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Medically reviewed on Apr 16, 2018

Scientific Name(s):Various species of Lathyrus , most commonly L. sativus L. (chickling vetch or chick-pea), L. odoratus L. (sweet pea), L. cicera L. (flat-podded vetch), L. hirsutus L. (caley pea), L. sylvestris L. (everlasting pea), L. clymenum (spanish vetchling), L. incanus (Smith and Rydb.) Rydb. (wild pea) and L. pusillus Elliott (singletary pea). Family: Fabaceae (beans) 1 , 2

Common Name(s): Chickling vetch , chick-pea , sweet pea , flat-podded vetch , caley pea , everlasting pea , spanish vetchling , wild pea , singletary pea and others, depending on species


Some Lathryus species are eaten.


There is no clinical evidence to support specific dosage recommendations for Lathryus .


Contraindications have not yet been identified.


Documented adverse effects. Avoid use.


None well documented.

Adverse Reactions

Research reveals little or no information regarding adverse reactions with the use of this product.


Some species are neurotoxic.


Lathyrus is a widespread genus with species that grow throughout the world.


The Lathyrus species are generally cultivated for food, fodder, and as ornamentals. For example, flowers of the sweet pea, L. odoratus (not to be confused with the common garden pea, Pisum spp.), are cultivated for their color and fragrance. The seeds of Lathyrus species are commonly eaten by large populations in India, parts of Africa, France, Italy, Spain, and other countries. 1 L. sativus is used to prepare unleavened Indian bread and is sometimes eaten raw as pasteballs or cooked. 1 However, ingestion of certain species, particularly L. sativus , L. cicera , and L. clymenum , can result in a toxic syndrome known as neurolathyrism. This disease has been recognized for more than a century in Europe, Africa and Asia; most commonly in Asia. Because of the potential for public health problems, the sale of L. sativus has been banned in many states in India; despite these efforts, distribution persists. 1 Lathyrism remains a common problem among grazing animals in some countries.


A variety of compounds with potential neurotoxic effects have been identified and are discussed below. Other compounds isolated from seeds of the Lathyrus species include phytates, divicine, and a mixture of alkaloids. The lack of vitamins A, B, and C from these seeds may enhance the neurotoxic potential. 1

Uses and Pharmacology

Lathyrism appears to be the result of toxicity caused by several compounds, including beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (ODAP) and beta-aminopropionitrile (BAPN).

ODAP is a neurotoxin that is associated with the animal and human neurotoxic manifestations of the disease neurolathyrism. BAPN induces skeletal abnormalities in animals; this compound and related compounds appear to be responsible for osteolathyrism (damage to the skeleton), which has not been observed in man. BAPN induces osteolathyrism and angiolathyrism (damage to the blood vessels) without inducing neurotoxic effects. 3 L. odoratus is more commonly associated with osteolathyrism than other species 1 and a separate term, odoratism, has been proposed for this syndrome.


There is no clinical evidence to support specific dosage recommendations for Lathryus .


Documented adverse effects. Avoid use. 4


None well documented.

Adverse Reactions

Research reveals little or no information regarding adverse reactions with the use of this product.


Osteolathyrism, evidenced by skeletal deformities and aortic rupture, has been induced in rats given a 50% diet of sweet peas or diets containing 0.1% to 0.2% BAPN. 1 The toxicity appears to be related to structural defects in collagen induced by the Lathyrus toxins.

Neurolathyrism occurs in many animal species, but some (eg, the squirrel monkey) appear to be particularly resistant to the toxic effects of Lathyrus . 5 Human neurolathyrism remains a significant public health problem in India, particularly among the poor for whom L. sativus forms the main part of the diet. The disease generally occurs when a diet consisting of one-third to one-half L. sativus seeds in consumed for 3 to 6 months. Muscular rigidity and spasticity, weakness, paralysis of leg muscles, weak pulse, shallow breathing, convulsions, or death may occur. 1 , 6 , 7 Prolonged neurotoxicity lasting more than 40 years, characterized by poor central motor coordination and reduced nerve conduction in the lower limbs, has been observed in persons suffering from the effects of neurolathyrism. 8

There does not appear to be a common mechanism for the mode of action of the neurolathyrogens. Some propose that these compounds may affect glutamine concentrations or activity in the central nervous system. 1

Pyramidal tract involvement has been observed in primates fed beta-N-oxalylamino-L-alanine (BOAA), a potent neuroexcitatory amino acid found in chickling peas and an inhibitor of glutamate. 9 Others have proposed that the neurotoxin may function as a zinc carrier and that cerebral zinc deficiency may play a role in the disease. 10

Several procedures have been used in an attempt to deactivate the toxin prior to ingestion. Typically, these involve soaking seeds in water, followed by steaming or sun drying. Roasting the seeds at high temperatures for 20 minutes also seems to help destroy the neurotoxic factors. These procedures, however, only destroy 80% to 85% of the toxin. 1

Preliminary findings suggest that treatment with the centrally acting muscle relaxant tolperisone can significantly reduce the spasticity in neurolathyrism. 11


1. Liener IE, ed. Toxic Constituents of Plant Foodstuffs , 2nd ed. New York: Academic Press; 1980.
2. Lewis WH, Elvin-Lewis MPF. Medical Botany: Plants affecting man's health . New York: John Wiley & Sons, 1977.
3. Spencer PS, Schaumburg HH. Lathyrism: a neurotoxic disease. Neurobehav Toxicol Teratol . 1983;5:625.
4. Wickersham RM, Novak KK, managing eds. Drug Facts and Comparisons . St. Louis, MO: Wolters Kluwer Heath, Inc.; 2003.
5. Mehta T, et al. The Lathyrus sativus neurotoxin: resistance of the squirrel monkey to prolonged oral high doses. Toxicol Appl Pharmacol . 1983;69:480.
6. Hardin JW, Arena JM. Human Poisoning from Native and Cultivated Plants . 2nd ed. Durham, NC: Duke University Press; 1974.
7. Misra UK, Pandey CM. H reflex studies in neurolatyrism. Electroencephalogr Clin Neurophysiol . 1994;93:281.
8. Hugon J, et al. Studies of the etiology and pathogenesis of motor neuron disease. III. Magnetic cortical stimulation in patients with lathyrism. Acta Neurol Scand . 1993;88:412.
9. Spencer PS, et al. Lathyrism: evidence for role of the neuroexcitatory aminoacid BOAA. Lancet . 1986;2:1066.
10. Lambein F, et al. From soil to brain: zinc deficiency increases the neurotoxicity of Lathyrus sativus and may affect the susceptibility for the motorneurone disease neurolathyrism. Toxicon . 1994;32:461.
11. Haque A, et al. New findings and symptomatic treatment for neurolathyrism, a motor neuron disease occurring in north west Bangladesh. Paraplegia . 1994;32:193.

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