Endemic Fungal Pathogens are making you crazy and then killing you: Cosmic Death Fungus Spotlight
An essay by Michael "myconull" Nolivos based on the research of Seth Peribsen and Cosmic Death Fungus.
Introduction
A problem well stated is a problem half solved - Charles Kettering
This is my unofficial sequel to Riva Tez’s essay on the single-cell parasite Toxoplasma Gondii. Inspired by Paul Ewald’s book Plague Time, Riva does a great job to layout this scaffolding: the microbial theory of mental and chronic disease; the factor of latency and delayed onset of sickness; the endemic classification of these issues; and the importance of wielding scientific and epistemic anarchism to help uncover new paradigms. Riva calls for more scientific anarchism in science. To this, I say: What did you think scientific anarchism meant? Vibes? Essays? Actually, yes. In this essay I’ll use the same scaffolding but based on endemic fungal pathogens.
Background and Disclaimer
I am not a biologist. I am an enthusiastic researcher who enjoys looking for assumption errors in different fields. - Riva Tez
Same! I'm Mike Nolivos. Software engineer by day, enthusiastic assumption error researcher by night. I’ve been researching fungal pathogen systems for 10 months now, following the public research of Seth Peribsen (a pen name). I’m not a biologist, but I have the curiosity and time to deep dive and absorb a large amount of information. I consider myself part of the massive wave of incoming AI-native researchers. I personally rely on Perplexity and frontier LLMs during my research journey. I’ve used AI to verify statements of fact, check connections, rapidly explore new lines of research. Even though this isn't my area of expertise, I'd like to think I've been able to get up to speed with the help of AI. Many of the sources I provide below are Perplexity links where you can continue the discussion or research yourself.
Obligatory Disclaimer: This essay should not be considered medical advice.
An Accidental Discovery
In science, sometimes it’s an accidental discovery that brings about progress. That’s what happened when researcher Seth Peribsen made an accidental discovery after a visit to the doctor. Upon taking prescribed anti-fungals that triggered significant relief from lifelong APECED (a rare genetic autoimmune disorder), Seth discovered that he was suddenly getting better. APECED had plagued him for his entire life up to that point. This led him to further pursue a theory where fungi were the root of the issue. You can learn more about Seth's journey from the several interviews he has given here.
What is the cosmic death fungus?
The “cosmic death fungus” is a catch-all phrase to describe a specific genera of human invasive fungal pathogens. These fungi include (but are not limited to): Candida, Aspergillus and Cryptococcus. The “Cosmic” prefix is based on the premise that these fungi may have cosmic origins, aligned with a panspermia theory. The origin of these fungi is not the focus of this essay. In case you’re interested though, this study estimates the Earth gets hit with roughly 100/tons per day of cosmic space dust. Space dust with extremophile microbes hitching a ride, and with smaller pieces that are light enough to slow down and avoid destructive fireballs upon atmospheric entry. But let’s set aside the origin story. The fungi are already here on Earth, and they're a problem.
It’s Plague Time
What inspired me to write this essay was Riva’s essay on t. gondii and the book “Plague Time: The new germ theory of disease” by Paul Ewald. For me, Plague Time is probably required reading for a serious exploration of chronic disease. Paul Ewald published Plague Time in 2002, and one of the criticisms in the preface of the book was that it was published “twenty years too early”. As I read that now in 2024, this timeline may yet turn out to be prophetic.
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Myco in biome?
I’ll argue that these fungal pathogens are (already) stealth endemic. They're making you crazy. And they’re ultimately killing us. Another title for this essay could be “We should really also be looking at endemic fungal pathogens!”
Fair warning: this might be a bit unsettling. If you are a brave epistemic researcher, read on.
Endemic fungal pathogens…
An epidemic refers to a disease spread across a local region: for example, an isolated flu outbreak in a city. We should all know what a pandemic is by now. It is an epidemic disease that has spread over a much larger area: for example, a country, a continent or the whole world. The next level up of disease spread is classified as endemic, and endemic diseases are the focus of this essay. An endemic disease has a level of permanence, but the term does not confine itself to a locality. - Riva Tez
Fungi pathogens are endemic. The fungi Cryptococcus neoformans (C. neoformans) is often described as ubiquitous in the environment:
Cryptococcus neoformans infection is acquired from the environment. Because it is ubiquitous in soil and dust, exposure to the organisms is practically unavoidable. The organism, most likely in an encapsulated form, is inhaled into the lungs and deposited in the small airways. Source
“Practically unavoidable”. Huh. Human exposure is thought to be as high as 70% by age five (Source). This determination of ubiquity can be found in multiple studies. This is an escalation of pathogen distribution compared to T. gondii. The infection pathway of T. gondii is based on food contamination and cats (allegedly). Now think about how often we played in the dirt as kids. It’s probably a tough pill to swallow, which is why this information can be a bit unsettling. You probably have some c. neoformans in your microbiome and don't even notice it. I talk more about the stealth latent nature of crypto later on.
Aspergillus is also considered ubiquitous in indoor and outdoor settings. It can be found in soil, decaying vegetation, seeds, grains and indoor and outdoor settings. One study tested 40 homes using air sampling methods and found invasive aspergillus in every single home. If you're gardening or doing lawn work, aspergillus is a concern and it is often suggested to wear N95 masks while gardening for this reason.
Candida albicans is so common it's traditionally been considered a normal part of the normal flora in humans. If you were to take a lab test, there is an "acceptable" threshold amount of antigens or anti-bodies before concerns would get flagged. The big system already assumes everyone has it, and maybe so should you. It is present in the mucous membranes, gastrointestinal tract and skin. This assumption of normality stands out considering that it is classified as a fungal pathogen in the literature.
Fungal pathogens are already endemic. There is an invisible world of microorganisms in the environment and within us, the microbiome. This might seem obvious, but it needs to be stated in context. Because it's usually bacteria, viruses or other parasites that have the attention from a biology perspective. To an amateur like me, fungi seemed to have been sidelined, except in popular culture (The Last of Us game franchise comes to mind). In a study on "Microbes and Mental Illness", the list of pathogens were identified and fungi were at the bottom of the list. Last, but not the least?
Fungi are making you crazy…
“Microbes and Mental Illness: Past, Present, and Future” is a massive review of over 400+ studies. It examines the premise that there may be a link from microbial infection to psychiatric outcomes including “autism, schizophrenia, bipolar disorder, depressive disorders, and anxiety disorders, as well as suicidality and aggressive or violent behaviors”. The links between psychiatric outcomes and microbes is startling.
Candida, Aspergillus and C. neoformans are included in the list of microbial pathogens in that study. Here is the unsettling truth: the fungi C. neoformans is known to cross the blood brain barrier, evade immune response and colonize the brain. There are several strategies for doing so, including the “Trojan horse” mechanism of hitching a ride *inside* a white blood cell. Another mechanism is the "seed cell" morphotype. Sized regularly at 5 microns, the C. neoformans seed cells morphotype goes even smaller to enable further host dissemination.
C. neoformans has a (horrifying) affinity for the brain and cerebral spinal fluid. It shows a predilection for certain brain areas including (but not limited to) the basal ganglia, cortex and cerebellum. This regional preference may be due to higher concentrations of nutrients like inositol and neurotransmitter precursors that C. neoformans can utilize, including dopamine.
C. neoformans can use dopamine as a precursor to synthesize melanin, which the fungi can use to increase virulence. Melanin for crypto acts like biological shielding. How much dopaminergic manipulation by fungi is happening in the neurobiome? If these fungi can get in the brain, as the data suggests, they must be doing something there. Probably nothing good. But the brain isn't the only place where fungi can have a negative impact.
The Second Brain
The enteric nervous system is a 500 million neuron network in the gut. It is often referred to as the "second brain" due to its size and complexity. This is roughly the same amount of neurons as in the spinal cord. It can operate independently of the brain and consists of layers throughout the gastrointestinal system. What impact do infectious fungal pathogens have on the second brain?
Steering of the Host
You may have heard of the cordyceps fungi, the so-called zombie fungus. These fungi achieve bio-mechanical control of a host ant after invasion, steering the ant to climb to treetops where the fungus can fruit and disseminate spores further. Absolutely terrifying for the ant. But could this also happen in some form to humans? Are fungi steering us like Paul Atreides? It was difficult to imagine in the Dune movie franchise how the hero, Paul, could steer a massive worm while riding it. That is until the director Denis Villeneuve showed the concept of opening and closing breathing holes on the worms body. Then it just made sense.
Fungi host steering in humans is a horrifying concept. There is a range of implementation details to consider. I think there is an anchoring bias to the depictions of zombie ant fungus in nature and mind-controlling fungi in gaming. That's what I would consider an extreme end. From another perspective, host steering by fungi could be as simple as an intervention of a single but important metabolic pathway. This type of steering could lead to an imbalance of the body's homeostatic equilibrium.
One such pathway under investigation by Seth is the tryptophan metabolic pathway. You can see in the image below the "fork in the road" that the tryptophan molecule can take. It's a simplification but it's useful for visualization. Depending on how tryptophan gets metabolized, it can lead to different outcomes. From an immune system perspective, these outcomes can be extremely consequential.
One study published in the Journal of Immunology in 2010 examined how candida can dampen the host defence by downregulating IL-17 production. I asked GPT-4o what IL-17 was:
IL-17, or Interleukin-17, is a pro-inflammatory cytokine that plays a crucial role in the immune system, particularly in the body’s defense against bacterial and fungal infections. IL-17 is involved in the recruitment and activation of neutrophils, which are essential for the clearance of extracellular pathogens. It also stimulates the production of other pro-inflammatory cytokines and chemokines, amplifying the immune response.
A pathogen messing with IL-17 seems like a major issue. And what did the study conclude?
...we found that live C. albicans shifts tryptophan metabolism by inhibiting IDO expression away from kynurenines and toward 5-hydroxytryptophan metabolites. In addition, we show that these latter 5-hydroxytryptophan metabolites inhibit IL-17 production. In conclusion, live C. albicans inhibits host Th17 responses by modulatory effects on tryptophan metabolism.
"Modulatory effects on tryptophan metabolism". There it is. See what I mean? So it seems like candida can manipulate the hosts immune response in a reinforcing feedback loop to its own benefit but at our expense. Another significant observation that Seth has frequently highlighted is the bufotenine connection. The following is the abstract of a 1995 study considering bufotenine as a diagnostic indicator for psychiatric disorders:
We have analyzed products of the serotonin-degradative pathway, in which both N-methylserotonin and bufotenine are formed in urine specimens of products with psychiatric disorders by three-dimensional HPLC with electrochemical detection. Bufotenine was detected in urine from all autistic patients with mental retardation and epilepsy (n = 18) and many autistic patients (32/47) with mental retardation. Bufotenine was detected in the urine of 15 of 18 patients with depression. Thirteen of 15 schizophrenic patients were also positive for bufotenine. N-methylserotonin was also detected in some cases of each disorder. Only two of 200 urine specimens from healthy controls were positive for bufotenine. Thus, the presence and levels of bufotenine might be useful and important markers of some psychiatric disorders.
This study design was replicated 15 years later in 2010 by the Department of Health Sciences of the University of Pavia, Italy.
Results: Urine bufotenine levels were significantly higher in ASD subjects (3.30 +/- 0.49 microg/L, p<0.05) and patients with schizophrenia (4.39 +/- 0.43 microg/L, p<0.001) compared with controls (1.53 +/- 0.30 microg/L). Among patients with ASD, there was a significant positive correlation between urine bufotenine and hyperactivity scores on the Vineland Adaptive Behavior Scale (r=0.479, p<0.05). No other associations were detected.
Let's return to the tryptophan metabolic pathway. Considering the below chart, tryptophan is a fork in the road where on the one hand leads to bufotenine (a type of DMT). On the other hand, on the right hand side, the path leads to endogenous DMT, NN-dimethyltryptamine. This is the type of DMT that the body naturally makes. Endogenous means originating from within (internal), in contrast to exogenous originating from without (external). The Hallucinogen _N,N_-Dimethyltryptamine (DMT) Is an Endogenous Sigma-1 Receptor Regulator. Sigma-1 is common receptor throughout the body and plays an important role in fungal pathogen resistance via calcium signalling. Calcium signalling is one of the ways how fungal pathogens "see" in the inner world that is our bodies.
This ENN-DMT connection is Seth's research which I am only paraphrasing here. The big takeaway here should be that fungal steering of human hosts doesn't need to be a dramatic Hollywood affair. It can happen at a microscopic level, one molecular interaction at a time.
Fungal steering is reinforcing feedback loops that would benefit fungi at our immune system expense. Whether these steering interactions are occurring, and how did these interaction come about are open research questions. How can we go about thinking about these questions from first principles? One way is to examine the concept of fungal intelligence.
Fungal Intelligence
If you were to map intelligence on a spectrum, it's important to understand where fungi fall in relation to viruses, bacteria and other parasites. This adds additional context when discussing virulence, immune evasion, and pathogenicity. It might also shed light on the possibility of fungal steering of human hosts.
Fungal intelligence is a thing. The focus has usually been on bacteria and then viruses, with fungi recently reaching more recognition. Fungal immune evasion strategies are very complex and dynamic. As a computer scientist, their biological programming seems to me like a vonn Neumann probe. Except instead of exploring and colonizing space, the space being colonized is our bodies. All of the elements are there: travel (candida hyphenation extension and spatial re-orientation), resource gathering (see candida albicans metabolic adaptions), immune evasion and self-replication. Take note in the below chart of decision making and spatial recognition abilities with candida, and the manipulation by fungi of other organisms.
If it can happen in nature, it can happen to us. We are a part of nature after all. A healthy human is normally too big of an organism to steer fully. But then again, have you ever wondered what schizophrenia actually is? I think about it a lot, and of fungi impacts on mental health in general.
Mental Health
Psychiatric manifestions of cryptococcal meningitis (brain infection) can include:
personality changes
irritability: increased agitation and restlessness
psychosis: some patients develop psychotic symptoms like hallucinations or delusions
depression and anxiety: mood disorders can emerge as part of the disease process
behavioural changes like aggression in some cases
It's important to highlight that cryptococcal infections can occur even in immunocompetent hosts. There is usually a disclaimer that these fungi are concerns for immunocompromised hosts. However, this could be an ascertainment bias as those with immune issues get more testing done. When was the last time you got checked for a fungal infection in your CNS?
Endemic fungal pathogens are making you crazy...
…and then killing you
Recent estimates have put the global death rate attributable to invasive fungal disease at 3.7 million deaths annually. This is subject to statistics and data collection that attribute deaths to fungal infections directly. Fungal infections are especially dangerous for covid-19 patients, CDC study warns. "During the pandemic patients dually infected with covid-19 and a fungal infection had 48.5% mortality, compared with 12.3% in patients who had only fungal infections." I think there's a lot of room for a larger total fungal death estimate than we realize.
The aspergillus fungi species produces a potent toxin (aflotoxin) that causes DNA damage. This afloxtoxin is considered a carcinogen and risk factor for liver cancer. The damage to DNA (particularly the guanine base pair) results in protein transcription errors. In addition, over expression of genes like STAT3 are implicated in autoimmune disorders. This is a "too much of a good thing is a bad thing scenario". A c. neoformans infection by itself can induce STAT3 activation and over expression (Source).
The "fungal pathogens are killing you argument" is informed from the other first principles of pathogenicity and biological entropy. If these pathogens are making us sick, affecting our body chemistry and even DNA, and they go unnoticed for a long time... eventually the bill becomes due. At this point you might be asking: Why were these fungal pathogens missed?
Stealth of the Chronic
Why didn't we realize before now?
Challenges in chronic disease study
difficulty in diagnoses. Remember C. neoformans affinity for cerebrospinal fluid? This means a lumbar puncture sample is key to a diagnosis.
The symptoms of cryptococcosis, such as headache, cough, and fever, are non-specific and can mimic other conditions, making it difficult to suspect the infection initially.
Candida is considered so common to everyone that lab testing thresholds assumes everyone already has it. Stop and think: Have you ever noticed your candida? Like Riva mentioned in her essay, we as society made great efforts for COVID-19. But latent pathogens already endemic are seemingly ignored. Even though their distribution and virulence is high, progression of disease can be slow. Their dormancy can also make infection hard to notice.
A 2019 study analyzing the microbiota of children with autism and their mothers found the same markers of fungi. This "dysbiotic" state of blood was determined:
a decisive argument for proven presence of Aspergillus fumigatus in almost all of the autistic children. As it was demonstrated in our previous study, filterable L-forms can be transmitted by vertical pathway from mother to child before birth. Thus, it can be suggested that autistic children may be born already colonized with fungi, while a “silent aspergillosis” could contribute or even be a leading cause for neurodevelopmental disorders in the early childhood. Source.
Silent. Stealth. Undetected at birth, born already colonized. Is autism fungal? The human body is extremely complex. Speaking with certainty on these topics seems dismissive of that complexity. The answers to a lot of chronic infectious disease aren't going to be simple. Still, the fungal connections are difficult to ignore.
Challenges in Chronic Disease Study
Riva explains the challenge in understanding pathogenic causes of chronic disease:
It’s tough to determine whether a pathogen plays a causal role in a given chronic disease. Maybe that’s why contemporary biomedical research doesn’t go after it with the same gumption it does for other causes. Firstly, the timing delay between exposure to an infectious pathogen and the appearance of a chronic disease could be decades. This creates a study timing problem, which can only be solved if you have a large enough population sample to correlate infectious disease antibodies and noncommunicable disease symptoms. But still, that’s not enough. Different genetic variants of infectious pathogens manifest in people differently. Furthermore, genes may play a role in the onset of a chronic illness.
…continued…
It’s largely unethical to infect humans with pathogens to study them, and how these pathogens manifest in laboratory animals may also be different. On top of that, we would expect pathogens to cause diseases indirectly, such as via autoimmune processes induced by the pathogen. This seems to be the case for several chronic illnesses, and it makes it hard to track. Biology is complex. Unfortunately, we reward researchers for finding one piece of the correlation puzzle and then rely too heavily on it, ignoring the forest for the trees.
Let's talk about pathogen dormancy now. C. neoformans evolved in the wild being swallowed by amoebas. So when this fungus encounters a white blood cell immune response (phagocytosis), it’s not a problem. It gets engulfed and sets up shop inside. Crypto can thrive and multiply within a white blood cell, lying dormant for years or even decades. This dormancy factor is critical to understand. From when infection initially occurs and symptoms start to appear much, much later could take a very long time. They also are known to survive the vomocytosis process (white blood cell expulsion) intact. This is what makes studying these types of pathogens as the root cause of chronic disease difficult. Something else later down the line can trigger reactivation. Then these dormant fungi are released by the white blood cell and go to work.
Dormancy in cryptococcus neoformans: 60 years of accumulating evidence
This dormancy factor screws with causal attribution. "It's the vaccine! It's Bill Gates nanotechnology! It's demons! It's the spike protein!"
Note on correlation and causation
In the preface to Plague Time, Paul Ewald commented on the common critique to his book that “correlation is not causation”. His response is so important that I copied it here in full:
Consider astronomy; where would we be today if astronomers were unwilling to draw conclusions about causation from correlative evidence? If astronomers could experimentally alter the speed or composition of stars and galaxies their conclusions could be more rigorously tested, but they have been able to make pretty good progress without such manipulations. The health sciences have a greater potential for experimental manipulation of proposed causes than astronomy, but this greater potential does not mean that experimental manipulation will resolve the validity of all causal hypotheses. Science, whether health or astronomy, needs to draw conclusions on the best evidence and reasoning that are available. Hypotheses about disease causation need to be accepted or rejected on correlative evidence when experimental manipulation is not feasible. One of the messages of Plague Time is that we have now entered a period of medical history when the best standard of evidence for disease causation must rely, as in astronomy, on correlational evidence.
Matters of health that involve the gut and brain are difficult to pin down causally. There is an irreducible complexity of the microbial reality and systems interactions in the body. I'm skeptical AGI will even be able to sort that out. Ethics are also a factor. The brain might as well be deep space, because while someone is alive it sounds difficult to really validate what is actually going on there. Even MRI can only bring us back certain information. I agree with Paul's epistemic approach. Sometimes it's ok to use correlation when it’s not practical to manipulate with experiments. This doesn't have to mean being dogmatic in pursuing correlation at the expense of causation. It just means understanding the practical reality of investigations in this type of field.
Studying chronic disease is a major challenge. When thinking about this, the parable of the blind men and the elephant comes to mind. Throughout history of the science of medicine, researchers have found or understood individual parts of a larger puzzle. But is it possible there is a unifying theory that would connect to all of the other puzzle pieces?
Fungal uTOE - Unified Theory of Everything
It’s easy enough to come up with a theory that fits all the evidence you’re working with. It’s hard to make a theory that will fit the evidence you’re unaware of. The real test of a theory happens when it comes in contact with something new and relevant. - slimemoldtimemold
As part of my 10-month research journey, I’ve made it a hobby to check fungi pathogenicity applied to other kinds of treatments and diseases. I believe fungal pathogen systems theory is truly a new lens of looking at the world of health. This might make certain people mad, but this is exactly what epistemic and scientific anarchism is. Riva's essay introduced me to the Thomas Khun model of scientific paradigms shifts to explain how science progresses.
Fungi, Lithium and Mental Health
Lithium has a long history being used as a neuropsychiatric treatment (another accidental discovery). Effects on mania, bipolar/mood disorders and even anti-suicidal effects have been noted in the literature. In multiple systematic reviews and meta analyses (here and here) looking at the lithium in America’s water systems and neuropsychiatric outcomes, more lithium in the water correlated to better psychiatric outcomes.
What is a possible mechanism of action? Through the fungal pathogen systems lens, lithiums effect on c. neoformans stands out. In addition to this effect on c. neroformans, lithium suppresses hyphen outgrowth in c. albicans. How much of mental health is rooted in microbes? Perhaps lithium’s anti-fungal effect is just another blind man finding one part of the elephant but not seeing the bigger picture.
Candida and Microplastics
Candida biofilms adhere to microplastic pieces, weaving it as part of their biofilms and increasing virulence. An analogy would be like a builder using steel rebar to reinforce concrete to make it stronger. Biofilms are a critical part of fungal virulence and immune evasion. Biofilms also can hinder the effectiveness of anti-fungal treatments. What does humanity do about the microplastics problem? I’m no Sun Tzu but it seems logical not to boost the defences of a microbiological endemic pathogen. Microplastics still are a concern, but the fact that candida can use it again just shows how complex the situation is.
Alzheimers
Researchers at Baylor College of Medicine and collaborating institutions showed in this study that Candida albicans can enter the brain in animal models by breaking down the blood-brain barrier. This is achieved through the production of enzymes called secreted aspartic proteases (Saps), which degrade the barrier, allowing the fungus access to brain tissue. Candida presence in the brain triggers the creation of amyloid-beta like peptide. Traditionally, amyloid beta plaques were considered as one of the causes of Alzheimer’s. Yet there is a link to fungal presence in the neurobiome and Alzheimer's. “Immunohistochemical analyses have revealed fungal material in about 10% of cells in the brains of AD patients, suggesting that while not ubiquitous, fungal infections are a notable feature in these individuals” (Source)
Recently it was revealed that Alzheimers research may have been fraudulent. 16 years and how many millions of dollars were spent pursuing a hypothesis that was based on evidence that looks to have been doctored. What a tragedy. Even if the research wasn’t fraudulent, the hypothesis pursued could still have been misguided. Is there an explanation considering an infectious origin hypothesis of Alzheimer’s? It turns out, the amyloid beta plaques have a role as an anti-microbial peptide.
Evidence from the current literature that amyloid beta, traditionally viewed as pathological, actually acts as an antimicrobial peptide, protecting the brain against pathogens. However, in case of a prolonged or excessive activation of a senescent immune system, amyloid beta accumulation and aggregation becomes damaging and supports runaway neurodegenerative processes in AD. Source
What came first, the fungi or the Alzheimers? My grandfather suffered from Alzheimer's and ultimately passed away some years ago. RIP abuelito. Alzheimer's is a terrible disease. Writing this, I shed grown man tears. If only I knew then what I know now. Oh and look at that: endogenous DMT ameliorates Alzheimer’s disease by restoring neuronal sigma-1 receptor-mediated endoplasmic reticulum-mitochondria crosstalk.
Ultrasound
The study “Effect of ultrasound on fungal cells” showed that candida albicans yeast cells can be disturbed enough by ultrasonic frequency enough to rupture the yeast cell. Researcher Sterling Cooley claimed that "Alzheimer’s is as good as cured” based on his witnessing ultrasonic treatment helping patients. This claim triggered a large public backlash for such a bold statement, including from Martin Shkreli. I suspect Sterling may have stumbled upon an unknown side effect on fungi in the neurobiome. Sterling may have been one of the blind men probing the elephant, thinking that it's microtubule stimulation that could help Alzheimer's but only seeing one part of the mechanism of action. I've learned a lot from that backlash, which is why I'm careful with words.
Hyperbaric Oxygen Therapy
In vitro studies have shown that hyperbaric oxygen therapy (HBOT) can inhibit the growth of Candida albicans within pressure and time ranges tolerated by humans. HBOT delivers high concentrations of oxygen deep into tissues, where it can attack and kill yeast, fungus, and other pathogens (Perplexity Page). The founder of Github Nat Friedman recently announced on X relief from chronic mild psoriasis with atmospheric hyperbaric oxygen therapy, but could only find one n=2 study about this. He issued a public request for mechanisms of action, and so I proposed candida and the oxygen effect on the fungi in the replies. I received no reply. Who would believe a random person on the Internet?
Cancer
A lot of alternative methods of cancer treatment are anti-fungal. Garlic, Pau d’arco, Coconut oil / MCT oil, carrots, baking soda, hydroxychlorquine. The list goes on and on. Is this merely a coincidence or is fungi a part of cancer progression? A study found fungi in all major types of cancer. We inevitably return to the inevitable correlation vs causation debate. What came first, the fungi or the cancer?
Recently in the Journal of Orthomolecular Medicine this study was published about a protocol consisting of Ivermectin, Fenbendazole and Mebendazole as a treatment for cancer. Any drug that ends in -azole is an anti-fungal class drug by categorical definition. The paper goes to great lengths to explain the mechanism of action. When looking through the endemic fungal pathogen lens, the mechanism of action looks different. "It's not what you're putting in, but what you're taking out" is a common phrase I've heard when discussing mechanism of actions. Yet if you search in the study for "fungal" or "fungi", there are 0 results. This cancer topic is much bigger than I can fit here so I’ll leave it there.
The Elephant in the Room
I understand the need to try to guard against confirmation bias, anchoring bias and other tricks the mind can play. If all of these correlations didn’t keep happening, that would be great. Instead what happened to me in my research journey is the correlations continued to stack up. And then I really did start wondering, has everyone got it wrong? Is this actually something that all of the world’s top scientists and doctors missed? I now think it's indeed quite possible. Chronic latent microbial infections are that much of a challenge to detect, and the fungi seem a lot smarter and more ubiquitous. I became sort of obsessed with this idea. How can you not be intrigued by this possibility? The implications would be revolutionary for our understanding of chronic disease. It would be Thomas Khun’s fourth phase.
The list of correlation goes on and on without an end: from compounds like methylene blue, lactoferrin, and IP6 all the way to fruits like coconuts and pomegranates. Feel free to check these for yourself. There’s an anti-fungal effect for each of those, and it’s not some kind of groundbreaking research. It’s already in the data. The theory of fungal pathogen systems proposes that a simpler explanation has largely been missed. Anti-fungal effects of these compounds combined with endemic fungal pathogens.
At some point, these fungi stop looking like any another pathogen. Fungal pathogen systems theory starts looking like a novel unified theory of everything (health related). The inflammation, toxicity and even genetic nucleotide damage caused by these fungal pathogens could explain the progression of chronic disease, and even aging.
To close the loop on t.gondii, I'll propose some first principles:
Fungi are more numerous in nature than single celled parasites
Though they are roughly the same size (4-8 microns for t.gondii), but as discussed C. neoformans can go even smaller with the seed cell morphotype (so they can get into tighter spots)
Like the Internet, more nodes in the network means more intelligence and capabilities. These fungi pathogens form colonies and the fungi species demonstrate advanced empirical intelligence. A colony is more dangerous and capable than a single-celled loner.
From these first principles, you can reason that pathogenic fungi are at least one order of magnitude worse than t. gondii. I realize it's not a clean comparison, as we're comparing multiple species of fungi against one, but you get the idea.
A problem well stated is a problem half solved
Endemic fungal pathogens are making you crazy and then killing you. It’s a black pill, but it's still just the beginning. There are real reasons to be optimistic: understanding a problem well enough is an important step to solving it. There are also other strategies to validate biological hypotheses. Another way to try to figure out what's happening in the body black box is by reverse engineering: Starting from the hypothesis and then working backwards. There is still so much more that I could have included in this essay. But this is the point where this essay ends, and the CDF protocol begins.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8929585/ - Lithium is also neuroprotective against dementia.