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A study comparing autistic children to their neurotypical siblings and unrelated neurotypical children revealed that autistic children often lack bifidobacteria, a crucial microbe abundant in newborns. The speaker is publishing a paper based on this research. Identical twins with autism, who were nonverbal and aggressive, shared elevated levels of three identical microbes and had zero bifidobacteria. After treatment focused on eliminating harmful microbes and increasing beneficial ones, both twins became fully verbal and non-aggressive within seven months. The speaker believes that the microbiome offers insights into the condition of these children, as microbes travel from the gut to the brain via nerves. The speaker emphasizes the need to focus on nonverbal, severely affected autistic children and criticizes the lack of research and therapeutics, especially in light of the high number of cases in California.

Remember that your microbiome are the different bacterias that reside and inhabit your gut, and the type of bacteria that you have in your gut is actually really important. There are specific bacteria that can lead to more inflammation and metabolic diseases like type two diabetes, like high blood pressure, high blood sugar, all of these things. And there are also different types of gut bacteria that lend itself to low levels of inflammation and good health. So ultimately, we understand that we can't metabolize these sugar substitutes. In general, they just pass through in our feces and in our urine, but they do impact the gut microbiome. And there was a mouse study looking at this, and it showed that the microbiome shift to favor species associated with metabolic and inflammatory diseases when we drink these sugar substitutes and eat a significant amount of these sugar substitute.

Speaker 0: What results kind are you seeing with this study, with the fecal transplants in autistic children? We published that case supervised by the FDA: it was giving one sibling to another and the kid started verbalizing and he's not aggressive. He came to my office banging his head, breaking his teeth, and now he's responding and he's responding to treatment. He's communicating better. He's listening. He's doing classes. He's developing. Obviously, this kid was old when we got him, it's much better, we get better results and I think Doctor James Adams will tell you we get better results the younger they are. So that's one kid. We are on to more precise manipulations, kind of, with two twins that we did. We won a research award at the American College of Gastro about two weeks ago. And basically what we showed was two identical twins that had the same exact microbes at baseline. We manipulated the microbiome and then those microbes disappeared. But what we showed, which has been my path and my mission, save the Biff, is those kids, two identical twins, nine months later, their Bifidobacteria increased with whatever we did. And now they're verbalizing, they're fully reading, fully verbal. This is a beginning. The judge that judged my presentation said this is a proof of concept, right? That when you actually attain an engraftment of Bifidobacteria, these kids are improving. This is obviously my hypothesis, has been my hypothesis. To get to that, to do that, unfortunately, we do not have a stool assay right now that is valid, verified and reproducible in the consumer product, right? So this is the problem because parents are going to say, well, I gave my kids these probiotics and my kid's not improving. So what is Doctor Hazen saying? Well, the problem is if you don't see the increase in the bifidobacteria, your kid's not going to improve. And unfortunately, the tests that are out there are not valid, verified, or reproducible or anything that I could say, oh yeah, use this consumer product. We are developing a consumer product in full transparency, but we are far from that because of the fact that there are trillions of microbes in the gut. And as a responsible physician, I feel that I cannot give a report to a patient that says you have eubacteria or you have Alistope sphingoldi, but I have no idea what Alistope Spine Goldie does, if it's a good bug or a bad bug, because here's what's gonna happen. You're gonna get this lab test from me, you're gonna go to like a thousand doctors and they're gonna say, I have no idea what this test means. Which was the problem, by the way, at the beginning when all these tests were starting. Remember, UBiome, the company that sold all these tests? All these patients would get all these testing and then they would go to the GI doctor and the GI doctors would say, what is this? What the hell?

The speaker ties stool and fecal transplant to the brain–gut axis, recalling an N-of-one observation: giving the microbiome of a happy person to a patient with suicidal tendencies, UTIs, C. difficile, psoriasis appeared to reduce suicidality. They stress the finding is not reproducible and suggest a donor component. They recount a case where the donor—a yoga instructor and vegetarian—was evaluated and deemed a perfect candidate, illustrating the importance of donor health and history. They warn that too often we assume a neighbor is a good donor, while we may not know the donor’s mental state. The field is promising but with unknowns. The speaker asserts there is nothing more important in this life than understanding the microbiome, which will affect your life, affect your kids’ lives, and warns that if we don’t pay attention, microbes are taking over our bodies when we die and put us back into ground.

"When fecal transplant showed more than, you know, improving C." "And one of my patients with Alzheimer's started remembering his daughter's date of birth, I said, what did I do? I just changed the microbiome." "I used the wife's microbiome to the husband." "It wasn't about pushing stools for Alzheimer's, but what was causing Alzheimer's? What microbes was the culprit?" "What microbes could suppress that microbe That's the culprit." "Babies have a lot of bifidobacteria, this important microbe that helps us decompose sugar." "And we saw a lot of Bifidobacteria in newborns." "There is obviously a consensus in the medical field because there's a lot of gynecologists now that are using the secretions from the vagina of the mom and smearing it on the baby that is born with C section to just make them healthier in a way."

The speaker envisions a future in which everything will be linked to microbes, including cancer. They point to current examples such as HPV cervical cancer, Epstein-Barr virus with Burkitt’s lymphoma, and Helicobacter pylori with gastric cancer to illustrate how specific microbes are associated with particular cancers. They suggest it is only a matter of time before doctors begin saying that certain cancers, like colon cancer, are associated with specific bacteria, referring to a hypothetical “colon cancer with X bacteria.” This framing implies that cancer development could be driven or influenced by the presence of particular microbial communities. From there, the speaker raises the question of how to neutralize a particular microbe in order to prevent it from contributing to cancer alongside another microbe. They emphasize that microbes are constantly present and interacting, describing a ongoing “war in our guts” where microbes compete and influence disease outcomes. The idea is that some microbes are beneficial, or “good ones,” and that understanding these relationships is key to prevention and treatment strategies. A central claim the speaker highlights is what has been learned from the COVID experience: it reveals the ability of a microbe to survive inside a virus, but also the ability of a virus to cause death in a person. This observation reinforces the notion of a complex battle between microbes themselves and between microbes and viruses, where outcomes depend on how different organisms interact with one another. The speaker stresses that the crucial insight lies in identifying which microbe neutralizes which other microbe, suggesting that these inter-microbial dynamics could determine disease progression and outcomes. Ultimately, the speaker defines this understanding as “the key to the whole research that I’m doing.” The emphasis is on mapping out the interactions between microbes and viruses, recognizing the dual role of microbes as potential drivers of disease and as possible targets for interception, and using that knowledge to guide the research trajectory aimed at preventing cancer and other illnesses by modulating the microbiome.

"everybody is different." "We all have a fingerprint of our microbiome." "families are different." "the mom with triplets had an overgrowth of a certain group of microbes and the triplets, two of the triplets didn't have that microbe, but the one with autism had twice the amount of microbes that the mom had." "Engraftment determines success of a fecal transplant." "The kid started speaking, verbalizing." "We discovered that those people that had severe COVID had zero Bifidobacteria." "autistic kids have loss of bifidobacteria." "two identical twins, same exact microbes disappeared after nine months, and the Bifidobacteria goes up." "these kids are verbalizing, they're reading, they're counting." "Restoring the microbiome, saving the Bif, improving the bifidobacteria, and the kids are verbalizing." "this is a new revelation." "And I think it's going to be one of the biggest discoveries of this century in my opinion."

Speaker 1 discusses a published case linking the gut microbiome to cognitive impairment. The paper centers on a patient with Clostridium difficile and a mini-mental state exam (MMSE) of 21, who could not remember much or engage in activities like golfing. The intervention involved transplanting the microbiome from the patient’s wife into the patient, after which the MMSE improved from 21 to 26 to 29, and the patient began remembering his daughter’s date of birth. This case was the first reported instance of using the wife’s fecal matter to implant into the husband. It prompted consideration of connections between Alzheimer's disease and gut problems. Dr. Sheldon Jordan encouraged analyzing the stools of patients with Alzheimer's to examine their microbiomes. Dr. Barodo (Barote), a pioneer of fecal transplant, explained that fecal transplant is the procedure where stools from a healthy donor are put into a patient with C. difficile; it is the only FDA-approved indication in America. While the transplant is used to treat C. difficile, in this case it appeared to improve Alzheimer's symptoms. The speaker contacted Dr. Barodi (Barodi) to publish the case, and it took a long time to publish. This experience contributed to the exploration of a gut–brain connection. The brain is connected to the bowels via blood vessels, nerves, and lymphatics, making it possible for gut contents to influence the brain and vice versa. Microbes secrete substances, including methane gas, which could affect the brain if overproduced by certain gut microbes. The case suggested there is something meaningful going on in the microbiome, leading to the idea that the best way forward is to advance science by studying the microbiome of the brain and the gut together. The speaker notes that microbiome research is in its infancy and much work remains to be done in this space.

In 2004, an experiment with mice revealed the impact of gut bacteria on stress response. One group of mice had their gut bacteria removed, while the other group was left untouched. When exposed to stress, the bacteria-free mice displayed an exaggerated response, which led to the discovery of the gut-brain axis. This connection between gut and brain also applies to humans. Countless nerves, including the vagus nerve, link the gut and the brain. The microbiome can communicate with the brain chemically. The gut and brain are also connected hormonally by the HPA axis, which regulates hormone balance and metabolism. Taking care of one benefits the other, while neglecting one causes the other to suffer.

Interviewer: But you you have had this case. I know that you're still working on publishing the research where you, you know, you did this with twins. And we know that, you know, the twin studies are very popular for a bunch of reasons because the genetics are identical. What happened? Researcher: So from COVID and from doing that N of one, which took time, and then from trying to get this familial FMT, I had these kids that were basically coming in with autism. And I have a lot of patients that come to me that have tried so many things. So this case was two twins with the mom flew in from Tennessee, and I basically innovated. And but I said to her, I said, me let look at the microbiome. What was amazing about this case, and it's going to be a breakthrough, I don't want to say too much because it's going to be published in October at the American College of Gastro, but essentially we saw the identical out of trillions of microbes, we saw elevation, relative abundance of microbes elevated the same three phylum in both identical kids. And as we refluralized the gut, not with fecal transplant, but with methods, we basically noticed that those microbes disappeared and the good bacteria came on at the same time as speech started. So this was a breakthrough case, and it's going to be a breakthrough for the FDA once they see that. And we're going to use that. So we're going to start doing familial fecal transplant with the FDA. But we're hoping that we can bring this other method after, while we're doing familial fecal transplant to get the data to understand because this could have been a fluke with these two kids kids. But we wanna try to reproduce these two kids to see if we can do this for other kids. Mhmm. And therefore, maybe run two protocols, one with familial FMT, fecal microbiota transplant or intestinal microbiota transplant, and then another one with this protocol to see can we do this more safer, better, less playing with poop? Because this doesn't play with poop. Interviewer: Well, the other aspect is also that, as we said at the beginning, everybody's different, And so I think this is actually kind of important. There isn't a of Researcher: one size fits Interviewer: all solution when it comes to this. Researcher: There isn't a microbiome. There's trillions of microbes. And I gave you the example with the fungus or it could be a fungal, you know, overgrowth. It could be a you know, even doctor Feingold, who was the beginning, who basically said, let's try vancomycin. Right? Researcher: He said, let's vancomycin for kids with autism, and he saw something with vancomycin. What he was seeing was a destruction of a microbiome and a suppression of microbes that secrete toxins, which decreased the aggressivity the aggressivity of the kid but did not restore the speech. It was but at least it gave a quality of life to the family to say, hey. Our kid is not banging his head on the wall. And so vancomycin got us to this level. Researcher: Right? But vancomycin is not a permanent solution. The solution is really to restore the gut to the way it was, and the challenge that we have is we do not know what it was before. So when you take a kid and he has a destroyed microbiome, you don't know what his fingerprint of his microbiome was before to reproduce him. Right? Researcher: And you're right. Everybody's different, so everybody may not need the same, but we need to be more precise.

When examining a person’s microbiome without any information about their history, the speaker asks if they are constipated or if there is a family history of Parkinson's. The response from the person is, “yeah, how'd you know?” The speaker notes that they have seen many samples with Parkinson's that look like this picture, implying a recognizable signature. The key claim is that if you begin having that signature microbiome and it persists, Parkinson's starts twenty years prior as constipation. In other words, the process begins with constipation as an early sign long before other symptoms emerge. The speaker references studies that look back in time: they took polyps out and noticed that those polyps had a certain stain that basically was the beginning of Parkinson's. This suggests that the early indicators can be traced back to initial changes related to the disease. A central idea is that the nervous system is involved in the disease, and it starts at the microbiome level. The speaker emphasizes that an imbalance in the microbiome—specifically in the microbes—basically starts the process of Parkinson's disease. In other words, the microbiome imbalance is proposed as the initiating factor. From these observations, the speaker concludes that you can predict what’s going to happen based on this early microbiome signature. The overarching point is that the disease process begins in the gut microbiome long before traditional Parkinson's symptoms appear, and that identifiable microbiome patterns can forecast the trajectory.

Severely autistic, nonverbal twins were observed to have identical microbiome compositions. After correcting their microbiomes to increase good microbes and decrease bad microbes, the twins became verbal and fully reading. This outcome is considered significant because clinical improvement was correlated with a measurable improvement in the microbiome assay.

Speaker 1 discusses probiotics and the current state of microbiome science: taking random probiotics may be questionable because the technology of the microbiome is not FDA-approved yet. The reason is that there are many bacteria in the microbiome and we don’t know what they are, what they do, whether they’re good or bad. For example, blotia and Rosaburia are poorly understood; 90% of GI colleagues don’t know blotia is a microbe, and 90% don’t know there’s such a thing as Rosaburia. Historically trained on Klebsiella pneumoniae, E. coli, Salmonella, C. difficile, Clostridium perfringens, but not on nonpathogenic microbes. The question remains: is blotia a good bug or a bad bug, and who has too high or too low levels? This represents the abyss of the microbiome and is still research, not consumer product or standard medical practice. Speaker 1 explains that doctors cannot be told to use a new stool test or to start using microbiome data broadly until researchers reproduce findings and doctors see the data for themselves. The idea is that oncologists may notice correlations, such as loss of bifidobacteria in invasive cancer, and observe improvements in cancer alongside bifidobacteria, which could influence acceptance of the gut-brain or microbiome link. However, such observations need replication to move from incidental findings to established conclusions. An example given is Colleen Kelly at Brown University, who published two cases of alopecia areata with C. difficile where hair grew back after fecal transplant. The question is whether fecal transplant for alopecia areata is valid; however, an academic center trying to reproduce the data could not. The speaker suggests uncertainty about whether a specific microbe caused hair regrowth or if exposure during treatment led to it. Until data are reproduced, no one can claim alopecia areata is improved by fecal transplant or microbiota transplant. Concluding guidance: if you’re healthy, keep doing what you’re doing and do nothing else; if you’re not healthy and have multiple diseases and you’ve tried a probiotic, if it works, continue, but if it doesn’t work, then it’s probably not a great probiotic. The overarching theme is careful interpretation, replication, and recognition that microbiome science is still evolving and not yet ready for universal clinical application.

Bifidobacteria are important for immunity, but they are not the only important microbe. The speaker notes that bifidobacteria are the microbe that is disappearing. Analyzing thousands of stool samples, out of 4,000 stool samples, there are only four that can be said with certainty “these are both microbiomes.” Out of the thousand samples analyzed, less than five percent have bifidobacteria. The speaker highlights that loss of bifidobacteria is not universally linked to all conditions. It is present in Alzheimer's disease, with Alzheimer's patients having lots of bifidobacteria; Lyme disease patients also have lots of bifidobacteria. Crohn’s patients that have never been treated have lots of bifidobacteria. In autistic kids, there is enough data now; they showed data initially, and now more data and more labs reproducing that data show that there are lots of bifidobacteria in autism. The speaker mentions that “Loss of bifidobacteria in autism” can be addressed by replenishing bifidobacteria, and refers to this as proof of concept that the judge at the American College of Gastroenterology acknowledged, noting that this is what is needed to advance science to understand. Loss of bifidobacteria was also noticed in patients with invasive cancer. The speaker says they published that data at the American College of Gastroenterology and presented at Digestive Disease Week, showing that if a patient had a non-aggressive cancer, they had a better level of bifidobacteria than a patient with invasive cancer who has zero. Regarding therapeutic implications, the speaker asks whether modulating the gut to improve bifidobacteria is feasible and notes collaboration with multiple centers, including MD Anderson. The implication is to start modulating the gut and improving bifidobacteria in cancer patients rather than relying solely on chemotherapy and immunotherapy. In summary, the research conducted at Progena Biome—a research lab—focuses on bifidobacteria, its variable presence across diseases, its potential replenishment in autism, and its association with cancer progression, highlighting ongoing work to modulate the gut microbiome as a therapeutic strategy.

The speaker investigated a commercially available microbe, typically given to infants in small doses. To increase the dosage, they created a yogurt-like substance to amplify the bacterial counts a thousandfold. The speaker observed effects in the mice they studied. Surprisingly, the speaker claims that every observation seen in mice has also been observed in humans.

The speaker observed three different groups of immune responses when examining data in more detail. One group experienced less inflammation overall, while two other groups had mixed results. The speaker found that individuals with the highest diversity in their gut microbiomes at the start of the study were the most likely to experience decreases in inflammation. The data suggests that a diverse microbiota, potentially better equipped to degrade various dietary fibers, may lead to a more positive response. Conversely, individuals with a depleted gut microbiome may not respond as well.

Two twins with severe autism and nonverbal communication are described; their microbiome is identically the same, with the same groups of microbes. After you correct their microbiome, you flip that formula to becoming good microbes high, low bad microbes down. And those kids are speaking and fully verbal, fully reading, that's the gold. Because now you know, well, have clinical significance, but I also have a microbiome assay that tells me that my kid has improved. The speaker emphasizes 'the gold' as the result of these changes and references a microbiome assay to demonstrate improvement. This is presented as significant.