• Maeve@kbin.earth
    link
    fedilink
    arrow-up
    1
    ·
    20 hours ago

    Eh, I’d bet alcohol is more on the everlasting schizophrenia risk side. But weed really does fuck up your thinking.

    Like every occasional sixth month or year in a conducive environment, yes, it may enhance thinking outside the box for an insight or few. Daily would be like a milder version of dropping hallucinogens.

    • BCsven@lemmy.ca
      link
      fedilink
      arrow-up
      1
      arrow-down
      1
      ·
      16 hours ago

      Studies have shown a direct link to weed induced schizo disorders and those with genetic markers susceptible for it. Getting a DNA test is not on most peoples priority list.

        • BCsven@lemmy.ca
          link
          fedilink
          arrow-up
          2
          ·
          14 hours ago

          I think the science paper I read was 7x higher rate on weed, ifyour had a certain gene. I will have to find it

          • Maeve@kbin.earth
            link
            fedilink
            arrow-up
            1
            ·
            14 hours ago

            That’s still not statistically significant, and correlation does not imply causation. It serves as a caution, and I’m inclined to agree it’s not wise to risk it, but let’s be honest with ourselves and others.

            • BCsven@lemmy.ca
              link
              fedilink
              arrow-up
              2
              ·
              11 hours ago

              Well correlation studiear say 37% risk, but I recognize that correlation is not causation, however they have found the mechanism that causes the increased psychosis with genes.

              https://www.mdpi.com/2076-3417/12/20/10464

              AKT1 gene polymorphism rs2494732 as the main genetic factor

              C allele homozygosity significantly increases psychosis risk in cannabis users.

              Mechanism: Cannabis consumption slows AKT1 functionality, releasing greater dopamine in the striatum through indirect mechanisms.

              COMT and DAT1 gene interactions compound the risk

              CB-1 receptor activation leading to increased dopamine release and GABA inhibition