- Email: [email protected]
The relationship of diet to nephritis in the tropics with special reference to the consumption of aroid plants
801 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MF_3)ICINE AND HYGIENE. VOI. XXVI. No. 3. November, 1932.
T H E R E L A T I O N S H I P O F D I E T TO N E P H R I T I S IN T H E T R O P I C S W I T H SPECIAL R E F E R E N C E T O T H E C O N S U M P T I O N OF AROID PLANTS. BY
ALFRED CL~RK, ~* London School of Hygiene and Tropical Medicine.
Two hundred years ago HANS SLOANE in his account of the conditions of life in the West Indies mentioned that he had observed that ill-health followed the excessive consumption of the tubers of the natural order Arace~e and described their acrid properties and their effects when eaten. He states that they produce the symptoms of dysentery, that they make people pale, and he mentions the importance of throwing away the first decoction when boiling them for food. These observations are all confirmed by my experimental feeding . of rats. The acrid properties of this order have been commented upon in botanical text books for many years and have been attributed to the mechanical irritation of minute acicular crystals of calcium oxalate. Acicular crystals are certainly present in both the tubers and leaves of the plants of this order and calcium and oxalic acid can be demonstrated chemically, but it seems to me highly improbable that so insoluble a compound as calcium oxalate could give rise to such intense burning of the tongue and desquamation of the hands as result when the cut tubers are chewed or handled. I have chewed calcium oxalate and put it in my eye without any discomfort ensuing. I fed rats upon sweet potato--an innocuous tuber--in which 5 per cent. of calcium oxalate was incorporated. They lived for fifty days without symptoms and when killed at the end of that time showed no abnormalities other than those usually found in animals fed upon a partly deficient diet. Moreover spinach contains 0-30 per cent. of oxalic acid in the form of the calcium salt and is certainly not acrid. The cause of the acridity must therefore be sought in some other body or bodies contained in the tubers. In two former papers published in these TRANSACTIONSt I have described the earlier experimental work carried out upon these and other edible tubers eaten in Trinidad and mentioned the constant production of nephritis in rats when they were fed on tannia. Since these papers were published more *I have recently received a grant from the Medical Research Council which will render further work on this subject possible. I am also grateful to the Surgeon-General of Trinidad for arranging continuous supplies of tubers for use in London. t Trans. Roy. Soc. Trop. Med., vol. xxii (5), 453 and xxiii (2), 167.
809,
THE RELATIONSHIP OF DIET TO NEPHRITIS I N THE TROPICS.
work has been done upon the pathological conditions found in rats poisoned by tannia at the London School of Hygiene and Tropical Medicine. Two impure fractions have been obtained from the tuber by Dr. R. B. WATERS. The first, A, when injected intravenously produces almost immediately a rise in blood sugar which attains in 50 min. a height of as much as 415 rag. per 100 c.c. At the same time the hepatic glycogen disappears altogether as a rule, or a mere trace too small to measure may be found. When, on the other hand, rats are fed upon the raw tuber the blood sugar is reduced in spite of the large quantity consumed by the animal. In two or three days it is reduced to 50 or 60 mg. per 100 c.c. and at the same time the glycogen of the liver has completely or practically disappeared. The second fraction, B, is so far only available in an impure form, but this is so toxic that a single drop, 0.05 c.c., injected intravenously kills a 60 gram rat immediately from cardiac and respiratory paralysis. When a similar dose is administered intraperitoneally death ensues in about eight minutes, the limbs being paralysed progressively and death, which occurs from paralysis of the heart and respiration, is preceded by a terminal convulsion in the same way as I have often observed in rats dying from eating tannia. The liver, lungs, heart and kidneys are found to be engorged with blood. I am greatly indebted to Dr. R. B. WATERSfor his work upon the biochemical problems involved. With regard to the character of the nephritis produced by the poison of tannia, it was pointed out to me by Dr. DOROTHY RUSSELL that the picture presented closely resembles that of acute uranium poisoning. A matter of great practical interest in its bearing on the much-debated question of the origin of nephritis in the West Indies, and possibly in other tropical colonies, arises from these facts. That nephritis is unduly prevalent in the West Indies is shown by the following table compiled from figures furnished by the Surgeon-General of Trinidad. Taking the rate of mortality from this disease in England and Wales as the standard the figures are as follows :-1.00 England and Wales. 2-86 U.S.A. 0.78 New Zealand. 3.70 Trinidad and Tobago. 1.29 New South Wales. 4.40 Barbados 1-89 St. Vincent. 7.62 British Guiana (whole colony). 2.13 Grenada. 9.08 ,, ,, (East Indian population) I think it must be conceded that amongst the native races of a tropical colony the official figures are likely for several reasons to underestimate the incidence of such diseases. I therefore undertook to make a number of postmortem examinations of the bodies in the mortuary in Port-of-Spain. In all 114 cadavers were so examined and in each case microscopical slides were made
ALFRED CLARK.
303
of the kidneys and in most cases of the liver and spleen also. Thirty-two of these were rejected on account of suspected postmortem changes, which speedily supervene in the tropics. The remaining eighty-two seemed to me to be above suspicion. The causes of death in these were arranged in three classes :-21 = 25.6 per cent. sudden or accidental deaths. 18 ~ 21.9 per cent. apparently due to malnutrition. 43 --~ 52.4 per cent. miscellaneous causes. The incidence of nephritis was as follows :-12 -~ 14.6 per cent. showed no signs of nephritis to the naked eye or microscopically. 4 ~- 4.8 per cent. acute nephritis. 26 ~ 31.7 per cent. sub-acute nephritis. 40 ~ 48.7 per cent. chronic nephritis--mostly interstitial. I am indebted to Dr. T. B. WELCH, at that time Medical Superintendent of the leper settlement at Chacachacare, (Trinidad)for figures showing the incidence of albuminuria in all new admissions to that institution during 1929 and 1930. Total number of admissions 132 Dying on admission .. 1 Not examined . . . . 13 Urine showed no albumin 6 ~ 5.08 per cent. Slight cloud .... 95 ~ 80.50 per cent. Well-marked cloud .. 16 = 13.55 per cent. Heavily loaded . . . . 1 -~ 0.84 per cent. To what extent the Bacillus leprae may account for the albuminuria in these cases I do not know and medical literature gives little help. No doubt there are many causes for the high nephritis rate of the West Indies. Malaria and other infections may account for much, but I am inclined to think that the nephrotoxic effect of the aroid tubers is a very important factor especially in people suffering from chronic malnutrition, a common enough combination, superior foods being hard to come by and these tubers cheap and abundant. That malaria is the principal factor in the etiology of this nephritis seems unlikely when one considers the figures for the disease in Barbados. It is known that prior to 1927 anopheline mosquitoes did not exist on the island and that no malaria, excepting imported cases, had occurred. Malaria was introduced in 1927. The diet is very similar to that of Trinidad, certainly no better. As an experimental community therefore the Barbadians offer a unique and invaluable opportunity for comparing the incidence of nephritis in two tropical countries in which the diet is similar but in one of which malaria has long been endemic and in the other absent. If malaria were the predominant cause then nephritis should be materially less frequent in Barbados than it is in Trinidad. What we find for the year 1926, the year before the appearance of malaria, is that the incidence of nephritis is almost as high as that in Trinidad and in
804
THE RELATIONSHIP OF DIET TO NEPHRITIS IN THE TROPICS.
1930 is slightly higher. Its importance as a cause of death in 1930 is shown by the following figures for some of the common diseases : Deaths
Malaria Malarial cachexia Dysentery
Deaths
0 3 45
Typhoid Pulmonary tuberculosis Nephritis
46 125 277
Even children under three years were not exempt from nephritis as in 1930, fifty-two died from this disease. T h e number of deaths per mille of the total population in 1930 was 1.63 (from nephritis), which compared with that of England and Wales is as 4.40 to 1. (These figures are from the official Report on Vital Statistics for the year 1930). SUMMARY
AND
CONCLUSIONS.
1.--(a) In rats a very acute nephritis not unlike that resulting from uranium poisoning- and involving chiefly the glomeruli and convoluted tubules is caused by eating raw tannia or the viscid decoction of these tubers. (b) A subacute nephritis or a chronic nephritis of the " nephritis repens " type is caused by eating the tubers when these are cooked by boiling for half an hour.
(c) The addition of sterol-containing foods to the tannia diet materially lessens, but does not entirely neutralise, the toxicity of the tubers. .(d) These tubers are largely eaten and a decoction of them taken as a soup in Trinidad. A pap prepared from tannia is given to infants. (e) Nephritis of all types is unduly prevalent in Trinidad. 2.--(a) Malnutrition, either qualitative or quantitative, and some diseases, such as malaria, also produce or favour the production of nephritis. (b) Malnutrition and malaria both exist in Trinidad. 3.--(a) In Barbados the economic and dietetic conditions are similar to those in Trinidad, but, until the year 1927, malaria was unknown there while nephritis was common. (b) The introduction of malaria into Barbados has not affected the nephritis rate for the island. 4 . ~ ( a ) The suprarenal glands are functionally destroyed by tannia. (b) The glycogenic function of the liver is destroyed and the blood sugar diminished by eating tannia. (c) A close relationship exists between the activity of the suprarenal glands and the glycogenic function of the liver. (d) Extirpation of the suprarenals does not affect the acidity of the gastric juices but is frequently followed in cats by the production of gastric ulcers. (T. R. ELLIOTT). (e) Ulceration and gastric bleeding are frequently found in the stomachs of rats fed on tannia.
ALFRED CLARK.
305
5.--Death in acute tannia poisoning is probably due to lesions of the suprarenal glands. 6 . - - T h e nature of the poison is at present unknown. 7 . - - T h e use of tannia and other aroid tubers as one of the principal articles of diet is an important factor in the causation of nephritis in Trinidad. 8.--Correction of the dietaries, especially those of the poor, might be expected to lessen the incidence of nephritis in Trinidad. I am indebted to Dr. MCCANCE for an analysis of the food factors of the tuber and the decoction. His figures are as follows : - 100 grams of decoction contains 100 grams of tuber contains T o t a l nitrogen . . . . 0-1 gram .. 0.361 gram Fat .. trace or none .. Carbohy¢lrate 'as glucose .. 7.8 .. 24.0 Sodium . . . . 0"040 .. 0.126 Potassium . . . . 0"270 .. 0-850 Calcium . . . . 0"0078 .. 0..024 Magnesium . . . . 0"011 .. 0.035 Iron 0-0013 0-0041 Phosphorus "" :: 0.018 . . . . 0"057 T a k i n g 5-6"8 as the proper factor for the estimation of the a m o u n t of ~rotein from the a m o u n t of nitrogen in vegetables we get a protein content of 0-56 per cent. in the decoction and of 1.79 per cent in the raw tuber. It should be stated that HURST'S estimate of the protein content of the tuber was calculated from the dried tuber. Also that McC~a,~cE's decoction was about 0.4 times the concentration of that employed in m y experiments. It is evident that the food value of both tuber and the decoction is by no means negligible. TABLE I. EFFECTS OF FEEDING WITH TANNIA TUBERS BOTH RAW AND BOILED FOR THIRTY MINUTES.
Animals e m p l o y e d :
standard
rats of average weight 60 grams. Percentages. W e i g h t of liver per cent. of body-weight N o r m a l diet . . . . . . 4.69 Diet B (28 days) . . . . 4.50 Raw tannia (3 days) .. 3-47 Boiled tannia (24 days) 3.89 (Diet B corresponds to the composition of the tannia as estimated by Dr. McCANcE, b u t without any toxic substance.) Percentages: Glycogen of liver per cent. of weight. N o r m a l diet . . . . 4.73 D i e t B (28 days) .. 4.24 Raw tannia (3 days) 0.22 Boiled tannia (24 days) 1.73 W e i g h t of suprarenals per cent. of bodyN o r m a l diet .. 0.0234 weight. Raw tannia (3 d a y s ) " 0.0387 Boiled tannia (24 days) 0-0258 W a t e r only (2 days).. 0.0234 Blood sugar in mg. per 100 c.c. N o r m a l diet .. 118.7 m g . 88.9 nag. Raw tannia (3 d a y s ) " Boiled tannia (24 days) 116.0 mg. W a t e r only (4 days).. 89.0 mg.
806
THE RELATIONSHIP OF DIET TO
NEPHRITIS IN THE TROPICS.
TABLE I I . C O R R E L A T I O N OF T H E H E P A T I C G L Y C O G E N W I T H THE TOTAL AMOUNT OF TANNIA C O N S U M E D , AND ITS P R O P O R T I O N COMPARED W I T H THAT OF A R A T F E D O N NORMAL DIET.
Glycogen content )er cent. of liver weight. Rat No. 1,029
1,034 1,042 1,048
1,049 1,050 1 051 1,052 1,064
1,070 1,082 1,085
Normal diet. 4.00% 2.90% 3.10% 3.30% 3.41% 4.78% 10.92% 4.63% 5.97% 4.81% 4.33% 4.61%
Rat No.
Total consumption per rat-gram.
Raw tannia.
1,024 1,025 1,030 1,040 1,041 1,062 1,071 1,072 1,073 1,074 1,077 1,079
0.00 0"00 0.00 0.00 0"00 0.00 trace
1.62%
trace 1.09% 0.00 0.00
~
0.50 gram 0.74 0.27 0.44 ~J 0-30 ,, 0.87 0-24 p~ 0.II 0"37 0"39 1.14 ~J 0.69 ,,
I W i t h a total consumption above 0.39 gram per rat-gram there is a complete disappearance of glycogen from the liver. TABLE I I I . RELATIONSHIP OF THE BLOOD SUGAR CONTENT TO THE AMOUNT OF TANNIA CONSUMED PER RAT-GRAM. Blood sugar in rag. per 100 c.c. Blood sugar over 100.0 mg. per cent.
Consumption of tannia I Blood sugar 100.0 per rat-gram. mg. per cent. and under.
111.0 rag. 107.3 106.7
0-39 grams 0.30 ~J 0.11
Average-108.3 rag.
0.26 grams
100.0 mg. 87-0 ~J 87.0 78.0 66.0 ~J 60.7 It 55.3
Consumption of tannia per rat-gram. 0-44 gram 0-69 1.14 J# 0"87 0"24 0 -44 0"37
76-2 mg. per cent. 0"59 gram per rat-gram.
T H E R E L A T I O N S H I P O F D I E T TO N E P H R I T I S IN T H E T R O P I C S W I T H SPECIAL R E F E R E N C E T O T H E C O N S U M P T I O N OF AROID PLANTS. BY
ALFRED CL~RK, ~* London School of Hygiene and Tropical Medicine.
Two hundred years ago HANS SLOANE in his account of the conditions of life in the West Indies mentioned that he had observed that ill-health followed the excessive consumption of the tubers of the natural order Arace~e and described their acrid properties and their effects when eaten. He states that they produce the symptoms of dysentery, that they make people pale, and he mentions the importance of throwing away the first decoction when boiling them for food. These observations are all confirmed by my experimental feeding . of rats. The acrid properties of this order have been commented upon in botanical text books for many years and have been attributed to the mechanical irritation of minute acicular crystals of calcium oxalate. Acicular crystals are certainly present in both the tubers and leaves of the plants of this order and calcium and oxalic acid can be demonstrated chemically, but it seems to me highly improbable that so insoluble a compound as calcium oxalate could give rise to such intense burning of the tongue and desquamation of the hands as result when the cut tubers are chewed or handled. I have chewed calcium oxalate and put it in my eye without any discomfort ensuing. I fed rats upon sweet potato--an innocuous tuber--in which 5 per cent. of calcium oxalate was incorporated. They lived for fifty days without symptoms and when killed at the end of that time showed no abnormalities other than those usually found in animals fed upon a partly deficient diet. Moreover spinach contains 0-30 per cent. of oxalic acid in the form of the calcium salt and is certainly not acrid. The cause of the acridity must therefore be sought in some other body or bodies contained in the tubers. In two former papers published in these TRANSACTIONSt I have described the earlier experimental work carried out upon these and other edible tubers eaten in Trinidad and mentioned the constant production of nephritis in rats when they were fed on tannia. Since these papers were published more *I have recently received a grant from the Medical Research Council which will render further work on this subject possible. I am also grateful to the Surgeon-General of Trinidad for arranging continuous supplies of tubers for use in London. t Trans. Roy. Soc. Trop. Med., vol. xxii (5), 453 and xxiii (2), 167.
809,
THE RELATIONSHIP OF DIET TO NEPHRITIS I N THE TROPICS.
work has been done upon the pathological conditions found in rats poisoned by tannia at the London School of Hygiene and Tropical Medicine. Two impure fractions have been obtained from the tuber by Dr. R. B. WATERS. The first, A, when injected intravenously produces almost immediately a rise in blood sugar which attains in 50 min. a height of as much as 415 rag. per 100 c.c. At the same time the hepatic glycogen disappears altogether as a rule, or a mere trace too small to measure may be found. When, on the other hand, rats are fed upon the raw tuber the blood sugar is reduced in spite of the large quantity consumed by the animal. In two or three days it is reduced to 50 or 60 mg. per 100 c.c. and at the same time the glycogen of the liver has completely or practically disappeared. The second fraction, B, is so far only available in an impure form, but this is so toxic that a single drop, 0.05 c.c., injected intravenously kills a 60 gram rat immediately from cardiac and respiratory paralysis. When a similar dose is administered intraperitoneally death ensues in about eight minutes, the limbs being paralysed progressively and death, which occurs from paralysis of the heart and respiration, is preceded by a terminal convulsion in the same way as I have often observed in rats dying from eating tannia. The liver, lungs, heart and kidneys are found to be engorged with blood. I am greatly indebted to Dr. R. B. WATERSfor his work upon the biochemical problems involved. With regard to the character of the nephritis produced by the poison of tannia, it was pointed out to me by Dr. DOROTHY RUSSELL that the picture presented closely resembles that of acute uranium poisoning. A matter of great practical interest in its bearing on the much-debated question of the origin of nephritis in the West Indies, and possibly in other tropical colonies, arises from these facts. That nephritis is unduly prevalent in the West Indies is shown by the following table compiled from figures furnished by the Surgeon-General of Trinidad. Taking the rate of mortality from this disease in England and Wales as the standard the figures are as follows :-1.00 England and Wales. 2-86 U.S.A. 0.78 New Zealand. 3.70 Trinidad and Tobago. 1.29 New South Wales. 4.40 Barbados 1-89 St. Vincent. 7.62 British Guiana (whole colony). 2.13 Grenada. 9.08 ,, ,, (East Indian population) I think it must be conceded that amongst the native races of a tropical colony the official figures are likely for several reasons to underestimate the incidence of such diseases. I therefore undertook to make a number of postmortem examinations of the bodies in the mortuary in Port-of-Spain. In all 114 cadavers were so examined and in each case microscopical slides were made
ALFRED CLARK.
303
of the kidneys and in most cases of the liver and spleen also. Thirty-two of these were rejected on account of suspected postmortem changes, which speedily supervene in the tropics. The remaining eighty-two seemed to me to be above suspicion. The causes of death in these were arranged in three classes :-21 = 25.6 per cent. sudden or accidental deaths. 18 ~ 21.9 per cent. apparently due to malnutrition. 43 --~ 52.4 per cent. miscellaneous causes. The incidence of nephritis was as follows :-12 -~ 14.6 per cent. showed no signs of nephritis to the naked eye or microscopically. 4 ~- 4.8 per cent. acute nephritis. 26 ~ 31.7 per cent. sub-acute nephritis. 40 ~ 48.7 per cent. chronic nephritis--mostly interstitial. I am indebted to Dr. T. B. WELCH, at that time Medical Superintendent of the leper settlement at Chacachacare, (Trinidad)for figures showing the incidence of albuminuria in all new admissions to that institution during 1929 and 1930. Total number of admissions 132 Dying on admission .. 1 Not examined . . . . 13 Urine showed no albumin 6 ~ 5.08 per cent. Slight cloud .... 95 ~ 80.50 per cent. Well-marked cloud .. 16 = 13.55 per cent. Heavily loaded . . . . 1 -~ 0.84 per cent. To what extent the Bacillus leprae may account for the albuminuria in these cases I do not know and medical literature gives little help. No doubt there are many causes for the high nephritis rate of the West Indies. Malaria and other infections may account for much, but I am inclined to think that the nephrotoxic effect of the aroid tubers is a very important factor especially in people suffering from chronic malnutrition, a common enough combination, superior foods being hard to come by and these tubers cheap and abundant. That malaria is the principal factor in the etiology of this nephritis seems unlikely when one considers the figures for the disease in Barbados. It is known that prior to 1927 anopheline mosquitoes did not exist on the island and that no malaria, excepting imported cases, had occurred. Malaria was introduced in 1927. The diet is very similar to that of Trinidad, certainly no better. As an experimental community therefore the Barbadians offer a unique and invaluable opportunity for comparing the incidence of nephritis in two tropical countries in which the diet is similar but in one of which malaria has long been endemic and in the other absent. If malaria were the predominant cause then nephritis should be materially less frequent in Barbados than it is in Trinidad. What we find for the year 1926, the year before the appearance of malaria, is that the incidence of nephritis is almost as high as that in Trinidad and in
804
THE RELATIONSHIP OF DIET TO NEPHRITIS IN THE TROPICS.
1930 is slightly higher. Its importance as a cause of death in 1930 is shown by the following figures for some of the common diseases : Deaths
Malaria Malarial cachexia Dysentery
Deaths
0 3 45
Typhoid Pulmonary tuberculosis Nephritis
46 125 277
Even children under three years were not exempt from nephritis as in 1930, fifty-two died from this disease. T h e number of deaths per mille of the total population in 1930 was 1.63 (from nephritis), which compared with that of England and Wales is as 4.40 to 1. (These figures are from the official Report on Vital Statistics for the year 1930). SUMMARY
AND
CONCLUSIONS.
1.--(a) In rats a very acute nephritis not unlike that resulting from uranium poisoning- and involving chiefly the glomeruli and convoluted tubules is caused by eating raw tannia or the viscid decoction of these tubers. (b) A subacute nephritis or a chronic nephritis of the " nephritis repens " type is caused by eating the tubers when these are cooked by boiling for half an hour.
(c) The addition of sterol-containing foods to the tannia diet materially lessens, but does not entirely neutralise, the toxicity of the tubers. .(d) These tubers are largely eaten and a decoction of them taken as a soup in Trinidad. A pap prepared from tannia is given to infants. (e) Nephritis of all types is unduly prevalent in Trinidad. 2.--(a) Malnutrition, either qualitative or quantitative, and some diseases, such as malaria, also produce or favour the production of nephritis. (b) Malnutrition and malaria both exist in Trinidad. 3.--(a) In Barbados the economic and dietetic conditions are similar to those in Trinidad, but, until the year 1927, malaria was unknown there while nephritis was common. (b) The introduction of malaria into Barbados has not affected the nephritis rate for the island. 4 . ~ ( a ) The suprarenal glands are functionally destroyed by tannia. (b) The glycogenic function of the liver is destroyed and the blood sugar diminished by eating tannia. (c) A close relationship exists between the activity of the suprarenal glands and the glycogenic function of the liver. (d) Extirpation of the suprarenals does not affect the acidity of the gastric juices but is frequently followed in cats by the production of gastric ulcers. (T. R. ELLIOTT). (e) Ulceration and gastric bleeding are frequently found in the stomachs of rats fed on tannia.
ALFRED CLARK.
305
5.--Death in acute tannia poisoning is probably due to lesions of the suprarenal glands. 6 . - - T h e nature of the poison is at present unknown. 7 . - - T h e use of tannia and other aroid tubers as one of the principal articles of diet is an important factor in the causation of nephritis in Trinidad. 8.--Correction of the dietaries, especially those of the poor, might be expected to lessen the incidence of nephritis in Trinidad. I am indebted to Dr. MCCANCE for an analysis of the food factors of the tuber and the decoction. His figures are as follows : - 100 grams of decoction contains 100 grams of tuber contains T o t a l nitrogen . . . . 0-1 gram .. 0.361 gram Fat .. trace or none .. Carbohy¢lrate 'as glucose .. 7.8 .. 24.0 Sodium . . . . 0"040 .. 0.126 Potassium . . . . 0"270 .. 0-850 Calcium . . . . 0"0078 .. 0..024 Magnesium . . . . 0"011 .. 0.035 Iron 0-0013 0-0041 Phosphorus "" :: 0.018 . . . . 0"057 T a k i n g 5-6"8 as the proper factor for the estimation of the a m o u n t of ~rotein from the a m o u n t of nitrogen in vegetables we get a protein content of 0-56 per cent. in the decoction and of 1.79 per cent in the raw tuber. It should be stated that HURST'S estimate of the protein content of the tuber was calculated from the dried tuber. Also that McC~a,~cE's decoction was about 0.4 times the concentration of that employed in m y experiments. It is evident that the food value of both tuber and the decoction is by no means negligible. TABLE I. EFFECTS OF FEEDING WITH TANNIA TUBERS BOTH RAW AND BOILED FOR THIRTY MINUTES.
Animals e m p l o y e d :
standard
rats of average weight 60 grams. Percentages. W e i g h t of liver per cent. of body-weight N o r m a l diet . . . . . . 4.69 Diet B (28 days) . . . . 4.50 Raw tannia (3 days) .. 3-47 Boiled tannia (24 days) 3.89 (Diet B corresponds to the composition of the tannia as estimated by Dr. McCANcE, b u t without any toxic substance.) Percentages: Glycogen of liver per cent. of weight. N o r m a l diet . . . . 4.73 D i e t B (28 days) .. 4.24 Raw tannia (3 days) 0.22 Boiled tannia (24 days) 1.73 W e i g h t of suprarenals per cent. of bodyN o r m a l diet .. 0.0234 weight. Raw tannia (3 d a y s ) " 0.0387 Boiled tannia (24 days) 0-0258 W a t e r only (2 days).. 0.0234 Blood sugar in mg. per 100 c.c. N o r m a l diet .. 118.7 m g . 88.9 nag. Raw tannia (3 d a y s ) " Boiled tannia (24 days) 116.0 mg. W a t e r only (4 days).. 89.0 mg.
806
THE RELATIONSHIP OF DIET TO
NEPHRITIS IN THE TROPICS.
TABLE I I . C O R R E L A T I O N OF T H E H E P A T I C G L Y C O G E N W I T H THE TOTAL AMOUNT OF TANNIA C O N S U M E D , AND ITS P R O P O R T I O N COMPARED W I T H THAT OF A R A T F E D O N NORMAL DIET.
Glycogen content )er cent. of liver weight. Rat No. 1,029
1,034 1,042 1,048
1,049 1,050 1 051 1,052 1,064
1,070 1,082 1,085
Normal diet. 4.00% 2.90% 3.10% 3.30% 3.41% 4.78% 10.92% 4.63% 5.97% 4.81% 4.33% 4.61%
Rat No.
Total consumption per rat-gram.
Raw tannia.
1,024 1,025 1,030 1,040 1,041 1,062 1,071 1,072 1,073 1,074 1,077 1,079
0.00 0"00 0.00 0.00 0"00 0.00 trace
1.62%
trace 1.09% 0.00 0.00
~
0.50 gram 0.74 0.27 0.44 ~J 0-30 ,, 0.87 0-24 p~ 0.II 0"37 0"39 1.14 ~J 0.69 ,,
I W i t h a total consumption above 0.39 gram per rat-gram there is a complete disappearance of glycogen from the liver. TABLE I I I . RELATIONSHIP OF THE BLOOD SUGAR CONTENT TO THE AMOUNT OF TANNIA CONSUMED PER RAT-GRAM. Blood sugar in rag. per 100 c.c. Blood sugar over 100.0 mg. per cent.
Consumption of tannia I Blood sugar 100.0 per rat-gram. mg. per cent. and under.
111.0 rag. 107.3 106.7
0-39 grams 0.30 ~J 0.11
Average-108.3 rag.
0.26 grams
100.0 mg. 87-0 ~J 87.0 78.0 66.0 ~J 60.7 It 55.3
Consumption of tannia per rat-gram. 0-44 gram 0-69 1.14 J# 0"87 0"24 0 -44 0"37
76-2 mg. per cent. 0"59 gram per rat-gram.