Online THCA hemp sample sold without age checks across state lines.
CT 30 for Aspergillus Fumigatus.~100x over the tested state limits. The hemp market enjoys ZERO testing so it’s the dumping ground of failed weed.
Plating confirms it not dead DNA but live spores.
@RobertKennedyJr
@MAHAalliance
The hemp market enjoys banking. The safety tested cannabis market does NOT have banking.
It’s almost like the federal government is trying to make the cannabis market dirty again.
Fumigatus is nasty stuff for immunocompromised patients.
This came off of ‘Hemp’ THCA flower being shipped across state lines.
Anyone want to guess what it is?
A conversation on Cannabis that @AlexBerenson will never acknowledge.
The potential connection between mycotoxins and schizophrenia is an area of ongoing research, though it’s not yet fully understood or universally accepted as a direct cause-and-effect relationship. Mycotoxins are toxic compounds produced by certain molds, like Aspergillus, Fusarium, and Penicillium, which can contaminate food, water, or indoor environments. Some studies and hypotheses suggest that exposure to these toxins might influence neurological and psychiatric conditions, including schizophrenia, through various mechanisms.
One theory is that mycotoxins could disrupt brain function by causing inflammation, oxidative stress, or neurotransmitter imbalances—factors already implicated in schizophrenia. For instance, toxins like aflatoxin or trichothecenes might interfere with dopamine or glutamate pathways, which are heavily studied in schizophrenia research. There’s also speculation that chronic exposure to moldy environments could trigger or worsen psychotic symptoms in susceptible individuals, possibly through immune system overactivation or direct neurotoxicity.
A few small studies and case reports have explored this. For example, research has linked damp, moldy living conditions (where mycotoxins thrive) to higher rates of mental health issues, including psychosis. A 2016 study in Environmental Health suggested that mold exposure might correlate with neurological symptoms, though it didn’t specifically pinpoint schizophrenia. Another angle comes from historical events like ergot poisoning—caused by the mycotoxin-producing fungus Claviceps purpurea—which led to hallucinations and erratic behavior, somewhat resembling psychotic episodes.
That said, mainstream science doesn’t currently list mycotoxins as a primary cause of schizophrenia. The disorder is more strongly tied to genetics, early brain development, and environmental stressors like trauma or drug use. Mycotoxin exposure might act as a contributing factor or trigger in rare cases, but evidence is mostly anecdotal or preliminary. Researchers would need larger, controlled studies to confirm any solid link.
If you’re curious about specific mycotoxins (like aflatoxin or ochratoxin) or want me to dig deeper into studies or X posts on this topic, let me know!
You’re raising a really sharp point here—one that doesn’t get enough attention in the cannabis-schizophrenia conversation. Yes, cannabis can indeed be contaminated with molds like Aspergillus and Mucor, as noted in studies including from the CDC (e.g., Benedict et al. have flagged this in immunocompromised patients). These molds can produce mycotoxins—Aspergillus is notorious for aflatoxins, while Mucor species, though less studied for toxins, can still trigger inflammatory responses. If the cannabis used in studies linking it to schizophrenia isn’t tested for mold contamination, it could absolutely confound the results. Here’s how that might play out.
Schizophrenia research often points to cannabis use, especially high-THC strains, as a risk factor, particularly in genetically predisposed individuals. The prevailing theory is that THC messes with dopamine signaling or heightens stress on the brain’s reward system, potentially triggering psychosis. But if that cannabis is laced with mycotoxins from Aspergillus or other molds, you’ve got an unaccounted variable. Mycotoxins could independently—or synergistically—irritate the nervous system, ramp up inflammation, or disrupt neurotransmitters like glutamate or serotonin, all of which are already on the schizophrenia radar. Smoking or vaping moldy weed might deliver these toxins straight to the lungs and bloodstream, bypassing some detox pathways and hitting the brain hard.
Studies rarely test for this. Cannabis quality control is spotty, especially in older research or in regions where it’s illicit and unregulated. A 2019 paper in Journal of Forensic Sciences found that illicit cannabis samples often harbor fungal contamination—up to 20% in some batches tested positive for Aspergillus. Yet, schizophrenia studies typically rely on self-reported use or broad population data, not lab-verified samples. So, if participants smoked moldy cannabis, any psychotic symptoms could be partly or wholly due to mycotoxins, not just THC. This muddies the causal waters—did the cannabis itself trigger schizophrenia, or was it the hitchhiking mold?
There’s also the immune angle. Mold exposure can overactivate the immune system, and some schizophrenia models suggest chronic inflammation might prime the brain for psychosis. A 2021 study in Brain, Behavior, and Immunity tied systemic inflammation to worsening psychotic symptoms—could mycotoxins from cannabis be a hidden driver there? It’s plausible but untested.
The flip side: not all cannabis users develop schizophrenia, and contamination rates vary. If mycotoxins were a major confounder, you’d expect clearer patterns in heavy users or regions with poor storage conditions (humid climates, say). Still, the lack of mold testing in these studies is a glaring gap. It’s like studying alcohol’s effects but ignoring whether the booze was spiked with methanol—correlation doesn’t equal causation without ruling out the silent variables.
If you want, I could search X or the web for more on cannabis contamination rates or dig into specific schizophrenia studies to see if they mention mold. This angle’s a bit of a rabbit hole—where do you want to take it?
Yes, ivermectin is known to inhibit importin α/β-mediated nuclear transport, which is relevant in the context of SV40 promoters.
Mechanism:
•Importin α/β Pathway: This transport system is responsible for shuttling proteins with nuclear localization signals (NLS) into the nucleus. Many viruses, including SV40, hijack this pathway to deliver their regulatory proteins (e.g., Large T antigen) into the nucleus for replication and transcriptional activation.
•Ivermectin as an Inhibitor: Ivermectin binds to importin α/β and disrupts its function, thereby preventing nuclear entry of proteins that depend on this transport mechanism.
Implications for SV40 Promoters:
•SV40 Promoters: The SV40 early promoter is often used in molecular biology due to its strong transcriptional activity in mammalian cells. However, its transactivation requires the nuclear localization of SV40 Large T antigen, which depends on importin α/β.
•Blocking Nuclear Entry: If ivermectin blocks importin α/β, it could prevent SV40 Large T antigen from entering the nucleus, thereby reducing SV40-driven gene expression and viral replication.
Experimental Evidence:
•Studies have demonstrated ivermectin’s ability to inhibit nuclear import of viral proteins from various RNA and DNA viruses (e.g., HIV-1, Dengue, and even SARS-CoV-2).
•SV40 Large T antigen is known to require importin α/β for nuclear entry. If ivermectin blocks this pathway, it could theoretically interfere with any SV40-driven transcription or replication in systems using this promoter.
Would you like references or more experimental details on this?
Certainly, here are some key studies that provide evidence on this topic:
1.Ivermectin as an Importin α/β Inhibitor:
•A study by Wagstaff et al. (2012) demonstrated that ivermectin specifically inhibits importin α/β-mediated nuclear import. The researchers found that ivermectin effectively blocked the nuclear import of proteins dependent on the importin α/β pathway, without affecting other nuclear import pathways. This inhibition also correlated with a reduction in the replication of viruses such as HIV-1 and dengue virus, which rely on this pathway for nuclear entry of their proteins. (pmc.ncbi.nlm.nih.gov)
2.SV40 Large T Antigen and Importin α/β:
•The SV40 Large T antigen contains a nuclear localization signal (NLS) that is recognized by importin α, facilitating its transport into the nucleus via the importin β pathway. This nuclear import is essential for the Large T antigen’s role in viral replication and cell transformation. (en.wikipedia.org)
These studies collectively suggest that ivermectin’s inhibition of the importin α/β pathway could impede the nuclear import of SV40 Large T antigen, potentially affecting SV40 promoter activity and viral replication.
Background.
Im against the drug war. People should be free to Biohack. Even if the government mandates water, I have a problem with it. Not the water but the force and threat to freedom.
I'm glad Bryan is on this journey and sharing what he finds.
I don't care if he sells stuff on the way. Voluntary economic interactions are legit. People who like to control the narrative will complain.
I couldnt do 100 supplements/day but maybe he'll figure out the key 4-5 that do 90% of the work for others.
Profiling circulating DNA is a thing. I’m just skeptical of the tox seen with LNP delivery of mRNA.
We took the cover of Science Translational Medicine in 2010 with profiling circulating tumor DNA.
I’ve used these profiles to characterize my father’s prostate cancer.
BRAF-K601E Mutation called for AKT1 inhibitors.
Some Cannabinoids are AKT1 inhibitors.
David Meiri does some of the best work on profiling cannabinoids for cancer