This is quote from Keeper Trout's "Ayahuasca: Alkaloids, Plants, Analogs" which is available as a free PDF on erowid.
I laughed when he calls previous research a "scientific circus", because it really is.
"Fungal products such as the ergot type alkaloids that are known from some fungal endophytes in grasses and sedges, as were mentioned in passing above, not only have threat of inherent toxicity but similarly have the potential for synergistic toxicity and adverse reactions if combined with MAOI's.
Other compounds like ring substituted gramines [Note 11], or the unsubstituted and/or ring-methoxylated tryptophols, indole acetic acids, tryptophans, and also a variety of β-carbolines (some of them quaternary), are all known from Phalaris strains. All are known to be toxic, or at least potentially toxic, to certain livestock even in the absence of MAO inhibitors.
Another potentially toxic factor that appears to have seen neither consideration nor toxicological evaluation is the reported, but apparently intermittent, presence of the N-methyl cations of DMT and 5-MeO-DMT [Note 12]. The first of these has been noted to comprise up to 5% of the total alkaloid content [By Frahn & Illman 1973] during those periods of active growth when they are produced. Neither the parameters surrounding their production nor their levels over the course of the seasons have been adequately elucidated. If these compounds entered into nervous system tissue and cyclized, it would not be surprising if any quaternary β-carbolines that resulted showed neurotoxic results, delayed onset and serious lasting toxicity. Both should be evaluated for their potential for green pigment formation. If they do, it would be surprising if it was not "at least closely related" structurally to pigmentation from 5-MeO-DMT or DMT. While lacking evaluation, these compounds cannot be dismissed without further study.
The contribution of Bromus, Cyperus, Scirpus, Fescue, Paspalum, Sorghum halepense, Tribulus, clovers and the many other possible components of pasturage similarly cannot be dismissed [Note 13].
While much of this is conjecture, it is amazing that this issue stands in need of clarification and resolution despite the fact that so many have apparently come to consider the issue cut and dried in what sometimes seems to be a fairly politicized scientific circus.
This is not an argument for any particular conclusion in this matter other than the obvious one that the issue is not yet closed and desperately needs objective investigation, despite how politically motivated people {Note 14] have presented and/or manipulated the data.
Many studies were undertaken which attempted to negatively correlate tryptamines' toxicity with palatability based on the premise that lowest palatability indicated the greatest toxicity [Note 15] despite the fact they were working with P. arundinacea and all deaths were occurring on P. tuberosa [Note 16]
Purporting to address the `tryptamine problem' 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 that is has been deliberately cultivated & utilized for forage for over 200 years. According to Marten & Heath 1973, successful reports of its use far out weigh any negative reports. It is widely and successfully used for forage, hay and silage. Its primary weakness appears to be its highly variable palatability.]
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)
When the correlation between tryptamines and staggers began to be questioned, and the lack of staggers occurrence in P. arundinacea noted, the reasons cited for the importance of such programs shifted to focus on addressing diarrhea in lambs, or watery eyes/ rough coats in cattle, and decreased weight gains in both, rather than stagger production, but never failed to mention staggers; stressing the `toxic' nature of the tryptamines and, in most cases, presented the tryptamine/ staggers connection as an already proven fact.
This is so pervasive that in Southon & Buckingham's 2 volume 1989 Dictionary of Alkaloids., under the entry for 5-MeO-DMT (as the methyl ether of bufotenine, O-Methylbufotenine), they flatly assert "Toxic agent causing staggers-like poisoning of sheep in Australia."
Do I really have to say who they cite as their reference?
This should not be a political issue; it is a very serious one both of economics and livestock toxicity. If these are not the areas which are effectively addressed in research, a great disservice is being done to the livestock producers who are depending on agricultural science not only to define the problem but to provide potential solutions.
The ability to reproduce many, but not all, symptoms of one manifestation of the syndrome and absolutely none of the other can hardly be considered to be a successful causal determination. `Almost' is usually considered the same as a miss in science, or a sign that more work needs to be done before making any conclusions. At the very least it would seem sensible that people first attempted to identify exactly what is in the grasses at the time of peak illness/fatalities and then attempt a toxicological assessment with each and all of the isolated components not just a selected few.
Despite much study and the best efforts of many, a clear and accurate understanding of the true origin of Phalaris staggers is lacking.
The majority of the evidence is strongly against chronic Phalaris staggers being a product of tryptamine ingestion but few seem to care for discovering the truth; politics rule.
Consult our forthcoming work on the Genus Phalaris for more details of some perplexingly bad science.
See Festi & Samorini and/or Shulgin & Shulgin 1997 for alternate scenarios that are AT LEAST as plausible, if not far better supported.
The major discrepancies in Gallagher's work that are seemingly contradicted by the rest of the world
1. DMT, bufotenine (5-OH-DMT) and 5-MeO-DMT were all said to be orally active
2. Over 1 mg/ kg was claimed to
"readily" produce death via heart failure if given intravenously to sheep. [Perhaps it is just a coincidence but this is also the usual dosage given in the literature as a normal intramuscular dose for humans.]
3. Subcutaneous administration was reported to be either equally or more readily fatal than intravenous administration
4. Bufotenine was more active than DMT and readily crossed the blood-brain barrier
5. Oral administration of 5-MeO-DMT took 6 minutes for onset"
Here are links to the above mentioned book on erowid, Festi and Samorini's work, and SST.
Trout-
Ayahuasca: alkaloids, plants & analogs by Keeper of the Trout (full text) title page
www.erowid.org
SST-
Festi & Samorini(mentions Phalaris staggers pages 3-7)
There is a load more literature out there in regards to ammonium uptake, cobalt poisoning, endophytes on grass...
Will post more eventually.
Hope that helps ya Intezam
