck and M. P. Cameron).London, 1962

6. Dreiling, D. A., Richman, A., Fradkin, N. T. Gastroenterology, 1952,20, 636.

The relevance of these findings to chronic pancreatitisis unknown. One difficulty is that chronic alcoholism isoften associated with chronic gastritis and achlorhydria,which would abolish the acid-secretin secretory reflex inthe pancreas. Moreover, though a long-continued increasein pancreatic-duct pressure sounds a likely cause of chronicpancreatitis, many workers disagree about this. While itcan be shown that continued pancreatic secretion againstan obstructed duct leads to a rise in serum-amylaselevels this does not necessarily imply acinar necrosis,for the blood levels of amylase are determined by the sumof the processes of production and elimination; and if theelimination is restricted, the blood level rises.

McCutcheon, summarising the evidence against theobstruction hypothesis, pointed to the fact that obstruc-tion of the major pancreatic duct in cats, dogs, and rabbitscauses atrophy of acini with preservation of the islets ofLangerhans, but not pancreatitis 8; and, according to

Thal et al.,9 experiments in which maximum secretoryactivity was provoked in the presence of complete ductobstruction failed to produce pancreatic necrosis.

Nevertheless, these observations have been concerned

largely with the production of acute pancreatitis, and theirrelevance to the chronic state is questionable.

Chemical as well as mechanical factors may operate.For example, an excess of ethyl radicals may competewith methyl groups in a metabolic pathway analogousto that followed when the administration of ethionine to

experimental animals is associated with severe pancreaticnecrosis.3 10

OBESITY IN CHILDHOOD

COMMENTING 11 on the treatmemt of obesity in childhood,we remarked that most obese children grow into evenmore obese adults. But some do not, and in a surveyGrant 12 has tried to distinguish between obesity inchildren which was likely to be temporary and that whichwould persist into adult life. Growth records of about1000 English children showed that somatic types wereremarkably constant over the whole period from below 8 toover 14 years of age. There was an average gain of 10% inweight with every 2 inches gained in height, and this wasobserved in children varying from l5O/., underweight to15’% overweight. Progressive obesity resulted when again in weight of more than 10%, was maintained for eightor more years. A few children had transient obesity whichwas different from progressive obesity in its abrupt onset,high initial rate of gain, and rapid slowing down with agradual return to the previous physique.The constancy of the individual growth-rates over long

periods suggests that internal constitutional factors ratherthan environment play the biggest part in their pro-duction. It also suggests that short-term treatment with

drugs or psychotherapy is unlikely to be of permanentvalue. The best chance of prophylactic success in

preventing progressive obesity may be found in detectinggrowth-rates in excess of 10%, at the earliest oppor-tunity, and regulating dietary intake from this stage tomaintain them at or below this critical level.

7. McCutcheon, A. D. Lancet, 1962, i, 710.8. Wang, C., Strauss, L., Adlersberg, D. Gastroenterology, 1958, 35, 465.9. Thai, A., Perry, J. F., Egner, W. Surgery Gynec. Obstet. 1957, 105, 191.

10. Meister, A. Biochemistry of the Ammo-acids. New York, 1965.11. Lancet, Aug. 6, 1966, p 327.12. Grant, M W. Med. Offr 1966, 115, 331