Format
Scientific article
Publication Date
Original Language

English

Country
United States
Keywords
marijuana
synthetic cannabinoids
SCBs
K2
spice

Synthetic Pot: Not Your Grandfather’s Marijuana

In the early 2000s in Europe and shortly thereafter in the USA, it was reported that ‘legal’ forms of marijuana were being sold under the name K2 and/or Spice. Active ingredients in K2/Spice products were determined to be synthetic cannabinoids (SCBs), producing psychotropic actions via CB1 cannabinoid receptors, similar to those of Δ9-tetrahydrocannabinol (Δ9-THC), the primary active constituent in marijuana. Often abused by adolescents and military personnel to elude detection in drug tests due to their lack of structural similarity to Δ9-THC, SCBs are falsely marketed as safe marijuana substitutes. Instead, SCBs are a highly structural diverse group of compounds, easily synthesized, which produce very dangerous adverse effects occurring by, as of yet, unknown mechanisms. Therefore, available evidence indicates that K2/Spice products are clearly not safe marijuana alternatives.

Trends

SCBs are a large collection of man-made chemicals, reported in the scientific literature over decades of research to have affinity for CB1 and CB2 cannabinoid receptors.

Products known as K2 or Spice contain a mixture of SCBs that have been illicitly synthesized and sprayed onto inert plant material, to mimic the appearance and psychotropic effects of Δ9-THC in marijuana.

K2/Spice products are falsely marketed to adolescent and other vulnerable populations as ‘safe’ and/or ‘legal’ alternatives to marijuana, and are widely known to avoid detection in standard drug screens due to their lack of structural similarity to Δ9-THC.

SCBs present in K2/Spice products produce a variety of dangerous acute and chronic adverse effects, including psychosis, seizures, tolerance, dependence, and death, with a greater severity and frequency than observed following marijuana use.

Very little is known about the mechanisms underlying the distinct toxic effects of SCBs compared to Δ9-THC, but it is likely that they result from actions at both CB1 and non-CB1 cannabinoid receptor targets.

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