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ATHEROGENICITY AND THE SUPERMARKET SHELF
534
Letters
to
the Editor
ATHEROGENICITY AND THE SUPERMARKET SHELF
SIR,-In the debate on dietary change in relation to coronary heart disease (CHD) the emphasis is invariably placed on lowering serum cholesterol; the limitations of this approach have been highlighted by Professor Ahrens (Dec. 22/29, p. 1345). There is, however, another aspect to this problem that has been ignored-the specific atherogenicity of certain vegetable fats which may be independent of their effect on serum cholesterol. In 1959 Wigand’ reported that in rabbits fed cholesterolfree diets supplemented with various fats the most severe atherosclerotic lesions were produced by coconut oil; less severe lesions were produced by butterfat, although it contained cholesterol. Extensive studies’have now been reported in primates fed peanut, coconut, butter, and corn oils supplemented with cholesterol, and in all the trials the most severe atherosclerotic lesions in both aorta and coronary arteries were produced by peanut oil; the next most atherosclerotic was coconut oil.2-4 Similar results were obtained when the oils were added to a cholesterol-free diet and fed to rabbits. Serum cholesterol levels remained low on peanut oil, and were increased to a comparable extent by butter and coconut oils, but coconut oil produced large increases in serum triglycerides. Peanut oil produced highly characteristic arterial lesions in which there is massive proliferation of smooth muscle cells and collagen but very little lipid accumulation. They closely resemble the abruptly raised, low lipid fibrous or gelatinous lesions that I see frequently in human aortas at autopsy, particularly in men aged 40-60 with CHD. Coconut oil lesions are both proliferative and lipid-rich, and again have their human counterparts, but I seldom see lesions resembling the non-proliferative fatty infiltration produced by butter oil. Peanut oil contains about 60% oleic acid (18:1) and 25% linoleic acid (18:2) so theoretically it should be a "good" oil, but it also contains about 7% of the long chain saturated fatty acids arachidic (20:0), behenic (22:0) and lignoceric (24:0), and these may be the atherogenic factors.6,7 Its atherogenicity is not related to aflatoxin content.8 Inexplicably, this work is totally ignored by advocates of dietary change although it emanates from a leading specialised centre of research (SCOR) laboratory in Chicago, and not from a crank in an obscure institute. It is ignored both at the clinical level, and by the many committees set up to make dietary recommendations, including the F.A.O./W.H.O. Expert Consultation on Dietary Fats and Oils in Human Nutrition.9 1. Wigand G. Production of hypercholesterolæmia and atherosclerosis in rabbits by feeding different fats without supplementary cholesterol. Acta Med Scand 1959; 166: suppl 351. 2. Wissler RW, Frazier LE, Hughes RH, Rasmussen RA. Atherogenesis in the cebus monkey: 1. A comparison of three food fats under controlled dietary conditions. Arch Pathol 1962; 74: 312-22. 3. Vesselinovitch D, Getz GS, Hughes RH, Wissler RW. Atherosclerosis in the rhesus monkey fed three food fats. Atherosclerosis 1974; 20: 303-21. 4. Wissler RW, Vesselinovitch D. Diet and experimental atherosclerosis. In: Chavez A, Bourges H, Basta S, eds. Nutrition vol I: Review of basic sciences. Basel: Karger, 1975: 333-39. 5. Kritchevsky D, Tepper SA, Kim HK, Story JA, Vesselinovitch D, Wissler RW. Experimental atherosclerosis in rabbits fed cholesterol-free diets: 5. Comparison of peanut, corn, butter and coconut oils. Exp Mol Pathol 1976;;24: 375-91. 6. Kritchevsky D, Tepper SA, Vesselinovitch D, Wissler RW. Cholesterol vehicle in experimental atherosclerosis. Atherosclerosis 1971; 14: 53-64 and 1973; 17: 225-43. 7. Renaud S. Thrombogenicity and atherogenicity of dietary fatty acids in rat.
The advocates of increased polyunsaturated fat diets do not spell out to the housewife what she is supposed to buy. By implication they support the formula: animal fat=butter=satura-
ted=bad ; polyunsaturated=vegetable=good. This is exemplified by Dr Ball (Dec. 1, p. 1182) in his remarks on the
promotional activities of the Butter Information Council. He should go into an ordinary supermarket and look carefully at the display of fats. In our supermarket about 20% of the space is occupied by butter and the remainder is margarine and shortening ; in this section not more than 10% is occupied by a known brand of polyunsaturated margarine which states that it is "high in polyunsaturates" but no longer names the oil used, nor the percentage of cis-cis-linoleic acid. The remaining 90%, some of which are "soft" and presumably emulsified, describe themselves as made from "pure vegetable oils" or "edible oils". Some of these may be all right, but many are highly saturated or contain large amounts of trans-acids, and, according to Ministry of Agriculture, Fisheries and Food statistics, over 40% of the oil used is of marine origin. Partially hydrogenated marine oils contain even more arachidic, behenic, and lignoceric acids than does peanut oil.9 The shortenings, which describe themselves as "pure solid vegetable oil", are almost certainly coconut oil, 95% saturated (butter is only 65% saturated and lard is only 30% saturated). Of the cooking oils, two out of five brands are named (corn oil and sunflower oil) and the remainder are "pure vegetable oil". I suspect that they are rapeseed oil; even the new strains with less than 5% erucic acid exhibit significant cardiac toxi-
city. 10
Even if the Government issued specific recommendations -and I agree with Professor Ahrens that this would be premature and unwise-how is the housewife to know what to buy? Dr Ball would do the public a much greater service by campaigning for full and proper labelling of fats with the proportions of total saturated, long chain saturated, cis-cis linoleic, long-chain monoenes (erucic), and trans acids than by campaigning for destruction of the dairy industry which produces, in milk, the cheapest source of first class protein available. Department of Chemical Pathology, University of Aberdeen, Aberdeen AB9 2ZD
ELSPETH B. SMITH
JAW WIRING FOR OBESITY SIR,- The paper by the Danish Obesity Group (Dec. 15, p 1255) highlights some of the problems of the treatment o obesity. However, in our opinion this paper and your editoria in the same issue underrate jaw wiring as a treatment for obes ity. The Adelaide Obesity Group has managed or has in hand some 300 cases of obesity being treated by this method. The indications, contraindications, and oral surgical methods have been reported (Br Dent J 1979; 146: 339) as has the weigh loss for some of the patients.We would like to present the pro gress of a cohort of 122 patients who had their jaws wire between February, 1975, and May, 1978. Of these, 13 (11’c were unwired because of intolerance of the wires (9) or medica reasons (4), and 11 (9%) were lost to follow-up. We have dat on 73 patients with characteristics similar to those of th Danish patients (see table). All patients lost weight, and the pattern of loss was simila to that in our earlier study,’ with an initial rapid weight lo (10 kg per month) followed by a plateau (2 kg per month) afte five or six months when the median weight loss was 42 (range 5-98) of the initial excess over ideal weight.
J Atheroscler Res 1968; 8: 625-36. 8. Vesselinovitch D, Wissler RW, Schaffner TJ, Borensztajn J. The effect of various diets on atherogenesis in rhesus monkeys. Atherosclerosis 1980;
35: 189-207. 9.
FAO/WHO Expert Consultation. Dietary fats and oils in human nutrition. FAO Food Nutr Paper 1977; No. 3.
10. Beare-Rogers JL, Nera EA. Nutritional effects ofpartially hydrogenated l erucic rapseseed oils. Lipids 1977; 12: 769-74. 1. Rodgers S, Burnett R, Goss A, Phillips P, Goldney R, Kimber C, Thoma D, Harding P, Wise P. Jaw wiring in treatment of obesity. Lancet 1977 i: 1221-23.
Letters
to
the Editor
ATHEROGENICITY AND THE SUPERMARKET SHELF
SIR,-In the debate on dietary change in relation to coronary heart disease (CHD) the emphasis is invariably placed on lowering serum cholesterol; the limitations of this approach have been highlighted by Professor Ahrens (Dec. 22/29, p. 1345). There is, however, another aspect to this problem that has been ignored-the specific atherogenicity of certain vegetable fats which may be independent of their effect on serum cholesterol. In 1959 Wigand’ reported that in rabbits fed cholesterolfree diets supplemented with various fats the most severe atherosclerotic lesions were produced by coconut oil; less severe lesions were produced by butterfat, although it contained cholesterol. Extensive studies’have now been reported in primates fed peanut, coconut, butter, and corn oils supplemented with cholesterol, and in all the trials the most severe atherosclerotic lesions in both aorta and coronary arteries were produced by peanut oil; the next most atherosclerotic was coconut oil.2-4 Similar results were obtained when the oils were added to a cholesterol-free diet and fed to rabbits. Serum cholesterol levels remained low on peanut oil, and were increased to a comparable extent by butter and coconut oils, but coconut oil produced large increases in serum triglycerides. Peanut oil produced highly characteristic arterial lesions in which there is massive proliferation of smooth muscle cells and collagen but very little lipid accumulation. They closely resemble the abruptly raised, low lipid fibrous or gelatinous lesions that I see frequently in human aortas at autopsy, particularly in men aged 40-60 with CHD. Coconut oil lesions are both proliferative and lipid-rich, and again have their human counterparts, but I seldom see lesions resembling the non-proliferative fatty infiltration produced by butter oil. Peanut oil contains about 60% oleic acid (18:1) and 25% linoleic acid (18:2) so theoretically it should be a "good" oil, but it also contains about 7% of the long chain saturated fatty acids arachidic (20:0), behenic (22:0) and lignoceric (24:0), and these may be the atherogenic factors.6,7 Its atherogenicity is not related to aflatoxin content.8 Inexplicably, this work is totally ignored by advocates of dietary change although it emanates from a leading specialised centre of research (SCOR) laboratory in Chicago, and not from a crank in an obscure institute. It is ignored both at the clinical level, and by the many committees set up to make dietary recommendations, including the F.A.O./W.H.O. Expert Consultation on Dietary Fats and Oils in Human Nutrition.9 1. Wigand G. Production of hypercholesterolæmia and atherosclerosis in rabbits by feeding different fats without supplementary cholesterol. Acta Med Scand 1959; 166: suppl 351. 2. Wissler RW, Frazier LE, Hughes RH, Rasmussen RA. Atherogenesis in the cebus monkey: 1. A comparison of three food fats under controlled dietary conditions. Arch Pathol 1962; 74: 312-22. 3. Vesselinovitch D, Getz GS, Hughes RH, Wissler RW. Atherosclerosis in the rhesus monkey fed three food fats. Atherosclerosis 1974; 20: 303-21. 4. Wissler RW, Vesselinovitch D. Diet and experimental atherosclerosis. In: Chavez A, Bourges H, Basta S, eds. Nutrition vol I: Review of basic sciences. Basel: Karger, 1975: 333-39. 5. Kritchevsky D, Tepper SA, Kim HK, Story JA, Vesselinovitch D, Wissler RW. Experimental atherosclerosis in rabbits fed cholesterol-free diets: 5. Comparison of peanut, corn, butter and coconut oils. Exp Mol Pathol 1976;;24: 375-91. 6. Kritchevsky D, Tepper SA, Vesselinovitch D, Wissler RW. Cholesterol vehicle in experimental atherosclerosis. Atherosclerosis 1971; 14: 53-64 and 1973; 17: 225-43. 7. Renaud S. Thrombogenicity and atherogenicity of dietary fatty acids in rat.
The advocates of increased polyunsaturated fat diets do not spell out to the housewife what she is supposed to buy. By implication they support the formula: animal fat=butter=satura-
ted=bad ; polyunsaturated=vegetable=good. This is exemplified by Dr Ball (Dec. 1, p. 1182) in his remarks on the
promotional activities of the Butter Information Council. He should go into an ordinary supermarket and look carefully at the display of fats. In our supermarket about 20% of the space is occupied by butter and the remainder is margarine and shortening ; in this section not more than 10% is occupied by a known brand of polyunsaturated margarine which states that it is "high in polyunsaturates" but no longer names the oil used, nor the percentage of cis-cis-linoleic acid. The remaining 90%, some of which are "soft" and presumably emulsified, describe themselves as made from "pure vegetable oils" or "edible oils". Some of these may be all right, but many are highly saturated or contain large amounts of trans-acids, and, according to Ministry of Agriculture, Fisheries and Food statistics, over 40% of the oil used is of marine origin. Partially hydrogenated marine oils contain even more arachidic, behenic, and lignoceric acids than does peanut oil.9 The shortenings, which describe themselves as "pure solid vegetable oil", are almost certainly coconut oil, 95% saturated (butter is only 65% saturated and lard is only 30% saturated). Of the cooking oils, two out of five brands are named (corn oil and sunflower oil) and the remainder are "pure vegetable oil". I suspect that they are rapeseed oil; even the new strains with less than 5% erucic acid exhibit significant cardiac toxi-
city. 10
Even if the Government issued specific recommendations -and I agree with Professor Ahrens that this would be premature and unwise-how is the housewife to know what to buy? Dr Ball would do the public a much greater service by campaigning for full and proper labelling of fats with the proportions of total saturated, long chain saturated, cis-cis linoleic, long-chain monoenes (erucic), and trans acids than by campaigning for destruction of the dairy industry which produces, in milk, the cheapest source of first class protein available. Department of Chemical Pathology, University of Aberdeen, Aberdeen AB9 2ZD
ELSPETH B. SMITH
JAW WIRING FOR OBESITY SIR,- The paper by the Danish Obesity Group (Dec. 15, p 1255) highlights some of the problems of the treatment o obesity. However, in our opinion this paper and your editoria in the same issue underrate jaw wiring as a treatment for obes ity. The Adelaide Obesity Group has managed or has in hand some 300 cases of obesity being treated by this method. The indications, contraindications, and oral surgical methods have been reported (Br Dent J 1979; 146: 339) as has the weigh loss for some of the patients.We would like to present the pro gress of a cohort of 122 patients who had their jaws wire between February, 1975, and May, 1978. Of these, 13 (11’c were unwired because of intolerance of the wires (9) or medica reasons (4), and 11 (9%) were lost to follow-up. We have dat on 73 patients with characteristics similar to those of th Danish patients (see table). All patients lost weight, and the pattern of loss was simila to that in our earlier study,’ with an initial rapid weight lo (10 kg per month) followed by a plateau (2 kg per month) afte five or six months when the median weight loss was 42 (range 5-98) of the initial excess over ideal weight.
J Atheroscler Res 1968; 8: 625-36. 8. Vesselinovitch D, Wissler RW, Schaffner TJ, Borensztajn J. The effect of various diets on atherogenesis in rhesus monkeys. Atherosclerosis 1980;
35: 189-207. 9.
FAO/WHO Expert Consultation. Dietary fats and oils in human nutrition. FAO Food Nutr Paper 1977; No. 3.
10. Beare-Rogers JL, Nera EA. Nutritional effects ofpartially hydrogenated l erucic rapseseed oils. Lipids 1977; 12: 769-74. 1. Rodgers S, Burnett R, Goss A, Phillips P, Goldney R, Kimber C, Thoma D, Harding P, Wise P. Jaw wiring in treatment of obesity. Lancet 1977 i: 1221-23.