Intensive breeding efforts to produce low tryptamine strains of Phalaris arundinacea were undertaken, in the US, ostensibly to decrease animal fatalities, in spite of the following demonstrable facts:
1. Highest numbers of animal deaths occur during the times when the tryptamine content was proven to be lowest (by
separate workers in Australia and US),
2. "Low alkaloid' strains of Phalaris aquatica are found to produce higher numbers of dead livestock than "high alkaloid' strains when compared directly,
3. Phalaris arundinacea has NEVER caused any occurrence of staggers in the US: and only two incidences worldwide
(Simpson et al. 1969 & Ulvund 1985] despite it clearly being on record as deliberately cultivated & utilized for forage for over 200 years.
Many workers appeared to operate as if the causative link between 5-MeO-DMT and Phalaris staggers was already
proven (almost as soon as the presence of dimethylated tryptamines was first reported). The known ability of DMT and 5-MeO-DMT to produce a green pigmentation in vitro using enzyme preparations of cells has caused a similar green pigmentation found in animals which died from chronic Phalaris staggers to become both regarded as diagnostic evidence and proof that such methylated tryptamines are the causative agents despite Gallagher's utter and complete failure to observe this pigmentation in any animals afflicted with acute or peracute staggers (This was true whether the
animals recovered or died).
It must be remembered that Gallagher was only able to mimic some of the acute stagger symptoms with the N-dimethylated tryptamines and was entirely unable to reproduce either the chronic effects or degenerative neurological changes like lesions.
I might also mention tha bufotenine was reported by Gallagher to be more active than DMT and produces a brown pigmentation (as does serotonin) under similar in vitro conditions. (Using bufotenine bioxalate. Gessner et al. 1960 reported that deaths of rodents given intraperitoneal administrations of 6 divided doses, of what WOULD have been a lethal dose of given all at once, were delayed by around a week with an apparent return to normalcy after the acute effects wore off.
They could not find anything unusual except for "acute thoracic kyphosis accompanied by a cervical hyperextension ofthe
spine" as well as dehydration and loss of around 1/3 of the totalbody weight. (4 out of 5 rats died this way) The length of time suggests it might be worth looking into some sort of secondary problem resulting from the mechanical aspects of the interperitoneal injection itself in terms of actual site of delivery or infection potential? I have witnessed this performed on rats a good number of times. A quick jab somewhere into the belly is about all the care in target selection that is usually given. It might be added that said rats are not totally compliant in this matter as evidenced by their struggling and screams.
Work by Gallagher is claimed to have established lethality using oral administration of pure compounds, but it must be stressed that at no point in Gallagher's work is it actually stated that any death or deaths were produced by oral administration although he docs claim effects began in 6 minutes via this route. [As opposed to the 6- 12-(72) hours known to be required for onset of symptoms, and up to months before death, after grazing. <Recovery from the effects of administered 5-MeO-DMT is complete within an hour.]
Interestingly, Gallagher also states that bufotenine readily crosses the blood brain barrier. Clearly something needs closer scrutiny.
One idea commonly tossed around is that the presence of B- carbolines orally activate DMT/5-MeO-DMT. While logical, this property is entirely unevaluated for any of the B-carbolines reported from Phalaris. Directly toxic effects are suspected from I or 2 of the quaternary B-carbolines.
The action of the quaternary N-methylated tryptamines that are known to sometimes represent up to 5% of the alkaloids
present in P. aquatica (under poorly defined circumstances must also be considered due to their potential for cyclization. IF the B-carbolines turn out to possess MAOI properties, their interaction with many other compounds present MUST also be considered.
Other alkaloids known to also be (at least sometimes) present in Phalaris: 3-methylindole (known to produce Bovine Pul-
monaty Emphysema in cattle), indoleacetic acid, 5-methoxy-indoleacetic acid, tryptophan, 5-methoxy-tryptophan, (the preceding 4 can be readily converted to 3-methylindole by the gut flora of cattle but not by sheep or goats), gramine, substituted gramine derivatives and hordenine.
Hordenine and gramine are both known to produce toxic effects in livestock and the combination of hordenine with a
MAOI would be more likely to precipitate a hypertensive crisis, than combining tryptamines with MAO inhibitors. (Also
more likely than if combining mescaline with an MAOI].
Another llictor to consider is the known anticholinesterase activity of bufotenine and several of the Phalaris B-carbolines ( see Ghosal et al. 1977.)
The potential presence of lysergic acid type fungal products, from not only grass ergotisms but also fungal endophytes of common pasturage components, would also contribute to toxicity, especially if combined with an MAOI. Combine this gut-full of chemicals with yet other compounds found in the mixed pasturage Phalaris invariably occurs in - Agrostis, Bromus, Carex, Cyperus, Fescue, Scirpus, Sorghum. Tribulus, Ryegrasses etc.. - all of which have been incredibly dismissed as trivial; yet, all are known to produce alkaloids toxic to livestock; most inducing stagger effects on their own], add the potential metabolites produced by gut flora, and there rapidly appears to be many potential sources of toxicity and contributing factors possibly involved with Phalaris; all of which, for the largest part, have been
entirely disregarded in the peculiar quest to blame dimethylated tryptamines.
My best guess is a complex of drug interactions may be involved; hordenine, lysergic acid derivatives, B-carbolines & mixed indoles are hardly a recommended combination.
Incredibly, perhaps due to the politics involved, we still do not fully understand this economically important disorder despite over 3 decades of work and a hell of a lot of money thrown at it attempting to address the tryptamine "problem".
Amazingly, Gallagher went on to further conclude that exposure to DMT/5-MeO-DMT produced a situation where later stimulation by dogs would induce death due to a sensitization to adrenaline somehow caused by prior exposure to the tryptamines.
Another not so insignificant point is that Phalaris staggers are known to be produced by strains that do not contain appreciable amounts of the N-dimethylated tryptamines, containing instead ~-carbolines and gramine and/or hordenine.
Other workers have put considerable effon into linkg decreased palatability with the tryptamines claiming the decrease in palatability was evidence of toxicity; the assumption that sheep would supposedly prefer to eat nontoxic plants.
If sheep were truly this discriminating, it would seem that tPhalaris staggers and a host of other livestock poisonings would be less of a problem. [I must note that, like hordenine and gramine, 5-MeO-DMT is a proven feeding deterrent. Due to their TASTE.]
The majority of the evidence is strongly against the chronic form of Phalaris staggers syndrome being a product of tryptamine ingestion but few seem to care for discovering the truth; politics rule.
See Festi & Samorini and/or Shulgin & Shulgin 1997 for alternate scenarios that are AT LEAST as plausible,if not far better supported.
More recent work strongly suggests that one or more, up to several novel furanobisindoles may be involved in the toxicity. Several have been characterized.
See the recent published accounts by N. Anderton, C.A. Bourke, S.M. Colegate and R. Oram for more
details concerning their research
