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GENETIC INFLUENCES ON SERUM-URIC-ACID
911 years the consumption of canned food and frozen has also increased, but there is no reason to supproducts this has caused the rise in the incidence of coronary that pose disease. As for saturated fat and cholesterol, my survey indicates that numerous experiments on animals have shown that these two factors have a strong atherogenic effect. On the other hand, evidence for the atherogenic effect of sugar is by no means so strong. We have succeeded in producing atherosclerosis in rabbits with saccharose, but only when we used a semisynthetic diet consisting of about 50% sugar and containing no fat at all (and, of course, no cholesterol). The atherosclerotic plaques in the aorta were insignificant compared with the striking changes in animals fed saturated fat and/or cholesterol. It would thus appear from these experiments that sugar plays, at most, a subordinate role in atherogenesis. McGandy et awl. arrived at the same conclusion after a thorough investigation of the atherogenic effect of dietary fats and carbohydrates. Sugar may, however, be of greater importance in the presence of hypertriglyceridamia induced by carbohydrates.6In some of these cases the consumption of sugar must be severely restricted, which is best achieved by substituting polyunsaturated fats for carbohydrates. As for the prevention of atherosclerotic disease on a national scale, it might be advisable to recommend a certain restriction of sugar, especially for overweight persons. In some quarters a low-fat diet has been recommended in the prophylaxis and treatment of atherosclerosis. This has often resulted in an undesirable increase in sugar consumption-e.g., the use of more marmalade, jam, and honey, instead of butter. Judging from his letter, Dr. Cleave harbours a dislike for sunflower and its seeds, and dislikes my suggestion that sunflower-seed oil could be used to improve certain foods by replacing saturated fat, a procedure which he calls unnatural substitution. Experience has, however, shown that it is possible to manufacture really palatable ice-cream and margarine with sunflower oil instead of the coconut fat, which has hitherto been widely used for such purposes. The use of sunflower oil has increased considerably in recent years. In 1968, three million tons were produced; it now ranks third among the edible vegetable oils traded. In the U.S.S.R. sunflower seed is the most important single source of fats and oils, contributing over 40% of the total domestic supply.
In
recent
Medical Research Laboratory for the Study of Atherosclerosis, University of Lund, Sweden.
later to renal failure. They have severe and extensive basement-membrane thickening with or without deposits. If benefit is to be expected from immunosuppressive treatment, this must be started early and continued for a long time. Unfortunately early recognition is not always possible because a long period of asymptomatic proteinuria may precede the clinical onset of nephrotic syndrome. J. CHURG T. EHRENREICH Mount Sinai School of Medicine, E. GRISHMAN. New York, N.Y.
PALLÆSTHESIOMETER reference to the article by Dr. Neilson and SIR,-With his colleagues (Sept. 27, p. 669) may I draw attention to the fact that a useful pallxsthesiometer is already on the market ? The ’Biothesiometer ’, obtainable from the Bio-medical Instrument Co., Munn Road, Newbury, Ohio, is a development of the apparatus described by Aring and Frohring in 1942.1 It operates at a frequency of 100 cycles per second, and constant pressure is obtained simply by letting the vibrating stylus rest on its own weight. The device is simple, cheap, and compact, and affords a more objective measurement of vibration threshold than the old tuning-forks. Department of Medicine, Arhus University School of Medicine, G. GREGERSEN. Denmark.
GENETIC INFLUENCES ON SERUM-URIC-ACID SiR,ŇThe article by Professor Acheson and Dr. Florey (Aug. 23, p. 391), and your annotation (p. 417), prompt us to report some of our observations on the subject of serumuric-acid level and genetic influence. As we have already recordedwe failed to detect any racial differences in serumuric-acid levels when comparing healthy Caucasian and Indian adults of similar age and sex. We have also failed to find any association between serum-uric-acid levels and ABO and rhesus (D) blood-groups in an investigation of 141 healthy adult Indians (see accompanying table). There is SERUM URIC ACID LEVELS IN RELATION TO BLOOD-GROUPS IN ADULT HEALTHY INDIANS
HAQVIN MALMROS.
MEMBRANOUS GLOMERULONEPHRITIS SIR,-May we add a small point to your comprehensive leader (Sept. 20, p. 626) ? Since 1957 we have studied over 100 cases of membranous glomerulonephritis (or as we prefer, membranous nephropathy, since it is not an inflammatory process). A review of the first 60 cases was published in the 1968 edition of the Pathology Annual (p. 145). During an average follow-up of three years (maximum 17 years), about one quarter of the 60 patients died, one quarter recovered clinically, and the remainder were unimproved. Recovery occurred in some who were treated with steroids and in some who were not. It is our impression that the histological equivalent of recovery is the disappearance of the subepithelial deposits. However, many patients heal " with defect ", and have a residual damage of the capillary wall manifested by focal or diffuse thickening of the basement membrane. Some apparently recover only to succumb 5. McGandy, R. B., Hegsted, D. M., Stare, F. J. New Engl. J. Med. 1967, 277, 417. 6. Fredrickson, D. S., Levy, R. J., Lees, R. S. ibid. 1967, 276, pp. 34 94, 148, and 215.
conclusive evidence of the familial
occurrence
of gout and
hyperuricaemia, so one would naturally expect serum-uricacid levels to be, in some way, genetically determined. But in view of the inconsistent results in the series reported by Professor Acheson and Dr. Florey, the negative findings of previous workers,3-5 and the inconclusive results of twin studiesprobably there is no such association. University Department of Physiology Singapore.
Åring,
N. SAHA B. BANERJEE.
C. D., Frohring, W. O. J. Lab. clin. Med. 1942, 28, 204. Banerjee, B., Saha, N. J. Indian med. Ass. 1967, 48, 207. Hauge, M., Harvald, B. Acta med. scand. 1955, 42, 247. Dunn, J. P., Brooks, G. W., Mausner, J., Rodnan, G. P., Cobbs, S. J. Am. med. Ass. 1963, 185, 431. 5. Florey, C. du V., Acheson, R. M. Am. J. Epidem. 1968, 88, 178. 6. Boyle, J. A., Greig, W. R., Jaseni, M. K., Duncan, A., Diver, M., Buchanan, W. W. Ann. rheum. Dis. 1967, 26, 234.
1. 2. 3. 4.
In
recent
Medical Research Laboratory for the Study of Atherosclerosis, University of Lund, Sweden.
later to renal failure. They have severe and extensive basement-membrane thickening with or without deposits. If benefit is to be expected from immunosuppressive treatment, this must be started early and continued for a long time. Unfortunately early recognition is not always possible because a long period of asymptomatic proteinuria may precede the clinical onset of nephrotic syndrome. J. CHURG T. EHRENREICH Mount Sinai School of Medicine, E. GRISHMAN. New York, N.Y.
PALLÆSTHESIOMETER reference to the article by Dr. Neilson and SIR,-With his colleagues (Sept. 27, p. 669) may I draw attention to the fact that a useful pallxsthesiometer is already on the market ? The ’Biothesiometer ’, obtainable from the Bio-medical Instrument Co., Munn Road, Newbury, Ohio, is a development of the apparatus described by Aring and Frohring in 1942.1 It operates at a frequency of 100 cycles per second, and constant pressure is obtained simply by letting the vibrating stylus rest on its own weight. The device is simple, cheap, and compact, and affords a more objective measurement of vibration threshold than the old tuning-forks. Department of Medicine, Arhus University School of Medicine, G. GREGERSEN. Denmark.
GENETIC INFLUENCES ON SERUM-URIC-ACID SiR,ŇThe article by Professor Acheson and Dr. Florey (Aug. 23, p. 391), and your annotation (p. 417), prompt us to report some of our observations on the subject of serumuric-acid level and genetic influence. As we have already recordedwe failed to detect any racial differences in serumuric-acid levels when comparing healthy Caucasian and Indian adults of similar age and sex. We have also failed to find any association between serum-uric-acid levels and ABO and rhesus (D) blood-groups in an investigation of 141 healthy adult Indians (see accompanying table). There is SERUM URIC ACID LEVELS IN RELATION TO BLOOD-GROUPS IN ADULT HEALTHY INDIANS
HAQVIN MALMROS.
MEMBRANOUS GLOMERULONEPHRITIS SIR,-May we add a small point to your comprehensive leader (Sept. 20, p. 626) ? Since 1957 we have studied over 100 cases of membranous glomerulonephritis (or as we prefer, membranous nephropathy, since it is not an inflammatory process). A review of the first 60 cases was published in the 1968 edition of the Pathology Annual (p. 145). During an average follow-up of three years (maximum 17 years), about one quarter of the 60 patients died, one quarter recovered clinically, and the remainder were unimproved. Recovery occurred in some who were treated with steroids and in some who were not. It is our impression that the histological equivalent of recovery is the disappearance of the subepithelial deposits. However, many patients heal " with defect ", and have a residual damage of the capillary wall manifested by focal or diffuse thickening of the basement membrane. Some apparently recover only to succumb 5. McGandy, R. B., Hegsted, D. M., Stare, F. J. New Engl. J. Med. 1967, 277, 417. 6. Fredrickson, D. S., Levy, R. J., Lees, R. S. ibid. 1967, 276, pp. 34 94, 148, and 215.
conclusive evidence of the familial
occurrence
of gout and
hyperuricaemia, so one would naturally expect serum-uricacid levels to be, in some way, genetically determined. But in view of the inconsistent results in the series reported by Professor Acheson and Dr. Florey, the negative findings of previous workers,3-5 and the inconclusive results of twin studiesprobably there is no such association. University Department of Physiology Singapore.
Åring,
N. SAHA B. BANERJEE.
C. D., Frohring, W. O. J. Lab. clin. Med. 1942, 28, 204. Banerjee, B., Saha, N. J. Indian med. Ass. 1967, 48, 207. Hauge, M., Harvald, B. Acta med. scand. 1955, 42, 247. Dunn, J. P., Brooks, G. W., Mausner, J., Rodnan, G. P., Cobbs, S. J. Am. med. Ass. 1963, 185, 431. 5. Florey, C. du V., Acheson, R. M. Am. J. Epidem. 1968, 88, 178. 6. Boyle, J. A., Greig, W. R., Jaseni, M. K., Duncan, A., Diver, M., Buchanan, W. W. Ann. rheum. Dis. 1967, 26, 234.
1. 2. 3. 4.