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Hypothesis: Heated milk protein and thrombosis
Journal of A therosclerosis Research
Elsevier Publishing Company, Amsterdam - Printed in The Netherlands
Short Communication H Y P O T H E S I S : H E A T E D M I L K P R O T E I N AND T H R O M B O S I S
J. c. ANNAND Camperdown House, Broughty Ferry, Dundee (Great Britain)
(Received September 21st, 1967)
On 1st J a n u a r y 1923 Holder pasteurisation became compulsory in the United Kingdom. Thereafter all milk classified and sold to the public as "pasteurised" was heated for a period of 30 min at not less than 145~ (63~ I t was then found at different times in different population groups that, within a period of at most 2 years after the introduction of Holder pasteurisation, a significant sudden rise occurred in the mortality ascribed to both arteriosclerotic heart disease (AHD) and to cerebral embolism and thrombosis (CET) (Table 1). On the other hand when Flash pasteurisation was introduced--the milk on this occasion being heated for a period of 16 seconds only at a temperature of 165~ (74~ greater part of the mortality rise that followed seemed to coincide with the changes in disease classification that were introduced at this time 1. Thus the possibility began to be entertained that milk which has been heated for a relatively long period of time m a y be a dietary factor especially involved in the pathogenesis of thrombosis. This hypothesis appeared to be supported b y the finding that these sudden increases in mortality in the United Kingdom during the decade 1920-1930 (Table 1) principally affected not only the urban population (as distinct from the rural), but also the expected social class (in this case the working class) who evinced a preference for pasteurised milk because of its low cost and because of its keeping properties 1,2. I t was decided therefore to re-examine all available and pertinent dietary surveys in the light of the hypothesis that heated milk, particularly milk that had been heated for a relatively prolonged period of time, might be a primary factor in the pathogenesis of thrombosis, and also to investigate whether either heated milk protein or milk fat or both might be at fault. The following is a s u m m a r y of some of the salient features of this survey. (1) The different population groups who consumed no milk protein (the Yemenitesa, the South VietnamesO, the Atiu Mitiaro 5 and the H u n j a 6) and, likewise, those who consumed only fresh milk--none of it being heated (the rural Zulu 7, the Masai 8, the Samburu~, the nomads of Nigeria 1~ and of Somaliland n , the West Africans ot Gabon 12 and the Congolese Pygmies 13) were all found to be free from the disease. j . Atheroscler. Res., 7 (1967) 797-801
798
SHORT
COMMUNICATION
TABLE 1 CORRELATION
OF HOLDER
Population group
Edinburghl, 2 Glasgowl, ~ Dundeel, 2 Aberdeenl, ~ Lanarkshire 2 (excluding Glasgow) County of Sutherland 2 County of Bute 2 London Admin. County a5
PASTEURISATION
AND THROMBOSIS
Holder pasteurisalion (year of introduction )
Angina pectoris ( A P ) (internat. list Nos. 89, 94 and z120) mortality per l, 000, 000 persons
Cerebral embolism and thrombosis ( C E T ) (internal. list Nos. 74b, 82b and 332) mortality per 1,O00,O00 persons
AP 1 AP 2 AP 3 AP 4
CET I
CET 2
1923 1924 1924 1926 1935-37 1947-50 1952-53
1925 1924 1925 1926 1937 1948 1954
67 56 42 91 188 685 1185
92 91 64 135 375 1185 1523
37.3 a 62.5 a 52.4 a 48.4 a 99.5 b 73.0 28.5
1924 1924 1925 1927 1938 1948 1954
174 77 162 121 153 298 518
236 101 188 227 193 518 680
35.6 31.2 16.0 87.6 26.1 73.8 31.3
1954
1954
963
1710
77.9
1954
610
823
34.9
1956
1956
1610
2848
76.9
1956
955
1398
46.4
1925
1925
31
112
261.3 c 1926
90
120
33.3
[Average total Oslo (Norway) 36
MORTALITY
1922
1922
3
81.8] 43
CET 3
CET 4
[41.6]
1333.3 d not available
Columns AP1 and CET1 denote the year of commencement of the sudden rise in the appropriate mortality. Columns AP2 and CET2 denote the appropriate average mortality for the 4 years immediately preceding the year of introduction of pasteurisation. Columns AP3 and CET3 denote appropriate average mortality for the 4 years immediately succeeding the introduction of pasteurisation. Columns AP4 and CET4 denote the %age increase between Columns AP2 and AP3 and between Columns CET2 and CET3. a Possibly low because deaths ascribed to "coronary thrombosis" were not included in International List No. 89 in Scotland until 1931. b Possibly enhanced as deaths ascribed to "coronary thrombosis" were now included in International List No. 94, e Possibly enhanced because (i) after 1927 all deaths ascribed to "coronary thrombosis" were included unlike those in Scotland--in International List No. 89 and (it) the large London creameries introduced Holder pasteurisation during this period. a Mortality ascribed to the following group of classifications: angina pectoris, infarctus cordis, sclerosis art. coron, cordis.
(2) O n t h e o t h e r h a n d t h e t w o l a c t o - v e g e t a r i a n g r o u p s
(i)
t h e E a s t I n d i a n s i 4 , is
a n d (it) t h e T r a p p i s t 16-19 m o n k s , b o t h of w h o m c o n s u m e d b o i l e d a n d / o r p a s t e u r i s e d milk a n d milk p r o d u c t s , were e i t h e r n o t p r o t e c t e d or were only p a r t i a l l y p r o t e c t e d b y their diet. (3) C o u n t r i e s o r p o p u l a t i o n g r o u p s w h o c o n s u m e d o n l y s m a l l q u a n t i t i e s of m i l k that had received relatively prolonged heat treatment, were found to suffer a correspondingly low mortality; and this finding appeared to apply both to "privileged" c o m m u n i t i e s s u c h a s i n F r a n c e a n d T h e N e t h e r l a n d s a n d t o d e v e l o p i n g c o u n t r i e s , e.g. ThailandZ0, 21 a n d S o u t h Korea22, 2~. I n t h e f o r m e r g r o u p , e v a p o r a t e d m i l k , p r o c e s s e d c h e e s e a n d c o o k e d m i l k g e n e r a l l y w e r e all r e l a t i v e l y u n p o p u l a r a n d i n T h a i l a n d a n d
J. Atheroscler. Res., 7 (1967) 797-801
SHORT COMMUNICATION
799
South Korea evaporated milk, taken in coffee, was the only dairy product commonly consumed. Random postmortem studies in these last two countries revealed a thrombosis incidence of 2.7 and 2.0 % respectively. The reverse obviously held good for such countries as Australia, New Zealand, Canada, Ireland, the United Kingdom and the USA. (4/) By custom the Yemenites discard their milk protein and consume only the milk fat which, after being boiled, is then used for cooking purposes; thus their intake of milk protein consists only of that portion contained in the milk fat (0.35 % milk protein). They were reported to be free from AHD a, although they consume milk fat which has received prolonged heat treatment. (5) Milk fat consumption generally has been found not to be correlated with the A H D incidence either at the clinical 24 or at the international level 2a. (6) During both wars the consumption of milk protein in the United Kingdom 26-2s, that had received prolonged heat treatment fell and rose again in direct relationship to the mortality graph, either preceding the latter b y one year or coinciding with i t - both during its fall and during its rise. Throughout the last war the same close parallelism in respect of the total milk protein consumption and mortality occurred in both Denmark 29 and Canada 3~ In the USA at this time neither the mortality nor the milk protein consumption deviated from their steady rise. Thus, from 1931 to 1945 the crude mortality (International List No. 94a) per 100,000 rose from 7.9 to 95.8. At the same time the per capita consumption of milk foods known to have been heated for a significant period of time (e.g. evaporated milk, ice cream etc.) rose b y 102.8 %. Cheese consumption also increased b y 68.4 % and an increasing but unknown proportion of the latter was either pasteurised or processed and/or cooked: at the same time coffee consumption rose b y 26.2 %. On the other hand, in the United Kingdom during both wars and in both Canada and Denmark during the last War, the graph depicting milk fat consumption failed in every case to correlate with that of mortality. Thus on 3 occasions in the United Kingdom the latter preceded the former in beginning to rise b y periods varying from 2 to 4 years. (7) Antibodies to milk protein have frequently been demonstrated in "healthy" adults al-34, but the relevance of this observation to atherogenesis or to thrombogenesis cannot be pursued from the present data. Although the evidence summarized above is circumstantial and does not prove a causal relationship, nevertheless the fact should be mentioned that clinical experience over a period of 10 years has consistently supported the possibility that milk protein that has received prolonged heat treatment m a y well be an important dietary factor in the pathogenesis of thrombosis. Thus, all patients suffering from A H D who maintained a diet devoid of heated milk protein either showed a sustained improvement in their condition or failed to deteriorate further. On the other hand, patients who for various reasons did not maintain their diet evinced a high incidence of thrombosis and/or cardiac irregularities together with congestive failure.
J. Atheroscler. Res., 7 (1967) 797-801
800
SHORT COMMUNICATION
REFERENCES
J. c., Atherosclerosis, t h e case against protein, continued, J. Coll. gen. Practit., 1961, 4: 567. ANNAND, J. C., Thrombosis, f u r t h e r evidence against heated animal protein, J. Coll. gen. Practit., 1964, 7: 386. BRUNNER D. AND K. LOBL, Serum cholesterol, electrophoretic lipid p a t t e r n a n d coronary artery disease. A s t u d y in coronary p a t i e n t s a n d in h e a l t h y m e n of different origins and occupations in Israel, Ann. intern. Med., 1958, 49: 732. Nutrition survey, Republic of Vietnam, 1959, A report b y t h e I n t e r d e p a r t m e n t Committee on Nutrition for National Defense, W a s h i n g t o n , D.C., USA. WALKER, J. D., Nutritional s u r v e y in t h e Cook islands, Nutrition, 1962, 16: 15. TOOMEY, E. G. AND P. D. WHITE, A brief s u r v e y of the health of aged Hunjas, Amer. Heart f . , 1964, 68: 841. CAMPBELL, G, D., Personal communication.
1 ANNAND,
2 3
4 5 6
7 8 MANN, G. V., R. D. SHAFFER, a . S. ANDERSON AND H. H. SANDSTEAD, C a r d i o v a s c u l a r di s e a s e
in t h e Masai, J. Atheroscler. Res., 1964, 4: 289. 9 SHAPER, A. G., Cardiovascular studies in t h e S a m b u r u tribe of Northern Kenya, Amer. Heart J.,
1962, 63: 437. 10 MANN, G. V., B. M. NICOL AND F. J. STARE, The fl-lipoprotein and cholesterol concentrations
in sera of Nigerians, Brit. reed. J., 1955, ii: 1008. 11 LAPPICCIRELLA, V., R. LAPPICCIRELLA, F. ABBONI AND S. LIOTTA, Clinical, biological a n d
12 13
14 15
16
cardiographic s u r v e y a m o n g t h e n o m a d tribes of Somaliland who subsist only on milk, Bull. Wld Hlth Org., 1962, 27: 681. MILLER, D. C., S. S. SPENCER AND P. D. WHITE, Survey of cardiovascular disease a m o n g Africans in t h e vicinity of Albert Schweitzer Hospital in 1960, Amer. J. Cardiol., 1962, 10: 432. MANN, G. V., O. A. ROLLS, D. L. PRICE AND J. M. MERRILL, Cardiovascular disease in African Pygmies, J. chron. Dis., 1962, 15: 341. NATH, H. P., N. K. GUPTA AND P. V. K. IYER, Increasing incidence of coronary artery t h r o m b o sis in I n d i a n A r m y personnel, Indian J. reed. Res., 1957, 45: 217. MALHOTRA, R. P. AND N. S. PATHANIA, Some aetiological aspects of coronary h e a r t disease, Brit. reed. J., 1958, ii: 528. McCULLAGH, E. P. AND L. A. LEWIS, A s t u d y of diet, blood lipids and vascular disease in Trappist monks, New Engl. J. Med., 1960, 263: 569.
17 GROEN,
18
19
2o 21 22 23
24 25 26 27
28 29 30 31
32
J. J ,
K. B. TIJONG, M. KOSTER, A. F. WILLEBRANDS, G. VERDONCKAND N. PIERLOOT,
The influence of nutrition a n d ways of life on blood cholesterol and the prevalence of hypertension and coronary heart disease a m o n g Trappist a n d Benedictine monks, Amer. J. clin. Nutr., 1962, 10: 456. GROEN, J. J., The habits of t h e Trappist m o n k s a n d their influence on t h e incidence of coronary heart disease and percentage of cholesterol in t h e blood, Voeding, 1964, 25: 310. KEYS, A., The diet a n d some characteristics of Trappist monks, Mal. Cardiovasc., 1962, 3: 1. Nutrition survey, 1960, the Kingdom of Thailand, A Report by the I n t e r d e p a r t m e n t Committee on Nutrition for National Defense, W a s h i n g t o n , D.C., USA. HIRST, A. E., P. PUJARATON AND I. GORE, A comparison of atherosclerosis of t h e aorta and coronary arteries in ]Bangkok a n d Los Angeles, Amer. J. clin. Path., 1962, 38: 162. JARMOLYNCH, J., A. S. DAOUD, K. T. LEE, L. G. JACOVIC AND O. ZUMBO, Chemico-pathologic s t u d y in geographic pathology, Fed. Proc., 1963, 22: 384. LEE, K. T., S. C. NAM, O. H. KWON, S. B. KIM AND F. GOODALE, Geographic pathology of atherosclerosis. A s t u d y of t h e critical level of dietary fats as related to myocardial infarction in Koreans, Exp. molec. Path., 1963, 2: 1. MORRIS, J. N., J. A. HEADY, G. L. MILLS AND T. R. E. PILKINGTON, Diet a n d plasma cholesterol in 99 b a n k men, Brit. reed. J., 1963, ii: 571. YUDKIN, J., Diet and coronary thrombosis, Lancet, 1957, ii: 155. PREST, A. R., Consumer's Expenditure in the United Kingdom, 1900-1919, Cambridge University Press, New York, London, 1954. STONE, R., Measurement of Consumer's Expenditure and Behaviour in the United Kingdom, 1920-1938, Cambridge University Press, New York, London, 1954. The Urban Working-Class Household Diet, 1940-1949, Ministry of Food, H . M . S . O . , London, 1951. Statistiske efterretninger, Danmarks Statistik, 1949, 41: 374. PAGE, H. G., Dominion Bureau of Statistics, Ottawa, Canada, personal communication. LAROSE, C., P. H. DELORME, M. RICHTER AND B. ROSE, Immunologic studies on milk a n d egg allergy, J. Allergy, 1962, 33: 306. ROTHBERG, R. M. AND R. S. FARR, The incidence a n d t h e a m o u n t of antibovine s e r u m a l b u m i n
J. Atheroscler. Res., 7 (1967) 797-801
SHORT COMMUNICATION
33 84 35 an
S01
(BSA) a n d a n t i - a - l a c t a l b u m i n (ALA) in t h e s e r u m of c h i l d r e n a n d a d u l t s , Clin. Res., 1962, 10: 219. GUNTHI~R, M., R. ASCHAFFENBURG, R. H. MATTHEWS, W. E. PARISH AND R. A. COOMBS, T h e level of a n t i b o d i e s to t h e p r o t e i n s of cow's milk in t h e s e r u m of n o r m a l h u m a n i n f a n t s , Immunology, 1960, 3: 296. PARISH, W. E., A. M. BARRETT, a . A. COOMBS, M. GUNTHER AND F. •. CAMPS,H y p e r s e n s i t i v i t y to m i l k a n d s u d d e n d e a t h in infancy, Lancet, 1960, ii: 1106. REGISTRAR-GENERAL, Statistical Review of England and Wales, 1920-1930, H. M. S. O., L o n d o n . BJERVE, P. J., C e n t r a l B u r e a u of Statistics, Oslo, N o r w a y , P e r s o n a l c o m m u n i c a t i o n .
J. Atheroscler. Res., 7 (1967) 797~801
Elsevier Publishing Company, Amsterdam - Printed in The Netherlands
Short Communication H Y P O T H E S I S : H E A T E D M I L K P R O T E I N AND T H R O M B O S I S
J. c. ANNAND Camperdown House, Broughty Ferry, Dundee (Great Britain)
(Received September 21st, 1967)
On 1st J a n u a r y 1923 Holder pasteurisation became compulsory in the United Kingdom. Thereafter all milk classified and sold to the public as "pasteurised" was heated for a period of 30 min at not less than 145~ (63~ I t was then found at different times in different population groups that, within a period of at most 2 years after the introduction of Holder pasteurisation, a significant sudden rise occurred in the mortality ascribed to both arteriosclerotic heart disease (AHD) and to cerebral embolism and thrombosis (CET) (Table 1). On the other hand when Flash pasteurisation was introduced--the milk on this occasion being heated for a period of 16 seconds only at a temperature of 165~ (74~ greater part of the mortality rise that followed seemed to coincide with the changes in disease classification that were introduced at this time 1. Thus the possibility began to be entertained that milk which has been heated for a relatively long period of time m a y be a dietary factor especially involved in the pathogenesis of thrombosis. This hypothesis appeared to be supported b y the finding that these sudden increases in mortality in the United Kingdom during the decade 1920-1930 (Table 1) principally affected not only the urban population (as distinct from the rural), but also the expected social class (in this case the working class) who evinced a preference for pasteurised milk because of its low cost and because of its keeping properties 1,2. I t was decided therefore to re-examine all available and pertinent dietary surveys in the light of the hypothesis that heated milk, particularly milk that had been heated for a relatively prolonged period of time, might be a primary factor in the pathogenesis of thrombosis, and also to investigate whether either heated milk protein or milk fat or both might be at fault. The following is a s u m m a r y of some of the salient features of this survey. (1) The different population groups who consumed no milk protein (the Yemenitesa, the South VietnamesO, the Atiu Mitiaro 5 and the H u n j a 6) and, likewise, those who consumed only fresh milk--none of it being heated (the rural Zulu 7, the Masai 8, the Samburu~, the nomads of Nigeria 1~ and of Somaliland n , the West Africans ot Gabon 12 and the Congolese Pygmies 13) were all found to be free from the disease. j . Atheroscler. Res., 7 (1967) 797-801
798
SHORT
COMMUNICATION
TABLE 1 CORRELATION
OF HOLDER
Population group
Edinburghl, 2 Glasgowl, ~ Dundeel, 2 Aberdeenl, ~ Lanarkshire 2 (excluding Glasgow) County of Sutherland 2 County of Bute 2 London Admin. County a5
PASTEURISATION
AND THROMBOSIS
Holder pasteurisalion (year of introduction )
Angina pectoris ( A P ) (internat. list Nos. 89, 94 and z120) mortality per l, 000, 000 persons
Cerebral embolism and thrombosis ( C E T ) (internal. list Nos. 74b, 82b and 332) mortality per 1,O00,O00 persons
AP 1 AP 2 AP 3 AP 4
CET I
CET 2
1923 1924 1924 1926 1935-37 1947-50 1952-53
1925 1924 1925 1926 1937 1948 1954
67 56 42 91 188 685 1185
92 91 64 135 375 1185 1523
37.3 a 62.5 a 52.4 a 48.4 a 99.5 b 73.0 28.5
1924 1924 1925 1927 1938 1948 1954
174 77 162 121 153 298 518
236 101 188 227 193 518 680
35.6 31.2 16.0 87.6 26.1 73.8 31.3
1954
1954
963
1710
77.9
1954
610
823
34.9
1956
1956
1610
2848
76.9
1956
955
1398
46.4
1925
1925
31
112
261.3 c 1926
90
120
33.3
[Average total Oslo (Norway) 36
MORTALITY
1922
1922
3
81.8] 43
CET 3
CET 4
[41.6]
1333.3 d not available
Columns AP1 and CET1 denote the year of commencement of the sudden rise in the appropriate mortality. Columns AP2 and CET2 denote the appropriate average mortality for the 4 years immediately preceding the year of introduction of pasteurisation. Columns AP3 and CET3 denote appropriate average mortality for the 4 years immediately succeeding the introduction of pasteurisation. Columns AP4 and CET4 denote the %age increase between Columns AP2 and AP3 and between Columns CET2 and CET3. a Possibly low because deaths ascribed to "coronary thrombosis" were not included in International List No. 89 in Scotland until 1931. b Possibly enhanced as deaths ascribed to "coronary thrombosis" were now included in International List No. 94, e Possibly enhanced because (i) after 1927 all deaths ascribed to "coronary thrombosis" were included unlike those in Scotland--in International List No. 89 and (it) the large London creameries introduced Holder pasteurisation during this period. a Mortality ascribed to the following group of classifications: angina pectoris, infarctus cordis, sclerosis art. coron, cordis.
(2) O n t h e o t h e r h a n d t h e t w o l a c t o - v e g e t a r i a n g r o u p s
(i)
t h e E a s t I n d i a n s i 4 , is
a n d (it) t h e T r a p p i s t 16-19 m o n k s , b o t h of w h o m c o n s u m e d b o i l e d a n d / o r p a s t e u r i s e d milk a n d milk p r o d u c t s , were e i t h e r n o t p r o t e c t e d or were only p a r t i a l l y p r o t e c t e d b y their diet. (3) C o u n t r i e s o r p o p u l a t i o n g r o u p s w h o c o n s u m e d o n l y s m a l l q u a n t i t i e s of m i l k that had received relatively prolonged heat treatment, were found to suffer a correspondingly low mortality; and this finding appeared to apply both to "privileged" c o m m u n i t i e s s u c h a s i n F r a n c e a n d T h e N e t h e r l a n d s a n d t o d e v e l o p i n g c o u n t r i e s , e.g. ThailandZ0, 21 a n d S o u t h Korea22, 2~. I n t h e f o r m e r g r o u p , e v a p o r a t e d m i l k , p r o c e s s e d c h e e s e a n d c o o k e d m i l k g e n e r a l l y w e r e all r e l a t i v e l y u n p o p u l a r a n d i n T h a i l a n d a n d
J. Atheroscler. Res., 7 (1967) 797-801
SHORT COMMUNICATION
799
South Korea evaporated milk, taken in coffee, was the only dairy product commonly consumed. Random postmortem studies in these last two countries revealed a thrombosis incidence of 2.7 and 2.0 % respectively. The reverse obviously held good for such countries as Australia, New Zealand, Canada, Ireland, the United Kingdom and the USA. (4/) By custom the Yemenites discard their milk protein and consume only the milk fat which, after being boiled, is then used for cooking purposes; thus their intake of milk protein consists only of that portion contained in the milk fat (0.35 % milk protein). They were reported to be free from AHD a, although they consume milk fat which has received prolonged heat treatment. (5) Milk fat consumption generally has been found not to be correlated with the A H D incidence either at the clinical 24 or at the international level 2a. (6) During both wars the consumption of milk protein in the United Kingdom 26-2s, that had received prolonged heat treatment fell and rose again in direct relationship to the mortality graph, either preceding the latter b y one year or coinciding with i t - both during its fall and during its rise. Throughout the last war the same close parallelism in respect of the total milk protein consumption and mortality occurred in both Denmark 29 and Canada 3~ In the USA at this time neither the mortality nor the milk protein consumption deviated from their steady rise. Thus, from 1931 to 1945 the crude mortality (International List No. 94a) per 100,000 rose from 7.9 to 95.8. At the same time the per capita consumption of milk foods known to have been heated for a significant period of time (e.g. evaporated milk, ice cream etc.) rose b y 102.8 %. Cheese consumption also increased b y 68.4 % and an increasing but unknown proportion of the latter was either pasteurised or processed and/or cooked: at the same time coffee consumption rose b y 26.2 %. On the other hand, in the United Kingdom during both wars and in both Canada and Denmark during the last War, the graph depicting milk fat consumption failed in every case to correlate with that of mortality. Thus on 3 occasions in the United Kingdom the latter preceded the former in beginning to rise b y periods varying from 2 to 4 years. (7) Antibodies to milk protein have frequently been demonstrated in "healthy" adults al-34, but the relevance of this observation to atherogenesis or to thrombogenesis cannot be pursued from the present data. Although the evidence summarized above is circumstantial and does not prove a causal relationship, nevertheless the fact should be mentioned that clinical experience over a period of 10 years has consistently supported the possibility that milk protein that has received prolonged heat treatment m a y well be an important dietary factor in the pathogenesis of thrombosis. Thus, all patients suffering from A H D who maintained a diet devoid of heated milk protein either showed a sustained improvement in their condition or failed to deteriorate further. On the other hand, patients who for various reasons did not maintain their diet evinced a high incidence of thrombosis and/or cardiac irregularities together with congestive failure.
J. Atheroscler. Res., 7 (1967) 797-801
800
SHORT COMMUNICATION
REFERENCES
J. c., Atherosclerosis, t h e case against protein, continued, J. Coll. gen. Practit., 1961, 4: 567. ANNAND, J. C., Thrombosis, f u r t h e r evidence against heated animal protein, J. Coll. gen. Practit., 1964, 7: 386. BRUNNER D. AND K. LOBL, Serum cholesterol, electrophoretic lipid p a t t e r n a n d coronary artery disease. A s t u d y in coronary p a t i e n t s a n d in h e a l t h y m e n of different origins and occupations in Israel, Ann. intern. Med., 1958, 49: 732. Nutrition survey, Republic of Vietnam, 1959, A report b y t h e I n t e r d e p a r t m e n t Committee on Nutrition for National Defense, W a s h i n g t o n , D.C., USA. WALKER, J. D., Nutritional s u r v e y in t h e Cook islands, Nutrition, 1962, 16: 15. TOOMEY, E. G. AND P. D. WHITE, A brief s u r v e y of the health of aged Hunjas, Amer. Heart f . , 1964, 68: 841. CAMPBELL, G, D., Personal communication.
1 ANNAND,
2 3
4 5 6
7 8 MANN, G. V., R. D. SHAFFER, a . S. ANDERSON AND H. H. SANDSTEAD, C a r d i o v a s c u l a r di s e a s e
in t h e Masai, J. Atheroscler. Res., 1964, 4: 289. 9 SHAPER, A. G., Cardiovascular studies in t h e S a m b u r u tribe of Northern Kenya, Amer. Heart J.,
1962, 63: 437. 10 MANN, G. V., B. M. NICOL AND F. J. STARE, The fl-lipoprotein and cholesterol concentrations
in sera of Nigerians, Brit. reed. J., 1955, ii: 1008. 11 LAPPICCIRELLA, V., R. LAPPICCIRELLA, F. ABBONI AND S. LIOTTA, Clinical, biological a n d
12 13
14 15
16
cardiographic s u r v e y a m o n g t h e n o m a d tribes of Somaliland who subsist only on milk, Bull. Wld Hlth Org., 1962, 27: 681. MILLER, D. C., S. S. SPENCER AND P. D. WHITE, Survey of cardiovascular disease a m o n g Africans in t h e vicinity of Albert Schweitzer Hospital in 1960, Amer. J. Cardiol., 1962, 10: 432. MANN, G. V., O. A. ROLLS, D. L. PRICE AND J. M. MERRILL, Cardiovascular disease in African Pygmies, J. chron. Dis., 1962, 15: 341. NATH, H. P., N. K. GUPTA AND P. V. K. IYER, Increasing incidence of coronary artery t h r o m b o sis in I n d i a n A r m y personnel, Indian J. reed. Res., 1957, 45: 217. MALHOTRA, R. P. AND N. S. PATHANIA, Some aetiological aspects of coronary h e a r t disease, Brit. reed. J., 1958, ii: 528. McCULLAGH, E. P. AND L. A. LEWIS, A s t u d y of diet, blood lipids and vascular disease in Trappist monks, New Engl. J. Med., 1960, 263: 569.
17 GROEN,
18
19
2o 21 22 23
24 25 26 27
28 29 30 31
32
J. J ,
K. B. TIJONG, M. KOSTER, A. F. WILLEBRANDS, G. VERDONCKAND N. PIERLOOT,
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