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 »  Abstract
 »  Introduction
 »  Material and Methods
 »  Results
 »  Discussion
 »  References

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ORIGINAL ARTICLE
Year : 2004  |  Volume : 52  |  Issue : 2  |  Page : 206-209

Possible relationship between phenylthiocarbamide taste sensitivity and epilepsy


Department of Anthropology, Panjab University, Chandigarh - 160014, India

Correspondence Address:
Department of Anthropology, Panjab University, Chandigarh - 160014, India
neelamkuki@yahoo.com

 » Abstract 

The study was based on the data of a sample of 400 epileptic patients (200 idiopathic and 200 symptomatic) and 100 normal healthy individuals serving as controls. The PTC threshold distribution was bimodal. The number of non-tasters among idiopathic epileptics (35.5%) and symptomatic epileptics (32.5%) was significantly higher than controls (20%). The relative incidence of non-tasters in idiopathic and symptomatic epilepsies was 2.20 and 1.93 respectively. There is evidence that non-tasters tend to ingest a greater quantity of bitter tasting goitrogenic substances present naturally in edible plants which in turn exert greater thyroid stress in non-tasters or less sensitive tasters. Such a stress during intrauterine or early childhood growth and development might have affected neurological maturation which in turn made them more susceptible to epilepsy than tasters, who faced lesser stress.

How to cite this article:
Pal S K, Sharma K, Pathak A, Sawhney I M, Prabhakar S. Possible relationship between phenylthiocarbamide taste sensitivity and epilepsy. Neurol India 2004;52:206-9


How to cite this URL:
Pal S K, Sharma K, Pathak A, Sawhney I M, Prabhakar S. Possible relationship between phenylthiocarbamide taste sensitivity and epilepsy. Neurol India [serial online] 2004 [cited 2019 Dec 14];52:206-9. Available from: http://www.neurologyindia.com/text.asp?2004/52/2/206/11044



 » Introduction Top


Phenylthiocarbamide (PTC) taste sensitivity is a genetically controlled trait, the gene (allele) for the ability to taste PTC being dominant over the non-taster allele. A review of the literature reveals that human populations show a tremendous variation in the frequency of tasters which ranges from 10% to 98%.[1],[2],[3] The thiocarbamides are known to be active goitrogenic substances, being inhibitors of thyroid function, and some of these are naturally present in the edible plants of the Brassica genus including cabbage, cauliflower, kale, brussel sprouts, turnips, etc.[4],[5],[6],[7],[8] The ability to taste these substances has been suggested as a possible balanced polymorphism related to the metabolic differences of thyroid activity.[7] Apart from goiter, several other diseases (diabetes, tuberculosis, mongolism, mucoviscidosis, duodenal and gastric ulcers) have been reported to be associated with the ability to taste PTC.[9],[10],[11] A high incidence of non-tasters has been reported in patients with nodular goiter,[12],[13] congenital athyreotic cretinism,[14],[15] and dental caries.[16] Sharma[17] has reported a higher frequency of non-tasters in epileptic twins.
Epilepsy is in fact not a disease but a manifestation of a disease. It is defined as a condition characterized by recurrent (two or more) afebrile seizures, unprovoked by any immediate identifiable cause.[18] Multiple seizures occurring in a 24-hour period are considered a single event. The etiology of the disease is heterogeneous, and epilepsy can be divided into two broad categories: idiopathic and symptomatic. It should be interesting to study the taste sensitivity to PTC among idiopathic and symptomatic epileptics. This formed the basis of the present study.


 » Material and Methods Top

The data for the present study were collected from Neurology outpatient department (OPD) and epilepsy follow-up clinic at the Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh. A total of 400 epileptic patients (200 idiopathic and 200 symptomatic) and 100 normal and healthy subjects, serving as controls, were studied. Both, patients and controls, belonged to the northwestern region of India (Punjab, Haryana and Himachal Pradesh) and were matched for castes/ethnic background. The patients were subjected to electroencephalography (EEG) and computed tomography (CT). A few doubtful cases were investigated for magnetic resonance imaging (MRI). On the basis of these investigations, the patients were categorized as idiopathic or symptomatic. The control sample was matched for age, sex and ethnic background with the sample of patients. The idiopathic category included 114 males and 86 females with a mean + S.D age of 23.22 + 9.92 years, while the symptomatic category included 119 males and 81 females with a mean age of 25.7 + 11.07 years. Hence, both the samples were comparable for age and sex.
The technique of using 13 solutions was used to determine the taste sensitivity to PTC as per standard procedures described by Harris and Kalmus.[19] The stock/standard solution containing 1.3 gm PTC diluted in one liter (L) of distilled water was labelled as 'Solution 1'. It was further diluted by 100%, i.e. 0.5L Solution 1 diluted with 0.5L distilled water to get 'Solution 2', and so on till 'Solution 13'. To determine taste sensitivity, sorting technique was used by starting with the weakest 'Solution 13'. A person who could not taste Solution 1 was grouped under the category threshold solution number (TSN) < 1. The distribution of the frequency of tasters and non-tasters is usually bimodal with antimode recording the lowest frequency separates the two distributions. The anitmodal point was taken to classify the subjects as tasters or non-tasters. To study the association between disease and PTC locus, relative incidence (RI) was calculated after Woolf.[20]


 » Results Top


The frequency distribution of the various threshold levels of PTC taste sensitivity among the epileptics and controls is given in [Table - 1]. The distribution of the threshold is biomodal as shown in [Table - 1] and [Figure - 1], [Figure - 2], [Figure:3]. The antimode point is at Solution 4 in idiopathic epileptics, and at Solution 3 in symptomatic epileptics and controls. The means and standard deviations of the thresholds for idiopathic epileptics, symptomatic epileptics and controls were: 5.36+3.18; 5.39+3.45, 6.62+3.03, respectively.
[Table - 2] shows the number and percentage of tasters and non-tasters, gene frequency and relative incidence (RI) among idiopathic and symptomatic epileptics. There were a greater number of non-tasters in both idiopathic and symptomatic epileptics than in the controls. The chi-square test shows significant differences between idiopathic epileptics and controls, between symptomatic epileptics and controls, but insignificant differences between idiopathic and symptomatic epileptics. The RI is about 14% higher in idiopathic epileptics than symptomatic epileptics. These results show a significant association between PTC locus and epilepsy. However, the type of epilepsy (idiopathic and symptomatic) does not seem to have any significant difference for PTC tasting ability.


 » Discussion Top


In the present study, there is a significantly higher incidence of PTC non-tasters among epileptics than controls. On the contrary, there are no differences between idiopathic and symptomatic epileptics for PTC sensitivity. The relative frequency of non-tasters among different diseases is given in [Table - 3]. The excessive number of non-tasters in cystic fibrosis has been speculated to be associated with alterations in the taste response due to local patho-physiological conditions, as the composition of glycoprotein in the saliva and mucus has been reported to be abnormal.[11] The high frequency of non-tasters among epileptics agree with the previous findings of Sharma[17] on twins. On the basis of these findings, it can now be generalized that there are no differences between twins and the general population in showing higher frequency of non-tasters in epileptics.
The present study reveals no differences in PTC taste sensitivity between idiopathic and symptomatic epileptics despite the fact that these have different etiologies. Of the diseases listed in [Table - 3], the ones which show higher frequency of non-tasters have neurological pathogeneses except cystic fibrosis. Greene[21] has hypothesized that PTC taste sensitivity is significantly correlated with maturation in visual-motor perception as tasters show greater maturation than non-tasters, who are more deficit in both sexes in the non-iodized population, but not in the iodized population. He further theorized on this basis that the more sensitive tasters may limit their ingestion of the bitter tasting goitrogens which in turn reduces the stress placed on the thyroid gland and therefore increases the likelihood of normal neurological maturation. On the contrary, the less sensitive tasters and non-tasters of PTC may ingest greater quantities of goitrogens present in edible plants which increases the stress on the thyroid glands, thus increasing the probability of intermittent hypothyrodism, which may adversely affect neurological maturation.[21]
The dietary history of the people in northwest India reveals that cabbage, turnips, cauliflower, Brassica leaves, etc. are consumed almost daily in large amounts by the people during the winter season. The less sensitive tasters and non-tasters undergo greater thyroid stress due to greater ingestion of goitrogens in the vegetables. The fetuses of non-taster mothers would also be experiencing some thyroid stress during their intrauterine growth and development. Sheppard and Gartler[14] suggested that non-taster fetuses may be susceptible to embryonic thyroidectomy on the basis of the evidence of an association between non-tasters and athyreotic cretins. The presence of normal non-tasting siblings of the cretins has been attributed to the variations in the time, dosage and duration of exposure of the fetus to maternally ingested goitrogens.[14] A similar etiology may exist for the association between non-tasters and epilepsy. The greater thyroid stress in non-tasters or less sensitive tasters during intrauterine and early childhood growth and development might affect neurological maturation and thus make them more susceptible to epilepsy.
The region covered by the present study has been declared as goiter prone and consequently the sale of iodized salt is mandatory under law. In the iodized populations, the correlation between goiter and higher frequency of non-tasters has not been found to be significant but the direction of the correlation is reported to be positive.[21],[28] So, in the populations covered under iodization programmes, many less sensitive tasting and non-tasting children are expected to be normal. Moreover, interaction between genetic and environmental factors specific to the area and population may play a more crucial role in determining the susceptibility of the non-taster to epilepsy.
The above account rules out any simple relationship between the higher frequency of non-tasters and epilepsy. This inference is further strengthened by the evidence that epileptic seizures lower the scholastic abilities of the affected person. Pal[29] has shown that about two-thirds of the idiopathic and symptomatic patients show either poor scholastic, social and vocational adjustment or loss of memory. This may indirectly interfere with the ability of such persons to correctly perceive the exact threshold of the PTC solution. This is an alternative hypothesis which can be forwarded. But the present series of data run contrary to this hypothesis, because the incidence of non-tasters is about 35% in the epileptics, while lowered scholastic abilities were witnessed in about 66% of the epileptic patients. However, there is further need to extend the present study to explore these aspects. 

 » References Top

1.Hulse F. The Human Species. New York: Random House 1963.  Back to cited text no. 1    
2.Mourant AE, Kopec AC, Domaniewska-Sobczak K. Blood group and disease Oxford: Oxford University Press; 1978.  Back to cited text no. 2    
3.Singh KS, Bhalla V, Kaul V. The biological variations in Indian populations. Delhi: Oxford University Press 1994.  Back to cited text no. 3    
4.Suk V. Cabbage and goiter in carpathian Ruthenia: A contribution to ethnic pathology. Anthropologie 1931;9:1-6.  Back to cited text no. 4    
5.Mackenzie CG, Mackenzie JB. Effect of sulfonamides and thioureas on the thyroid gland and basal metabolism. Endocrinology 1943;32:185.  Back to cited text no. 5    
6.Riddel WJB, Wybar KC. Taste of thiouracil and phenylthiocarbamide. Nature 1944;154:669.  Back to cited text no. 6    
7.Harris H, Kalmus H. Genetical differences in taste sensitivity to phenylthiourea and to anti-thyroid substances. Nature 1949;163:878-9.  Back to cited text no. 7    
8.Van Etten CH. Goitrogens. In: Liener IE, (Ed). Toxic constituents of plant food stuffs. New York: Academic Press 1969:103-42.  Back to cited text no. 8    
9.Terry MC. Taste blindness and diabetes in the colored population of Jamaica. J Hered 1950;41:306-7.  Back to cited text no. 9    
10.Saldanha PH. Apparent pleiotropic effect of genes determining taste thresholds for phenylthiourea. Lancet 1956;271-4.  Back to cited text no. 10    
11.Manlapas FC, Stein AA, Pagliara AS, Apicelli AA, Porter IH, Patterson PR. Phenylthiocarbamide taste sensitivity in cystic fibrosis. J Pediatr 1965;66:8-11.  Back to cited text no. 11    
12.Kitchin FD, Howel-Envas W, Clarke CA, MC Connell RR, Sheppard PM. PTC taste response and thyroid disease. Brit Med J 1959;1:1069-74.  Back to cited text no. 12    
13.Facchini F, Abbati A, Campagnoni S. Possible relations between sensitivity to phenylthiocarbamide and goiter. Hum Biol 1990;62:545-52.  Back to cited text no. 13    
14.Sheppard TH, Gartler SM. Increased incidence of non-tasters of phenylthiocarbamide among congenital athyreotic cretins. Science 1960;131:929.  Back to cited text no. 14    
15.Fraser GR. Cretinism and taste sensitivity to phenylthiocarbamide. Lancet 1961;280:964-5.  Back to cited text no. 15    
16.Chung CS, Witkop CJ, Henry JL. A genetic study of dental caries with special reference to PTC taste sensitivity. Am J Hum Genet 1964;16:231-45.  Back to cited text no. 16    
17.Sharma K. Genetic epidemiology of epilepsy: A twin study. Neurology India 2004.  Back to cited text no. 17    
18.Commission on classification and terminology of the International League gainst epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;32:199-208.  Back to cited text no. 18    
19.Harris H, Kalmus H. The measurement of taste sensitivity to PTC. Ann Eugen 1949;15:24-31.  Back to cited text no. 19    
20.Woolf B. On Estimating the relation between blood groups and diseases. Ann Hum Genet 1955;19:251-3.  Back to cited text no. 20    
21.Greene LS. Physical growth and development, neurological maturation and behavioural functioning in two Ecuadorian Andean Communities in which goiter is endemic. II. PTC taste sensitivity and neurological maturation. Am J Phys Anthropol 1974;41:139-52.  Back to cited text no. 21    
22.Hollingsworth DR. Phenylthiourea taste testing in Hiroshima subjects with thyroid disease. J Clin Endocrinol 1963;23:961-3.  Back to cited text no. 22    
23.Brand N. Taste sensitivity and endemic goiter in Israel. Ann Hum Genet 1963;26:321-4.  Back to cited text no. 23    
24.Azevedo EH, Krieger H, Mi MP, Morton NE. PTC taste sensitivity and endemimc goiter in Brazil. Am J Hum Genet 1965;17:87-90.   Back to cited text no. 24    
25.De Luca F, Cramarossa L. Phenylthiourea and endemic goiter. Lancet 1965.  Back to cited text no. 25    
26.Mendez de Araujo HM, Salzano FM, Wolf H. New data on the association between PTC and thyroid disease. Human genetik 1972;15:136-44.  Back to cited text no. 26    
27.Kaplan AR, Fischer R., Glanville E. Powell, W. Kamionkowski M, Flesher B Differential taste sensitivities in duodenal and gastric ulcer patients gastroenterology 1964;47:604-9.  Back to cited text no. 27    
28.Delange F, Thilly C, Pourbaix P, Ermans ANN. Treatment of Idjwi islandendemic goiter by iodized oil. In: Stanbury B, (Ed). Endemic Goiter. Washington: Pan American Health Organization Scientific Publication No. 193, WHO; 1969:118-31.  Back to cited text no. 28    
29.Pal SK. Biomedical - Anthropological investigations on epileptics. Ph.D thesis (unpublished) Chandigarh: Panjab University 2002.  Back to cited text no. 29    

 

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