Ackee toxicity is associated with consumption of the fruit of the tree
Blighia sapida. The problem is endemic in Jamaica, and a number of ca
ses have been reported in the U.S. among Jamaican immigrants. Illness
is associated with the method of preparation of the fruit and its ripe
ness. Malnourished individuals and children appear to be the most susc
eptible. Levels of the toxic compound, hypoglycin, which are found in
the arils and seeds of the fruit, significantly decrease in the arils
with ripeness (from 1000 ppm to <0.1 ppm). Symptoms of ackee poisoning
in humans occur 6 to 48 hours after ingestion and include vomiting, m
uscular and mental exhaustion, hypoglycemia, coma and death. Intraveno
us glucose relieves the hypoglycemia. The most likely mechanism of act
ion occurs through the incorporation of hypoglycin into fatty acid met
abolic pathways. Hypoglycin or its primary metabolite methylenecyclopr
opylacetyl-CoA inhibits the oxidation of fatty acids and leucine and t
he activity of acyl-CoA dehydrogenases. The dose required to elicit ac
ute responses is not known with any precision, nor is it possible to e
liminate the likelihood of adverse effects with long-term ingestion of
the toxin. Ingestion of unripe aril or pod and seeds represents a sig
nificant health hazard; this hazard diminishes considerably with the c
onsumption of properly processed or prepared ripe fruit.