stimulant and visual effect comes from the high boiling point fraction of nutmeg essential oil, ie > 210 degC (myristicin, safrole, elemicin). The sedative and almost narcotic and rather toxic effect appears to be from the lower boiling fractions.

Rubbing the oil on the leg muscles seemed to be the most effective and efficient method. It reduced any physical discomfort, eliminated flavoured burps, and sped up absorption, the effects of nutmeg (pre 1997 only) and sassafras oil are almost identical to MDA, but only last for about 20 to 30 minutes after strenuous muscle excercise. It is now clear that we only need to look at safrole and myristicin. Given the lower potency of MMDA it may turn out to be mostly a matter of safrole. When the sassafras oil was still freely available it was a popular way of getting the effects--an idea I started after hearing about the bioamination of myristicin. An no, you won't find bioamination of safrole in the papers---you have to do it yourself.

Crunch's initial questions is extremely valid. There are many traditional preparations that contain allylbenzenes such as safrole which are consumed for their activity. While the jury is still out on nutmeg's activie constituent, my own research and that of people close to me suggests that the 'nice', stimulant and visual effect comes from the high boiling point fraction of nutmeg essential oil, ie > 210 degC (myristicin, safrole, elemicin). The sedative and almost narcotic and rather toxic effect appears to be from the lower boiling fractions.

I have personally had some very hard trips on sassafrass oil, nutmeg oil and parsley oil. My own research indicates that ingestion is not required. In fact maximum effect can be achieved by applying to major muscles. Our group also found that ingestion or application of allylbenzenes without *strong* muscle activity produced negligible results.

As for comparison to MDA, I can confirm that effects can become so strong as to cause temporary blindness (the type of visual problems seen on high dose MDA) and even passing out. The strength of the trip can be controlled by the amount of muscle activity.

Sasha Shulgin mentions the amination of myristicin to MMDA several times in PIHKAL (eg #157). The good doctor also makes it clear that there would be no difference in the process for the varying allylbenzenes (eg safrole, elemicin etc). The experiment where the direct in vitro amination of myristicin was performed used rabbit liver tissue. Since then discussion centers around the amination of allylbenzenes in liver tissue only. I presonally tend to think that muscle tissue is a more efficient converter, but that is speculation.

Safrole is NOT a proven carcinogen in humans. The trials that caused safrole to be labelled a carcinogen were done on rats. Rats lack the enzyme that deals with the hydroxylated derivative that is actually the carcinogenic metabolite. Humans have this enzyme and hence would not have the same problems of build up. (note, personally I think there is plenty of other reason to assume safrole is carcinogenic, but at this stage science tells us otherwise).
More recent research that shows adducts being formed by regular consumption of myristicin or safrole does not prove cardinogenic effect. It merely shows adducts, which could have various results.

Before we all repeat the mantra that safrole is bad and gives you cancer we need to take a critical look at the research. It is the same hysteria that gives us the WOD!.If anything, the recent research has shown that myristicin has the same adduct causing activity as safrole. Safrole's research was done due to the safrole content in the betel quid chewed all throughout asia. But more importantly the myristicin research was done because of the use of myristicin in coca cola, a product consumed in all parts of the world. If science ruled supreme in this rather than just hysteria, then myristicin would be banned the same as safrole, but I think Coca Cola might have some objections to that.

I should mention that on my last trip to germany many of the freaks I was hanging out with were consuming sassafras root tea in rather large amounts. They claimed pleasant stimulating effects from it. Given that most of them didn't like the taste one would have to assume that the effect was at least good enough to make them endure the yucky tea.

sure, it may be placebo, but why are similar quantities of safrole (or other allylbenzene) consumption found in many traditional preparations acttributed with the same pleasant stimulating effects?

some of my early nutmeg experiments were also hit and miss even though I was using the same oil each time. This led me to experiment to find out what triggers the amination. My discovery was serendipitous. I took nutmeg oil early one morning and spent the day playing on the computer. I had no effects all day. Then at 5 to 5 I realised I had to get to the post office and I ran a few blocks to make it. By the time I got to the shop my vision suddenly turned into bright swirls and I could not even see as far as putting an address on an envelope. I walked out of the shop and my knees gave way. I sat in front of the post office for about 20 minutes totally off my face, having an absolute ball - with about a dozen concerned onlookers standing above me. Almost as quick as it turned on it also turned off again. The effect was very high dose MDA like, both visually and physically.

It didn't take long to work out that the oil can sit in your body for ages and not be activated until metabolism is stimulated. Further experiments moved away from eating the oil, in favour of applying it to relevant muscles (eg leg muscles for dancing, arm muscles for sex, etc). The more strenuous the 'excercise', the stronger the effect would be.

My friends and I went to many raves and parties smelling like christmas puddings. if we weren't sure if we liked the party we would use oil instead of pills. With oil you can go home to sleep within half an hour of strong effects. But if you want to stay you just turn the drugs on by dancing hard.

My experiments fell into disarray when we ran out of that batch of oil. Future batches gave mostly narcotic and toxic effects and never the amphetamine/MDA type feeling. Sadly I did not retain a sample of the original oil. I have been searching for a high myristicin oil for over a decade now with no success. usually the allylbenzene content of mutmeg oil is much less than 1%. Turns out that indonesian oil is actually fractionally distilled and the myristicin sold separately sad.gif It is not something I would like to try and import into australia though.

before and during the nutmeg study period we also did a few safrole experiments. Ingestion of 1ml of sassy oil is extremely unpleasant, so we mostly concentrated on nutmeg experiments.

Re: mace--- I'm not ashamed to say that in my younger days I occasionally consumed more nutmeg than is seemly. I eventually found that a 1:1 mix of mace and nutmeg (both purchased preground) seemed rather more worthwhile than just nutmeg. Much less palatable, though, if that's possible.

It should be remembered that deaths have occurred from anything as little as a single nutmeg, and is quite common from doses as high as 3 whole nutmegs. The toxic principle may well not be in the essential oil.... or it might. I intend to only work with essential oils to eliminate at least some possibilities. Furthermore I will only experiment with the 200+degC fraction of the oil. This eliminates most substances other than allylbenzenes.

One of these days I will hopefully get to purify a small amount of pure myristicin and other allylbenzenes and then experiment on these in double blind trials. I have achieved good effects from consuming small amounts of sassafras oil (80%+ safrole), dill and parsley seed oil, as well as lots of experiments on nutmeg. The effects of nutmeg and sassafras oil are almost identical to MDA, but only last for about 20 mins after strenuous muscle excercise. This has me convinced of two things.
1) that the allylbenzenes are responsible for the nice effects.
2) that the conversion is dependent on muscle activity.

Point 2 would mean that resting liver tissue in vitro will not give an appropriate picture of how fast and comprehensive the conversion can be. My liver at rest will not convert enough to even feel I have taken anything. It is not until metabolism is accelerated substantially that effects start.

I would like to have tissue samples removed from my body during an experience and to have these analysed. Obviously this will not be from my liver, but I think we will get more meaningful numbers from muscle areas anyway.

I should also note that a couple of weeks ago I got a bottle of mace essential oil (in the assumption it would be high in myristicin). Turns out it had 0% constituents with boiling ooint over 200 degC ie no myristicin whatsoever. This only reinforces my belief that all processed nutmeg and mace oils are fractionally distilled and the myristicin sold separately. Some oil producers in Indonesia have openly admitted this, so it appears common and accepted practice.

Myristicin's psychoactive properties were confirmed by a study on ten human participants in 1961 (Hallstrom & Thuvander 1997, citing Truitt et al. 1961). Each of the participants was administered 400mg of myristicin, or approximately 6-7 mg/kg by body weight. Only four of the participants experienced psychoactive effects, including euphoria, anxiety, and trouble concentrating. That only four participants experienced psychoactive effects at this level suggests that 400mg or (6-7mg/kg) is a threshold effective dose for nearly half of the population. Time of onset was between two and three hours after ingestion. Interestingly, 400mg of myristicin is around twice the amount of myristicin that would be present in a moderate-high psychoactive dose of nutmeg. Myristicin generally makes up 4-8% of nutmeg's volatile oil and has been found in concentrations as high as 1.3% of nutmeg by weight (C.E.F.S. 2005). the myristicin content of mace is generally double that of nutmeg, making it potentially more potent than nutmeg.

The subject took her 400mg capsule of myristicin at 7:30 am. At 8:45 during a psychoanalytic hour there was flushing, sweating, a sense of light-headedness and a feeling of being detached. The subject felt that she talked more freely and had less of a tendency to weigh and measure her words. She experienced a mild perceptual distortion and a general feeling that the physical surroundings were somewhat fluid. Distances seemed variable. On leaving the analytic hour there was a sense of detachment which the subject felt led to reckless driving and a feeling that nothing would happen. Throughout the day the subject experienced periodic flushing and a feeling of euphoria. The subject was talkative, laughed a great deal and felt rather insensitive about what others might think or say. There was some difficulty in concentrating and a general feeling of restlessness.

Ammonia is produced as a byproduct of muscle activity. As exercise intensity or exercise duration increases ammonia production rate also increases (Graham et al. 1995). During high intensity exercise ammonia production comes from the purine nucleotide cycle (PNC) this cycle typically occurs in the fast-twitch fibers (MacLean et al. 1991). In prolonged sub-maximal exercise ammonia production comes from the breakdown of branched chain amino acids. The production site for ammonia during branch chain amino acid metabolism is generally in the slow-twitch fibers (Graham et al. 1995). Not much is known about the pathway of ammonia from blood to the sweat glands. Czarnowski and Gorski (1991) theorize that the ammonia in perspiration is due to diffusion from high pH in the blood to a lower pH in the sweat glands.

Yuan and Chan (2000) found that after fifteen seconds of intense sprinting exercise ammonia production is at its peak. Also, during their study higher blood ammonia levels were collected when exercised on the bicycle ergometer than from a treadmill. They theorize that this was due to a larger recruitment of the fast-twitch fibers in relation to running on a treadmill. Ammonia is postulated to play a role in muscle fatigue. Muscular fatigue is commonly defined as a failure to maintain the required or expected force or power output (Fushimi et al. 2001). The causes of muscular fatigue involve specific impairments within the muscle itself, including transmission of the neural stimulus to the muscle at the motor end plate and propagation of that stimulus throughout the muscle. Other events that result in muscle fatigue include disruption of calcium release and uptake within the sarcoplasmic reticulum, substrate depletion and various other metabolic events that impair energy provision and muscle contraction. Fatigue can also result from alterations within the central nervous system (CNS). Although essentially nothing is known about the specific mechanisms underlying this type of fatigue, ammonia build-up in the CNS could lead to altered function, which would impair motor function, lethargy, convulsions, ataxia and even coma (Davis 1995).

Peripheral fatigue may also play a role in muscle fatigue. This occurs at the level of the sarcomere and involves failure at the neuromuscular junction, sarcolemma and transverse tubules. Muscle fatigue desensitizes muscle spindle threshold, thereby decreasing afferent feed-back to the CNS (Meyers et al. 1999).

At rest, the liver removes ammonia as urea (Wagenmakers 199. During exercise, blood is shunted from the liver and kidneys to supply muscles with more oxygen. This means that the liver is removing little or no ammonia. Some of the ammonia is released into the blood and another portion is retained in the muscle then released into the blood during recovery. Ammonia is also utilized in the formation of alanine and glutamine within the muscle (Czarnowski and Gorski 1991). In the branch chain amino acid cycle an amine group is removed and a carbon skeleton is left. The carbon skeleton is oxidized to make glucose through gluconeogenesis or converted into fat for storage. The amine group picks up another hydronium ion and leaves as ammonia (Houston 1995).

Possible clearance routes for ammonia in the blood are sweat and expiration (Graham et al. 1995). As blood ammonia increases the equilibrium concentrations are changed and the need for ammonia to be cleared increases. Ammonia then diffuses from the plasma to the sweat glands where it is excreted (Czarnowski and Gorski 1991).

Branched-chain amino acids augment ammonia metabolism. Contribution of BCAA in ammonia production:

net ammonia production after 1 leg muscle exercised: 1,112 mumol/kg
net ammonia production when taking BCAA supplement at 77mg/kg (and exercising same leg muscle) = 1,670 mumol/kg