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Acacia confusa

Acacia confusaAcacia confusa is Uncontrolled in the United States, however, it is not approved for human consumption. This is a gray area of the law because the plant contains DMT, which is classified as a Schedule I drug.

Addictive Potential: None

Emergency Room Visits Yearly: Unknown

Mandatory Minimum Sentence: Unknown

Mechanism of Action: Increases Serotonin when combined with an MAOI

Overview:

Acacia confusa is also known as Acacia Petit Feuille, Small Philippine Acacia, Formosa Acacia (Taiwan Acacia) and Formosan Koa. It is a perennial tree native to South-East Asia. Although it has become very common in many tropical Pacific areas, including Hawaii. In recent years, there have been reports of Acacia confusa root bark being boiled into a tea along with peganum harmala in order to make acaciahuasca, which reportedly produces psychoactive effects similar to those of traditional ayahuasca. The root bark of Acacia confusa contains NMT (1.43%) and DMT (1.15%) (Liu et al., 1977).

Acacia confusa is currently legal to buy, sell, and possess in the United States.

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Warnings:

The toxicity of Acacia confusa seeds. The seeds of Acacia confusa contain a chemical called neurolathryogen, or α-amino-β-oxalylaminopropionic acid (Quereshi et al., 1977). Neurolathryogen is considered to be neurotoxic (Evans et al., 1977) and should be avoided.

General MAOI warnings. When ingested orally, MAOIs inhibit the catabolism of dietary amines. Sufficient intestinal MAO-A inhibition can lead to hypertensive crisis, when foods containing tyramine are consumed (so-called “cheese syndrome”), or hyperserotonemia if foods containing tryptophan are consumed. The amount required to cause a reaction exhibits great individual variation and depends on the degree of inhibition, which in turn depends on dosage and selectivity.

The exact mechanism by which tyramine causes a hypertensive reaction is not well understood, but it is assumed that tyramine displaces norepinephrine from the storage vesicles. This may trigger a cascade in which excessive amounts of norepinephrine can lead to a hypertensive crisis. Another theory suggests that proliferation and accumulation of catecholamines causes hypertensive crises.

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