- Email: [email protected]
BRAN AND BLOOD-LIPIDS
800 believe is related to these effects. From the pituitary, a factor was isolated with fat-mobilising activity (L.M.F.) which induced a rise in non-esterified fatty acids (N.E.F.A.) after intravenous injection in rabbits.8 Later, th’s factor was purified and the structure determined.9 With high doses of L.M.F., at N.E.F.A. concentrations of 3000-4000 µeq. per 1. serum some of the animals became comatose and remained unconscious for several hours with signs of respiratory distress. These effects resemble those occurring after the administration of A.A .7 A similar phenomenon was observed by Woods and Kellner/" who found that after the infusion of corticotrophin into obese rabbits, most of the animals died after showing signs of weakness, lethargy, and tachypnoea. There was a relation between the mortality and the level of N.E.F.A. in the blood. The most likely explanation for these observations is that large amounts of A.A., which is one of the fatty acids mobilised from adipose tissue, are transformed into the aggregation-inducing intermediate, thus leading to the formation of thrombi in the
lungs. One of the metabolic defects in diabetes is
an
enhanced
lipolysis. Spontaneous platelet aggregation was reported in a patient with diabetes and hyperlipw-mia.11 Other factors also seem to play a role.12 It would seem of considerable clinical importance to determine whether A.A. in normal or increased concentrations could act as a thrombosis-inducing substance in these circumstances. Large-scale clinical trials are being conducted in which the effect of the daily administration of aspirin upon the incidence of myocardial infarction is investigated. The first results indicate a favourable trend.13 Aspirin treatment prevents the thrombosis-inducing effects of A.A.7 We observed that the platelet-aggregation inhibiting effects of indomethacin, and to a lesser extent of aspirin, are considerably reduced in the plasma of rats deficient in essential fatty acids.14 These observations indicate that A.A. may be one of the thrombosis-inducing agents in disease states. Department of Pharmacology, Erasmus University Rotterdam, Rotterdam, Netherlands.
J. E. VINCENT.
BRAN AND BLOOD-LIPIDS SIR The paper by Professor Connell and his colleagues (March 1, p. 496) might have been a more valuable contribution to an understanding of the role of dietary fibre in modifying lipid metabolism if we had more information on the nutritional aspects of the study. Dietary fibre is clearly defined in the introduction and the limitations of crude fibre " analysis are recognised. However, in the body of the paper the authors fail to define what they actually measured in the diets eaten. We presume that all the fibre intakes quoted relate to the crude-fibre content of the diet and not to the " total dietary fibre " intake; thus the pectic substances and hemicellulose fractions, potentially of particular importance in cholesterol meta"
were not assessed. We also infer that the study
bolism,
was uncontrolled, reliance being placed on a dietary history before and during the test period on the unspecified breakfast cereal. No evidence is presented to show that table i warrants the
inclusion of standard-error values for what appears 8. 9.
to
be
Sim, A. W., de Vries, J. W., Vincent, J. E. Biochem. J. 1964, 92, 590. Li, C. H., Barnafi, L., Chretien, M., Chung, D. Nature, 1965, 208, 1093.
Woods, K. R., Kellner, A. ibid. 1964, 202, 157. Kwaan, H. C., Colwell, J. A., Suwanwela, N. Diabetes, 1972, 21, 108. Kwaan, H. C., Colwell, J. A., Cruz, J., Suwanwela, N., Dobbie, J. G. J. Lab. clin. Med. 1972, 80, 236. 13. McNicol, G. P., Mitchell, J. R. A., Reuter, H., van de Loo, J. Thromb. Diath. hœmorrh. 1974, 31, 379. 14. Vincent, J. E., Zijlstra, F. J., Bonta, I. L. Unpublished.
10. 11. 12.
a
very
fat,
or
content
approximate estimate of dietary energy, protein, carbohydrate. Furthermore, the estimated fibre of the control diets and the increase
on
the addition
fibre-containing cereal do not support the authors’ description of the diet as a high-fibre one. No estimate of the other fibre components in the diet is given although total " fibre might have been we would estimate that the 10-5 g. with an increase of 7-5 g. on the " high " fibre diet. of the
"
This compares with an intake of 16-2 g. total fibre in a Glaswegian study of subjects on a mixed diet with wholemeal bread, vegetables, and fruit, and an intake of 32 g. 1 on a vegetarian-type diet. An African living on a homemaize diet may ingest 45 g. or more of fibre pounded each day,but no actual measurements are available. We are not therefore surprised that no response was apparent on feeding extra cereal, but we would have more confidence in the results if they were the product of detailed and careful dietary control. An increased intake of dietary fibre above virtually any control value will result in an increased weight of stool and there is no a-priori reason to reject the hypothesis that a very much higher intake of dietary fibre would have had a different effect. Is it not time that studies on the role of " fibre " in metabolism developed some research respectability with measurements being made of what subjects eat and with clear statements documenting the nature of the fibre used ? We need controlled trials of different types of fibre fed to volunteers and not, as is often the case, a motley collection of patients with undefined problems. Professor Connell and his colleagues’ use of medical students as " normal " subjects is welcome, but " crude fibre " measurements are not relevant to any present-day clinical investigation with fibre. Dunn Nutritional Laboratories, Milton Road, Cambridge CB4 1XJ.
W. P. T. JAMES D. A. T. SOUTHGATE.
SIR,-Professor Connell and his colleagues claim that " the addition of a tolerable amount of dietary fibre to the diet does not affect serum-lipids ". This, they say, is in contrast to our findings 3 that raw bran lowered serumHowever, there are three triglycerides significantly. important ways in which their study differed from ours. (1) Their subjects were American medical students and therefore presumably mostly young and male (age and sex data were not given). They started with low plasma-triglyceride levels-mean 71 mg. per 100 ml. Our subjects were mostly middle-aged and female. They started with plasma-triglycerides which averaged 118 mg. per 100 ml. As we pointed out, all our 8 subjects whose initial level was over 100 showed a fall with bran. Those starting below 100 showed no significant change. Thus, the findings of Professor Connell and his colleagues are not in contrast but in agreement with ours. Its nature (2) Connell used a bran-rich breakfast cereal. was not specified, but presumably the bran was cooked in the manufacture of the cereal. Our results were obtained with raw bran. Cooking could affect the properties of bran. (3) Connell’s subjects took all their bran in one dose. Ours took bran in divided doses with meals. We felt this was a more logical procedure when we were trying to influence metabolic events within the intestinal lumen. The only conclusion to be drawn from the paper by Professor Connell and his colleagues is that a large helping of a commercial bran cereal at breakfast time does not affect the serum-triglycerides of young men-that is, of subjects with initially low triglyceride levels. This is perhaps not very surprising, since it is presumably difficult to lower a level which has not had a chance to rise in the first place. It would be unfortunate therefore if this paper discouraged 1. 2. 3.
Southgate, D. A. T., Durnin, J. V. G. A. Br. J. Nutr. 1970, 24, 517. James, W. P. T. J. Coll. gen. Practnrs (in the press). Heaton, K. W., Pomare, E. W. Lancet, 1974, i, 49.
801 further work on the effect of bran or other fibre-rich materials upon blood-lipids. We would respectfully suggest that all workers in this field are careful to observe the differences between bran, fibre, and crude fibre. Bran is 35-40% fibre (that is, unavailable polysaccharides and lignin), but only 8-10% crude fibre (that is, the fraction which resists boiling with dilute acid and dilute alkali). Our subjects ate about 38 g. bran per day, not, as Professor Connell stated, 38 g. crude fibre. Department of Medicine, Bristol Royal Infirmary, Bristol BS2 8HW.
K. W. HEATON E. W. POMARE.
SiR,-Professor Connell and his colleagues reported that wheat bran, supplementing a low-fibre Western-type diet of crude fibre 0-2 g. per 100 kcal., the resultant food containing crude fibre 04 g. per 100 kcal., did not reduce serum-lipids of healthy normolipidaemic medical students. Their mean serum-cholesterol was 165 mg. per 100 ml. It would indeed have been surprising if bran, which is a portion of normal food, reduced normal bloodlipid levels. From a review of the existing literature in 1973,1 it was stated that it was unlikely that " breakfast cereals rich in cereal fibre would reduce serum lipids or increase bile salt excretion ". This was because experiments in hypercholesterolaemic rats had shown that fibre-rich whole ground rice was about four times as hypocholesterolasmic as an equal amount of crude fibre in rice bran, large amounts (16% daily calories) supplementing low-fibre white-rice diets.2 Fibre is an extremely complex group of substances. It plant foods. It is normally packages all unprocessed " possible, but unproved, that the package " is much more effective when it remains in its natural physicochemical relationship to the cell contents than when the two are separated. Attention should be paid to experiments which reported that large supplements of a mixture of fibre-rich vegetables composed of starchy roots, such as sweet potatoes, and leafy vegetables, such as cabbage, supplementing a low-fibre Western-type diet, the resultant food containing crude fibre 0-6 g. per 100 kcal., significantly reduced serum-lipids of male students. Their mean serum-cholesterol level was 194 mg. per 100 ml.3. This level represented hyperlipidaemia in young men. The Committee on Medical Aspects of Food Policy (Nutrition) has reported4 that " Populations who eat a diet rich in fibre (particularly fibre from cereals and legumes) usually have a lower serum cholesterol concentration and a lower mortality from I.H.D. (ischaemic heart disease) than those who eat a Western-type diet relatively low in this kind of fibre. There is also some evidence that the serum cholesterol concentration of healthy persons can be reduced by increasing the consumption of food rich in fibre ". Might I suggest that reduction of serum-lipids occurs only in certain persons who are members of a group having a high risk of developing I.H.D. ? They are unhealthy persons. Animal experiments, planned to assess the action of different varieties of fibre, have reported that serum-cholesterol levels are reduced, feecal excretion of steroids is increased,5 bile-salt excretion 1. 2.
3. 4.
5. 6. 7.
Trowell, H. C. Plant Foods for Man, 1974, 1, 91. K. S., Kurup, P. A. Atherosclerosis, 1973 17, 156. Grande, F., Anderson, J. T., Keys, A. Am. J. clin. Nutr. 1974, 27, 1043. Report of Advisory Panel of Committee on Medical Aspects of Food Policy (Nutrition) on Diet in Relation to Cardiovascular and Cerebrovascular Disease. Department of Health and Social Security; p. 18. London, 1974. Balmer, J., Zilversmit, D. B. J. Nutr. 1974, 104, 1319. Morgan, B., Heald, M., Atkin, S. D., Green, J., Chain, E. B. Br. J. Nutr. 1974, 32, 447. Kritchevsky, D., Story, J. A. J. Nutr. 1974, 104, 458.
Vijayagopal, P., Devi,
is increased,6 and bile salts in vitro are bound.’7 The epidemiological association of diverticular disease and ischaemic heart-disease suggests that fibre deficiency is a factor in both diseases.8 Woodgreen, Fordingbridge, Hants SP6 2AZ.
HUGH TROWELL.
BOWEL-TRANSIT TIMES AND DIET SIR,-Much interest has focused lately on the effect of dietary fibre on bowel-transit times and stool weights. The relation between gastrointestinal behaviour and the prevalence of various gastrointestinal, venous, and cardiovascular disorders has also been considered.9 Reports relating bowel-transit times to dietary fibre have come from several African regions.1O I made a limited study of the subject during a recent stay at the Hospital Amazonico, Pucallpa, Peru. As far as I am aware, few such studies have been done in South America. I noted a low prevalence of the aforementioned diseases and decided, therefore, to measure bowel-transit times to see if there was a similar association between these diseases and diet in a remote and primitive Shipibo Indian village, San Francisco. The villagers ate an unrefined diet consisting mostly of fish, yucca (a root crop), and fresh fruits. Water was drunk from a nearby lake. Bowel-transit times were measured by a modification of a method first used by Hinton et al.ll 20 volunteers were asked to swallow eight small plastic beads. The time taken to excrete the first four beads was accepted as the bowel-transit time. The weights of the faeces passed were measured, and 24-hour excretion-rates were calculated. The subjects’ diets remained unchanged during the period of the experiment, and all faeces passed were considered by them to be within normal limits by local standards. The wet weight of faeces excreted in 24 hours was within the range 60-650 g. (average 325 g.). The average for Englishmen is under 120 g.1S The average bowel-transit time was 23-7 hours (range 12-42 hours). The corresponding time for Englishmen is approximately 70 hours. 12 The effects of the Shipibo Indian’s unrefined diet on bowel-transit times and stool weight are thus consistent with findings in other areas.12 Of the 20 subjects in this survey, 17 had parasitic infestations-Ascaris 9, Trichocephalus 9, and Ankylostoma 8. This limited study suggests an association between bowel-transit times and diet; whether parasites have any effect on bowel-transit times remains to be seen. 12
Pilgrims Court,
Kidbrooke Grove, London SE3.
TREVOR JOHN CROFTS.
TREATMENT OF LEPROSY
SIR,—Since the publication of my letter (Feb. 15, p. 405) I have had inquiries from doctors in India about the exact composition and availability of the drug I used. Perhaps this is because the second component in the combination is known to doctors in India as brobenzoxaldine and not as broxaldine. The product I used was ’ Intestopan Forte’ capsules (Sandoz [India]) (broxyquinoline 500 mg., brobenzoxaldine [broxaldine] 100 mg.). 79/81 Anna Salai, Madras 600006, India.
C. S. GANGADHAR SHARMA.
11.
Trowell, H. C., Painter, N. S., Burkitt, D. P. Am. J. dig. Dis. 1974, 19, 864. Burkitt, D. P. Clin. Radiol. 1973, 24, 271. Walker, A. R. P., Walker, B. F., Richardson, B. D., Woolford, A. Postgrad, med. J. 1973, 49, 243. Hinton, J. M., Lennard-Jones, J. E., Young, A. C. Gut, 1969, 10,
12.
Burkitt, D. P., Walker, A. R. P., Painter, N. S. Lancet, 1972, ii,
8.
9. 10.
842. 1408.
lungs. One of the metabolic defects in diabetes is
an
enhanced
lipolysis. Spontaneous platelet aggregation was reported in a patient with diabetes and hyperlipw-mia.11 Other factors also seem to play a role.12 It would seem of considerable clinical importance to determine whether A.A. in normal or increased concentrations could act as a thrombosis-inducing substance in these circumstances. Large-scale clinical trials are being conducted in which the effect of the daily administration of aspirin upon the incidence of myocardial infarction is investigated. The first results indicate a favourable trend.13 Aspirin treatment prevents the thrombosis-inducing effects of A.A.7 We observed that the platelet-aggregation inhibiting effects of indomethacin, and to a lesser extent of aspirin, are considerably reduced in the plasma of rats deficient in essential fatty acids.14 These observations indicate that A.A. may be one of the thrombosis-inducing agents in disease states. Department of Pharmacology, Erasmus University Rotterdam, Rotterdam, Netherlands.
J. E. VINCENT.
BRAN AND BLOOD-LIPIDS SIR The paper by Professor Connell and his colleagues (March 1, p. 496) might have been a more valuable contribution to an understanding of the role of dietary fibre in modifying lipid metabolism if we had more information on the nutritional aspects of the study. Dietary fibre is clearly defined in the introduction and the limitations of crude fibre " analysis are recognised. However, in the body of the paper the authors fail to define what they actually measured in the diets eaten. We presume that all the fibre intakes quoted relate to the crude-fibre content of the diet and not to the " total dietary fibre " intake; thus the pectic substances and hemicellulose fractions, potentially of particular importance in cholesterol meta"
were not assessed. We also infer that the study
bolism,
was uncontrolled, reliance being placed on a dietary history before and during the test period on the unspecified breakfast cereal. No evidence is presented to show that table i warrants the
inclusion of standard-error values for what appears 8. 9.
to
be
Sim, A. W., de Vries, J. W., Vincent, J. E. Biochem. J. 1964, 92, 590. Li, C. H., Barnafi, L., Chretien, M., Chung, D. Nature, 1965, 208, 1093.
Woods, K. R., Kellner, A. ibid. 1964, 202, 157. Kwaan, H. C., Colwell, J. A., Suwanwela, N. Diabetes, 1972, 21, 108. Kwaan, H. C., Colwell, J. A., Cruz, J., Suwanwela, N., Dobbie, J. G. J. Lab. clin. Med. 1972, 80, 236. 13. McNicol, G. P., Mitchell, J. R. A., Reuter, H., van de Loo, J. Thromb. Diath. hœmorrh. 1974, 31, 379. 14. Vincent, J. E., Zijlstra, F. J., Bonta, I. L. Unpublished.
10. 11. 12.
a
very
fat,
or
content
approximate estimate of dietary energy, protein, carbohydrate. Furthermore, the estimated fibre of the control diets and the increase
on
the addition
fibre-containing cereal do not support the authors’ description of the diet as a high-fibre one. No estimate of the other fibre components in the diet is given although total " fibre might have been we would estimate that the 10-5 g. with an increase of 7-5 g. on the " high " fibre diet. of the
"
This compares with an intake of 16-2 g. total fibre in a Glaswegian study of subjects on a mixed diet with wholemeal bread, vegetables, and fruit, and an intake of 32 g. 1 on a vegetarian-type diet. An African living on a homemaize diet may ingest 45 g. or more of fibre pounded each day,but no actual measurements are available. We are not therefore surprised that no response was apparent on feeding extra cereal, but we would have more confidence in the results if they were the product of detailed and careful dietary control. An increased intake of dietary fibre above virtually any control value will result in an increased weight of stool and there is no a-priori reason to reject the hypothesis that a very much higher intake of dietary fibre would have had a different effect. Is it not time that studies on the role of " fibre " in metabolism developed some research respectability with measurements being made of what subjects eat and with clear statements documenting the nature of the fibre used ? We need controlled trials of different types of fibre fed to volunteers and not, as is often the case, a motley collection of patients with undefined problems. Professor Connell and his colleagues’ use of medical students as " normal " subjects is welcome, but " crude fibre " measurements are not relevant to any present-day clinical investigation with fibre. Dunn Nutritional Laboratories, Milton Road, Cambridge CB4 1XJ.
W. P. T. JAMES D. A. T. SOUTHGATE.
SIR,-Professor Connell and his colleagues claim that " the addition of a tolerable amount of dietary fibre to the diet does not affect serum-lipids ". This, they say, is in contrast to our findings 3 that raw bran lowered serumHowever, there are three triglycerides significantly. important ways in which their study differed from ours. (1) Their subjects were American medical students and therefore presumably mostly young and male (age and sex data were not given). They started with low plasma-triglyceride levels-mean 71 mg. per 100 ml. Our subjects were mostly middle-aged and female. They started with plasma-triglycerides which averaged 118 mg. per 100 ml. As we pointed out, all our 8 subjects whose initial level was over 100 showed a fall with bran. Those starting below 100 showed no significant change. Thus, the findings of Professor Connell and his colleagues are not in contrast but in agreement with ours. Its nature (2) Connell used a bran-rich breakfast cereal. was not specified, but presumably the bran was cooked in the manufacture of the cereal. Our results were obtained with raw bran. Cooking could affect the properties of bran. (3) Connell’s subjects took all their bran in one dose. Ours took bran in divided doses with meals. We felt this was a more logical procedure when we were trying to influence metabolic events within the intestinal lumen. The only conclusion to be drawn from the paper by Professor Connell and his colleagues is that a large helping of a commercial bran cereal at breakfast time does not affect the serum-triglycerides of young men-that is, of subjects with initially low triglyceride levels. This is perhaps not very surprising, since it is presumably difficult to lower a level which has not had a chance to rise in the first place. It would be unfortunate therefore if this paper discouraged 1. 2. 3.
Southgate, D. A. T., Durnin, J. V. G. A. Br. J. Nutr. 1970, 24, 517. James, W. P. T. J. Coll. gen. Practnrs (in the press). Heaton, K. W., Pomare, E. W. Lancet, 1974, i, 49.
801 further work on the effect of bran or other fibre-rich materials upon blood-lipids. We would respectfully suggest that all workers in this field are careful to observe the differences between bran, fibre, and crude fibre. Bran is 35-40% fibre (that is, unavailable polysaccharides and lignin), but only 8-10% crude fibre (that is, the fraction which resists boiling with dilute acid and dilute alkali). Our subjects ate about 38 g. bran per day, not, as Professor Connell stated, 38 g. crude fibre. Department of Medicine, Bristol Royal Infirmary, Bristol BS2 8HW.
K. W. HEATON E. W. POMARE.
SiR,-Professor Connell and his colleagues reported that wheat bran, supplementing a low-fibre Western-type diet of crude fibre 0-2 g. per 100 kcal., the resultant food containing crude fibre 04 g. per 100 kcal., did not reduce serum-lipids of healthy normolipidaemic medical students. Their mean serum-cholesterol was 165 mg. per 100 ml. It would indeed have been surprising if bran, which is a portion of normal food, reduced normal bloodlipid levels. From a review of the existing literature in 1973,1 it was stated that it was unlikely that " breakfast cereals rich in cereal fibre would reduce serum lipids or increase bile salt excretion ". This was because experiments in hypercholesterolaemic rats had shown that fibre-rich whole ground rice was about four times as hypocholesterolasmic as an equal amount of crude fibre in rice bran, large amounts (16% daily calories) supplementing low-fibre white-rice diets.2 Fibre is an extremely complex group of substances. It plant foods. It is normally packages all unprocessed " possible, but unproved, that the package " is much more effective when it remains in its natural physicochemical relationship to the cell contents than when the two are separated. Attention should be paid to experiments which reported that large supplements of a mixture of fibre-rich vegetables composed of starchy roots, such as sweet potatoes, and leafy vegetables, such as cabbage, supplementing a low-fibre Western-type diet, the resultant food containing crude fibre 0-6 g. per 100 kcal., significantly reduced serum-lipids of male students. Their mean serum-cholesterol level was 194 mg. per 100 ml.3. This level represented hyperlipidaemia in young men. The Committee on Medical Aspects of Food Policy (Nutrition) has reported4 that " Populations who eat a diet rich in fibre (particularly fibre from cereals and legumes) usually have a lower serum cholesterol concentration and a lower mortality from I.H.D. (ischaemic heart disease) than those who eat a Western-type diet relatively low in this kind of fibre. There is also some evidence that the serum cholesterol concentration of healthy persons can be reduced by increasing the consumption of food rich in fibre ". Might I suggest that reduction of serum-lipids occurs only in certain persons who are members of a group having a high risk of developing I.H.D. ? They are unhealthy persons. Animal experiments, planned to assess the action of different varieties of fibre, have reported that serum-cholesterol levels are reduced, feecal excretion of steroids is increased,5 bile-salt excretion 1. 2.
3. 4.
5. 6. 7.
Trowell, H. C. Plant Foods for Man, 1974, 1, 91. K. S., Kurup, P. A. Atherosclerosis, 1973 17, 156. Grande, F., Anderson, J. T., Keys, A. Am. J. clin. Nutr. 1974, 27, 1043. Report of Advisory Panel of Committee on Medical Aspects of Food Policy (Nutrition) on Diet in Relation to Cardiovascular and Cerebrovascular Disease. Department of Health and Social Security; p. 18. London, 1974. Balmer, J., Zilversmit, D. B. J. Nutr. 1974, 104, 1319. Morgan, B., Heald, M., Atkin, S. D., Green, J., Chain, E. B. Br. J. Nutr. 1974, 32, 447. Kritchevsky, D., Story, J. A. J. Nutr. 1974, 104, 458.
Vijayagopal, P., Devi,
is increased,6 and bile salts in vitro are bound.’7 The epidemiological association of diverticular disease and ischaemic heart-disease suggests that fibre deficiency is a factor in both diseases.8 Woodgreen, Fordingbridge, Hants SP6 2AZ.
HUGH TROWELL.
BOWEL-TRANSIT TIMES AND DIET SIR,-Much interest has focused lately on the effect of dietary fibre on bowel-transit times and stool weights. The relation between gastrointestinal behaviour and the prevalence of various gastrointestinal, venous, and cardiovascular disorders has also been considered.9 Reports relating bowel-transit times to dietary fibre have come from several African regions.1O I made a limited study of the subject during a recent stay at the Hospital Amazonico, Pucallpa, Peru. As far as I am aware, few such studies have been done in South America. I noted a low prevalence of the aforementioned diseases and decided, therefore, to measure bowel-transit times to see if there was a similar association between these diseases and diet in a remote and primitive Shipibo Indian village, San Francisco. The villagers ate an unrefined diet consisting mostly of fish, yucca (a root crop), and fresh fruits. Water was drunk from a nearby lake. Bowel-transit times were measured by a modification of a method first used by Hinton et al.ll 20 volunteers were asked to swallow eight small plastic beads. The time taken to excrete the first four beads was accepted as the bowel-transit time. The weights of the faeces passed were measured, and 24-hour excretion-rates were calculated. The subjects’ diets remained unchanged during the period of the experiment, and all faeces passed were considered by them to be within normal limits by local standards. The wet weight of faeces excreted in 24 hours was within the range 60-650 g. (average 325 g.). The average for Englishmen is under 120 g.1S The average bowel-transit time was 23-7 hours (range 12-42 hours). The corresponding time for Englishmen is approximately 70 hours. 12 The effects of the Shipibo Indian’s unrefined diet on bowel-transit times and stool weight are thus consistent with findings in other areas.12 Of the 20 subjects in this survey, 17 had parasitic infestations-Ascaris 9, Trichocephalus 9, and Ankylostoma 8. This limited study suggests an association between bowel-transit times and diet; whether parasites have any effect on bowel-transit times remains to be seen. 12
Pilgrims Court,
Kidbrooke Grove, London SE3.
TREVOR JOHN CROFTS.
TREATMENT OF LEPROSY
SIR,—Since the publication of my letter (Feb. 15, p. 405) I have had inquiries from doctors in India about the exact composition and availability of the drug I used. Perhaps this is because the second component in the combination is known to doctors in India as brobenzoxaldine and not as broxaldine. The product I used was ’ Intestopan Forte’ capsules (Sandoz [India]) (broxyquinoline 500 mg., brobenzoxaldine [broxaldine] 100 mg.). 79/81 Anna Salai, Madras 600006, India.
C. S. GANGADHAR SHARMA.
11.
Trowell, H. C., Painter, N. S., Burkitt, D. P. Am. J. dig. Dis. 1974, 19, 864. Burkitt, D. P. Clin. Radiol. 1973, 24, 271. Walker, A. R. P., Walker, B. F., Richardson, B. D., Woolford, A. Postgrad, med. J. 1973, 49, 243. Hinton, J. M., Lennard-Jones, J. E., Young, A. C. Gut, 1969, 10,
12.
Burkitt, D. P., Walker, A. R. P., Painter, N. S. Lancet, 1972, ii,
8.
9. 10.
842. 1408.