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Poverty and malnutrition
The cause of the disease has been attributed to poverty and malnutrition in combination with the presence of the neurotoxin (184.108.40.206 14:46, 8 July 2007)
Yes, poverty and malnutrition are two major etiological factors associated with lathyrism. But as it is written now it can be thought that ingestion of the neurotoxin alone is not sufficient to cause the poisoning, as according to the present wording in addition to eating the toxic beans one would also need to be poor and malnourished to get the disease. However, all of the symptoms can be artificially reproduced in the laboratory by feeding the purified toxin to otherwise well fed animals. In fact, ignorance is certainly the main cause of the poisoning, as not knowing the involved legumes to be toxic may justify their ingestion, wheter by rich and well nourished individuals or not.
Sophos II 08:41, 9 July 2007 (UTC)
Hi Sophos II
Food for thought.
Ingestion of the neurotoxin alone does not seem to produce the disease. While some laboratory studies have demonstrated neurological effects of the toxin; the neurodegenerative effects leading to permanent crippling, have not been successfully produced under experimental conditions.
Every day millions of people eat grasspea and hence ingest significant amounts of the toxin with no apparent ill effects.
Overconsumption of grasspea leads to the disease. I think the current estimate for overconsumption is 50% of the diet for a period of at least 4 weeks.
The argument, let's call it a hypothesis, is precisely that well nourished individuals won't get poisoned by grasspea, a) because they eat sufficient other foods and b) these foods have a protective effect.
Ref Getahun,H,Lambien F,Vanhoome M,Van Der Stuyft P(2003).Food-aid cereals to reduce neurolathyrism related to grass-pea preparations during famine.The Lancet,vol 362,Nov 2003,pp 1808-1810.Full text available free online at:http://www.thelancet.com/journal/vol362/iss9398/
Dirk.Enneking 08:11, 29 September 2007 (UTC)
- Hi Dirk,
- If oxalyldiaminopropionate (ODAP) was not toxic, as you suggest, it would not be called a toxin.
- If ODAP would not interfere with the glutamate-mediated neurotransmission, it would also not be called a neurotoxin.
- There is a vast amount of litterature showing evidence that ODAP is produced by plants of the genus Lathyrus, that ODAP is present in the seeds of these plants, and that ODAP it is the main cause of the (maybe occasional) symptoms of lathyrism, an illness by definition only suffered by those who have been ingesting beans from these plants. I estimate that it is not necessary to show proof of this but if absolutely required, this could easily be sorted out.
- Now of course, that doesn't mean that nothing can be done to make these beans less toxic. In fact there are many other foods that can be toxic or even lethal if they are not prepared correctly or if they are ingested in wrong quantities or in a wrong combination: coprinus, fugu and cassava are just three examples that just come to my mind...
- Sophos II 22:57, 21 October 2007 (UTC)
No mention of treatment or even if the damage is permanent. This is a severe lack. Halfelven 20:04, 9 November 2007 (UTC)
Dr Enneking, I have noticed that too much importance is given to effects of ODAP on glutamate receptors.But the most significant effect of ODAP is its inhibition of Tyrosine amino transferase and is not referred to by most researchers. Why ?. In fact this inhibition explains several features of ODAP toxicity to experimental animals SLN Rao —Preceding unsigned comment added by Slnrao213 (talk • contribs) 16:16, 5 December 2007 (UTC)