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Jamaican vomiting sickness: A theoretical investigation
JAMAICAN
VOMITING SICKNESS: INVESTIGATION
A THEORETICAL
ANTHONY THOMAS and LAURIE KRIEGER Department
of Anthropology,
University of North Carolina at Chapel Hill, U.S.A.
Abstract-Jamaican Vomiting ‘Sickness has been investigated for over sixty years, and yet this acute disease remains an epidemiological mystery. In this article, we have ciitically examined the toxin hypotheses emphasized in the literature-particularly the ackee and yam theories of causation. Because of the inadequacies of the conventional toxin hypotheses, we suggest that more attention should be given to a malnutrition hypothesis and a psychogenic hypothesis. Jamaican Vomiting Sickness (JVS), a reportedly culture bound syndrome, may very well have multiple causation. That is. toxin, malnutrition, and psychogenic etiologies may be operative independently and sometimes jointly in the epidemics and family outbreaks of acute and often fatal Jamaican Vomiting Sickness.
The “Vomiting Sickness” of Jamaica was first recorded in 1885 by Bowrey, the Island Chemist [l]. The first medical report on the illness was published in 1904 by Turton [2] who gave a description of Jamaican Vomiting Sickness which is remarkably similar to contemporary summaries. By the second decade of,this century there was a heated controversy over the causes.of this baffling disease. Most of the major explanations for the cause of this illness emerged during the course of this initial controversy and these explanations are still being debated today. This paper describes the disease and its incidence, discusses possible causes. and suggests areas for further research. EPIDEMIOLOGY Jamaican Vomiting Sickness (JVS) appears in family outbreaks, sporadic cases, and in epidemic form. Of the 721 cases described in the literature under review by Kenneth Hill [3], the greatest incidence is in the age group from two to five years, with a considerable number being between five and ten years. Infants who have not yet been weaned are rarely affected, and the incidence among individuals over ten years of age is low. The incidence of the disease among boys and girls is approximately equal. Young adult women are also occasionally affected, and there are rare reports of adult men falling prey to JVS. Vomiting Sickness is reported almost exclusively during the colder winter months (December-March). JVS by folk definition and medical observation tends to be unique to Jamaica. However, there are a few poorly documented accounts of JVS occurring among Jamaican emigrants [3.4]. Furthermore, the illness tends only to be diagnosed in Jamaicans of African ancestry and tends to occur in rural rather than urban areas [S]. Throughout the literature an emphasis is placed upon the frequent occurrence of family outbreaks. The causes of Jamaican Vomiting Sickness are not the only controversial aspects of the disease; the very quality of the epidemiological data is questionable. In particular. the system of record keeping has been inadequate. As Cicely Williams points out. the current 111
seasonal incidence of JVS may be explained by the practice of closing the file for health officers’ reports of this illness from April through October [6]. Early to present day researchers have consistently emphasized the failure of health officers to accurately identify and record cases of JVS. One problem is that it is often very difficult to decide whether a patient is actually a victim of JVS, especially in the sporadic cases, as symptoms are often accompanied by severe worm infestation, malnutrition, malaria, and other disorders [7]. In 1952, a reliable diagnosis of Jamaican Vomiting Sickness was not possible; yet health officers were required at that time to submit a monthly list of JVS patients in their parish [6]. In the early part of this century, all mysterious serious ailments among rural Jamaican children tended to be associated with JVS-including yellow fever and spinal meningitis [S]. SYMPTOMOLOGY Jelliffe [9] and Stuart [lo] found in their clinical observations during 1953 that the most outstanding feature of JVS is sudden and severe hypoglycemia. Blood glucose levels characteristically range from &20mg. There appear to be two typical forms of JVS. In the first type, the patient, most often a young child, complains of discomfort in the stomach and vomits. The vomitus is usually the content of the child’s last meal. The child may vomit several more times. If this is the case, the vomitus changes to clear or frothy mucus. The patient begins to feel better and falls asleep. The remission may last several hours. When the patient awakens, or later the following day, (s)he is seized by sudden, effortless vomiting which is rapidly succeeded by collapse, convulsions, coma and death. The vomitus in the final attacks is again clear or frothy mucus that is occasionally bloodstained. The shortest fatal case of JVS was reported to last one hour: however the average duration is about 12 l/2 hours [3]. In the cases examined by Stuart ef al., often the liver was impalpable upon admission to a hospital, but tended to enlarge and become palpable during recovery [lo]. In neither
ANTHONY THOMAS and LAURIE KRIEGER
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form of Vomiting Sickness does the temperature exceed 100” or 101’F unless accompanied by a bacterial or viral infection. The temperature is almost always normal or subnormal. Usually a cyclical clouding of consciousness is a feature of the disease. The second. or fulminating form, is not usually accompanied by vomiting. “A fulminating variety of so-called Vomiting Sickness is recognized in which vomiting does not occur, the patient being precipitated dramatically into the stage of collapse, drowsiness, convulsions, stupor, twitching of the limbs and fatal coma” [lo]. The second form of JVS is usually of short duration, i.e. fatal within l-24 hr. Scott’s data indicate that 85% of fatal cases show signs of convulsions [3]. JVS has been treated successfully with large amounts of glucose administered intravenously and by glucose drinks if the patient is conscious. However, this therapy is usually unsuccessful with the very rapid fulminating form or in cases where the patient has experienced severe hypoglycemia for an extended period of time-24 hr or longer [S]. The glucose treatment was not initiated in Jamaica until the discovery of a connection between hypoglycemia and JVS in 1953; therefore there is much published on postmortems of JVS victims [ 1 l-191. POSTMORTEM
Many of the early workers were quite observant and maintained precise records of autopsies. Consequently, later accounts differ little from their earlier counterparts. Typically, a postmortem examination of the JVS victim reveals a fatty metamorphosis of the liver and kidney. The liver glycogen is depleted. Generalized hyperaemia is usually observed. Hemorrhages may be found over the heart, in the lungs and over the liver and spleen. The meninges, as well as parts of the brain, are often inflamed and may be hemorrhagic (especially if death was preceded by convulsions). Oedema of the connective tissues is commonly found. There is swelling and hyperaemia of lymph nodes throughout the body and hyperaemia of the alimentary lymph nodes may exist as well. Necrobiosis of the pancreatic, renal and liver epithelia is often found. It is very rare to find bacteria in the vomitus. stomach contents. viscera or heart’s blood. On rare occasions when bacteria are present, they are invariably S. aureus. POSSIBLE
CAUSES
In the next portion of the paper, we will discuss possible causal mechanisms. Many have been proposed by physicians and other investigators. Several toxin hypotheses have been proposed by physicians who have worked in Jamaica. In addition to evaluating the toxin etiologies, we will discuss two additional hypotheses: a malnutrition hypothesis and possible psychogenic causative factors. Jamaican Vomiting Sickness, reportedly a culture bound syndrome, may very well have multiple causation. Consequently, all of these hypotheses may be operative independently and sometimes jointly in the epidemics and family outbreaks of acute and often fatal Jamaican Vomiting Sickness.
SUSPECTED
TOXINS
Certain plant poisons are known to cause sudden and severe hypoglycemia in experimental animals. The plants implicated in JVS are ackee. yams. cassava. unidentified plants used in bush teas and poisonous plants that young children may eat when alone. Presently, it is widely held that the disease is due to the ingestion of a toxic substance w-hich pioduces a block (often temporary) in the enzyme system responsible for gluconeogenests [20.21]. Harold Scott suspected ackees as the cause of the mysterious Jamaican vomiting disease in an article submitted for publication in October of 1915 [ 131. In the 1970s the ackee is still a prime suspect [‘I]. The ackee is an evergreen (Blighiu sapida) bearing a fruit that is widely eaten in Jamaica and forms the basis for ackee and saltfish. Jamaica’s national dish. The tree bears fruit perennially. In 1970 it was estimated that there were 200 acres of cultivated ackees and mangoes respectively. The Jamaican Ministry of Agriculture’s 1975 targets for these crops were 1300 additional acres for ackees and 700 added acres for mangoes [22]. The ackee was brought to Jamaica from West Africa in the late 18th century and is found throughout the Caribbean as well as in Florida and Central America. Jamaica is the only area where the fruit is a popular article of diet, although tinned ackee is eaten by Jamaicans who have migrated to other parts of the world. The fruit of the ackee is 7-10 cm long. It is normally divided into three compartments (loculi). Each of these contains one seed. The fruit splits into three valves at maturity exposing the black seeds. Each seed has a large cream colored arillus which is the edible portion of the ackee [23]. The poisonous quality of the ackee is appreciated wherever it grows. Jamaica is no exception. People general/y in this island [Jamaiccc] are convinced that ackres, under certain conditions are poisonous; among these conditions may be mentioned: (i) Unopened ackees, and by consequence: (ii) Ackees which have not opened naturally, but hare been forced after falling unopened: (iii) Fruit gathered jr0171 u decayed branch; (iv) Ackees with some soft spot in nn otherwise apparently sound fruit [ 131. The toxic principle was isolated by Hassall. Reyle. and Feng and first reported in 1954 [24]. They isolated two water-soluble toxins from the ackee: hypoglycin A and hypoglycin B. Hypoglycin A is the more potent toxin. The toxins are found in the seeds of the ackee fruit. A very small quantity of hypoglycin A is found in the ripe arillus, while the unripe arillus contains a larger concentration. These toxins cause severe and sudden hypoglycemia in experimental animals [24,25]. (For an explanation of how the hypoglycins produce hypoglycemia, see Feng [25] and Bondy and Rosenberg [4]). The water-solubility of the toxin is significant because in Jamaica older children and adults frequently consume the solid parts of the cooked ackee, while young children eat ackee soup or the “pot water” in which the ackees have been cooked.
Jamaican vomiting sickness The known toxicity of the unripe ackee and its prevalence and popularity in Jamaica create strong temptations for many researchers to accept the ackee as the villain in JVS. However, all this evidence is circumstantial. Perhaps no one is more aware of this than Cicely Williams, who argues forcefully against an easy solution to the problem if based on circumstantial evidence [S-7]. Unfortunately the arguments against ackees as the causative agent are also circumstantial. It is accepted that ackees may contain a toxic principle-they certainly are not ‘fool proof’, and in some cases of vomiting are associated with the consumption of ackees; but it is equally certain that there are many people today who are eating unripe, unopened or raw ackees and drinking the pot-water, in which these are cooked, without ill effect [7]. Williams calls for investigation of this problem by an expert in food poisoning and an epidemiologist [5,61. W. L. Bamett is the primary proponent of a toxic principle in yams as the cause of JVS [26]. He blames a toxic glucoside in St. Vincents yam for many cases of JVS. Barnett shows the toxicity of certain types of yam-stems by experimental evidence using fish as the subjects. He links the JVS peak with the digging of early varieties of yam. Further he holds the drying effect of yam storage and transportation practices accountable for the lack of yam poisoning and JVS in urban centers. His epidemiological methods are questionable and his work has been subject to criticism. Hill criticizes Barnett’s statement that summer JVS coincides with harvesting of the summer yam crop because there is no agreement that Vomiting Sickness occurs at all during the summer. Hill also points out that many islands in the West Indies grow yams, none report a toxicity and nowhere but Jamaica is the JVS ,syndrome reported [3]. Stuart, Jelliffe and Hill feel yams are not responsible [lo]. Williams points out that the yam’s cyanogenic glucoside, “. . is found mainly in the yam head, or stem end of the yam, which is not generally consumed, but kept for replanting”[6]. Cassava is grown and eaten in much of the tropical world. Though not a common crop in Jamaica today, cassava is part of the rural food inventory. Cassava is known to contain HCN. another toxic cyanogenic glucoside. Wherever cassava is grown and eaten, some method of rendering the food nontoxic is practiced. There are two kinds of cassava: bitter and sweet. In sweet cassava most of the HCN is found in the rind. Since the HCN in bitter cassava is distributed throughout the fruit, techniques are used to leach out the poisonous agent. Seidelin ruled out cassava poisoning because no prussic acid could be found in the viscera of JVS victims [12]. Nevertheless. cassava poisoning is not uncommon in Jamaica’s history and is due primarily to insufficient leaching out of HCN [3]. Cassava poisoning produces vomiting. In order to link cassava poisoning more firmly with JVS. it would be helpful to know if HCN is capable of producing the kind of hypoglycemia associated with JVS: this answer is not apparent from the literature. The argument that cassava is the dominant causative agent of JVS suffers from
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some of the same fallacies as the argument that it is yams. Cassava is eaten in many parts of the world, but JVS appears to be specific to Jamaica. Jamaica’s ethnomedicine often involves the use of “bush teas”. Bush teas are infusions of parts of various plants. These teas are consumed widely not only for medicinal purposes, but as part of the first meal of the day. Jamaica has a wide variety of plants and many of these are poisonous to humans. Some other plants are easily confused with those that are regular components of many bush teas. Furthermore, since congeries of plants are used to make the different types of bush teas, it would be difficult to separate out any one toxic agent. Some ingredients are known to be capable of producing hypoglycemia. Toxic bush teas are considered as possible sources of the cirrhosis following veno-occlusive disease in Jamaica [27,28]. Frequently, bush teas are suspected as a contributory factor in JVS [6,9, 10, IS]. Hill questions the bush tea explanation because of the seasonal incidence of JVS [3]. However, it may be possible that some of the plants regularly used or mistakenly used in bush teas are of seasonal occurrence. Williams seems to express the belief that’the various types of JVS outbreaks may have different causes. In this view, bush teas may be just one causal factor. Bush teas form part of the diet of many age groups in Jamaica, not just those of the population at greatest risk of contracting JVS. K. L. Standard reports that, “Mint and cercie are the most popular ‘bush teas’ used . . . and are often given as early as the first week of life [29]. If these bush teas are administered to young infants, it is possible that other bush teas may be similarly given to infants. JVS is virtually absent among young infants. The bush tea argument, while plausible, has many problems. Children in rural Jamaica, particularly those from poor families, are often left unsupervised by adults during the day. They may spend much time finding, cooking and eating their own food. This custom is very important to consider in the etiology of JVS. Jamaican babies are usually weaned before one year of age [29]. However, children are not usually susceptible to JVS until two years. This age coincides with the toddling stage-the time at which children are mobile enough to search for food. Several cultural factors are directly relevant to this possible etiology. The children’s practice of cooking a “private pot” provides a multitude of opportunities to ingest toxic plants. The private pot consists of any scraps of food and foodstuffs gathered by the child who takes them, cooks and eats them without adult supervision [3]. Vomiting Sickness occurs during the time of the year that is traditionally the “hungry” season. Food is less plentiful during the winter. Williams writes: The families in which vomiting sickness is most frequently reported are those that sufir from chronic, often marginal malnutrition. The children have little supervision, and go foraging on their own for a portion of the day.. . . The universal habit of using a variety of local herbs for making tea, and the fact that vomiting sickness nearly always comes from rural areas, and very often the children are afSected while adults escape, probably indicates that this supplementation of food supply is often responsible for the tragedies [S].
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ASTHONY THOMAS and LACRIEKRIEGER
Certainly there are many potentially hypoglycemiaproducing plants indigenous to Jamaica [ 10,271. The possibility also exists that the children may be ingesting some form of chemical poison. Certain chemicals reputedly produce hypoglycemia when consumed e.g. guanadine, carbon tetrachloride, chloroneoarsphenamine phosphorus hydazine, fol-lll. [S, 30-321. However it is difficult to explain epidemic forms of JVS and family outbreaks including the mother, if some type of juvenile pica were the sole cause of JVS. Williams emphasizes the neglect of Jamaican children from poor families. However, she provides little documentation [S, 63. Thus, the supplementation of diet by children involves a good deal of conjecture. It appears that no one has ever observed Jamaican children regularly to see what their eating habits are. There are other cultural factors involved in the children’s dietary intake. Children often do not live with their mothers, but reside with other relatives (due to marriage and residence customs in Jamaica). While the biological parents may not be providing for a child, other relatives assume the responsibilities of “parental roles” [33]. Such customs are directly relevant to the degree of supervision and the kind of botanical training that a child receives. MALNUTRITION
HYPOTHESIS
Most authors agree that chronic malnutrition is endemic to small children in rural Jamaica [S, 6.7.20. 34. 35, 361. Protein Calorie Malnutrition (PCM) is noted by Fonaroff to be highest in urbanplantation environments [35]. Standard finds PCM. but the results are not differentiated by location [29]. Alleyne studied seriously under- and malnourished infants [36]. His population at risk (children 10-12 months old) is considerably younger than that of JVS (2-10 years), but his study is helpful in underscoring the presence of serious nutritional disease in Jamaica. Back reports in his 1956 article that, “It was found that the nutritional state of the small farmer and his family was good in most districts and that gross malnutrition was far less common than in the poorer districts of Kingston.. . .” [37]. He obtains these results by medical examination of a sample. However, in a subsequent and more comprehensive year-long survey including weekly recall nutritional data and medical examination, Back reports low vitamin A intake and low riboflavin intake [38]. Miall et al., demonstrate that, “infections adversely influence the state of nutrition and are themselves more serious where the nutritional state is poor” [34]. Malnutrition may be related to JVS in several possible ways. Malnutrition by itself may be a cause of JVS or the cause may be the combined effect of one of several toxins and malnutrition. If the cause of JVS is primarily infectious, malnutrition would enter into the interactions of host and invading organism. Mainzer presents experimental evidence illustrating the role that malnutrition, i.e. pellagra, plays in production of hypoglycemia; “In a quarter of the experiments [injection of insulin into human subjects suffering from pellagra] severe cerebral manifestations of hypoglycemia would appear abruptly, often preceded by autonomic phenomena” [39]. Josephs notes
that. “It is the common experience of those who have studied large series of children to find lower values for blood sugar in infancy during fasting and to fmd greater variation under different conditions.. As the child grows older. this liability disappears, and in adults it is rarely found, although it does occur” [40]. Williams considers that malnutrition may be linked to JVS by at least two chains: (1) chronic malnutrition complicated by a short period without food or some upset of the digestive system may produce hypoglycemia; (2) a high carbohydrate meal (such as the sugar cane of which Jamaican children are so fond) may’ precipitate hypoglycemia in people with a fatty liver [S]. A sore mouth and/or mouth tissues are occasionally found in association with JVS [i. 131. This symptom is characteristic of some vitamin deficiencies especially a deficiency of riboflavin (Bz). Toxins are absorbed more effectively in under nourished or malnourished animals [42]. Poorly nourished humans. especially children [S], are also more susceptible to the effects of toxins [7,42]. Jamaica has an unusually high prevalence of forms of malnutrition that disrupt liver function. It is well known that malnutrition is prevalent in Jamaica, particularly in those forms which damage the liver. A large proportion of the population is therefore peculiarly susceptible to toxins of’ various sorts [7]. Examination of JVS victims and their emissions has so far yielded little evidence implicating bacteria in this syndrome. Yet it is of interest that the ackee provides a good environment for haemolytic staphylococcus [S]; it is possible that the toxin produced by this organism may, in part. be responsible for JVS. Although bacteria are seldom found in association with JVS, the possibility of viral infection had not been ruled out as of 1953 [43]. A worm infestation may interfere with nutrition and may also independently produce vomiting. Ascarids have been reported for many years as present in the intestines of a large number of JVS victims [Z. 3,211. PSYCHOGENESIS
Psychological causation of sudden death is undoubtedly a controversial subject in the field of social science and medicine. However, there are numerous descriptions and discussions of social-psychological stress dramatically leading to death and/or complicating an existing illness [44-571. Engel lists life settings where a person is at greatest risk of sudden death. These are: 1. 011the impact oj’ the collapse or death of’ a close person: -7. during acute grief 3. on threat of loss of a close person: 4. during mourning or on an anniuersary; 5. on loss of’ Status or selfesteem: 6. personal danger or threat of’ injury: 7. after the danger is over: 8. reunion, triumph, or happy ending. Common to all is that they involve events impossible for the victims to ignore and to which their resporw is overwhelming excitation or giving up, or both [53]. Christian and Ratcliffe report animals the condition [shock
that ‘I.. . in free wild disease resulting in
181
Jamaican vomiting sickness sudden death] develops when environmental demands exceed maximum native capacity” [45]. Similar mechanisms may possibly operate in humans. Jamaicans are known to view certain types of food such as ackee as poisonous-particularly when the food is in a certain stage or state (e.g. unripe, bruised). Consequently it is possible that the fear of having eaten a poisonous substance may cause shock disease in either children or adults. Significantly, Christian and Ratcliffe report that of fourteen animals dying of shock disease resultant from stress, all were pathologically characterized by acute hypoglycemia with livers depleted of glycogen [45]. Some JVS victims may die from the psychophysiological reaction to the consumption of a substance believed to be poisonous. The young victims’ mothers may sicken for this reason also, or due to the sudden shock from the loss or grave illness of one or several of their children. The many reports show that mothers often fall prey to JVS after one or more of their children have succumbed. Witchcraft may also be implicated in JVS. Belief in sorcery presumes that a person may harm another person by wishing him or her ill or by performing certain magical acts designed to cause misfortune to the intended victim or his or her family. In the American South, the Caribbean, and Africa the cognitive pattern associated with witchcraft is found when a victim or patient believes him or herself to be “hexed”. This type of belief is a powerful psychological force in the production of or in association with many illnesses: pseudocyesis [SS], madness [59,60], asthma [47], cardiorespiratory disease [48], cardiovascular malfunction [53], abdominal pain and vomiting [60] to name a few. The logic of witchcraft is very much operative in Jamaica today. As in some other parts of the Caribbean, the indigenous term for witchcraft in Jamaica is obeah. Its curers and practitioners are obeah (wo)men, and the obeah belief complex is tied in with religious practices on the island [61-643. Anthropologists and other social scientists have found that socialization plays an important part in channeling the somatization of psychological states: Batesori and Mead.. show how the training of Balinese children to withdraw from expression of an) strong emotion may be a cultural factor predisposing them to the susceptibility to trance experience which is then used culturally.. There maJ be some similariries to this in the hexing culture, where a child is reared in the certain knowledge that the world is a dangerous place-ecil spells can be cast with great ease as punishment for even minor transgressions and the possibility of death from such a hex is very real [65]. It is common world-wide to find descriptions of parents ascribing the illness or death of their children to supernatural causes. Seldom if ever is this disease process reported from the child’s point of view. If socialization into witchcraft beliefs begins early in the child’s development, young children may succumb to sorcery. This possibility should be kept in mind by investigators because JVS occurs in a rural context where oheali beliefs prevail.
SUGGESTIONS
FOR
FURTHER
RESEARCH
Whereas heretofore, research into JVS was conducted by practicing physicians anti chemists, a crossdisciplinary approach with emphasis in the social sciences might begin to unravel some of the mysteries in Jamaican Vomiting Sickness. Anthropologists, with their participant-observation approach, could usefully study exactly what children eat and how parents socialize their offspring in food acquisition practices. The information gathered by anthropologists might be used to answer questions such as: How early and to what extent do children learn the ethno-botanical system, i.e. learn to distinguish between edible and non-edible materials? What do rural Jamaican children do when left alone? What is the structure of their associations with other children? Do poor rural parents sometimes neglect their children? And if there is neglect, what is the nature of this neglect by adults? Furthermore, the cultural anthropologist could elicit important information on the cultural significance of vomiting and stomach ailments. How and at what age are these meanings learned? Anthropologists and other experts skilled in ethnobotany might help unravel some of these dietary intake problems. Medical geographers and social epidemiologists would also contribute much to the study of Jamaican Vomiting Sickness. Maps are needed to illustrate incidences of JVS according to geographical studies area, elevation, and season. Nutritional already demonstrate that diet in Jamaica varies with geography, so a research team might explore the relationship of this variation to the occurrence of JVS. Particularly intense outbreaks of JVS might be correlated with climatic changes. Certainly, field investigators should give high priority to gathering data on the normative folk etiologies ascribed to Jamaican Vomiting Sickness. Furthermore, as JVS outbreaks occur, the presence of a physician-anthropologist clinical-research team would be very helpful. The team could, in the process of treatment and research, elicit from the affected people their understanding of what factors brought on the particular outbreak or sporadic case. Psychiatrists with training in anthropology and anthropologists with training in medicine could work together to explore the psychogenic hypotheses relevant to JVS. Current work on the autonomic nervous system and pathological symptoms is advancing our knowledge of mind-body interactions [66], but field studies are needed to gain an understanding of these interactions in natural social environments. Furthermore, recent work by psychologists on biofeedback processes is especially relevant to this whole topic of mind-body interactions [67,68]. As of this date, all the explanations for the outbreaks of JVS are based on very limited evidence and remain open to question. A more satisfactory explanation might be found with the combined effort of researchers from the several relevant disciplines. It seems that until a field study of broad dimensions is undertaken, Jamaican Vomiting Sickness will remain an epidemiological mystery. REFERENCES 1. Bowrey
J. J. Jamaica Gar.
10.
481, 1887.
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THOMAS
2 Turton R. S. The ‘vomiting sickness’ of Jamaica. J Trop. -Med. Hyg. 1. 163. 1904. 3. Hill K. R. The vomitine sickness of Jamaica. II!l. med. J. 1, 243, 1952. 4. Bondy P. K. Disorders of carbohydrate metabolism. In Duncan’s Diseases of Metabolism. 6th Edition (Edited by Bondy P. K. in association with Rosenberg L. I?.) p. 271. W. B. Saunders. Philadelphia. 1969. 5. Williams C. The vomiting sickness of Jamaica. J. the Med. Worn. Fed. 43. 1954. 6. Williams C. Report of the vomiting sickness study. Medical Department, Jamaica, 1953. 7. Williams C. Vomiting in children. WI. med. J. 1, 265, 1952. 8. Vomiting Sickness in Jamaica. In Yellow Fever Bulletin 2, 1913. 9. Jelliffe D. B. and Stuart K. L. Acute toxic hypoglycemia in the vomiting sickness of Jamaica. Br. Med. J. 1. 75. 1954. 10. Stuart K. L.. Jelliffe D. B. and Hill K. R. Acute toxic hypoglycemia occurring in the vomiting sickness of Jamaica. J. Tree. fed. 1. 69, 1955. sickness in Jamaica. Jamaica 1 I. Potter T. J. Vomiting Gaz. (Supplement) 34;695, 1912. sickness’ in Jamaica. Ann. 12. Seidlin H. On ‘vomiting Trop. Med. & Parasit. 7,377. 1913. 13. Scott H. H. On the ‘vomiting sickness’ of Jamaica. Ann. Trop. Med. & Parasit. 10, 1, 1916. 14. Scott H. H. The vomiting sickness of Jamaica. Trans. R. Sot. Trop. Med. Hyg. 10. 47, 1917. File HB 517 No. 15. Evans K. L. Medical Department 30, Kingston, Jamaica, 1943. H. D. The syndrome called ‘vomiting sick16. Chambers ness.’ I+![. med. J. 2. 37, 1953. 17. Fitzmaurice L. W. The Vomiting Sickness of Jamaica Symposium. IU. med. J. 2, 93, 1953. and fatty metamorphosis 18. Hill K. R. Hypoglycaemia of the liver in the vomiting sickness of Jamaica. J. Path. Bact. 35. 334. 1953. K. P. Acute toxic 19. Hill K. R.. Bras G., and Clearkin hypoglycaemia in the vomiting sickness of Jamaica. WI. med. J. 4, 91, 1955. 20. Patrick S. J., Jelliffe D. B., Stuart K. L. The hepatic glycogen content in acute toxic hypoglycaemia. J. Trop. Ped. 1, 88, 1955. 21. Stuart K. L. Vomiting sickness of Jamaica. In Diseases of Children in the Subtropics urld Tropics (Edited by Jeliffe D. G.). Edward Arnold Ltd. London, 1970. and Fisheries. Crop acreage 22. Ministry of Agriculture targets by general location 1970-75. (The authors of this article have a copy of this map in their files). 23. Parry J. H. Salt fish and ackee. Cur. Q. 8. 30. 1962. Seaforth C.E. The ackee Int. f?. Scient. 3. 51, 1962. Cooked ackee looks and tastes like lightly scrambled eggs. A.B: 24. Hassall C. H.. Reyle K. and Feng P. Hypoglycin Biologically active polypeptides from Blighia sapida. Nature. Lond. 173. 456. 1954. ackee: a review. I+!:!. 25. Feng P. C. Hypoglycin-from med. J. 18. 23X. 1969. 26. Barnett W. L. Investigatton into the “vomiting sickness” of Jamaica in 1943. Department of Government Chemist. (A copy is available at the Jamaica Institute, Kingston, Jamaica.) C. S. Nutrition, geography, and liver dis27. Davidson eases. Am. J. c/in. Nutr. 23. 427, 1970. Disease. In Disruses of 28. Stuart K. L. Veno-occlusive Children in the Subtropics und Tropics. (Edited by Jelliffe D. B.) Edward Arnold Ltd. London, 1970. 29. Standard K. L. A pilot nutrition survey in five lowincome areas in Jamaica. B!f. med. _f. 7, 215. 195X. 30. Minot A. S. and Cutler J. T. Studies of the response to calcium medication in the hypoglycemia of carbon tetrachloride boisoning. Am. J. Phvsio. xiii. 674. 1930.
and LXRIE
KRIEC~ER
31. Cross J. B. and Blackford L. M. Fatal hepatogenic hypoglycemia following neoarsphenamine. J.A.M..4. 94. 1739. 1930. 32. Minot A. S. The mechanism of the hypoglycemia produced by guanadine and carbon tetrachloride poisoning and its relief by calcium medication. J. P/w. E.\-p. Med. 43. 295. 1931. M,I, Mother IV/IOFtrthvred 33. Smith M. G. Introduction. me: A Study of the Family irl Three Selected Cornrrtw~iries irt Jamaica. Bv Edith Clarke. 1966. 34. Miall W. E., Desai P. and Standard K. L. Malnutrition, infection and child growth in Jamaica. J. biosoc. xi. 2, 31, 1970. 35 Fonaroff L. S. Settlement typology and infant malnutrition in Jamaica. Trop. yeogr. .ktMrd.21, 177. 1969. 36 Alleyne G. A. 0. Some features of infantile malnutrition. IU. med. J. 19, 32. 1970. survey of small farmers in 37 Back E. H. A nutritional Jamaica in 1955. w1. med. J. 5. 189. 1956. 38 Back E. H. The dietary of small farmers in Jamaica. WI. med. J. 10. 28. 1961. in pellagrins and 39 Mainzer F. Insulin-hypersensitivity its significance. Trans. R. Sot. Trap. Med. & HJ~. 43. 329, 1949. hypoglycemia in childhood. 40 Josephs H. Spontaneous Am. J. Dis. Child. 38, 746, 1929. 41 Bodansky M. The production of hypoglycemia in experimental derangements of the liver. Aer. J. Phxsiol. 66. 375. 1923. 42 Brown T. M. and Harvey A. M. Spontaneous hypoglycemia in “smoke” drinkers. J.A.M.A. 117, 12, 1941. L. S. and Caselitz F. H. Comment [in the 43 Grant Vomiting Sickness of Jamaica Symposium. Chairman: L. W. Fitzmauricel. w1. med. J. 2. 104. 1953. 44 Cannon W. B. -Voodoo” death. ilm. .4nthrop. 44. 169. 1942. 45 Christian J. J. and Ratctiffe, H. L. Shock disease in captive wild mammals. Am. J. Pathol. 28. 725. 1952. of sudden death 46. Richter C. P. On the phenomenon in animals and man. Psychosom Med. 19. 191. 1957. 47 Mathis J. L. A sophisticated version of voodoo death. Psvchosom. Med. 26. 104, 1964. conference. Case 48 Boitnott J. (Editor) Ctinicopathologic presentation. The Johns Hopkins Hospital. The Jonrrlal. pp. 186-199. 1967. 49. Burrell R. J. W. The possible bearing of curse .death and other factors in Bantu culture on the etiology of myocardial infarction. In The Etiology of Myocardial Infitrction. (Edited by James T. N. and Keyes J. N.). Little-Brown. Boston. 1963. 50 Engel G. L. A Life setting conducive to illness. Bulletirt of the Mrnirqet Clinic. 32. 355. 1968. 51 Dynes J. B. Sudden death. Discuses of the Nervous System. 30. 24. 1969. 52. Editorial notes. Scared to death. Ann. irtterrl. Med. 14. 789. 1971. 53. Engel G. L. Sudden and rapid death during psychological stress. Atw. interu. Med. 74. 771, 1971. on an old 54. Lester D. Voodoo death: some thoughts phenomenon. Am. Anthrop. 74. 386, 1972. 55. Clune F. J. A comment on voodoo deaths. Am. Anthrap. 75, 312, 1973. on an 56. Lex Barbara W. Voodoo death: New thoughts old explanation. Am. Amhrop. 76. 818. 1974. 57. Thomas Anthony E. Oaths. ordeals and the Kenyan courts: a policy analysis. Hum. Org. 33. 59, 1974. C. P. A case of pseudocyesis caused by 5x. Kimball “roots.” Am. J. Obstet. Gynrc. 107. 801. 1970. of psychosis in four East 59. Edgerton R. B. Conceptions African societies. 4m. Anthrop. 68. 408, 1966. 60. Timing D. C. Voodoo, root work, and medicine. Psychosom. Med. 29, 483. 1967. 61. Williams J. J. Voodoos nud Obeuhs. Phases of‘ West Indiut1 Witchcraft. Dial Press, London. 1932.
Jamaican 62. Kerr M. Persormliry and Cmflicr in Jamaica. (Revised Edition). Collins, London, 1963. 63. Hogg D. The convince cult in Jamaica. In Papers in Caribbean Attthropoloyp. Compiler: Mintz, S. Yale University Publications in Anthropology Reprints 58. 1970. 64. Bryce-La Porte. R. S. Crisis, contraculture. and religion among West Indians in the Panama Canal Zone. In Afro-American Anthropology. (Edited by Whitten N. and Szwed J.). The Free Press. New York, 1970. 65. Snell J. E. Hypnosis in the treatment of the ‘hexed’ patient. Am. J. Psychiar. 124, 311, 1967.
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66. Gelhorn E. and Kiely W. F. Autonomic nervous system in psychiatric disorder. In Biological Psychiatry. (Edited by Joseph Mendels). Wiley, New York, 1973. 67. Green E. E., Green A. M. and Walters E. D. Voluntary control of internal states: psychological and physiological. In Biqfeedback und Selj’ControL (Edited by Barbe T., et al.) Aldine-Atherton. New York, 1974. 68. Davidson R. and Krippner, S. Biofeedback research: the data and their implications. In Bi@edhack and Self Control. (Edited by Barbe T.. Decara L. V., Kamiya J.. Miller N., Shapiro D. and Stoyva J.) Aldine-Atherton. Chicago, 1974.
VOMITING SICKNESS: INVESTIGATION
A THEORETICAL
ANTHONY THOMAS and LAURIE KRIEGER Department
of Anthropology,
University of North Carolina at Chapel Hill, U.S.A.
Abstract-Jamaican Vomiting ‘Sickness has been investigated for over sixty years, and yet this acute disease remains an epidemiological mystery. In this article, we have ciitically examined the toxin hypotheses emphasized in the literature-particularly the ackee and yam theories of causation. Because of the inadequacies of the conventional toxin hypotheses, we suggest that more attention should be given to a malnutrition hypothesis and a psychogenic hypothesis. Jamaican Vomiting Sickness (JVS), a reportedly culture bound syndrome, may very well have multiple causation. That is. toxin, malnutrition, and psychogenic etiologies may be operative independently and sometimes jointly in the epidemics and family outbreaks of acute and often fatal Jamaican Vomiting Sickness.
The “Vomiting Sickness” of Jamaica was first recorded in 1885 by Bowrey, the Island Chemist [l]. The first medical report on the illness was published in 1904 by Turton [2] who gave a description of Jamaican Vomiting Sickness which is remarkably similar to contemporary summaries. By the second decade of,this century there was a heated controversy over the causes.of this baffling disease. Most of the major explanations for the cause of this illness emerged during the course of this initial controversy and these explanations are still being debated today. This paper describes the disease and its incidence, discusses possible causes. and suggests areas for further research. EPIDEMIOLOGY Jamaican Vomiting Sickness (JVS) appears in family outbreaks, sporadic cases, and in epidemic form. Of the 721 cases described in the literature under review by Kenneth Hill [3], the greatest incidence is in the age group from two to five years, with a considerable number being between five and ten years. Infants who have not yet been weaned are rarely affected, and the incidence among individuals over ten years of age is low. The incidence of the disease among boys and girls is approximately equal. Young adult women are also occasionally affected, and there are rare reports of adult men falling prey to JVS. Vomiting Sickness is reported almost exclusively during the colder winter months (December-March). JVS by folk definition and medical observation tends to be unique to Jamaica. However, there are a few poorly documented accounts of JVS occurring among Jamaican emigrants [3.4]. Furthermore, the illness tends only to be diagnosed in Jamaicans of African ancestry and tends to occur in rural rather than urban areas [S]. Throughout the literature an emphasis is placed upon the frequent occurrence of family outbreaks. The causes of Jamaican Vomiting Sickness are not the only controversial aspects of the disease; the very quality of the epidemiological data is questionable. In particular. the system of record keeping has been inadequate. As Cicely Williams points out. the current 111
seasonal incidence of JVS may be explained by the practice of closing the file for health officers’ reports of this illness from April through October [6]. Early to present day researchers have consistently emphasized the failure of health officers to accurately identify and record cases of JVS. One problem is that it is often very difficult to decide whether a patient is actually a victim of JVS, especially in the sporadic cases, as symptoms are often accompanied by severe worm infestation, malnutrition, malaria, and other disorders [7]. In 1952, a reliable diagnosis of Jamaican Vomiting Sickness was not possible; yet health officers were required at that time to submit a monthly list of JVS patients in their parish [6]. In the early part of this century, all mysterious serious ailments among rural Jamaican children tended to be associated with JVS-including yellow fever and spinal meningitis [S]. SYMPTOMOLOGY Jelliffe [9] and Stuart [lo] found in their clinical observations during 1953 that the most outstanding feature of JVS is sudden and severe hypoglycemia. Blood glucose levels characteristically range from &20mg. There appear to be two typical forms of JVS. In the first type, the patient, most often a young child, complains of discomfort in the stomach and vomits. The vomitus is usually the content of the child’s last meal. The child may vomit several more times. If this is the case, the vomitus changes to clear or frothy mucus. The patient begins to feel better and falls asleep. The remission may last several hours. When the patient awakens, or later the following day, (s)he is seized by sudden, effortless vomiting which is rapidly succeeded by collapse, convulsions, coma and death. The vomitus in the final attacks is again clear or frothy mucus that is occasionally bloodstained. The shortest fatal case of JVS was reported to last one hour: however the average duration is about 12 l/2 hours [3]. In the cases examined by Stuart ef al., often the liver was impalpable upon admission to a hospital, but tended to enlarge and become palpable during recovery [lo]. In neither
ANTHONY THOMAS and LAURIE KRIEGER
178
form of Vomiting Sickness does the temperature exceed 100” or 101’F unless accompanied by a bacterial or viral infection. The temperature is almost always normal or subnormal. Usually a cyclical clouding of consciousness is a feature of the disease. The second. or fulminating form, is not usually accompanied by vomiting. “A fulminating variety of so-called Vomiting Sickness is recognized in which vomiting does not occur, the patient being precipitated dramatically into the stage of collapse, drowsiness, convulsions, stupor, twitching of the limbs and fatal coma” [lo]. The second form of JVS is usually of short duration, i.e. fatal within l-24 hr. Scott’s data indicate that 85% of fatal cases show signs of convulsions [3]. JVS has been treated successfully with large amounts of glucose administered intravenously and by glucose drinks if the patient is conscious. However, this therapy is usually unsuccessful with the very rapid fulminating form or in cases where the patient has experienced severe hypoglycemia for an extended period of time-24 hr or longer [S]. The glucose treatment was not initiated in Jamaica until the discovery of a connection between hypoglycemia and JVS in 1953; therefore there is much published on postmortems of JVS victims [ 1 l-191. POSTMORTEM
Many of the early workers were quite observant and maintained precise records of autopsies. Consequently, later accounts differ little from their earlier counterparts. Typically, a postmortem examination of the JVS victim reveals a fatty metamorphosis of the liver and kidney. The liver glycogen is depleted. Generalized hyperaemia is usually observed. Hemorrhages may be found over the heart, in the lungs and over the liver and spleen. The meninges, as well as parts of the brain, are often inflamed and may be hemorrhagic (especially if death was preceded by convulsions). Oedema of the connective tissues is commonly found. There is swelling and hyperaemia of lymph nodes throughout the body and hyperaemia of the alimentary lymph nodes may exist as well. Necrobiosis of the pancreatic, renal and liver epithelia is often found. It is very rare to find bacteria in the vomitus. stomach contents. viscera or heart’s blood. On rare occasions when bacteria are present, they are invariably S. aureus. POSSIBLE
CAUSES
In the next portion of the paper, we will discuss possible causal mechanisms. Many have been proposed by physicians and other investigators. Several toxin hypotheses have been proposed by physicians who have worked in Jamaica. In addition to evaluating the toxin etiologies, we will discuss two additional hypotheses: a malnutrition hypothesis and possible psychogenic causative factors. Jamaican Vomiting Sickness, reportedly a culture bound syndrome, may very well have multiple causation. Consequently, all of these hypotheses may be operative independently and sometimes jointly in the epidemics and family outbreaks of acute and often fatal Jamaican Vomiting Sickness.
SUSPECTED
TOXINS
Certain plant poisons are known to cause sudden and severe hypoglycemia in experimental animals. The plants implicated in JVS are ackee. yams. cassava. unidentified plants used in bush teas and poisonous plants that young children may eat when alone. Presently, it is widely held that the disease is due to the ingestion of a toxic substance w-hich pioduces a block (often temporary) in the enzyme system responsible for gluconeogenests [20.21]. Harold Scott suspected ackees as the cause of the mysterious Jamaican vomiting disease in an article submitted for publication in October of 1915 [ 131. In the 1970s the ackee is still a prime suspect [‘I]. The ackee is an evergreen (Blighiu sapida) bearing a fruit that is widely eaten in Jamaica and forms the basis for ackee and saltfish. Jamaica’s national dish. The tree bears fruit perennially. In 1970 it was estimated that there were 200 acres of cultivated ackees and mangoes respectively. The Jamaican Ministry of Agriculture’s 1975 targets for these crops were 1300 additional acres for ackees and 700 added acres for mangoes [22]. The ackee was brought to Jamaica from West Africa in the late 18th century and is found throughout the Caribbean as well as in Florida and Central America. Jamaica is the only area where the fruit is a popular article of diet, although tinned ackee is eaten by Jamaicans who have migrated to other parts of the world. The fruit of the ackee is 7-10 cm long. It is normally divided into three compartments (loculi). Each of these contains one seed. The fruit splits into three valves at maturity exposing the black seeds. Each seed has a large cream colored arillus which is the edible portion of the ackee [23]. The poisonous quality of the ackee is appreciated wherever it grows. Jamaica is no exception. People general/y in this island [Jamaiccc] are convinced that ackres, under certain conditions are poisonous; among these conditions may be mentioned: (i) Unopened ackees, and by consequence: (ii) Ackees which have not opened naturally, but hare been forced after falling unopened: (iii) Fruit gathered jr0171 u decayed branch; (iv) Ackees with some soft spot in nn otherwise apparently sound fruit [ 131. The toxic principle was isolated by Hassall. Reyle. and Feng and first reported in 1954 [24]. They isolated two water-soluble toxins from the ackee: hypoglycin A and hypoglycin B. Hypoglycin A is the more potent toxin. The toxins are found in the seeds of the ackee fruit. A very small quantity of hypoglycin A is found in the ripe arillus, while the unripe arillus contains a larger concentration. These toxins cause severe and sudden hypoglycemia in experimental animals [24,25]. (For an explanation of how the hypoglycins produce hypoglycemia, see Feng [25] and Bondy and Rosenberg [4]). The water-solubility of the toxin is significant because in Jamaica older children and adults frequently consume the solid parts of the cooked ackee, while young children eat ackee soup or the “pot water” in which the ackees have been cooked.
Jamaican vomiting sickness The known toxicity of the unripe ackee and its prevalence and popularity in Jamaica create strong temptations for many researchers to accept the ackee as the villain in JVS. However, all this evidence is circumstantial. Perhaps no one is more aware of this than Cicely Williams, who argues forcefully against an easy solution to the problem if based on circumstantial evidence [S-7]. Unfortunately the arguments against ackees as the causative agent are also circumstantial. It is accepted that ackees may contain a toxic principle-they certainly are not ‘fool proof’, and in some cases of vomiting are associated with the consumption of ackees; but it is equally certain that there are many people today who are eating unripe, unopened or raw ackees and drinking the pot-water, in which these are cooked, without ill effect [7]. Williams calls for investigation of this problem by an expert in food poisoning and an epidemiologist [5,61. W. L. Bamett is the primary proponent of a toxic principle in yams as the cause of JVS [26]. He blames a toxic glucoside in St. Vincents yam for many cases of JVS. Barnett shows the toxicity of certain types of yam-stems by experimental evidence using fish as the subjects. He links the JVS peak with the digging of early varieties of yam. Further he holds the drying effect of yam storage and transportation practices accountable for the lack of yam poisoning and JVS in urban centers. His epidemiological methods are questionable and his work has been subject to criticism. Hill criticizes Barnett’s statement that summer JVS coincides with harvesting of the summer yam crop because there is no agreement that Vomiting Sickness occurs at all during the summer. Hill also points out that many islands in the West Indies grow yams, none report a toxicity and nowhere but Jamaica is the JVS ,syndrome reported [3]. Stuart, Jelliffe and Hill feel yams are not responsible [lo]. Williams points out that the yam’s cyanogenic glucoside, “. . is found mainly in the yam head, or stem end of the yam, which is not generally consumed, but kept for replanting”[6]. Cassava is grown and eaten in much of the tropical world. Though not a common crop in Jamaica today, cassava is part of the rural food inventory. Cassava is known to contain HCN. another toxic cyanogenic glucoside. Wherever cassava is grown and eaten, some method of rendering the food nontoxic is practiced. There are two kinds of cassava: bitter and sweet. In sweet cassava most of the HCN is found in the rind. Since the HCN in bitter cassava is distributed throughout the fruit, techniques are used to leach out the poisonous agent. Seidelin ruled out cassava poisoning because no prussic acid could be found in the viscera of JVS victims [12]. Nevertheless. cassava poisoning is not uncommon in Jamaica’s history and is due primarily to insufficient leaching out of HCN [3]. Cassava poisoning produces vomiting. In order to link cassava poisoning more firmly with JVS. it would be helpful to know if HCN is capable of producing the kind of hypoglycemia associated with JVS: this answer is not apparent from the literature. The argument that cassava is the dominant causative agent of JVS suffers from
179
some of the same fallacies as the argument that it is yams. Cassava is eaten in many parts of the world, but JVS appears to be specific to Jamaica. Jamaica’s ethnomedicine often involves the use of “bush teas”. Bush teas are infusions of parts of various plants. These teas are consumed widely not only for medicinal purposes, but as part of the first meal of the day. Jamaica has a wide variety of plants and many of these are poisonous to humans. Some other plants are easily confused with those that are regular components of many bush teas. Furthermore, since congeries of plants are used to make the different types of bush teas, it would be difficult to separate out any one toxic agent. Some ingredients are known to be capable of producing hypoglycemia. Toxic bush teas are considered as possible sources of the cirrhosis following veno-occlusive disease in Jamaica [27,28]. Frequently, bush teas are suspected as a contributory factor in JVS [6,9, 10, IS]. Hill questions the bush tea explanation because of the seasonal incidence of JVS [3]. However, it may be possible that some of the plants regularly used or mistakenly used in bush teas are of seasonal occurrence. Williams seems to express the belief that’the various types of JVS outbreaks may have different causes. In this view, bush teas may be just one causal factor. Bush teas form part of the diet of many age groups in Jamaica, not just those of the population at greatest risk of contracting JVS. K. L. Standard reports that, “Mint and cercie are the most popular ‘bush teas’ used . . . and are often given as early as the first week of life [29]. If these bush teas are administered to young infants, it is possible that other bush teas may be similarly given to infants. JVS is virtually absent among young infants. The bush tea argument, while plausible, has many problems. Children in rural Jamaica, particularly those from poor families, are often left unsupervised by adults during the day. They may spend much time finding, cooking and eating their own food. This custom is very important to consider in the etiology of JVS. Jamaican babies are usually weaned before one year of age [29]. However, children are not usually susceptible to JVS until two years. This age coincides with the toddling stage-the time at which children are mobile enough to search for food. Several cultural factors are directly relevant to this possible etiology. The children’s practice of cooking a “private pot” provides a multitude of opportunities to ingest toxic plants. The private pot consists of any scraps of food and foodstuffs gathered by the child who takes them, cooks and eats them without adult supervision [3]. Vomiting Sickness occurs during the time of the year that is traditionally the “hungry” season. Food is less plentiful during the winter. Williams writes: The families in which vomiting sickness is most frequently reported are those that sufir from chronic, often marginal malnutrition. The children have little supervision, and go foraging on their own for a portion of the day.. . . The universal habit of using a variety of local herbs for making tea, and the fact that vomiting sickness nearly always comes from rural areas, and very often the children are afSected while adults escape, probably indicates that this supplementation of food supply is often responsible for the tragedies [S].
180
ASTHONY THOMAS and LACRIEKRIEGER
Certainly there are many potentially hypoglycemiaproducing plants indigenous to Jamaica [ 10,271. The possibility also exists that the children may be ingesting some form of chemical poison. Certain chemicals reputedly produce hypoglycemia when consumed e.g. guanadine, carbon tetrachloride, chloroneoarsphenamine phosphorus hydazine, fol-lll. [S, 30-321. However it is difficult to explain epidemic forms of JVS and family outbreaks including the mother, if some type of juvenile pica were the sole cause of JVS. Williams emphasizes the neglect of Jamaican children from poor families. However, she provides little documentation [S, 63. Thus, the supplementation of diet by children involves a good deal of conjecture. It appears that no one has ever observed Jamaican children regularly to see what their eating habits are. There are other cultural factors involved in the children’s dietary intake. Children often do not live with their mothers, but reside with other relatives (due to marriage and residence customs in Jamaica). While the biological parents may not be providing for a child, other relatives assume the responsibilities of “parental roles” [33]. Such customs are directly relevant to the degree of supervision and the kind of botanical training that a child receives. MALNUTRITION
HYPOTHESIS
Most authors agree that chronic malnutrition is endemic to small children in rural Jamaica [S, 6.7.20. 34. 35, 361. Protein Calorie Malnutrition (PCM) is noted by Fonaroff to be highest in urbanplantation environments [35]. Standard finds PCM. but the results are not differentiated by location [29]. Alleyne studied seriously under- and malnourished infants [36]. His population at risk (children 10-12 months old) is considerably younger than that of JVS (2-10 years), but his study is helpful in underscoring the presence of serious nutritional disease in Jamaica. Back reports in his 1956 article that, “It was found that the nutritional state of the small farmer and his family was good in most districts and that gross malnutrition was far less common than in the poorer districts of Kingston.. . .” [37]. He obtains these results by medical examination of a sample. However, in a subsequent and more comprehensive year-long survey including weekly recall nutritional data and medical examination, Back reports low vitamin A intake and low riboflavin intake [38]. Miall et al., demonstrate that, “infections adversely influence the state of nutrition and are themselves more serious where the nutritional state is poor” [34]. Malnutrition may be related to JVS in several possible ways. Malnutrition by itself may be a cause of JVS or the cause may be the combined effect of one of several toxins and malnutrition. If the cause of JVS is primarily infectious, malnutrition would enter into the interactions of host and invading organism. Mainzer presents experimental evidence illustrating the role that malnutrition, i.e. pellagra, plays in production of hypoglycemia; “In a quarter of the experiments [injection of insulin into human subjects suffering from pellagra] severe cerebral manifestations of hypoglycemia would appear abruptly, often preceded by autonomic phenomena” [39]. Josephs notes
that. “It is the common experience of those who have studied large series of children to find lower values for blood sugar in infancy during fasting and to fmd greater variation under different conditions.. As the child grows older. this liability disappears, and in adults it is rarely found, although it does occur” [40]. Williams considers that malnutrition may be linked to JVS by at least two chains: (1) chronic malnutrition complicated by a short period without food or some upset of the digestive system may produce hypoglycemia; (2) a high carbohydrate meal (such as the sugar cane of which Jamaican children are so fond) may’ precipitate hypoglycemia in people with a fatty liver [S]. A sore mouth and/or mouth tissues are occasionally found in association with JVS [i. 131. This symptom is characteristic of some vitamin deficiencies especially a deficiency of riboflavin (Bz). Toxins are absorbed more effectively in under nourished or malnourished animals [42]. Poorly nourished humans. especially children [S], are also more susceptible to the effects of toxins [7,42]. Jamaica has an unusually high prevalence of forms of malnutrition that disrupt liver function. It is well known that malnutrition is prevalent in Jamaica, particularly in those forms which damage the liver. A large proportion of the population is therefore peculiarly susceptible to toxins of’ various sorts [7]. Examination of JVS victims and their emissions has so far yielded little evidence implicating bacteria in this syndrome. Yet it is of interest that the ackee provides a good environment for haemolytic staphylococcus [S]; it is possible that the toxin produced by this organism may, in part. be responsible for JVS. Although bacteria are seldom found in association with JVS, the possibility of viral infection had not been ruled out as of 1953 [43]. A worm infestation may interfere with nutrition and may also independently produce vomiting. Ascarids have been reported for many years as present in the intestines of a large number of JVS victims [Z. 3,211. PSYCHOGENESIS
Psychological causation of sudden death is undoubtedly a controversial subject in the field of social science and medicine. However, there are numerous descriptions and discussions of social-psychological stress dramatically leading to death and/or complicating an existing illness [44-571. Engel lists life settings where a person is at greatest risk of sudden death. These are: 1. 011the impact oj’ the collapse or death of’ a close person: -7. during acute grief 3. on threat of loss of a close person: 4. during mourning or on an anniuersary; 5. on loss of’ Status or selfesteem: 6. personal danger or threat of’ injury: 7. after the danger is over: 8. reunion, triumph, or happy ending. Common to all is that they involve events impossible for the victims to ignore and to which their resporw is overwhelming excitation or giving up, or both [53]. Christian and Ratcliffe report animals the condition [shock
that ‘I.. . in free wild disease resulting in
181
Jamaican vomiting sickness sudden death] develops when environmental demands exceed maximum native capacity” [45]. Similar mechanisms may possibly operate in humans. Jamaicans are known to view certain types of food such as ackee as poisonous-particularly when the food is in a certain stage or state (e.g. unripe, bruised). Consequently it is possible that the fear of having eaten a poisonous substance may cause shock disease in either children or adults. Significantly, Christian and Ratcliffe report that of fourteen animals dying of shock disease resultant from stress, all were pathologically characterized by acute hypoglycemia with livers depleted of glycogen [45]. Some JVS victims may die from the psychophysiological reaction to the consumption of a substance believed to be poisonous. The young victims’ mothers may sicken for this reason also, or due to the sudden shock from the loss or grave illness of one or several of their children. The many reports show that mothers often fall prey to JVS after one or more of their children have succumbed. Witchcraft may also be implicated in JVS. Belief in sorcery presumes that a person may harm another person by wishing him or her ill or by performing certain magical acts designed to cause misfortune to the intended victim or his or her family. In the American South, the Caribbean, and Africa the cognitive pattern associated with witchcraft is found when a victim or patient believes him or herself to be “hexed”. This type of belief is a powerful psychological force in the production of or in association with many illnesses: pseudocyesis [SS], madness [59,60], asthma [47], cardiorespiratory disease [48], cardiovascular malfunction [53], abdominal pain and vomiting [60] to name a few. The logic of witchcraft is very much operative in Jamaica today. As in some other parts of the Caribbean, the indigenous term for witchcraft in Jamaica is obeah. Its curers and practitioners are obeah (wo)men, and the obeah belief complex is tied in with religious practices on the island [61-643. Anthropologists and other social scientists have found that socialization plays an important part in channeling the somatization of psychological states: Batesori and Mead.. show how the training of Balinese children to withdraw from expression of an) strong emotion may be a cultural factor predisposing them to the susceptibility to trance experience which is then used culturally.. There maJ be some similariries to this in the hexing culture, where a child is reared in the certain knowledge that the world is a dangerous place-ecil spells can be cast with great ease as punishment for even minor transgressions and the possibility of death from such a hex is very real [65]. It is common world-wide to find descriptions of parents ascribing the illness or death of their children to supernatural causes. Seldom if ever is this disease process reported from the child’s point of view. If socialization into witchcraft beliefs begins early in the child’s development, young children may succumb to sorcery. This possibility should be kept in mind by investigators because JVS occurs in a rural context where oheali beliefs prevail.
SUGGESTIONS
FOR
FURTHER
RESEARCH
Whereas heretofore, research into JVS was conducted by practicing physicians anti chemists, a crossdisciplinary approach with emphasis in the social sciences might begin to unravel some of the mysteries in Jamaican Vomiting Sickness. Anthropologists, with their participant-observation approach, could usefully study exactly what children eat and how parents socialize their offspring in food acquisition practices. The information gathered by anthropologists might be used to answer questions such as: How early and to what extent do children learn the ethno-botanical system, i.e. learn to distinguish between edible and non-edible materials? What do rural Jamaican children do when left alone? What is the structure of their associations with other children? Do poor rural parents sometimes neglect their children? And if there is neglect, what is the nature of this neglect by adults? Furthermore, the cultural anthropologist could elicit important information on the cultural significance of vomiting and stomach ailments. How and at what age are these meanings learned? Anthropologists and other experts skilled in ethnobotany might help unravel some of these dietary intake problems. Medical geographers and social epidemiologists would also contribute much to the study of Jamaican Vomiting Sickness. Maps are needed to illustrate incidences of JVS according to geographical studies area, elevation, and season. Nutritional already demonstrate that diet in Jamaica varies with geography, so a research team might explore the relationship of this variation to the occurrence of JVS. Particularly intense outbreaks of JVS might be correlated with climatic changes. Certainly, field investigators should give high priority to gathering data on the normative folk etiologies ascribed to Jamaican Vomiting Sickness. Furthermore, as JVS outbreaks occur, the presence of a physician-anthropologist clinical-research team would be very helpful. The team could, in the process of treatment and research, elicit from the affected people their understanding of what factors brought on the particular outbreak or sporadic case. Psychiatrists with training in anthropology and anthropologists with training in medicine could work together to explore the psychogenic hypotheses relevant to JVS. Current work on the autonomic nervous system and pathological symptoms is advancing our knowledge of mind-body interactions [66], but field studies are needed to gain an understanding of these interactions in natural social environments. Furthermore, recent work by psychologists on biofeedback processes is especially relevant to this whole topic of mind-body interactions [67,68]. As of this date, all the explanations for the outbreaks of JVS are based on very limited evidence and remain open to question. A more satisfactory explanation might be found with the combined effort of researchers from the several relevant disciplines. It seems that until a field study of broad dimensions is undertaken, Jamaican Vomiting Sickness will remain an epidemiological mystery. REFERENCES 1. Bowrey
J. J. Jamaica Gar.
10.
481, 1887.
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ANTHONY
THOMAS
2 Turton R. S. The ‘vomiting sickness’ of Jamaica. J Trop. -Med. Hyg. 1. 163. 1904. 3. Hill K. R. The vomitine sickness of Jamaica. II!l. med. J. 1, 243, 1952. 4. Bondy P. K. Disorders of carbohydrate metabolism. In Duncan’s Diseases of Metabolism. 6th Edition (Edited by Bondy P. K. in association with Rosenberg L. I?.) p. 271. W. B. Saunders. Philadelphia. 1969. 5. Williams C. The vomiting sickness of Jamaica. J. the Med. Worn. Fed. 43. 1954. 6. Williams C. Report of the vomiting sickness study. Medical Department, Jamaica, 1953. 7. Williams C. Vomiting in children. WI. med. J. 1, 265, 1952. 8. Vomiting Sickness in Jamaica. In Yellow Fever Bulletin 2, 1913. 9. Jelliffe D. B. and Stuart K. L. Acute toxic hypoglycemia in the vomiting sickness of Jamaica. Br. Med. J. 1. 75. 1954. 10. Stuart K. L.. Jelliffe D. B. and Hill K. R. Acute toxic hypoglycemia occurring in the vomiting sickness of Jamaica. J. Tree. fed. 1. 69, 1955. sickness in Jamaica. Jamaica 1 I. Potter T. J. Vomiting Gaz. (Supplement) 34;695, 1912. sickness’ in Jamaica. Ann. 12. Seidlin H. On ‘vomiting Trop. Med. & Parasit. 7,377. 1913. 13. Scott H. H. On the ‘vomiting sickness’ of Jamaica. Ann. Trop. Med. & Parasit. 10, 1, 1916. 14. Scott H. H. The vomiting sickness of Jamaica. Trans. R. Sot. Trop. Med. Hyg. 10. 47, 1917. File HB 517 No. 15. Evans K. L. Medical Department 30, Kingston, Jamaica, 1943. H. D. The syndrome called ‘vomiting sick16. Chambers ness.’ I+![. med. J. 2. 37, 1953. 17. Fitzmaurice L. W. The Vomiting Sickness of Jamaica Symposium. IU. med. J. 2, 93, 1953. and fatty metamorphosis 18. Hill K. R. Hypoglycaemia of the liver in the vomiting sickness of Jamaica. J. Path. Bact. 35. 334. 1953. K. P. Acute toxic 19. Hill K. R.. Bras G., and Clearkin hypoglycaemia in the vomiting sickness of Jamaica. WI. med. J. 4, 91, 1955. 20. Patrick S. J., Jelliffe D. B., Stuart K. L. The hepatic glycogen content in acute toxic hypoglycaemia. J. Trop. Ped. 1, 88, 1955. 21. Stuart K. L. Vomiting sickness of Jamaica. In Diseases of Children in the Subtropics urld Tropics (Edited by Jeliffe D. G.). Edward Arnold Ltd. London, 1970. and Fisheries. Crop acreage 22. Ministry of Agriculture targets by general location 1970-75. (The authors of this article have a copy of this map in their files). 23. Parry J. H. Salt fish and ackee. Cur. Q. 8. 30. 1962. Seaforth C.E. The ackee Int. f?. Scient. 3. 51, 1962. Cooked ackee looks and tastes like lightly scrambled eggs. A.B: 24. Hassall C. H.. Reyle K. and Feng P. Hypoglycin Biologically active polypeptides from Blighia sapida. Nature. Lond. 173. 456. 1954. ackee: a review. I+!:!. 25. Feng P. C. Hypoglycin-from med. J. 18. 23X. 1969. 26. Barnett W. L. Investigatton into the “vomiting sickness” of Jamaica in 1943. Department of Government Chemist. (A copy is available at the Jamaica Institute, Kingston, Jamaica.) C. S. Nutrition, geography, and liver dis27. Davidson eases. Am. J. c/in. Nutr. 23. 427, 1970. Disease. In Disruses of 28. Stuart K. L. Veno-occlusive Children in the Subtropics und Tropics. (Edited by Jelliffe D. B.) Edward Arnold Ltd. London, 1970. 29. Standard K. L. A pilot nutrition survey in five lowincome areas in Jamaica. B!f. med. _f. 7, 215. 195X. 30. Minot A. S. and Cutler J. T. Studies of the response to calcium medication in the hypoglycemia of carbon tetrachloride boisoning. Am. J. Phvsio. xiii. 674. 1930.
and LXRIE
KRIEC~ER
31. Cross J. B. and Blackford L. M. Fatal hepatogenic hypoglycemia following neoarsphenamine. J.A.M..4. 94. 1739. 1930. 32. Minot A. S. The mechanism of the hypoglycemia produced by guanadine and carbon tetrachloride poisoning and its relief by calcium medication. J. P/w. E.\-p. Med. 43. 295. 1931. M,I, Mother IV/IOFtrthvred 33. Smith M. G. Introduction. me: A Study of the Family irl Three Selected Cornrrtw~iries irt Jamaica. Bv Edith Clarke. 1966. 34. Miall W. E., Desai P. and Standard K. L. Malnutrition, infection and child growth in Jamaica. J. biosoc. xi. 2, 31, 1970. 35 Fonaroff L. S. Settlement typology and infant malnutrition in Jamaica. Trop. yeogr. .ktMrd.21, 177. 1969. 36 Alleyne G. A. 0. Some features of infantile malnutrition. IU. med. J. 19, 32. 1970. survey of small farmers in 37 Back E. H. A nutritional Jamaica in 1955. w1. med. J. 5. 189. 1956. 38 Back E. H. The dietary of small farmers in Jamaica. WI. med. J. 10. 28. 1961. in pellagrins and 39 Mainzer F. Insulin-hypersensitivity its significance. Trans. R. Sot. Trap. Med. & HJ~. 43. 329, 1949. hypoglycemia in childhood. 40 Josephs H. Spontaneous Am. J. Dis. Child. 38, 746, 1929. 41 Bodansky M. The production of hypoglycemia in experimental derangements of the liver. Aer. J. Phxsiol. 66. 375. 1923. 42 Brown T. M. and Harvey A. M. Spontaneous hypoglycemia in “smoke” drinkers. J.A.M.A. 117, 12, 1941. L. S. and Caselitz F. H. Comment [in the 43 Grant Vomiting Sickness of Jamaica Symposium. Chairman: L. W. Fitzmauricel. w1. med. J. 2. 104. 1953. 44 Cannon W. B. -Voodoo” death. ilm. .4nthrop. 44. 169. 1942. 45 Christian J. J. and Ratctiffe, H. L. Shock disease in captive wild mammals. Am. J. Pathol. 28. 725. 1952. of sudden death 46. Richter C. P. On the phenomenon in animals and man. Psychosom Med. 19. 191. 1957. 47 Mathis J. L. A sophisticated version of voodoo death. Psvchosom. Med. 26. 104, 1964. conference. Case 48 Boitnott J. (Editor) Ctinicopathologic presentation. The Johns Hopkins Hospital. The Jonrrlal. pp. 186-199. 1967. 49. Burrell R. J. W. The possible bearing of curse .death and other factors in Bantu culture on the etiology of myocardial infarction. In The Etiology of Myocardial Infitrction. (Edited by James T. N. and Keyes J. N.). Little-Brown. Boston. 1963. 50 Engel G. L. A Life setting conducive to illness. Bulletirt of the Mrnirqet Clinic. 32. 355. 1968. 51 Dynes J. B. Sudden death. Discuses of the Nervous System. 30. 24. 1969. 52. Editorial notes. Scared to death. Ann. irtterrl. Med. 14. 789. 1971. 53. Engel G. L. Sudden and rapid death during psychological stress. Atw. interu. Med. 74. 771, 1971. on an old 54. Lester D. Voodoo death: some thoughts phenomenon. Am. Anthrop. 74. 386, 1972. 55. Clune F. J. A comment on voodoo deaths. Am. Anthrap. 75, 312, 1973. on an 56. Lex Barbara W. Voodoo death: New thoughts old explanation. Am. Amhrop. 76. 818. 1974. 57. Thomas Anthony E. Oaths. ordeals and the Kenyan courts: a policy analysis. Hum. Org. 33. 59, 1974. C. P. A case of pseudocyesis caused by 5x. Kimball “roots.” Am. J. Obstet. Gynrc. 107. 801. 1970. of psychosis in four East 59. Edgerton R. B. Conceptions African societies. 4m. Anthrop. 68. 408, 1966. 60. Timing D. C. Voodoo, root work, and medicine. Psychosom. Med. 29, 483. 1967. 61. Williams J. J. Voodoos nud Obeuhs. Phases of‘ West Indiut1 Witchcraft. Dial Press, London. 1932.
Jamaican 62. Kerr M. Persormliry and Cmflicr in Jamaica. (Revised Edition). Collins, London, 1963. 63. Hogg D. The convince cult in Jamaica. In Papers in Caribbean Attthropoloyp. Compiler: Mintz, S. Yale University Publications in Anthropology Reprints 58. 1970. 64. Bryce-La Porte. R. S. Crisis, contraculture. and religion among West Indians in the Panama Canal Zone. In Afro-American Anthropology. (Edited by Whitten N. and Szwed J.). The Free Press. New York, 1970. 65. Snell J. E. Hypnosis in the treatment of the ‘hexed’ patient. Am. J. Psychiar. 124, 311, 1967.
vomiting
sickness
183
66. Gelhorn E. and Kiely W. F. Autonomic nervous system in psychiatric disorder. In Biological Psychiatry. (Edited by Joseph Mendels). Wiley, New York, 1973. 67. Green E. E., Green A. M. and Walters E. D. Voluntary control of internal states: psychological and physiological. In Biqfeedback und Selj’ControL (Edited by Barbe T., et al.) Aldine-Atherton. New York, 1974. 68. Davidson R. and Krippner, S. Biofeedback research: the data and their implications. In Bi@edhack and Self Control. (Edited by Barbe T.. Decara L. V., Kamiya J.. Miller N., Shapiro D. and Stoyva J.) Aldine-Atherton. Chicago, 1974.