- Email: [email protected]
DIET AND CARDIOVASCULAR DISEASE
831 free diet with
Letters
to
magnesium supplementation may be more generally applicable. The evidence for these speculations
the Editor
MULTIPLE SCLEROSIS AND DIET Sir,- am a biochemist working on the development of analytical methods in nutrition. Five years ago I was told I had multiple sclerosis. I believe my experience and ideas may be of some value to those working on the disease. From diagnosis in 1969 until early 1973 I became slowly worse, though I have never been immobile or unable to carry out research work. However, I felt apathetic, I tired easily, I had backache, my balance was bad, I had flickering in my eyes, and one hand was numb and sensory paralysis was creeping up my arm. In March, 1973, I began to take a gluten-free diet with a vitamin and mineral supplement. In two months I felt more alert and a few months later the flickering in my eyes and the backache had gone and numbness was now confined to my fingers. Even now, after having the treatment for about a year and a half, I still have patches of numbness on the finger tips of one hand, my balance is rather poor, and I tire easily, though I am better than before. My improvement and my taking the diet might well have been coincidental, but Roger MacDougall, who originated this type of diet for multiple sclerosis and who was in a wheel-chair and almost blind, is now completely free of symptoms; several patients in a home in Godalming, Surrey, have improved while on the diet (data from the home) as have many other individuals
(Roger MacDougall, personal communication). In the diet I take, the subject avoids eating wheat, oats, rye, and barley (and anything containing them), takes less saturated fat, replacing it in part by unsaturated fat, reduces his sugar intake, replacing the remaining white sugar by Barbados sugar, and supplements his intake of food with vitamins and minerals Daily supplement*
.
as
follows:
Vitamin Bl Vitamin B2 Vitamin Be Nicotinamide Calcium pantothenate Vitamin C Vitamin E Calcium gluconate
Magnesium hydroxide Vitamin
24 12 60 1 120 600 180 900 900 150
mg. mg. mg. g. mg. mg. mg. mg. mg. ng.
B12 supplement is available from the Cantassium Company, 225 Putney Bridge Road, London SW15, under the National Health Service or privately; a modified version is also available privately from Regenics Ltd, 450 Edgware Road, London W2 1EG. *
This
In various malabsorption disorders, the symptoms can be cleared up by a gluten-free diet and magnesium supplements.’ Some of the symptoms in the magnesium-deficiency syndrome2 are strikingly like those I have experienced. I have now found that I can replace the supplement with the equivalent amount of magnesium hydroxide alone; progress continues and is perhaps a little faster than when I took the entire supplement. The latter contains much calcium, which is known to be antagonistic to the absorption of magnesium in the gut and to the reabsorption of magnesium in the renal tubules.3It may be significant that the magnesium content of the public water-supply in Godalming is about forty times that in Aberdeen. Further, high tea, a gluten-rich. meal, is popular in Scotland where the incidence of multiple sclerosis is high. A diet on the lines advocated by Roger MacDougall has helped many sufferers from multiple sclerosis but has been of no apparent benefit in other cases. The use of a gluten1
Booth, C. C., Hanna, S., Barbouris, N., McIntyre, I. Br. med. J. 1963, ii, 141. 2. Hanna, S., Harrison, M., McIntyre, I., Fraser, R. Lancet, 1960, ii, 172. 3
McIntyre, I. Proc. R. Soc. Med. 1960, 53, 1037.
is not strong and no firm conclusions can be drawn. The diet helps decrease the intensity of the symptoms in some cases, and the fact that dietary treatment sometimes helps suggests several lines of research. I thank
Roger MacDougall, whose diet made it possible for
to carry out
me
these observations.
36
Salisbury Terrace, Aberdeen AB1 6QH.
NORMAN A. MATHESON.
DIET AND CARDIOVASCULAR DISEASE
SIR,-In view of the long official silence in this country concerning the role of diet in the prevention of coronary heart-disease (when other countries have long ago made definitive statements 1-9) the report 10 of the Committee on Medical Aspects of Food Policy is all the more disappointing in its avoidance of the practical issues. Dietary advice, if it is to be taken, must be practicable. It must allow the dieter to choose from readily available foodstuffs so that his diet need not be extreme or faddist ", and not significantly more expensive than the food he would normally buy. The major scientific findings should have been presented in such a way that he can readily appreciate those foods he should avoid and those he can take. Our first criticism of the report is its lack of practicability. We are told that the total amount of saturated fat in the diet should be reduced. Three points arise here. First, a general reduction in fat content of diets, particularly saturated fat, will lead to a reduction in palatability that most people have now come to regard as acceptable or Second, there is no indication of how this necessary. reduction is to be achieved. Dietary fat is either " visible " " or hidden ". Have the committee the courage to openly recommend rejection of butter or hardened margarine-if so, why do they not say so? Do they recommend that we cut down our egg and milk consumption (thereby losing out on high-quality protein and vitamins) ? Do they recommend cutting off the visible fat in meat ? This last point is important because the half-informed would-be dieter may think in terms of cutting down on animal meat products generally, in which case he will certainly reduce his intake of saturated fat, but more seriously, a prime source of the essential fatty acid, arachidonic acid, will be eradicated. Most people forget that the hidden fats in lean meat are a rich source of the polyunsaturated fatty acids so scorned by the committee. "
1.
2. 3. 4.
5.
6. 7. 8. 9. 10.
Primary Prevention of Atherosclerotic Diseases: Report of InterSociety Commission for Heart Disease Resources. Circulation, 1970, 42, A-55. Alfin-Slater, R. B. J. Am. diet. Ass. 1969, 54, 486. Nutr. Rev. 1968, 26, 259. Diet and Coronary Heart Disease: a joint statement of the Food and Nutrition Board, Division of Biology and Agriculture, National Academy of Sciences—National Research Council, and the Council on Food and Nutrition, American Medical Association. ibid. 1972, 30, 223. Dietary Fat and Coronary Heart Disease. Standing Subcommittee appointed by National Heart Foundation of Australia. Med. J. Aust. 1967, i, 309. Coronary Heart Disease: Report of a committee of the Royal Society of New Zealand, 1971. Coronary Heart Disease: A New Zealand Report. National Heart Foundation of New Zealand, 1971. The Nutrition Report, 1972. German Society for Nutrition, 1972. Recommendations on Amount and/or Nature of Dietary Fats. Netherlands Nutrition Council, 1973. Diet and Coronary Heart Disease: report of the Advisory Panel of the Committee on Medical Aspects of Food Policy (Nutrition) on Diet in Relation to Cardiovascular and Cerebrovascular Disease. Rep. Hlth Soc. Subj. no. 7. H.M. Stationery Office, 1974. See Lancet, 1974, i, 1177.
832 not all potential or actual heart-disease sufferers obese. Reduction of total fat calories, therefore, can almost certainly be equated with an increase in carbohydrate calories, unless the person is ready to reduce his calorie intake, which if he is slim anyway is not a reasonable recommendation. It appears, from the report, that the committee are not in favour of extra carbohydrate calories either and therefore have not considered sufficiently the practical implications of their recommendations. Our second main criticism of the report is the apparently narrow interpretation of its terms of reference. Whereas the committee was asked to advise on the significance of any relation between nutrition and cardiovascular disease (para. 1.1), reference is made throughout the report only to death-rates and not to other coronary events. Dietary trials which may not show a convincing decrease in death-rate after modification of dietary fat consumption nevertheless show significant beneficial effects when all coronary events are considered." Other expert panels have taken the view that when these results are coupled with evidence from basic studies of biochemical mechanisms, it is prudent to recommend those at risk to modify dietary fat intake by increasing the P/S ratio. This committee has expressly excluded consideration of such basic
Third,
are
studies.
Paragraph 2.1.2 states: " An examination of any relationship between diet and disease does not necessitate a consideration of the intimate mechanisms involved. We have therefore agreed to consider the evidence linking diet with the development of cardiovascular disease without any examination of the pathways which may be implicated...." Surely it is just in those cases where scientific evidence is open to many interpretations that the intimate biochemistry, physiology, and pathology should be examined very closely. Basic knowledge in these areas must surely strengthen opinion one way or another, yet this committee has specifically chosen to ignore it. Finally, there would seem to be two basic approaches to dietary management in connection with public-health problems of this magnitude. (i) To conclude that the problem is so widespread that everyone is potentially at risk even though not showing clinical signs of the disease and recommend educational programmes at a national level to encourage the general population to modify its eating habits. (ii) To lay the problem at the door of clinicians to determine which of the population are at risk. Only those at risk would then be recommended to modify dietary habits. That this can be done in an eminently practical way has been shown by recent studies with hyperlipidsemic people in this country.12 No clear indication of which approach is the more useful has come from this report. In a field where a large number of scientific " facts are open to such wide differences in interpretation, it may not always be appreciated by readers of the report that it itself represents only one possible interpretation. Indeed another entirely different panel from this country would almost certainly have come up with a different inter’
pretation. The committee’s report
was
for the guidance of Govern-
ment, food manufacturers, the medical profession, and potential and actual sufferers from coronary heart-disease. It is regrettable that this report has avoided the practical issues and provided no clear guidance for any of these
sections of
society.
1 The Drive,
Sharnbrook, Bedford MK44 1HU.
11. 12.
M. I. GURR D. W. LARBEY
Nestel, P. J. Search, 1974, 5, 94. Evans, D. W., Turner, S. M., Ghosh, P. Lancet, 1972, i, 172.
FOOD ANTIBODIES AND MYOCARDIAL INFARCTION SIR,-Davies and his co-workers1 postulated a causal relationship between food antigenicity and myocardial infarction. Furthermore, they claimed that" the possession of antibody to cow’s milk protein and egg white in bloodsamples taken soon after infarction seems, therefore, to be highly predictive of death. Mortality was increased almost threefold if either antibody was present". After reading this paper I waited for the ridiculous to happen, and it has. I have received a request for a serumegg level from an astute clinician who prides himself on keeping up with the literature. To prevent this from happening elsewhere, I should like to publish my response to this request. The data of Davies et al. do not support their conclusions when re-evaluated in the predictive value format 23 for
analysing laboratory Food
Antibody
-7L z Milk Ab
Total
as a
tests.
Predictor
of Death Following Myocardial lnfarction
Total Die Live M.l. 80 +29 .. -10 94 104 Egg Ab 39 174 213 Total
109 egg
Sensitivity 29/39=74-4% Specificity 94/174=54-0% Predictive (prognostic) value for death 29/109=26-6% EHiciency= 123/213=57-7% (correct diagnosis)
Die +11 -22 33
Live 29 108 137
Total M.l. 40 130 170
Sensitivity 11/33=33-3% Specificity 108/137=78-8% Predictive (prognostic) value for death 11/40=27,5% Efficiency =119/170=70% (correct diagnosis)
The predictive or prognostic values of the presence of milk or egg antibody are approximately 27% for each. Approximately three-quarters of all positive results will be false-positives. Neither test appears to be of clinical value, let alone " highly predictive of death ". Furthermore, it is difficult to see how one could formulate a causal hypothesis after studying these results. Department of Pathology, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, U.S.A.
ROBERT S. GALEN.
ANGINA PECTORIS WITH NORMAL CORONARY ARTERIES
SIR,-The paper by Dr Richardson and his colleagues (Sept. 21, p. 677) must arouse great interest. The descriptive term " angina pectoris " and the disease ischxmic heart-disease " for many years have been considered synonymous. Demonstration of normal coronary arteries in patients with angina pectoris highlights the importance of discovering the mechanism(s) that produce(s) angina. Because ischaemic heart-disease is found in most patients with angina it is assumed that hypoxia or products of anaerobic metabolism such as lactic acid stimulate nervefibres in the myocardium.4 However, it is just as probable that such receptors are stimulated by changes in muscle tension. Any acute change of compliance in the left ventricle could be the cause of angina pectoris. The association of angina pectoris with hypertrophic obstructive cardiomyopathy and congestive cardiomyopathy without coronary-artery disease is easily explained. Such a postulate will also explain the paradoxical response of some patients with ischxmic heart-disease to 3-blocking therapy Davies, D. F., Johnson, A. P., Rees, B. W. G., Elwood, P. C Abernethy, M. Lancet, 1974, i, 1012. 2. Vecchio, T. J. New Engl. J. Med. 1966, 274, 1171. 3. Holland, W. W., Whitehead, T. P. Lancet, Aug. 17, 1974, p. 391 4. Friedburg, C. K. Diseases of the Heart; p. 724. Philadelphia, 1960 1.
Letters
to
magnesium supplementation may be more generally applicable. The evidence for these speculations
the Editor
MULTIPLE SCLEROSIS AND DIET Sir,- am a biochemist working on the development of analytical methods in nutrition. Five years ago I was told I had multiple sclerosis. I believe my experience and ideas may be of some value to those working on the disease. From diagnosis in 1969 until early 1973 I became slowly worse, though I have never been immobile or unable to carry out research work. However, I felt apathetic, I tired easily, I had backache, my balance was bad, I had flickering in my eyes, and one hand was numb and sensory paralysis was creeping up my arm. In March, 1973, I began to take a gluten-free diet with a vitamin and mineral supplement. In two months I felt more alert and a few months later the flickering in my eyes and the backache had gone and numbness was now confined to my fingers. Even now, after having the treatment for about a year and a half, I still have patches of numbness on the finger tips of one hand, my balance is rather poor, and I tire easily, though I am better than before. My improvement and my taking the diet might well have been coincidental, but Roger MacDougall, who originated this type of diet for multiple sclerosis and who was in a wheel-chair and almost blind, is now completely free of symptoms; several patients in a home in Godalming, Surrey, have improved while on the diet (data from the home) as have many other individuals
(Roger MacDougall, personal communication). In the diet I take, the subject avoids eating wheat, oats, rye, and barley (and anything containing them), takes less saturated fat, replacing it in part by unsaturated fat, reduces his sugar intake, replacing the remaining white sugar by Barbados sugar, and supplements his intake of food with vitamins and minerals Daily supplement*
.
as
follows:
Vitamin Bl Vitamin B2 Vitamin Be Nicotinamide Calcium pantothenate Vitamin C Vitamin E Calcium gluconate
Magnesium hydroxide Vitamin
24 12 60 1 120 600 180 900 900 150
mg. mg. mg. g. mg. mg. mg. mg. mg. ng.
B12 supplement is available from the Cantassium Company, 225 Putney Bridge Road, London SW15, under the National Health Service or privately; a modified version is also available privately from Regenics Ltd, 450 Edgware Road, London W2 1EG. *
This
In various malabsorption disorders, the symptoms can be cleared up by a gluten-free diet and magnesium supplements.’ Some of the symptoms in the magnesium-deficiency syndrome2 are strikingly like those I have experienced. I have now found that I can replace the supplement with the equivalent amount of magnesium hydroxide alone; progress continues and is perhaps a little faster than when I took the entire supplement. The latter contains much calcium, which is known to be antagonistic to the absorption of magnesium in the gut and to the reabsorption of magnesium in the renal tubules.3It may be significant that the magnesium content of the public water-supply in Godalming is about forty times that in Aberdeen. Further, high tea, a gluten-rich. meal, is popular in Scotland where the incidence of multiple sclerosis is high. A diet on the lines advocated by Roger MacDougall has helped many sufferers from multiple sclerosis but has been of no apparent benefit in other cases. The use of a gluten1
Booth, C. C., Hanna, S., Barbouris, N., McIntyre, I. Br. med. J. 1963, ii, 141. 2. Hanna, S., Harrison, M., McIntyre, I., Fraser, R. Lancet, 1960, ii, 172. 3
McIntyre, I. Proc. R. Soc. Med. 1960, 53, 1037.
is not strong and no firm conclusions can be drawn. The diet helps decrease the intensity of the symptoms in some cases, and the fact that dietary treatment sometimes helps suggests several lines of research. I thank
Roger MacDougall, whose diet made it possible for
to carry out
me
these observations.
36
Salisbury Terrace, Aberdeen AB1 6QH.
NORMAN A. MATHESON.
DIET AND CARDIOVASCULAR DISEASE
SIR,-In view of the long official silence in this country concerning the role of diet in the prevention of coronary heart-disease (when other countries have long ago made definitive statements 1-9) the report 10 of the Committee on Medical Aspects of Food Policy is all the more disappointing in its avoidance of the practical issues. Dietary advice, if it is to be taken, must be practicable. It must allow the dieter to choose from readily available foodstuffs so that his diet need not be extreme or faddist ", and not significantly more expensive than the food he would normally buy. The major scientific findings should have been presented in such a way that he can readily appreciate those foods he should avoid and those he can take. Our first criticism of the report is its lack of practicability. We are told that the total amount of saturated fat in the diet should be reduced. Three points arise here. First, a general reduction in fat content of diets, particularly saturated fat, will lead to a reduction in palatability that most people have now come to regard as acceptable or Second, there is no indication of how this necessary. reduction is to be achieved. Dietary fat is either " visible " " or hidden ". Have the committee the courage to openly recommend rejection of butter or hardened margarine-if so, why do they not say so? Do they recommend that we cut down our egg and milk consumption (thereby losing out on high-quality protein and vitamins) ? Do they recommend cutting off the visible fat in meat ? This last point is important because the half-informed would-be dieter may think in terms of cutting down on animal meat products generally, in which case he will certainly reduce his intake of saturated fat, but more seriously, a prime source of the essential fatty acid, arachidonic acid, will be eradicated. Most people forget that the hidden fats in lean meat are a rich source of the polyunsaturated fatty acids so scorned by the committee. "
1.
2. 3. 4.
5.
6. 7. 8. 9. 10.
Primary Prevention of Atherosclerotic Diseases: Report of InterSociety Commission for Heart Disease Resources. Circulation, 1970, 42, A-55. Alfin-Slater, R. B. J. Am. diet. Ass. 1969, 54, 486. Nutr. Rev. 1968, 26, 259. Diet and Coronary Heart Disease: a joint statement of the Food and Nutrition Board, Division of Biology and Agriculture, National Academy of Sciences—National Research Council, and the Council on Food and Nutrition, American Medical Association. ibid. 1972, 30, 223. Dietary Fat and Coronary Heart Disease. Standing Subcommittee appointed by National Heart Foundation of Australia. Med. J. Aust. 1967, i, 309. Coronary Heart Disease: Report of a committee of the Royal Society of New Zealand, 1971. Coronary Heart Disease: A New Zealand Report. National Heart Foundation of New Zealand, 1971. The Nutrition Report, 1972. German Society for Nutrition, 1972. Recommendations on Amount and/or Nature of Dietary Fats. Netherlands Nutrition Council, 1973. Diet and Coronary Heart Disease: report of the Advisory Panel of the Committee on Medical Aspects of Food Policy (Nutrition) on Diet in Relation to Cardiovascular and Cerebrovascular Disease. Rep. Hlth Soc. Subj. no. 7. H.M. Stationery Office, 1974. See Lancet, 1974, i, 1177.
832 not all potential or actual heart-disease sufferers obese. Reduction of total fat calories, therefore, can almost certainly be equated with an increase in carbohydrate calories, unless the person is ready to reduce his calorie intake, which if he is slim anyway is not a reasonable recommendation. It appears, from the report, that the committee are not in favour of extra carbohydrate calories either and therefore have not considered sufficiently the practical implications of their recommendations. Our second main criticism of the report is the apparently narrow interpretation of its terms of reference. Whereas the committee was asked to advise on the significance of any relation between nutrition and cardiovascular disease (para. 1.1), reference is made throughout the report only to death-rates and not to other coronary events. Dietary trials which may not show a convincing decrease in death-rate after modification of dietary fat consumption nevertheless show significant beneficial effects when all coronary events are considered." Other expert panels have taken the view that when these results are coupled with evidence from basic studies of biochemical mechanisms, it is prudent to recommend those at risk to modify dietary fat intake by increasing the P/S ratio. This committee has expressly excluded consideration of such basic
Third,
are
studies.
Paragraph 2.1.2 states: " An examination of any relationship between diet and disease does not necessitate a consideration of the intimate mechanisms involved. We have therefore agreed to consider the evidence linking diet with the development of cardiovascular disease without any examination of the pathways which may be implicated...." Surely it is just in those cases where scientific evidence is open to many interpretations that the intimate biochemistry, physiology, and pathology should be examined very closely. Basic knowledge in these areas must surely strengthen opinion one way or another, yet this committee has specifically chosen to ignore it. Finally, there would seem to be two basic approaches to dietary management in connection with public-health problems of this magnitude. (i) To conclude that the problem is so widespread that everyone is potentially at risk even though not showing clinical signs of the disease and recommend educational programmes at a national level to encourage the general population to modify its eating habits. (ii) To lay the problem at the door of clinicians to determine which of the population are at risk. Only those at risk would then be recommended to modify dietary habits. That this can be done in an eminently practical way has been shown by recent studies with hyperlipidsemic people in this country.12 No clear indication of which approach is the more useful has come from this report. In a field where a large number of scientific " facts are open to such wide differences in interpretation, it may not always be appreciated by readers of the report that it itself represents only one possible interpretation. Indeed another entirely different panel from this country would almost certainly have come up with a different inter’
pretation. The committee’s report
was
for the guidance of Govern-
ment, food manufacturers, the medical profession, and potential and actual sufferers from coronary heart-disease. It is regrettable that this report has avoided the practical issues and provided no clear guidance for any of these
sections of
society.
1 The Drive,
Sharnbrook, Bedford MK44 1HU.
11. 12.
M. I. GURR D. W. LARBEY
Nestel, P. J. Search, 1974, 5, 94. Evans, D. W., Turner, S. M., Ghosh, P. Lancet, 1972, i, 172.
FOOD ANTIBODIES AND MYOCARDIAL INFARCTION SIR,-Davies and his co-workers1 postulated a causal relationship between food antigenicity and myocardial infarction. Furthermore, they claimed that" the possession of antibody to cow’s milk protein and egg white in bloodsamples taken soon after infarction seems, therefore, to be highly predictive of death. Mortality was increased almost threefold if either antibody was present". After reading this paper I waited for the ridiculous to happen, and it has. I have received a request for a serumegg level from an astute clinician who prides himself on keeping up with the literature. To prevent this from happening elsewhere, I should like to publish my response to this request. The data of Davies et al. do not support their conclusions when re-evaluated in the predictive value format 23 for
analysing laboratory Food
Antibody
-7L z Milk Ab
Total
as a
tests.
Predictor
of Death Following Myocardial lnfarction
Total Die Live M.l. 80 +29 .. -10 94 104 Egg Ab 39 174 213 Total
109 egg
Sensitivity 29/39=74-4% Specificity 94/174=54-0% Predictive (prognostic) value for death 29/109=26-6% EHiciency= 123/213=57-7% (correct diagnosis)
Die +11 -22 33
Live 29 108 137
Total M.l. 40 130 170
Sensitivity 11/33=33-3% Specificity 108/137=78-8% Predictive (prognostic) value for death 11/40=27,5% Efficiency =119/170=70% (correct diagnosis)
The predictive or prognostic values of the presence of milk or egg antibody are approximately 27% for each. Approximately three-quarters of all positive results will be false-positives. Neither test appears to be of clinical value, let alone " highly predictive of death ". Furthermore, it is difficult to see how one could formulate a causal hypothesis after studying these results. Department of Pathology, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032, U.S.A.
ROBERT S. GALEN.
ANGINA PECTORIS WITH NORMAL CORONARY ARTERIES
SIR,-The paper by Dr Richardson and his colleagues (Sept. 21, p. 677) must arouse great interest. The descriptive term " angina pectoris " and the disease ischxmic heart-disease " for many years have been considered synonymous. Demonstration of normal coronary arteries in patients with angina pectoris highlights the importance of discovering the mechanism(s) that produce(s) angina. Because ischaemic heart-disease is found in most patients with angina it is assumed that hypoxia or products of anaerobic metabolism such as lactic acid stimulate nervefibres in the myocardium.4 However, it is just as probable that such receptors are stimulated by changes in muscle tension. Any acute change of compliance in the left ventricle could be the cause of angina pectoris. The association of angina pectoris with hypertrophic obstructive cardiomyopathy and congestive cardiomyopathy without coronary-artery disease is easily explained. Such a postulate will also explain the paradoxical response of some patients with ischxmic heart-disease to 3-blocking therapy Davies, D. F., Johnson, A. P., Rees, B. W. G., Elwood, P. C Abernethy, M. Lancet, 1974, i, 1012. 2. Vecchio, T. J. New Engl. J. Med. 1966, 274, 1171. 3. Holland, W. W., Whitehead, T. P. Lancet, Aug. 17, 1974, p. 391 4. Friedburg, C. K. Diseases of the Heart; p. 724. Philadelphia, 1960 1.