Marijuana (Cannabis sativa) is a fascinating plant, especially for those who focus on its psychological and medicinal effects without prejudice. For example, a molecular study of the compound cannabidiol (CBD) details the biochemical pathways of what has been suggested as a use to combat psychosis.
What do you mean, the herb is not contraindicated in adolescents and people with psychotic tendencies precisely because of its potential to trigger outbreaks? Truth. But in this case the undesirable influence of tetrahydrocannabinol (THC) comes.
Here’s the paradox of marijuana: its most popular ingredients go in opposite directions in psychosis. Consumption of strains high in THC, like Skunk, has been shown to be linked to a higher incidence of psychotic disorders.
The link is shown in an article by several authors, including Brazilians, published in The Lancet Psychiatry in 2019: the lifetime risk of developing this type of disorder is 3.2 higher for those who smoke the herb daily and 1.6 higher for those on skunk and the like.
At the other end is the CBD, which helps children with severe epilepsy, patients on chemotherapy, and chronic pain. These are indications that have led several countries and American states to license the medicinal use of marijuana, and there are also those suggesting CBD as an antipsychotic.
The group of Daniel Martins-de-Souza and Valéria de Almeida from Unicamp has teamed up with the group of Jaime Hallak, Antonio Zuardi and José Crippa from the USP in Ribeirão Preto to analyze the physiological mechanisms behind this potential. The work was published on May 28 in the journal Frontiers in Molecular Neuroscience.
I do not want to bore the reader here with the details of the complicated methodology. In short, neuroscientists analyzed the profiles of proteins secreted by nerve cells after cultures were treated with antipsychotics and CBD.
The drugs tested were clozapine and haloperidol, which belong to the atypical and typical classes of antipsychotic drugs, respectively.
The typical, or first generation, attack more psychotic symptoms that are mistakenly labeled positive. The term for psychological manifestations that do not occur in a healthy person, such as delusions and hallucinations.
The second generation, that of atypical antipsychotics, goes even further: it tries to contain both positive and negative symptoms. In the second case, it is the diminution of important psychological functions that leads to affective blunting, social isolation, and cognitive loss.
Unicamp’s partnership with USP found that the CBD-induced proteome profile was more like the effect of the atypical than the typical.
Based on some evidence, it was also investigated whether the marijuana compound has an impact on metabolic pathways involved in demyelination. This damage to the nerve sheath is critical to the transmission of nerve impulses and has been linked to schizophrenia.
Protein analysis showed that CBD appears to help with remyelination. “Another thing we want to investigate is the biochemical events triggered by topical antipsychotics rather than CBD, as it is precisely these events that may be responsible for the side effects,” says Martins-de-Souza.
“If a new drug can eliminate them, voilà!” He enthuses. “What CBD and traditional antipsychotics have in common must be good for treating disease; What is biochemically specific for traditional antipsychotics is perhaps exactly what we don’t want in new drugs. “
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