- Email: [email protected]
Coronary risk factors in people from the Indian subcontinent
Under general anaesthetic a gastroscope is passed, the stomach inflated, and the optimum point of gastrostomy insertion determined. Two Cope needles are placed 2 cm from this site and pulled up to control the stomach. A 20F "pull type" percutaneous endoscopic gastrostomy tube is partly inserted in the usual way, such that only the cone and the first 5 cm of tube are protruding from the anterior abdominal wall, and the other end is still protruding from th mouth. The cone is cut off and the button inserted into the end of the tube. The tube is gently pulled out of the mouth as the button is pushed through the abdominal wall. An assistant provides counter traction on the stomach via the Cope needles. With the button fully inserted, the balloon is inflated, and the tube twisted off and removed. The gastroscope is reinserted to confirm that the balloon is correctly inflated within the stomach. The Cope needles are then cut off and allowed to pass through the bowel. This method of insertion is a substantial advance because it allows primary percutaneous insertion of a gastrostomy button, and avoids a second procedure, probably under a second anaesthetic. The "push" technique with a guide wire and dilators might be an alternative approach. M Griffiths Regional
Wessex
Centre for Paediatric
Surgery, Southampton General Hospital,
Southampton SO16 6YD, UK
Coronary risk factors in people from the Indian subcontinent SIR Bhatnagar and colleagues (Feb 18, p 405) ignore some oddities in their data; their summary, which does not mention the sex differences in the results, is thereby
misleading. Women in west London had a much higher BMI (24-4 22-7) than their Punjabi controls, yet had almost identical concentrations of serum triglycerides, blood pressure, serum insulin, and insulin sensitivity. The men in west London also had a higher BMI (26-8 vs 22-9) but had concentrations of triglycerides and high-density lipoprotein (HDL) cholesterol that were similar to those of the Punjabi controls, despite having higher insulin concentrations and lower insulin sensitivity. In both sexes, cholesterol and apolipoprotein B values were higher in the west London population, but these lipid abnormalities are not components of the insulin resistance syndrome. The most consistent accompaniment of insulin resistance-reduced HDL cholesterol-was recorded in the west London women, but they were not insulin resistant. There are thus two incorrect statements in Bhatnagar’s concluding paragraph: "body weight, serum cholesterol, and blood pressure are increased in Indians who migrate to the UK" (blood pressure was not increased in women), and "their insulin resistance is exposed as an increase in blood glucose and decrease in HDL cholesterol" (HDL cholesterol was not reduced in men). The higher values of lipoprotein (a) in both Indian populations are of interest. However, though significant, the differences are not great. Are they sufficient to account for the increased CHD risk? R J Jarrett 45 Bishopsthorpe Road, London SE26 4PA, UK
their investigation of coronary risk factors, Bhatnagar and colleagues did not include a comparison of the diets of the 59 West London migrants of Punjabi origin with those of their 117 siblings living in the Indian Punjab. There should be concern particularly about milk consumption, which in international comparisons SiR-In
982
consistently correlates positively with mortality from coronary heart disease (CHD).’"’ The Punjabis and other north Indians are traditionally dairying and milk-consuming people, and have a high prevalence of adult lactose absorbers (>70%); CHD has been recognised as not uncommon in some rural as well as urban areas in the Indian Punjab since at least 1958. In Britain, milk is an important item in the diet of most migrant groups from the Indian subcontinent.’ Afro-Caribbeans, Pima Indians, South African Bantu, and Sri Lankans, like migrants from the Indian subcontinent, have a high prevalence of insulin resistance and/or noninsulin-dependent diabetes, but they have a low prevalence of adult lactose absorbers, which is associated with low intake of milk; and they experience less CHD than both migrants from the Indian subcontinent and the white
lactose-absorbing, milk-drinking populations of northern Europe and their overseas descendants.5 This is a global paradox that Bhatnagar and colleagues and other investigators should not ignore. I suggest that the research needed now is for prospective studies on intending migrants, to include dietary assessment and lactose-absorbing status. In the short term, we need to know any dietary differences, whether of milk consumption or otherwise, between Punjabi migrants and their siblings in the Punjab, which might account for the greater body-mass index of the migrants, and perhaps also for their higher serum cholesterol and fasting blood glucose levels. The South Asian people of West London also have a need to know of any such dietary differences. Jeffrey J Segall 308 Cricklewood Lane, London NW2 2PX, UK
1 2
3 4 5
Is milk a coronary health hazard? Br J Prev Soc Med 1977; 31: 81-85. Artaud-Wild SM, Connor SL, Sexton G, Connor WE. Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. Circulation 1993; 88: 2771-79. Segall JJ. Dietary lactose as a possible nsk factor for ischaemic heart disease: review of epidemiology. Int J Cardiol 1994; 46: 197-207. Senewiratne B, Thambipillai S, Perera H. Intestinal lactase deficiency in Ceylon (Sri Lanka). Gastroenterology 1977; 72: 1257-59. Mendis S, Ekanayake EM. Prevalence of coronary heart disease and cardiovascular risk factors in middle aged males in a defined population in central Sri Lanka. Int J Cardiol 1994; 46: 135-42.
Segall JJ.
SIR-Bhatnagar and colleagues and Williams in his accompanying commentary (p 401) discuss factors underlying the increased frequency of CHD, insulin resistance, and non-insulin-dependent diabetes mellitus (NIDDM) among people from the Indian subcontinent who are settled in the UK. It is surprising how these reports and many others do
not show interest in nutritional factors the observed increased tendency to insulin resistance, CHD, and NIDDM-namely, chromium. Trivalent chromium is an essential nutrient required for normal glucose and lipid metabolism, and insufficient dietary chromium is associated with maturity-onset diabetes and cardiovascular diseases. Chromium supplementation of the sucrose-based diet of diabetic rats has resulted in amelioration of the cardinal signs of diabetes such that they become indistinguishable from those of the matched rats fed the high chromium diet.’ The results of double-blind,
closely related
to
crossover studies of chromium supplementation showed beneficial effects in human subjects with impaired glucose tolerance,2 and the beneficial effect of supplemental chromium in NIDDM patients has been shown by other trials.3 Chromium deficiency leads to raised blood lipid of rats and to the deposition of aortic plaques. The feeding of
chromium to rats prevents both the formation of aortic plaques and the age-related rise in serum cholesterol. The aortas of people who died from atherosclerotic heart disease were generally depleted of chromium, whereas chromium was present in most aortas of people dying from other causes such as car accidents. The relation of serum chromium concentration to coronary artery disease was thoroughly investigated in two independent studies’5 with a total of 122 patients, of whom 82
were
diagnosed by cine-arteriography
as
having
coronary
artery disease. The reported chromium levels differed significantly (by 41% in the first study and 12% in the second) in subjects with and without coronary artery disease. On the other hand, there is evidence that human tissue chromium levels decline with advancing age. Dietary chromium intake, even by affluent apparently healthy people is suboptimum. Modern methods of food processing lead to significant losses of chromium from staple foods. In addition, stress, including strenuous exercise, high sugar diet, and physical trauma all lead to increased chromium losses. As in many other studies, Bhatnagar and colleagues did not measure the chromium content of the diets consumed by the patients. Chromium content of the diet should perhaps be assessed in all investigations in which insulin resistance, glucose intolerance, and cardiovascular disease are being examined. Ghanim S Mahdi School of Life, Basic Medical and Health Sciences, Department of Nutrition and Dietetics, King’s College London, London W8 7AH. UK
1 Mahdi GS, Naismith DJ. Role of chromium in barley in modulating the symptoms of diabetes. Ann Nutr Metab 1991; 35: 65-70. 2 Anderson RA, Polansky MM, Bryden NA, Canary JJ. Supplementalchromium effect on glucose, insulin, glucagon, and unnary chromium losses in subjects consuming controlled low-chromium diets. Am J Clin Nutr 1991; 54: 909-16. 3 Abraham AS, Brook BA, Eylath U. The effects of Cr supplementation on serum glucose and lipids in patients with and without non-insulin dependent diabetes. Metabolism 1992; 41: 768-71. 4 Newman HAI, Leighton RF, Lanese RR, Freeland NA. Serum chromium and angiographically-determined coronary artery disease. Clin Chem 1978; 24: 541-44. 5 Simonoff M, Llabador Y, Hamon C, Peers AM, Simonoff GN. Low plasma chromium in patients with coronary artery and heart disease. Biol Trace Elem Res 1984; 6: 431-39.
Authors’ reply is right to draw attention to the sex differences recorded in our study, but, as he suggests, they are not oddities. There are well-known variations in the clinical presentation and course of coronary heart disease (CHD) between men and women, which might result from differences in the pathogenesis of CHD that remain unclear. We did not show major differences in blood pressure in women, but Keil and colleagues’ have noted that blood pressure was higher in immigrant Punjabi women in the UK than in those in Punjab. Jarrett also refers to the apparent dissociation of insulin resistance, high-density lipoprotein cholesterol concentrations and body-mass index in some of our subjects. In patients with insulin resistance syndrome it is not uncommon to find that the clinical features that constitute the syndrome do not present at the same time or in a particular order; this is likely to be the case in our study. In fact we do not mention the term insulin resistance syndrome. Nor do we seek to explain our results seamlessly or otherwise by the existence of such a syndrome. Insulin. resistance might be part of the explanation of the greater CHD risk of Indians in the UK, but the increase in serum cholesterol, apolipoprotein B, and perhaps blood pressure
SIR-Jarrett we
associated with their migration is common to other migrant populations that move from areas of low CHD incidence to areas of high CHD incidence. We cannot agree with Jarrett that the serum lipoprotein (a) (Lp [a]) concentrations we recorded are not strikingly raised in Indians. Median values in Indians are almost twice those in white European populations in the UK. It is hard to think of many variables displaying such striking ethnic variation and we are not alone in this view.2 It is noteworthy that the median serum Lp (a) in middle-aged British men of European descent with established CHD is almost twice that of disease-free controls.3 We did compare the diets (and measures of psychological stress) of the two populations in our study, but we felt that it would be best to present these data in full in separate reports. There were major differences in lifestyle and diet between siblings in India and the UK. We are reluctant to accept Segall’s hypothesis of milk consumption to the exclusion of other dietary habits. A dairy-based culture has been known to exist in the area of the Punjab since at least 800 BC,4 and it is unlikely that a single dietary habit is to blame. In fact, preliminary analysis indicates that Punjabis in the UK regularly drink less milk (84%) than their siblings in India (100%), but consume more eggs and meat. Mahdi contends that chromium deficiency is an important cause of glucose intolerance, but this has mainly been shown to be the case in animals, in children with severe proteincalorie malnutrition, and in the occasional patient on total parenteral feeding.’ The chromium content of milled grains is low, but in most people, particularly in societies in which overnutrition is a problem, meat, whole grain, brewers’ yeast, and cooking in metal utensils (especially stainless steel) are more than likely to make up for any losses.
*Deepak Bhatnagar, Paul N Durrington, George C Sutton of Medicine, Manchester Royal Infirmary, Manchester M13 9WL, UK; and Department of Cardiology, Hillingdon
*University Department
Hospital,
Uxbridge
Keil JE, Britt RP, Weinrich MC, Hollis Y, Keil BW. Hypertension in Punjabi females: comparison between migrants to London and natives in India. Hum Biol 1980; 52: 423-33. 2 Sandholzer C, Saha N, Kark JD, et al. Apo (a) isoforms predict risk for coronary heart disease: a study in six populations. Arteriosclerosis Thromb 1992; 12: 1214-26. 3 Durrington PN, Ishola M, Hunt L, Arrol S, Bhatnagar D. Apolipoprotein (a), A1 and B and parental history in men with early onset ischaemic heart disease. Lancet 1988; i: 1070-73. 4 Achaya KT. Foods of the Gods. In: Achaya KT, ed. Indian food: a historical companion. Delhi: Oxford University Press, 1994: 34-35. 5 Milne DB. Trace elements. In: Burtis CA, Ashwood ER, eds. Tietz textbook of clinical chemistry. Philadelphia: WB Saunders Company, 1994: 1342-43. 1
Bubonic 1994
plague outbreak in Mozambique,
SIR-An outbreak of plague was reported in September, 1994, in Mozambique. The first suspected cases were identified on Sept 2, 1994, and a total of 226 cases and 3 deaths were recorded up to November, 1994, with an attack rate of 4-5%. There were no sex differences (M:F=0’8:1), and 56-5% of cases were aged between 4 and 15 years old. All cases were treated on the basis of clinical diagnosis. The criteria for clinical diagnosis were high fever and tender lymph nodes, sometimes suppurative. When at least 1 case was confirmed, the locality, village, or district was considered affected. Diagnosis was through smears stained with Giemsa; cultures were not possible because of difficulty in reaching the affected area. The outbreak occurred in 983
Wessex
Centre for Paediatric
Surgery, Southampton General Hospital,
Southampton SO16 6YD, UK
Coronary risk factors in people from the Indian subcontinent SIR Bhatnagar and colleagues (Feb 18, p 405) ignore some oddities in their data; their summary, which does not mention the sex differences in the results, is thereby
misleading. Women in west London had a much higher BMI (24-4 22-7) than their Punjabi controls, yet had almost identical concentrations of serum triglycerides, blood pressure, serum insulin, and insulin sensitivity. The men in west London also had a higher BMI (26-8 vs 22-9) but had concentrations of triglycerides and high-density lipoprotein (HDL) cholesterol that were similar to those of the Punjabi controls, despite having higher insulin concentrations and lower insulin sensitivity. In both sexes, cholesterol and apolipoprotein B values were higher in the west London population, but these lipid abnormalities are not components of the insulin resistance syndrome. The most consistent accompaniment of insulin resistance-reduced HDL cholesterol-was recorded in the west London women, but they were not insulin resistant. There are thus two incorrect statements in Bhatnagar’s concluding paragraph: "body weight, serum cholesterol, and blood pressure are increased in Indians who migrate to the UK" (blood pressure was not increased in women), and "their insulin resistance is exposed as an increase in blood glucose and decrease in HDL cholesterol" (HDL cholesterol was not reduced in men). The higher values of lipoprotein (a) in both Indian populations are of interest. However, though significant, the differences are not great. Are they sufficient to account for the increased CHD risk? R J Jarrett 45 Bishopsthorpe Road, London SE26 4PA, UK
their investigation of coronary risk factors, Bhatnagar and colleagues did not include a comparison of the diets of the 59 West London migrants of Punjabi origin with those of their 117 siblings living in the Indian Punjab. There should be concern particularly about milk consumption, which in international comparisons SiR-In
982
consistently correlates positively with mortality from coronary heart disease (CHD).’"’ The Punjabis and other north Indians are traditionally dairying and milk-consuming people, and have a high prevalence of adult lactose absorbers (>70%); CHD has been recognised as not uncommon in some rural as well as urban areas in the Indian Punjab since at least 1958. In Britain, milk is an important item in the diet of most migrant groups from the Indian subcontinent.’ Afro-Caribbeans, Pima Indians, South African Bantu, and Sri Lankans, like migrants from the Indian subcontinent, have a high prevalence of insulin resistance and/or noninsulin-dependent diabetes, but they have a low prevalence of adult lactose absorbers, which is associated with low intake of milk; and they experience less CHD than both migrants from the Indian subcontinent and the white
lactose-absorbing, milk-drinking populations of northern Europe and their overseas descendants.5 This is a global paradox that Bhatnagar and colleagues and other investigators should not ignore. I suggest that the research needed now is for prospective studies on intending migrants, to include dietary assessment and lactose-absorbing status. In the short term, we need to know any dietary differences, whether of milk consumption or otherwise, between Punjabi migrants and their siblings in the Punjab, which might account for the greater body-mass index of the migrants, and perhaps also for their higher serum cholesterol and fasting blood glucose levels. The South Asian people of West London also have a need to know of any such dietary differences. Jeffrey J Segall 308 Cricklewood Lane, London NW2 2PX, UK
1 2
3 4 5
Is milk a coronary health hazard? Br J Prev Soc Med 1977; 31: 81-85. Artaud-Wild SM, Connor SL, Sexton G, Connor WE. Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. Circulation 1993; 88: 2771-79. Segall JJ. Dietary lactose as a possible nsk factor for ischaemic heart disease: review of epidemiology. Int J Cardiol 1994; 46: 197-207. Senewiratne B, Thambipillai S, Perera H. Intestinal lactase deficiency in Ceylon (Sri Lanka). Gastroenterology 1977; 72: 1257-59. Mendis S, Ekanayake EM. Prevalence of coronary heart disease and cardiovascular risk factors in middle aged males in a defined population in central Sri Lanka. Int J Cardiol 1994; 46: 135-42.
Segall JJ.
SIR-Bhatnagar and colleagues and Williams in his accompanying commentary (p 401) discuss factors underlying the increased frequency of CHD, insulin resistance, and non-insulin-dependent diabetes mellitus (NIDDM) among people from the Indian subcontinent who are settled in the UK. It is surprising how these reports and many others do
not show interest in nutritional factors the observed increased tendency to insulin resistance, CHD, and NIDDM-namely, chromium. Trivalent chromium is an essential nutrient required for normal glucose and lipid metabolism, and insufficient dietary chromium is associated with maturity-onset diabetes and cardiovascular diseases. Chromium supplementation of the sucrose-based diet of diabetic rats has resulted in amelioration of the cardinal signs of diabetes such that they become indistinguishable from those of the matched rats fed the high chromium diet.’ The results of double-blind,
closely related
to
crossover studies of chromium supplementation showed beneficial effects in human subjects with impaired glucose tolerance,2 and the beneficial effect of supplemental chromium in NIDDM patients has been shown by other trials.3 Chromium deficiency leads to raised blood lipid of rats and to the deposition of aortic plaques. The feeding of
chromium to rats prevents both the formation of aortic plaques and the age-related rise in serum cholesterol. The aortas of people who died from atherosclerotic heart disease were generally depleted of chromium, whereas chromium was present in most aortas of people dying from other causes such as car accidents. The relation of serum chromium concentration to coronary artery disease was thoroughly investigated in two independent studies’5 with a total of 122 patients, of whom 82
were
diagnosed by cine-arteriography
as
having
coronary
artery disease. The reported chromium levels differed significantly (by 41% in the first study and 12% in the second) in subjects with and without coronary artery disease. On the other hand, there is evidence that human tissue chromium levels decline with advancing age. Dietary chromium intake, even by affluent apparently healthy people is suboptimum. Modern methods of food processing lead to significant losses of chromium from staple foods. In addition, stress, including strenuous exercise, high sugar diet, and physical trauma all lead to increased chromium losses. As in many other studies, Bhatnagar and colleagues did not measure the chromium content of the diets consumed by the patients. Chromium content of the diet should perhaps be assessed in all investigations in which insulin resistance, glucose intolerance, and cardiovascular disease are being examined. Ghanim S Mahdi School of Life, Basic Medical and Health Sciences, Department of Nutrition and Dietetics, King’s College London, London W8 7AH. UK
1 Mahdi GS, Naismith DJ. Role of chromium in barley in modulating the symptoms of diabetes. Ann Nutr Metab 1991; 35: 65-70. 2 Anderson RA, Polansky MM, Bryden NA, Canary JJ. Supplementalchromium effect on glucose, insulin, glucagon, and unnary chromium losses in subjects consuming controlled low-chromium diets. Am J Clin Nutr 1991; 54: 909-16. 3 Abraham AS, Brook BA, Eylath U. The effects of Cr supplementation on serum glucose and lipids in patients with and without non-insulin dependent diabetes. Metabolism 1992; 41: 768-71. 4 Newman HAI, Leighton RF, Lanese RR, Freeland NA. Serum chromium and angiographically-determined coronary artery disease. Clin Chem 1978; 24: 541-44. 5 Simonoff M, Llabador Y, Hamon C, Peers AM, Simonoff GN. Low plasma chromium in patients with coronary artery and heart disease. Biol Trace Elem Res 1984; 6: 431-39.
Authors’ reply is right to draw attention to the sex differences recorded in our study, but, as he suggests, they are not oddities. There are well-known variations in the clinical presentation and course of coronary heart disease (CHD) between men and women, which might result from differences in the pathogenesis of CHD that remain unclear. We did not show major differences in blood pressure in women, but Keil and colleagues’ have noted that blood pressure was higher in immigrant Punjabi women in the UK than in those in Punjab. Jarrett also refers to the apparent dissociation of insulin resistance, high-density lipoprotein cholesterol concentrations and body-mass index in some of our subjects. In patients with insulin resistance syndrome it is not uncommon to find that the clinical features that constitute the syndrome do not present at the same time or in a particular order; this is likely to be the case in our study. In fact we do not mention the term insulin resistance syndrome. Nor do we seek to explain our results seamlessly or otherwise by the existence of such a syndrome. Insulin. resistance might be part of the explanation of the greater CHD risk of Indians in the UK, but the increase in serum cholesterol, apolipoprotein B, and perhaps blood pressure
SIR-Jarrett we
associated with their migration is common to other migrant populations that move from areas of low CHD incidence to areas of high CHD incidence. We cannot agree with Jarrett that the serum lipoprotein (a) (Lp [a]) concentrations we recorded are not strikingly raised in Indians. Median values in Indians are almost twice those in white European populations in the UK. It is hard to think of many variables displaying such striking ethnic variation and we are not alone in this view.2 It is noteworthy that the median serum Lp (a) in middle-aged British men of European descent with established CHD is almost twice that of disease-free controls.3 We did compare the diets (and measures of psychological stress) of the two populations in our study, but we felt that it would be best to present these data in full in separate reports. There were major differences in lifestyle and diet between siblings in India and the UK. We are reluctant to accept Segall’s hypothesis of milk consumption to the exclusion of other dietary habits. A dairy-based culture has been known to exist in the area of the Punjab since at least 800 BC,4 and it is unlikely that a single dietary habit is to blame. In fact, preliminary analysis indicates that Punjabis in the UK regularly drink less milk (84%) than their siblings in India (100%), but consume more eggs and meat. Mahdi contends that chromium deficiency is an important cause of glucose intolerance, but this has mainly been shown to be the case in animals, in children with severe proteincalorie malnutrition, and in the occasional patient on total parenteral feeding.’ The chromium content of milled grains is low, but in most people, particularly in societies in which overnutrition is a problem, meat, whole grain, brewers’ yeast, and cooking in metal utensils (especially stainless steel) are more than likely to make up for any losses.
*Deepak Bhatnagar, Paul N Durrington, George C Sutton of Medicine, Manchester Royal Infirmary, Manchester M13 9WL, UK; and Department of Cardiology, Hillingdon
*University Department
Hospital,
Uxbridge
Keil JE, Britt RP, Weinrich MC, Hollis Y, Keil BW. Hypertension in Punjabi females: comparison between migrants to London and natives in India. Hum Biol 1980; 52: 423-33. 2 Sandholzer C, Saha N, Kark JD, et al. Apo (a) isoforms predict risk for coronary heart disease: a study in six populations. Arteriosclerosis Thromb 1992; 12: 1214-26. 3 Durrington PN, Ishola M, Hunt L, Arrol S, Bhatnagar D. Apolipoprotein (a), A1 and B and parental history in men with early onset ischaemic heart disease. Lancet 1988; i: 1070-73. 4 Achaya KT. Foods of the Gods. In: Achaya KT, ed. Indian food: a historical companion. Delhi: Oxford University Press, 1994: 34-35. 5 Milne DB. Trace elements. In: Burtis CA, Ashwood ER, eds. Tietz textbook of clinical chemistry. Philadelphia: WB Saunders Company, 1994: 1342-43. 1
Bubonic 1994
plague outbreak in Mozambique,
SIR-An outbreak of plague was reported in September, 1994, in Mozambique. The first suspected cases were identified on Sept 2, 1994, and a total of 226 cases and 3 deaths were recorded up to November, 1994, with an attack rate of 4-5%. There were no sex differences (M:F=0’8:1), and 56-5% of cases were aged between 4 and 15 years old. All cases were treated on the basis of clinical diagnosis. The criteria for clinical diagnosis were high fever and tender lymph nodes, sometimes suppurative. When at least 1 case was confirmed, the locality, village, or district was considered affected. Diagnosis was through smears stained with Giemsa; cultures were not possible because of difficulty in reaching the affected area. The outbreak occurred in 983