Cannabis is widely popular due to its capacity to alter sensory perception and produce euphoria. And when it comes to cannabis and sex…
Science has yet to harness the neurobiological mechanism of sexual activity, to better enable us to control it, and cure those who are deficient so that we may offer our patients not just normal blood pressure, control of blood glucose, and optimum respiratory function, but also what can be otherwise called “sexual satisfaction.”
It is hard to perform controlled studies on sexual behavior in animals and then extrapolate them to humans, as humans are vastly more complicated sexual beings than animals.
Exogenous cannabinoids are produced by plants. Endogenous cannabinoids are produced by humans. The connection between them are the cannabinoid receptors located in the central nervous system and the peripheral nervous system respectively – CB1 and CB2. The endogenous cannabinoids are called AEA (Anandamide) and 2-AG (2-Arachinoylglycerol).
The main enzyme that degrades AEA and 2-AG is FAAH (fatty acid amide hydrolase).
THC (Δ9 tetrahydrocannabinol) the exogenous (plant) cannabis when ingested, binds to CB1, stimulates AEA and 2-AG and through its psychoactive effect controls sexual behavior.
Sexual activity is a motivated behavior and consists of two phases: precopulatory and copulatory. It is difficult to perform a study on an animal’s sexual “appetite” and extrapolate it to humans. For one, animals have no prior knowledge or experience in using cannabis. For another, humans have a more complicated frontal lobe with capacity for emotions such as ambivalence, guilt, judgment and impulse control. These qualities are unique to the human, but are absent in animals, yet in humans they clearly affect sexual behavior.
Regardless of the fundamental differences between non-human and human subjects, rats have been studied to find the root cause and cure for sexual function and dysfunction. When rats were given HU-210, which blocks CB1 and CB2, they demonstrated decreased sexual activity. However, other studies, also performed on rats, demonstrated the opposite response after administering HU-210. The only consistent findings in the studies done on non-human subjects were the effects of low dose versus high dose cannabinoid ingestion.
Low levels of AEA stimulate sexual functioning and high doses of AEA inhibit sexual functioning. The mechanism of this biphasic response is thought to be through activation of TPRV channels. The hypothesis is that the CB1 receptors are located very close to the TPRV receptors. When cannabinoids are ingested in a low dose, CB1 is stimulated, but when high doses are ingested, CB1 is “overwhelmed” and TPRV is stimulated instead, resulting in negative sexual desire and activity.
There are no randomized controlled clinical studies of cannabis on human subjects in regard to sexual behavior. The only studies performed on human subjects consist of interviews of people who use cannabis. Consistently found is that chronic low dose use, of about two joints a week, is associated with aphrodisiac affects and heightened pleasure in both males and females. However, regardless of the landmark study consisting of patient interviews dating back to 1970, there has been no further advancement in our knowledge.
Human sexual behavior is very complex. We do not have the brain of a rat or mouse or a hamster. As such, discovering what cannabinoids do to the brain of a rat, mouse, or hamster cannot be extrapolated to what cannabinoids can do to the brain of a human.
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