Malassezia as a causative agent in paranoid schizophrenia
SERIOUS TRIGGER WARNING
I believe my paranoid schizophrenia was caused by a common fungus known as Malassezia, most likely M. furfur, which may manifest itself in Tinea versicolor (self-diagnosed).
What’s written in here has two parts to it. The first is based on personal stuff/knowledge mixed with some unreferenced information; this part may be seen as delusional crap given that am a schizophrenic. The other part contains passages from quality articles/case reports which may help me put forward an argument regarding my case. If you feel there is too much schizophrenia in the first part then skip through till the first referenced title below.
I think Malassezia fungus began a colonization process a long time ago slowly spreading to my organs so it can end up with a body perfect for optimal, sustained growth. I suspect it manipulates the hypothalamus and the endocrine system. In nature, there are many examples of germs manipulating hosts’ behaviour like in zombie ants while certain infections in humans can lead to psychoses.
Schizophrenia is a whole-body illness and this fungus covers humans from head to toe and is also found in the GI tract. It doesn’t normally provoke immune system reactions and little is known about it because it’s not easily isolated and grown in laps.
I believe it’s also behind many health issues because it causes chronic swelling around the body. This fungus is highly responsive to (based on personal observations):
Diet. For example: loves dairy/fats and hates coffee/citrus fruits/water.
Hormones; like sex and stress hormones.
Air; grows in humid and germy atmosphere such as the bathroom especially closer to a floor drain (gases coming out of the sewage system). This factor along with diet seem to produce the biggest impact on Malassezia in my body.
Smoking.
Immune system weakness.
Some research findings about schizophrenia may be explained while considering Malassezia as a cause:
Schizophrenia is more common in the city. This may be the result of having an extensive sewage network and much more sewer gases compared to a rural area.
Schizophrenics in developed countries are less likely to get better. Developing countries lack sewer infrastructures which is good for schizophrenics given that this hinders the growth of Malassezia.
Countries in Southeast Asia have the highest rate of schizophrenia. It’s hot and humid in these countries in addition to the type of toilet used in the region.
Seasonality of birth in schizophrenia may be attributed to humidity in the months before or during giving birth when the fungus colonization increases and is more easily transmitted to newborns before their immune system fully develop.
Simple personal observations about Malassezia (many bizarre stuff; I believe it’s very capable of doing things):
When it gets into a favorable atmosphere for it to grow; it will induce a feeling of sleep in the host. For example; opening the window when its humid outside or using the toilet. I could literally hear abdominal sounds by simply walking into the bathroom just to wash my hands. It should be the fungus changing the endocrine system so that I stay longer in there by making me feel relaxed. It does it maybe by squeezing on the glands or through the hypothalamus or just because of rapid growth. I think it has the ability to make muscles and tissues contract and relax maybe by using tissue fat/lipids or by collective binding/adhesion. The human brain in 60% fat.
If I eat something it likes like eggs then it will immediately narrow my GI tract so it can feed better and keep it for longer. This lead to bacterial overgrowth which weakens the host. A study found that schizophrenics have different throat bacteria while lactic acid bacteria was at least 400 times higher than in control subjects. On the other hand, drinking black coffee will widen the digestive system because the fungus is aversive to it and will try to eliminate it quickly. This is similar to IBS. Fasting alleviate my negative symptoms.
Lime has been my greatest weapon against this fungus and I aim to convince others like me to at least consider Malassezia as the cause of their schizophrenia by performing the following experiment. At least 15 kg of fresh whole lime will be needed (I used 40 kg). Spread the lime on the floor according to your body so you can lie down on them, with your head, all the way down till the thighs, is touching the lime. Try to do this for few hours and change between laying on stomach and back; try to listen to any abdominal sounds. Ideally, you should be without clothes and use a blanket to cover yourself. Doing this will make you lose internal fats rapidly and drive a lot of the fungus out of your system (taking antifungal medications will do the same but this is quicker and more effective). Fat is what Malassezia feeds on. It will also halt what the fungus is doing to your body and you should be able to feel much better afterwards. You can also ingest lime peel; cut into small pieces. People drink lemon water to flush their digestive tract; I think this happens because Malassezia doesn’t like lemon and will try to avoid it. After your finish, keep the lime near the bed for no longer than a couple of days before it begins to grow fungus. Having the lime around you will still have an impact on the fungus even you aren’t physically touching the lime. Think of lime as a kryptonite to Malassezia (lime peel contains phytochemicals which are released by plants to thwart pathogens; maybe this is why it works). Another way to manipulate the fungus is to pour thick black coffee into a number of buckets and keep them close to you (I surround myself with 8 small buckets; 200 g of black coffee with minimal water in each; coffee will last longer than lime).
If your schizophrenia is caused by this fungus and you want to observe how its impacting your body then it’s important that you make enough recovery first so that you become capable of noticing the things it does as it attempts to regain control of the body.
It targets the immune system. I successfully got rid of a tinea versicolor patch at the base of my lumbar spine and immediately it felt as if some sort connection was reestablished within the spinal cord (I make the patches burst by applying heat using a metal; they release some kind of odorous gas as they burst; feeling the applied heat on the skin is instantly regained as these patches burst; I wonder if Malassezia produce and hold such gas inside the body). After a short while I can tell my immune system is more active in attacking the fungus throughout the body. These fungal patches have an adverse impact on internal organs including the brain and I suspect they greatly lower blood supply by constricting blood vessels/arteries. All of these fungal spots work within connected networks, so if you rub a lime against a particular spot for long enough, other spots will also be irritated somewhere else in the body. I believe a master patch which forms under the skin around the nasal bone, where there is increased sebum production, is what controls these fungal networks because it’s the most established and active of all. Fungal networking is known in mycorrhiza.
It is careful not to expose what it does. It causes sickness very slowly over the years so the host remains unsuspecting and when the immune system becomes weak enough it begins a process that lead to psychoses. It won’t attempt to take over the host unless it has developed the necessary networks throughout the body. The first episode is when it takes control and risk exposing its pathogenesis but at the same time it desensitizes the host. We become numb, hardly itch, sneeze or cough; the mouth and eyes become dry while blood and fluids have a hard time circulating the body and it never allows the immune system to make a proper recovery.
The way this fungus reclaims my brain after stopping the treatment feels like it constricts or tightens the sides and back of my neck area and the scalp feels as if it’s being pulled upwards. It feels as if the fungus forms an invisible circle round the head then I become oblivious again. In this way, my schizophrenia has its basis outside the brain; in the skin which is the largest body organ and has a role in both nonspecific and specific immune responses.
It undertakes a process to make the host psychotic. The few weeks after my positive symptoms disappear is a time during which I feel most friendly and calm. I think this is due to having overall less of Malassezia formations in the body because inducing psychoses requires the master patch (the fungus in its developed form) to release many of these formations so that a number of selected processes, functions and secretions within the body resume while it retains other formations just to initiate a state of bodily chaos. As time passes my health, immunity and anxiety deteriorate gradually as the lost formations are built again. Hours before my psychoses begin it causes sepsis-like symptoms until I become paranoid and this happens after many patches appear at once for a short time throughout my body. Maybe this large release or activation of these fungal formations is what causes the mild sepsis or some kind of systemic inflammatory response.
It becomes very active/pathogenic in the days before psychoses start and this is the time when I can feel it the most as my immune system is compromised. I can literary feel the fungus being active in my ears and when it comes into contact with my body during, for example, getting closer to another person or a floor drain in the bathroom. Things like passing by the sewer pipes in the building car space or being near the sea will wear me down. A member of the forum said that schizophrenia is “a yeast infection that grows in your ear”. I believe this is very true in my case but it also goes beyond the ear and deeper into the body.
This fungus manipulates the hypothalamus to allow for better growth throughout the body. My body temperature remains elevated for a long time which is good for the fungus. It also causes fluids retention in the midsection and face as well as dehydration without making me feel thirsty. There is also insomnia. These functions are supposedly regulated by the hypothalamus. Moreover, sometimes it deliberately sends troops through the nose to the lungs so that they spread there without causing an overt infection; it just causes a slight occasional pain in the lungs. This happens before my psychoses or after taking a course of fluconazole.
It will make new formations in any cuts in the skin or inside the body like in a tooth extraction. I get a rapid recovery due to antifungals but at the same time I get itchy knees; this happened twice. During the second time, I thought I could apply an antiseptic salve on the knees so I made 4 small cuts in the skin around each knee. The next day I can see new Malassezia formation on each of these cuts. With the use of antifungal cream, Malassezia formations became visible on and around previous surgical cuts around the body particularly in the abdominal area. In addition, increased Malassezia growth worsens pain associated with a herniated disc in my lumbar spine; I don’t know if Malassezia is already there or this happens because of reduced circulation due to its overgrowth. Moreover, my diabetes mellitus worsened before schizophrenia started; this could be a factor in fungal overgrowth.
I think it causes the organs to be saturated with sebum, thus the swelling. My Fordyce spots dissipate as Malassezia decreases. During the lime and antifungal treatment, there was increased urination and expulsion of both hard and soft sebum through the skin from different sites of the body while the GI tract was getting rid of some sort of a substance.
Skin sensory receptors where the major fungal formation sets near the nasal bone were almost inactive. There were two white strips hardly visible under the skin and nothing seemed to help against them. I used something a bit invasive to get rid of them; hardly any pain was felt and there was no blood flow to the surface of the formation site. It was common to have a clear fluid coming down from the nose after my first psychotic episode.
Supplements helps the immune system against this fungus. In particular, selenium, vitamins E/D/C, and omega 3 are most useful. Any vitamins/minerals that play a role in immunity seem to help.
I have had always noticed a change in the alignment of my eyes after my first psychotic episode; most likely because of inflammation behind the eye and in the brain. During a course of antifungals, I experienced a feeling of readjustment in my right eyes followed by tears. At one point I also felt blood rushing to my head from the chest area. I don’t know if I was delusional but I also felt a connection being reestablished between the heart and the parietal lobe. I tend to lie down for hours when I try any treatment; it helps me feel any changes in the body.
It targets the thyroid gland. I remember having slight pain in the thyroid area during the two weeks before my first psychotic episode. I noticed a single fungal spot where the thyroid is after the first time my positive symptoms ended; this spot became more established with each psychotic episode. Before schizophrenia, I never gave much thought to what I assumed to be eczema on my scalp for years. The appearance of a lone fungal spot so close to the thyroid coinciding with my first psychoses made me a bit suspicious of it.
It may sound crazy likening what happens to zombie ants to some schizophrenics. Nevertheless, it happens in nature and we are part of nature while schizophrenia remains a mystery. What gave me the courage to write and post this is the fact that I’ve been making a great recovery from the brink of having psychoses and I do it by simply considering Malassezia as the culprit and subsequently doing whatever I could to fight it off. Please keep in mind that tinea versicolor may not be visible. I thought it was only on my scalp but with the treatment I found out it was all over my body specially the back while Malassezia is also associated with a number of different skin conditions like dandruff. Am hoping those who suspect their illness is caused by some sort of microorganism will experiment with a pile of lime and report what happens to the forum.
A lot of what is mentioned in this informal writing may be irrelevant details but it’s an effort to first find schizophrenic patients who can relate to anything mentioned here and then to entice relevant professionals to become suspicious of Malassezia as a causative agent in the illness. As to why I believe such a common fungus is causing my schizophrenia, I simply think it developed into an advanced form which puts my immune system in a constant jeopardy; I can think of some unique subtle ways I helped it get there. Nevertheless, I find it easy after my initial recovery to manipulate Malassezia due to its overgrowth while I understand it cannot be totally eradicated from the body. For me, there is nothing more encompassing than this fungus in trying to explaining my schizophrenia as it affects the whole body and is responsive to many factors both external and internal. Furthermore, it feels tempting to start hypothesizing how Malassezia could impact the brain. For example, given it has the ability to manipulate lipids and fluids, it could have an impact on blood-brain barrier integrity or find pathways to absorb gray matter elements, thus causing structural changes in the brain.
The following is from the internet with some elaborations; it may be relevant to what is mentioned above.
Title: Seborrheic dermatitis flare in a Dutch male due to commensal Malassezia furfur overgrowth (Oxford University Press; 2008).
“A 57-year- old male from the Netherlands… was hospitalized for bilateral weakness of his extremities and irregular fever. These symptoms were suspected to be the result of a brain embolism. Brain CT and MRI showed multiple, low-density lacunae in bilateral basal nuclei, thalami and frontal lobes denoting a brain embolism. Chest X-ray, abdominal ultrasound check, blood cultures, and serum HIV antibody were negative… Cerebrospinal fluid (CSF) examination included culture and smear for bacteria (Gram stain) and fungi (India ink examination) and Mycobacterium tuberculosis antibody. All tests were negative. Since the reasons for fever were not clear, the patient was not given any antibiotics. A dermatology consultant was requested since he presented with bilateral erythema and desquamation that was distributed on his cheeks and submaxilla area. Although the erythema was present for 10 years, the patient did not experience any discomfort and thus he had ignored it. However, the erythema had become more severe within recent weeks, extending to the post aurems, temples and the hair line with increased numbers of greasy scales…. These results indicated Malassezia furfur… Since a clinical and mycological diagnosis of Seborrheic Dermatitis (SD) was made…. The condition was treated with itraconazole capsules… Moreover, the patient was instructed to wash his face with 2% ketoconazole shampoo and to topically apply a cream containing 1% naftifine hydrochloride and 0.25% ketoconazole. His temperature almost immediately returned to normal within one day of treatment and the erythema was lighter with less scaling after 7 days. Direct microscopy and culture were performed once a week for 3 weeks during therapy and one week after discontinuation of systemic and topical therapy. All examinations were negative and no-side effects were noticed with a total of 5.8 gram of itraconazole…. It is accepted that there are three interrelated factors in SD: Malassezia overgrowth, sebaceous glands over secretion, and abnormal host response to Malassezia yeasts on the skin…. The case described herein shows that M. furfur is involved in SD because this patient had a large number of yeast cells in the scales… Additionally, the patient was cured with a combination of antifungal agents. Direct microscopic examination and culture after antifungal treatment were negative, which further implicates M. furfur as the etiologic agent of SD in this case… It is difficult to demonstrate a relationship between the flare of SD and the fever, but the patient’s fever was unexpectedly alleviated through the use of itraconazole, without receiving any other antibiotics. This may indicate an undetected Malassezia fungemia as blood and CSF cultures were negative for bacteria and neutrophil count was within normal limits”.
This case report above is very relevant in terms of making an association between brain abnormalities and Malassezia.
The basal ganglia/nuclei “are the site of most of the dopamine neurons in the brain” (Basal ganglia pathology in schizophrenia: dopamine connections and anomalies; Journal of neurochemistry).
Title: Research Sheds Light on the Risks and Causes of Schizophrenia (WKSU org; 2018).
“Still, Messamore acknowledges that our explanations for schizophrenia remain vague, its mysteries only deepened by bizarre clues, beginning with our skin…. Messamore is among a handful of researchers who have looked in the unique response people with schizophrenia have to what’s called the niacin flush…. Messamore has a theory. He says it has something to do with the way our body signals inflammation, both in the skin and in the brain…”.
Dr. Erik Messamore runs the Best Practices in Schizophrenia at Northeast Ohio Medical university.
A study involving 163 patients with schizophrenia found a third of them displayed a blunted response to niacin skin flushing test (Simple Skin Test May Help Identify Schizophrenia; Medscape; 2017).
Title: Schizophrenia as a membrane lipid disorder which is expressed throughout the body (NCBI; US National Library of Medicine; 1996).
“Clinical, biochemical and genetic evidence now indicates that schizophrenia is a disorder of membrane phospholipid metabolism associated with increased loss of highly polyunsaturated fatty acids from membranes owing to enhanced activity of a phospholipase A2. This changes the properties of membranes throughout the body and is responsible for such physical abnormalities as reduced vasodilator responses to niacin and histamine and altered immunological functions. A modest membrane abnormality is likely to produce its most serious consequences in the brain….”.
Phospholipase is necessary for the growth and pathogenicity of Malassezia (The lipolytic enzymes activities of Malassezia species; NCBI; US National Library of Medicine; 2009).
“Malassezia furfur is a lipophilic yeast that has been related to inflammatory skin conditions such as seborrhoeic dermatitis and psoriasis. We have previously reported that this yeast secretes enzymes capable of metabolizing complex lipids. This lipolytic system is critical for M. furfur growth, since the yeast has a strict dependence on an exogenous source of fatty acids…. M. furfur secretes enzymes having phospholipase A2 activity…. This enzyme liberates arachidonic acid from Hep-2 cells…. Arachidonic acid metabolites are well-known mediators of skin inflammation… we established that M. furfur can trigger an inflammatory response per se by releasing metabolic products” (Arachidonic acid released from epithelial cells by Malassezia furfur phospholipase A2: A potential pathophysiologic mechanism; Indiana University; 1998).
Arachidonic acid has been also implicated in schizophrenia (Arachidonic Acid: A Common Link in the Biology of Schizophrenia; JAMA Psychiatry; 1994)
Title: Brain’s immune cells hyperactive in schizophrenia (The Guardian; 2015).
“Although the causes of schizophrenia are unknown, inflammatory processes have already been implicated in it. Patients with schizophrenia exhibit elevated levels of small, pro-inflammatory proteins called cytokines…. Microglia are the brain’s resident immune cells, which form its first line of defense against infection and injury. In any such event, damaged neurons emit a distress signal, which activates microglial cells and attracts them to the damaged or infected site, where they proceed to engulf and neutralize pathogens…. This occurs by a process called phagocytosis…. We now know that microglia eliminate unwanted synaptic connections in the same way that the remove pathogens and damaged cells, engulfing them by phagocytosis. This process, called synaptic pruning…”.
Malassezia causes the production of cytokines; this is mentioned in the following article.
Title: The Malassezia Genus in Skin and Systemic Diseases (American Society for Microbiology; 2012).
“Malassezia yeasts demonstrate a species-specific ability to interact with cells that are constitutive members of the skin… or cell lineages that are involved in immune functions, including antigen-presenting dendritic cells, macrophages, eosinophils, and neutrophils. The exposure of the above-mentioned cells to Malassezia yeasts or their products has been shown to induce the production of a variety of cytokines… Interestingly, the contact of Malassezia cells with serum and subsequent opsonization increased their ability to induce IL-8 expression in a macrophage cell line and a granulocytic cell line… The involvement of Malassezia yeasts in the development of pityriasis versicolor illustrates the excellent adaptive mechanisms which this yeast possesses… In the two most common clinical forms of this disease, the hyperpigmented and hypopigmented forms, there is a significant fungal load on the skin but without any inflammatory alterations being observed. This has been partly attributed to the production of an array of indolic compounds produced by Malassezia species, in particular M. furfur, that have the ability to downregulate aspects of the inflammatory cascade. Thus, indoles like pityriarubins impede the respiratory burst of human neutrophils, while indirubin and indolo carbazole inhibit the phenotypic maturation of human dendritic cells. Additionally, malassezin was proposed to induce apoptosis in human melanocytes… Other metabolites that have been linked to the clinical presentation of pityriasis versicolor include melanin, azelaic acid, and other products of skin lipid peroxidation… The aberrant production of Malassezia phospholipases on the skin could result in the removal of epidermal lipids, disruption of the epidermal barrier function, and the development of seborrheic dermatitis when sebum production is constitutionally decreased. Phospholipase production is a well-established virulence factor in Candida albicans”.
Title: Fungal meningitis caused by a Malassezia species masquerading as painful ophthalmoplegia (NCBI; US National Library of Medicine; 1993).
“The patient, an otherwise healthy 42-year-old woman, developed non-throbbing periorbital pain and abducens nerve palsy of the right side two weeks prior to the present admission… On admission, neurologic examination revealed bilateral abducens nerve palsy, incomplete bilateral oculomotor paresis, and hypalgesia in the first and the second branch of the left trigeminal nerve. On CSF examination there were 742/mm3 white blood cells of which about 80% of the cells were neutrophils…. Although repeated cultures for bacteria or fungi were negative, PAS stains for CSF sediments showed a large number of yeasts morphologically consistent with a Malassezia species. Anti-fungal treatment with fluconazole and flucytosine resulted in dramatic improvement both in neurologic signs and laboratory findings. According to morphological criteria, the yeasts found in CSF sediments from this patient differed from those described previously as being pathogenetic in the CNS fungal infection. By contrast, these yeasts were similar to a Malassezia species in all aspects. Because some Malassezia requires oil for its growth in culture, it is possible that it failed to grow in the standard media and thus escaped recognition”.