Root crops, in common with most plants, contain small amounts of potential toxins and antinutritional factors such as trypsin inhibitors. Apart from cassava, which contains cyanogenic glucosides, cultivated varieties of most edible tubers and roots do not contain any serious toxins. Wild species may contain lethal levels of toxic principles and must be correctly processed before consumption. These wild species are useful reserves in times of famine or food scarcity. Local people are aware of the potential risks in their use and have developed suilable techniques for detoxifying the roots before consumption.

Cassava toxicity
The main toxic principle which occurs in varying amounts in all parts of the cassava plant is a chemical compound called linamarin (Nartey, 1981). It often coexists with its methyl homologue called methyl-linamarin or lotaustralin. Linamarin is a cyanogenic glycoside which is converted to toxic hydrocyanic acid or prussic acid when it comes into contact with linamarase, an enzyme that is released when the cells of cassava roots are ruptured. Otherwise linamarin is a rather stable compound which is not changed by boiling the cassava. If it is absorbed from the gut to the blood as the intact glycoside it is probably excreted unchanged in the urine without causing any harm to the organism (Philbrick, 1977). However, ingested linamarin can liberate cyanide in the gut during digestion.
Hydrocyanic acid or HCN is a volatile compound. It evaporates rapidly in the air at temperatures over 28 C and dissolves readily in water. It may easily be lost during transport, storage and analysis of specimens. The normal range of cyanogen content of cassava tubers falls between 15 and 400 mg HCN/kg fresh weight (Coursey, 1973). The concentration varies greatly between varieties (Fig. 7.1) and also with environmental and cultural conditions. The concentration of the cyanogenic glycosides increases from the centre of the tuber outwards (Bruijn, 1973). Generally the cyanide content is substantially higher in the cassava peel. Bittemess is not necessarily a reliable indicator of cyanide content.
Traditional processing and cooking methods for cassava can, if efficiently carried out, reduce the cyanide content to non-toxic levels. An efficient processing method will release the enzyme linamarase by disintegrating the microstructure the cassava root. On bringing this enzyme into contact with linamarin the glucoside is converted into hydrogen cyanide. The liberated cyanide will dissolve in the water when fermentation is effected by prolonged soaking, and will evaporate when the fermented cassava is dried. Sun drying fresh cassava pieces for short periods is an inefficient detoxification process. Cyanide will not be completely liberated and the enzyme will be destroyed during drying. Sun drying processing techniques reduce only 60 to 70 percent of the total cyanide content in the first two months of preservation. Cyanide residues can be quite high in the dry tubers, from 30 to 100 mg/kg (Casadei, 1988). Simple boiling of fresh root pieces is not always reliable since the cyanide may be only partially liberated, and only part of the linamarin may be extracted in the cooking water. The reduction of cyanides depends on whether the product is placed in cold water (27°C) or directly into boiling water (100°C). After 30 minutes cooking, the remaining cyanides are, in the first case, 8 percent of the initial value, and in the second case about 30 percent (Easers, 1986).
Figure 7-1 - Effect of traditional processing of four varieties of cassava tuberous roots in the preparation of gari, on total and free cyanide content at each respective stage of processing
Various authors have suggested different minimal levels for toxicity. Rosling (1987) was of the opinion that an intake of over 20 mg per 100 g of cassava is toxic, while Bolhuis (1954) set the toxic level at an intake of 50 to 60 mg daily for a European adult.
Table 7.1 shows the HCN content of various processed cassava products. It indicates that a dramatic reduction in the hydrocyanic acid content of the raw cassava has occurred during processing. Soaking in water improves detoxification as cells are broken by osmosis and fermentation, which facilitates hydrolysis of the glycosides. Short soaking (four hours) is ineffective, but when longer periods are used (18 to 24 hours) cyanide levels can be reduced by 50 percent (Table 7.2). Squeezing the product is a fundamental step in the elimination of the soluble cyanides.
Pathophysiology of cyanide intoxication
Cyanide is detoxicated in the body by conversion to thiocyanate, a sulphurcontaining compound with goitrogenic properties. The conversion is catalysed by an enzyme thiosulphate cyanide sulphur transferase (rhodanase) present in most tissues in humans, and to a lesser extent by mercaptopyruvate cyanide sulphur transferase which is present in red blood cells (Fielder and Wood, 1956). The essential substrates for conversion of cyanide to thiocyanate are thiosulphate and 3-mercaptopyruvate, derived mainly from cysteine, cystine and methionine, the sulphur-containing aminoacids. Vitamin B12 in the form of hydroxycobalamin probably influences the conversion of cyanide to thiocyanate. Hydroxycobalamin has been reported to increase the urinary excretion of thiocyanate in experimental animals given small doses of cyanide (Wokes and Picard, 1955; Smith and Duckett, 1965). About 60 to 100 percent of the injected cyanide in toxic concentration is converted to thiocyanate within 20 hours and enzymatic conversion accounts for more than 80 percent of cyanide detoxification (Wood and Cooley, 1956). Thiocyanate is widely distributed throughout body fluids including saliva, in which it can readily be detected. In normal health, a dynamic equilibrium between cyanide and thiocyanate is maintained. A low protein diet, particularly one which is deficient in sulphurcontaining amino-acids may decrease the detoxification capacity and thus make a person more vulnerable to the toxic effect of cyanide (Oke 1969, 1973). Excessive consumption of cassava, as the sole source of dietary energy and main source of protein, could thus increase vulnerability to cyanide toxicity.
TABLE 7.1 - HCN content of various cassava products during processing Remaining HCN
Food item
Detoxification stage
Remaining HCN

Mean (mg/kg)
Fresh leaves

Washed leaves (cold waler)

Dried leaves

Boiled leaves (15 min in water)

Boiled leaves (30 min in water)

Boiled cassava

Fresh roots (sweet)

Boiled roots (20 min In water)
Fresh roots (sweet and bitter)

Soaked roots (3 days)

Dried roots (3 days)

Uncooked fufu (flour and water)

Cooked fufu
Fresh roots (sweet)

Uncooked fuku (heated)

Cooked fuku

24 h fermentation

48 h fermentation

48 h pressing


5 day soaking

5-day soaking + 48 h drying

5-day soaking + 96 h drying
Source: Bourdoux et al. 1982; Oke, 1984.
Diseases related to cassava toxicity
Several diseases have been associated with the toxic effects of cassava. Its causative role has been confirmed in the pathological condition of acute cyanide intoxication and in goitre. There is also some evidence linking two types of paralysis to the combined effects of a high cyanide and low sulphur intake, such as could result from a diet dominated by inefficiently processed cassava. In these two diseases, tropical atoxic neuropathy and epidemic spastic paraparesis, paralysis follows damage to the spinal cord. The role of cyanide toxicity in the causation of tropical diabetes, and in congenital malformation has not been established. Similarly its supposed beneficial effects on sickle cell anaemia, shistosomiasis and malignancies are still hypothetical.
Acute cyanide intoxication. Symptoms appear four to hours after after of raw or insufficiently processed cassava and consist of vertigo, vomiting, collapse and in some cases death within one or two hours. Treatment is quite effective and cheap. The principle is to increase the detoxicating capacity of the patient by giving an intravenous injection of thiosulphate and thereby making more sulphur available for conversion of cyanide to thiocyanate.
Endemic goitre. Cyanide taken in the diet is detoxified in the body, resulting in the production of thiocyanate. Thiocyanate has the same molecular size as iodine and interferes with iodine uptake by the thyroid gland (Bourdoux et al., 1978). Under conditions of high ingestion of inefficiently processed cassava, there may be a chronic cyanide overload leading to a high level of serum thiocyanate of 1 to 3 mg/100 ml, compared to a normal level of about 0.2 mg/100 ml. Under such conditions there is an increased excretion of iodine and a reduced iodine uptake by the thyroid gland, resulting in a low thiocyanate/iodine (SCN/I) excretion ratio. The value of the threshold level for this ratio seems to be three (Derange et al., 1983) after which endemic goitre appears. This phenomenon can occur only when the iodine intake is below about 100 mg per day. At SCN/I ratios of lower than two there is a risk of endemic cretinism, a condition characterized by severe mental retardation and severe neurologic abnormalities (Ermans et al., 1983).
Studies in Zaire have shown that the population of Ubangi, who consume a high amount of sun dried but unfermented cassava products, have a low SCN/I ratio of 2 to 4 and suffer from endemic goitre and cretinism. Whereas in Kim, where fermented and dried cassava paste is eaten, the SCN/I ratio goes up to three to five and there is a low incidence of goitre. In Bas Zaire, where properly processed cassava products are eaten, the SCN/I ratio is higher than seven and there is no goitre. A low ratio leads to abnormal levels of the thyroid stimulating hormone (TSH) and low thyroxine (T4). Ayangade et al., (1982) found that in pregnant women the thiocyanate level of the cord blood was proportional to the maternal serum thiocyanate level, indicating that thiocyanate can cross the placental barrier and affect the foetus. However, there is very little thiocyanate in breast milk indicating that the mammary gland does not concentrate thiocyanate and so breast-fed infants are not affected.
When iodine supplements are given, for example, by adding potassium iodide to local supplies of salt, goitre is reduced in spite of a continued high intake of cassava products. Where salt intake is small or variable, iodized oil, given by mouth, provides protection for one to two years. In the Amazon jungle some tribal people eat as much as one kg of cooked fresh cassava per person per day and consume up to three litres of fermented cassava beer, but there have been no reported eases of either goitre or ataxic neuropathy. These tribes also consume a considerable amount of animal and fish protein and thus have high levels of sulphur-amino acids and iodine in their diet.
Neurological disorders
Cyanide intake from a cassava-dominated diet has been proposed as a contributing factor in two forms of nutritional neuropathies, tropical ataxic neuropathy in Nigeria (Osuntokun, 1981) and epidemic spastic paraparesis (Cliff et al., 1984). These disorders are also found in some cassava growingareas of Tanzania and Zaire.
Tropical ataxic neuropathy. This disease is common in a particular area in Nigeria where a lot of cassava is consumed without the addition of sufficient protein-rich supplementary foods to provide an adequate supply of sulphur amino-acids for the detoxification of ingested cyanide. The consumed cassava product, called purupuru, is processed by an insufficient fermentation of the cassava, which leaves a residual cyanide content of up to 0.10 M mole/g. As much as two kg of this foodstuff is consumed daily, leading to the ingestion of about 50 mg of cyanide. The toxic level for an adult is about 60 ma. The clinical picture is dominated by damage to one of the sensory tracts in the spinal cord resulting in an uncoordinated gait called ataxia.
When patients are brought to the hospital they have a high plasma thiocyanate level. On admission they are put on a hospital diet which is highly nutritious and includes cassava only twice a week. Within a short period the plasma thiocyanate level returns to normal, and the patients recover. However, on discharge, they go back to their original diet of cassava and so the condition reappears (Osuntokun, 1968).
All the cases reported came from the area where cassava is cultivated and eaten in large quantities, with no cases in the nearby areas where yam predominates. A change in the diet of the population at risk in Nigeria has reduced the incidence of this disease.
Epidemic spastic paraparesis. This is a situation of depending on very toxic varieties of cassava as a food security crop (Cliff et al., 1984). In parts of Mozambique a bitter toxic type of cassava is often planted as a food reserve because of its high yield. As cassava constitutes about 80 percent of the basic diet, there is nominally a standard method of preparation which makes the cassava safe for consumption. Cassava, containing about 327 mg HCN/ kg, is peeled, sliced and sun dried for about three weeks after which the cyanide level is reduced to about 95 mg/kg. It is then pounded to a flour which is mixed with hot water to make a paste called chima. This paste is normally eaten with a relish of beans, fish or vegetables, to provide a well balanced meal.
During a prolonged period of drought all the food crops in this area were lost except the toxic variety of cassava. The foodstores were depleted and many families had no alternative, but to resort to the toxic cassava. Normal processing time was reduced because of the emergency and so there was no proper detoxification. The people knew this but they had no other choice of action except to die of starvation. On eating the underprocessed chima without their usual protein-rich supplement they complained that it was more bitter than normal. After about four to six hours they suffered from nausea, vertigo and confusion. Sufferers showed a high serum thiocyanate level and a urinary thiocyanate excretion of about ten times that of non-cassava-eating groups in Mozambique. There followed a sudden appearance of many cases of spastic paraparesis, indicating an extensive epidemic. This disease affects mainly women and children. It damages the nerve tract in the spinal cord that transmits signals for movement, thus causing a spastic paralysis of both legs (Rolling, 1983). Outbreaks have been reported during the dry season from two areas in Zaire (Nkamany and Kayinge, 1982) and during droughts in one area in Mozambique (Cliff et al., 1984) and one area in Tanzania (Howlett, 1985).
During these drought periods about 500 g of dried cassava, or 1.5 kg on a fresh weight basis, is consumed daily, representing an intake of 1 500 kcal and 50 mg cyanide per day. This level approaches the toxic level of 60 ma. The body can safely detoxify about 20 mg cyanide per day but when this level increases to 30 mg symptoms of acute intoxication develop in many consumers and hence the epidemics. If there is a period during which a high cassava intake and a low protein-rich food intake, to supply sulphur amino-acids for detoxification, coincide, this combination precipitates the outbreak of this disease. The situation may be compared to the epidemics of lathyrism that occured in drought-affected areas of India owing to the high-level intake of the drought-resistant pea, Lathyrus saliva.
Production of low-cyanide foods
The development of a more sensitive method for cyanide determination in foods by Cooke (1978a) and an in-depth study of some traditional cassava foods have led to a better understanding of the detoxification mechanism of cyanide in foods and to improved recommendations for processing cassava.
Cyanide occurs in cassava and cassava products in two forms, the glucosidic form, which is the linamarin itself, and the non-glucosidic or bound form which is cyanohydrin. Under normal conditions of hydrolysis, when the enzyme linamarase reacts with linamarin, it is hydrolysed to cyanohydrin which, on decomposition, gives acetone and hydrocyanic acid. However, under acid conditions, of pH4 or less, which tend to occur in some lactic acid fermentations of cassava, the cyanohydrin decomposition is hindered and it becomes stable. It is relatively easy to get rid of free cyanide, which is present at about 10 percent in both peeled and fresh cassava, especially in solution, but the non-glucosidic cyanide may hydrolyse very slowly and result in a lot of residual cyanide in cassava products. Thus drying cassava chips in an air oven at 47° and 60°C causes a decrease in the bound cyanide content of 25 to 30 percent, whereas faster drying at 80°C or 100°C gave only a 10 to 15 percent decrease of the bound cyanide. However, losses of free cyanide were 80 to 85 percent and 95 percent respectively (Cooke and Maduagwu, 1978b). Drying results in an apparent increase in cyanide concentration because of loss of water (Bourdoux et al., 1982). The longer the drying the higher the amount of water removed. About 14 percent of the water can be removed during the first day, reaching a level of up to 70 percent after eight days. This leads to an increase in cyanide concentration from 70 mg/kg on the first day to 91 mg/kg after eight days.
Soaking in water at 30°C, boiling or cooking removes free cyanide but only about 55 percent of the bound cyanide is released after 25 minutes. However, the bound cyanide is removed by prolonged soaking as fermentation begins (Table 7.2) through the action of the enzyme linamarase which is released by disruption of the tuberous tissues. If water is added at this stage most of the cyanide is removed. Meuser and Smolnik (1980) were able to improve the production of gari by washing the mash after fermentation to remove the residual bound cyanide which was still present as cyanohydrin because of its higher stability at the lower pH.
The result of different drying techniques is shown in Table 7.3. Freeze drying or rash-drying eliminated only the free cyanide, which accounted for about 50 percent of the total cyanide present. Roller-drying of the fresh pulp at a pH of 5.5 to 5.7 removed virtually all the cyanide, whereas if the fermented pulp was dried on rollers or on drums high amounts of cyanide were retained in the dried product because of the acid condition (pH 3.8) of the fermented pulp. In the detoxification of cassava products fermentation is most effective when accompanied by squeezing and washing of the acidic pulp. Residual cyanide can be reduced further by sun drying or frying. This had been confirmed by Hahn (1983) as shown in Fig. 7.1. In traditional preparations of various food products from cassava, there may be some residual cyanide because of insufficient tissue disintegration during processing and insufficient washing. It is the residual cyanide that is responsible for toxicity. Some of these preparations have been simulated in the laboratory and modified to give much lower cyanide levels (Bourdoux et al., 1983).
TABLE 7.2 - Effects of soaking on the HCN content of six bitter cassava roots
Soaking period (days)
Remaining HCN (percentage)
Source: Bourdoux et al., 1983
Sweet potato
Sweet potato contains raffinose, one of the sugars responsible for flatulence. Three of the sugars which occur in plant tissues, raffinose, stachyose and verbascose are not digested in the upper digestive tract, and so are fermented by colon bacteria to yield the flatus gases, hydrogen and carbon dioxide. The level of raffinose present depends on the cultivar. In some parts of Africa the cultivars used are considered too sweet and cause flatulence (Palmer, 1982), Lin et al. (1985) have established that sweet potato shows trypsin inhibitor activity (TIA) ranging from 90 percent inhibition in some varieties to 20 percent in others. There is a significant correlation between the trypsin inhibitor content and the protein content of the sweet potato variety. Heating to 90°C for several minutes inactivates trypsin inhibitors. Lawrence and Walker (1976) have implicated TIA in sweet potato as a contributory factor in the disease enteritis necroticans. This seems doubtful since sweet potato is not usually eaten raw and the activity of the trypsin inhibitor present is destroyed by heat.
In response to injury, or exposure to infectious agents, in reaction to physiological stimulation or on exposure of wounded tissue to fungal contamination, sweet potato will produce certain metabolites. Some of these compounds, especially the furano-terpenoids are known to be toxic (Uritani, 1967). Fungal contamination of sweet potato tubers by Ceratocystis fimbriata and several Fusarium species leads to the production of ipomeamarone, a hepatoxin, while other metabolites like 4-ipomeanol are pulmonary toxins. Baking destroys only 40 percent of these toxins. Catalano et al. (1977) reported that peeling blemished or diseased sweet potatoes from 3 to 10 mm beyond the infested area is sufficient to remove most of the toxin.
TABLE 7.3 - Effect of drying on HCN consent of cassava
Drying process

HCN (ppm)
Freeze drying
Flash drying
Air drying 40°C
Chips. pulp
Heated air drying 180°C

Fermented pulp
Drum drying

Fermented pulp
HCN of pulp
free and bound
Source: Meuser & Smolnik, 1980.
Potato contains the glycoalkaloids alpha-solanine and alpha-chaconine (Maya, 1980), concentrated mainly in the flowers and sprouts (200 to 500 mg/100 g). In healthy potato tubers the concentration of the glycoalkaloids is usually less than 10 mg/100 g and this can normally be reduced by peeling (Wood and Young, 1974; Bushway et al., 1983). In bitter varieties the alkaloid concentration can go up to 80 mg/100 g in the tuber as a whole and up to 150220 mg/100 g in the peel. The presence of these glycoalkaloids is not perceptible to the taste buds until they reach a concentration of 20 ma/100 g when they taste bitter. At higher concentrations they cause a burning and persistent irritation similar to hot pepper. At these concentrations solanine and other potato glycoalkaloids are toxic. They are not destroyed during normal cooking because the decomposition temperature of solanine is about 243 C.
Levels of glycoalkaloids may build up in potatoes which are exposed to bright light for long periods. They may also result from wounding during harvest or during post-harvest handling and storage, especially at temperatures below 10°C (Jadhav and Salunkhe, 1975). Glycoalkaloids are inhibitors of choline esterase and cause haemorrhagic damage to the gastrointestinal tract as well as to the retina (Ahmed, 1982). Solanine poisoning has been known to cause severe illness but it is rarely fatal (Jadhav and Salunkhe, 1975).
Potato also contains proteinase inhibitors which act as an effective defense against insects and micro-organisms but are no problem to humans because they are destroyed by heat. Lectins or haemogglutenins are also present in potato. These toxins are capable of agglutinating the erythocytes of several mammalian species including humans (Goldstein and Hayes, 1978), but this is of minimal nutritional significance as haemogglutenins are also destroyed by heat, and potatoes are normally cooked before they are eaten.
The high content of calcium oxalate crystals, about 780 mg per 100 g in some species of cocoyam, Colocasia and Xanthosoma, has been implicated in the acridity or irritation caused by cocoyam. Oxalate also tends to precipitate calcium and makes it unavailable for use by the body. Oke (1967) has given an extensive review of the role of oxalate in nutrition including the possibility of oxalaurea and kidney stones. The acridity of high oxalate cultivars of cocoyam can be reduced by peeling, grating, soaking and fermenting during processing.
Acridity can also be caused by proteolytic enzymes as in snake venoms. Attempts have been made to isolate such enzymes from taro, Colocasia esculenta, and the principal component has been called "taroin" by Pena et al. (1984).
Banana and plantain
Banana and plantain do not contain significant levels of any toxic principles. They do contain high levels of serotonin, dopamine and other biogenic amines. Dopamine is responsible for the enzymic browning of sliced banana. Serotonin intake at high levels from plantain has been implicated in the aetiology of endomyocardial fibrosis (EMF) (Foy and Parratt, 1960). However, Ojo (1969) has shown that serotonine is rapidly removed from the circulating plasma and so does not contribute to elevated levels of biogenic amines in healthy Nigerians. It has been confirmed by Shaper (1967) that there is insufficient evidence for regarding its level in plantain as a factor in the aetiology of EMF.
The edible, mature, cultivated yam does not contain any toxic principles. However, bitter principles tend to accumulate in immature tuber tissues of Dioscorea rotundata and D. cayenensis. They may be polyphenols or tanninlike compounds (Coursey, 1983). Wild forms of D. dumetorum do contain bitter principles, and hence are referred to as bitter yam. Bitter yams are not normally eaten except at times of food scarcity. They are usually detoxified by soaking in a vessel of salt water, in cold or hot fresh water or in a stream. The bitter principle has been identified as the alkaloid dihydrodioscorine, while that of the Malayan species, D. hispida, is dioscorine (Bevan and Hirst, 1958). These are water soluble alkaloids which, on ingestion, produce severe and distressing symptoms (Coursey, 1967). Severe cases of alkaloid intoxication may prove fatal. There is no report of alkaloids in cultivated varieties of D. dumetorum.
Dioscorea bulbifera is called the aerial or potato yam and is believed to have originated in an Indo-Malayan centre. In Asia detoxification methods, involving water extraction, fermentation and roasting of the grated tuber are used for bitter cultivars of this yam. The bitter principles of D. bulbifera include a 3furanoside norditerpene called diosbulbin. These substances are toxic, causing paralysis. Extracts are sometimes used in fishing to immobolize the fish and thus facilitate capture. Toxicity may also be due to saponins in the extract. Zulus use this yam as bait for monkeys and hunters in Malaysia use it to poison tigers. In Indonesia an extract of D. bulbifera is used in the preparation of arrow poison (Coursey, 1967).
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