Integration into the genome... yet. They need long read Whole genome sequencing to prove that which Im sure is currently underway. Rudi showed it was integrated but was critiqued that it could be an artifact of making sequencing libraries. This paper fills in many questions.
The study was well controlled with RNAse confirmation that the target is in fact DNA and not RT of RNA.
Team "Scientific Censorship" has a lot of explaining to do. Many people on this team were vocal opponents of the CRISPR baby experiments run in China. Now they are guilty of
Advocating such experiments on a billion people. It is amazing how pliable their ethics are with a pinch of fear.
We covered this in our PrePrint with Dr. McCullough. @P_McCulloughMD
In a sane world this would lead to immediate moratorium on mRNA transfections until WGS are complete.
We are no longer in a sane world and you should take protection into your own hands osf.io/bcsa6/
You can find them at the below link on the bioRxiv preprint.
A good question from a fellow cat...
When will Whole Genome Sequence Moon?
I think they will need long read sequencing to sort out LINE-1 integration. That usually requires >100ng of DNA.
Human genome is 6pg so 10,000-100,000 cells of DNA are needed to sequence.
Each cell is unlikely to carry integrations in the same location of the genome. So they can't use consensus sequencing (ensemble of all 10,000 cells DNA sequencing) to sort it out. PacBio HiFi sequencing can deliver 150Gb in a single flow cell or 50X coverage per flow cell
More recent studies are pushing this number down to 5ng for PacBio, so they maybe able to get away with 1,000 cells. pacb.com/wp-content/upl…
This might require multiple flow cells. 10 would give you 500X. Either way, this could be over $25K in sequencing but the accuracy of the HiFi reads means each 20Kb read is as good as Sanger sequencing but 30X longer and better for mapping in LINE-1 regions.
They improve at a faster than Moore's law rate and they may be able to better speak to current yields. Will need to be done in those Huh7 cell lines and ultimate in patient biopsies. @PacBio pacb.com/wp-content/upl…
I did leave a comment in Rudi preprint that suggested DNAse and RNAse controls.
It had some push back.
The DNAse and RNAse experiments we just done on BNT162b2 and further move this from conspiracy towards Fact.
Before we get overly focused on Integration….
We should pause to realize this paper has data that should concern us today.
The paper demonstrates vax induced elevated LINE-1 expression.
It is worth reading the Back and Forth on the Jaenisch labs paper (Zhang et al).
They suggest integration with the virus is 2-5 integrations per 10,000 cells.
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?