---

The very first comment concerns the published accounts of D.M. Turner; while his intrepid exploration and brave reporting is of great value, it should be stressed that multiple drug combinations introduce a much greater degree of risks, possible strengthening of effects, unexpected reactions, and side-effects than does the administration of the exact same drugs if taken independently.

For these reasons it is urged that a person first acquire familiarity with their intended choices before attempting to combine them. Even if chosing to combine only two drugs they should study the issue very well and start with very small doses to familiarize themselves with the territory and assess potential side-effects. Synergism can work for OR against you. A fatal error in judgement cannot be undone.

If a person's intention is to see "how high they can get" I strongly urge that they chose substances other than those that are being discussed. I know of only the rare individual ingesting a whopping dose of DMT or ayahuasca analog who has appreciated it as much as something more reasonable. Most people have a wretched result and usually remember little of the event.

When taking DMT orally, it might be preferred to ingest the β-carboline prior to the tryptamine. While co-administration can obviously work, my opinion is that the best effects may be had by allowing the harmine to take full effect before administering the DMT. (This is disupted by some psychonauts who report oral activity only when fresh MAOI is taken along with the tryptamine source)

The limited attempts to delineate the ceiling seem to indicate that oral harmine/harmaline will only orally activate DMT for up to 3 or 4 hours after ingestion. More work is needed for precise definition.

A misunderstood point is that while harmine orally activates DMT and prolongs its duration, it significantly diminishes the intensity of the effects rather than actually potentiating them.

On the other hand, harmine and harmaline will both substantially potentiate LSD and also mushrooms. [The most commonly encountered primary criticism of this reported observation seems to revolve around the wide variability in response to a given dose of mushrooms, even within a single batch or by a single individual.

This is NOT a factor when administering harmala alkaloids on top of an already full-blown mushroom peak nor is it a factor when using known doses of LSD-25.

This area needs some serious work not a knee-jerk rejection bereft of any direct evaluation. In fact if people have not tried the combination it seems odd for them to have such strongly held opinions concerning its lack of efficacy]

Claims to the contrary do appear in print pointing to a published evaluation of LSD administration performed on individuals pretreated with an MAOI and reporting a serious diminishment of effects.

There are two crucial points that are glossed over:

1) these individuals were predosed every day for a week prior to the ingestion of substance (this would produce an internal situation of neuronal saturation that was almost certain to preclude any sort of good activity whether daily repeated predosing was done with an MAOI, an SSRI or even other psychedelic compounds) and 2) the disturbing fact that the person who has repeated claimed this both in print and lecture has NEVER tried the actual combinations that is being so casually dismissed.

Combining LSD (or Psilocybe) and harmala alkaloids in an individual who has not been predosed with MAOIs or SSRIs simply does not diminish the effectiveness of the LSD (or the mushrooms) and instead has quite the opposite effect.

This is very easy for anyone to evaluate but I would suggest only hard heads try the blend. Another way to evaluate this would be to smoke harmala alkaloids during an acid or mushroom intoxication (for instance smoking a joint rolled out of B. caapi leaf or a pipe of shredded bark). Despite only trivial amounts being ingested via this route the results are profound and dramatic.

Evidence strongly suggests that a similar potentiation effect also occurs with mescaline but this is a rather poorly evaluated area [Two human bioassays using pure materials are known; one involved 60 and the other 100 mg of mescaline hydrochloride. Both were taken with the equivalency of 130 mg of harmine base (150 mg of the hydrochloride) See Ott 1993 and/or 1994.

Other bioassays using San Pedro (and apparently peyote) have appeared in the Entheogen Review].

As have voiced concerns cautioning against the combination probably due to concerns about MAOI interactions with phenethylamines leading to a possible hypertensive crisis [Preliminary evidence suggests that this may not be a problem with harmine, harmaline or moclobemide, or, if it is, it is so to a far lesser degree of risk than with the nonselective, irreversible MAOIs which are known for such problems as food reactions. This is discussed in the enclosed excerpt from Sacred cacti in the chapter on Mescaline Pharmacology, in the section titled `drug interactions', included elsewhere here. See also the excellent treatment by Ott 1994 concerning mescaline and ayahuasca.] See discussion above.

They are interactive if ingested orally with or after acid or shrooms; or the harmine may be smoked after onset of the other alkaloids. In this last case, effective dosages of harmine are far lower when smoked on top of the other drugs than when orally administered.

If smoking it with the short DMT and the ultra-short 5-MeO-DMT, harmine or harmaline should be smoked (or drank) first. Harmine is not necessary to allow either tryptamine to work (when smoked) but adds another dimension that smoking straight DMT free base does not have. [It is commonly said to add a strong visual component to the 5-MeO-DMT experience.]

It also limits (gives some control over?) some of the dimension that it interacts with and contributes greatly towards purposeful applications.

Besides, it is exceedingly difficult to do very much in the physical while the peak is occurring on either DMT or 5-MeO-DMT. Trying to smoke anything after onset would almost require an automatic pipe and someone else to administer the smoke. (Rarely a good idea since another person can have no idea where you are at.)

Nausea is a common side-effect. Vomiting also occurs frequently in many people; some experience diarrhoea as well. Smoking only to the point when nausea starts to appear may help to minimize this for many people.

An unrelated side note: Combining LSD and Psilocybe together decreases the wave-like nature of the mushrooms, making it much more of a steady state, and adds a very nice dimension (and increased duration) to the Psilocybian elements of the experience but has left this observer feeling quite fried after the fact. If using this combination a substantial lowering of both dosages is suggested.

If drinking harmine with smoked DMT, the harmine can be ingested from 45 minutes up to several hours prior to smoking the tryptamine. [3 or 4 hours seems to be the upper limit for a noticeable interaction.]

Some people feel that nausea and suffering are important. While there may indeed be much to be learned from suffering, there is much to be learned when minimizing it as well.

Some people claim that vomiting is vital to being able to actually trip. As with cactus I suspect this idea arises from the fact that a person is most likely to vomit being immediately before or during onset or else is a result of the relief they experience when vomiting enhancing their appreciation of the event.

It should be remembered that long time ayahuasceros have frequently reported a lessening or disappearance of the intensity of nausea and vomiting as they grew "re-made" through their experience. As with some peyote using people, these appear to regard purging as a sign that the human vessel stands in need of further purification.

Whether smoking ayahuasca alkaloids can orally activate DMT is unknown and the likelihood is that it will not (due to the extremely low dosage of β-carbolines). Combining smoked harmine with subsequently smoked free-base DMT produces effects that more closely resemble those of oral ayahuasca than smoked free-base DMT taken alone. [A similar interaction results when smoking DMT after ingesting harmine orally.] While the character of the experience is significantly altered towards that experienced by oral administration, any lengthening of the DMT effects falls radically short of that resulting from oral ingestion of DMT following oral pre-administration of harmine.

While Gracie & Zarkov reported a lengthening of effects when predosing with 50 mg of smoked harmine extracts, I have not found this to be true when smoking smaller equivalencies of B. caapi or when orally predosing with P. harmala and following either with smoked DMT. Similarly with smoking DMT or 5-MeO-DMT after predosing with acid, or when smoking DMT after predosing with Psilocybe. In the case of acid, there was a persistent residual flavor to the experience and a substantial enhancement of the effects-per-dosage-level but no prolongation of the peak itself.) [Predosing with acid or mushrooms not only allows a far stronger reaction to smoked DMT or 5-MeO-DMT but also enables normally trivial amounts to be fully active. This combination at normal dosage levels is recommended for hardheads only.]

The disparity between my results and those of Gracie & Zarkov may reflect their smoking much larger amounts.

If a person makes a smoking blend incorporating Banisteriopsis leaf and/or bark with 30-50% DMT by weight suspended into it (after first being made into a slurry with ethanol or isopropanol and mixed with the dry herb then air dried prior to rolling into joints) the results and duration are noticeably different and longer lasting than with the same amount of DMT placed on a nonintoxicating herbal blend such as mullein and/or speamint and/or raspberry although, for me, it is not as prolonged as with oral ayahuasca.

The combination of ayahuasca with chacruna additionally mixed with LSD noticeably enhanced the strength and the intensity of the electronic components. Nausea was intense and lengthy. Much of the resulting combination had many of the better subjective components of mescaline but was considerably more electric.

A handful of reports exist claiming substantial enhancement for both the intensity and the duration of Psilocybin mushrooms by use of harmine and/or harmaline (usually P. harmala seeds or purified alkaloids) in a psilocybian based ayahuasca analog. At least one extreme and lengthy bad reaction involving this mixture (P. cubensis and Ayahuasca stem) has been reported, but whether this was more the result of the drug combination or other factors was never unraveled. See True Hallucinations by Terence McKenna.

At least one other bad interaction has been reported after combining Peganum harmala seeds and Psilocybe.

The duration of a mushroom experience is easily prolonged by smoking small amounts of harmine containing materials during the peak. This may be repeated a number of times. It seems to prolong whatever stage it is administered during and substantially enhances the auditory components of the trip. A commonly reported phenomenon is a rushing roar or wind sound behind the ears. [It also stimulates auditory hallucinations, like a rushing roar or wind sounds, when smoked on top of LSD.]

Pure alkaloids can be used but the smoking of ayahuasca bark or leaf will also work fine if larger amounts are smoked.

Smoking P. harmala seeds also works but the smoke is harsh and thick. Probably also due to other substances present, P. harmala seeds also produce more somatic distress than ayahuasca when smoked. The choking smoke of it burned as an incense in a closed spaces is almost certain to induce psychoactive effects if only of a mildly enhanced sedated nature. Anadenanthera peregrina seeds are sold for incense purposes in parts of Brazil. It would be interesting to burn the two or vaporize them, together, on hot rocks in a sweat lodge and see how they combined. Assuming adequate monitoring and life support was available.

A curious feature of this drug interaction is that when smoking such plant material, the activity is apparently caused by what should be pharmacologically insignificant amounts of harmine. Unfortunately, this is not yet a well explored area. Whether normally inactive amounts of harmine is enabled to become active by the LSD or DMT or whether the mode of administration enhances the effectivenss of drug delivery or whether smoking produces other products which show greater activity is not presently known.

There is also the intriguing report [Callaway 1995] that tetrahydroharmine is active when smoked or if taken orally after MAO inhibition. Clearly there is some need for better pharmacological definition.

Gracie and Zarkov also experimented with the smoking of these alkaloids but they consumed around 50 mg and did so prior to ingesting DMT or LSD. Oral potentiation of LSD by Peganum harmala seeds and alkaloids extracted from Passiflora incarnata were also evaluated. In all cases, they reported a rough doubling or more of effects from that established for a baseline. A prolonged peak was also reported.

In the case of the Passiflora they experienced strong, lasting and unpleasant side-effects. Whether these are a result of other harman-type alkaloids that are the major alkaloids in Passiflora species or another factor is not known.

This is an exciting new frontier but one that should be approached with a great deal of caution. There are always risks when exploring the unknown but a slow and cautious approach, always acquiring as much information as possible at all stages before proceeding further, can help minimize potential problems.

There have been no reported injuries or deaths from this area of interest. It would be nice if it stays that way.