Detection of Mycotoxins in Patients with CFS
- Thread starter slayadragon
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Forebearance
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It depends on how extreme you want to go, and on what ends up bothering you.
I would be more strict about anything that you sleep near. If your old house had a mold issue, it would seem wise to at least replace mattress, pillows, bedding, pajamas, etc. Also I'd like to note that you don't have to get rid of things that are coated with toxins that bother you. You can put them in storage. You just have to get them away from your new living space.
I would be more strict about anything that you sleep near. If your old house had a mold issue, it would seem wise to at least replace mattress, pillows, bedding, pajamas, etc. Also I'd like to note that you don't have to get rid of things that are coated with toxins that bother you. You can put them in storage. You just have to get them away from your new living space.
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Agreed with you there, I am looking at it the same way, hopefully I get better, but living in the house where I am now certainly isn't going to make me any better so it's at least a worthy variable to test out. Good luck to you as time goes on, I really hope to hear you find the cause and get better.
Well in this instance would I ever be able to be around them if I put them in storage? I mean, if I can never wear the clothes again then it is best to just get rid of them, and ultimately if that is what I have to do then so be it. If that means getting my health back then it is the least of my concerns, I just wanted to find out the general consensus before I went around throwing things away just because. I have a new mattress that I will be sleeping on and won't sleep on/near anything that was part of the moldy house. That is basically what I was planning, thank you a ton for the information. I suppose worst case, if my stuff keeps me sick, then I could get rid of it afterwards? Or would the mycotoxins be all throughout the house at that point causing me to need to move yet again?
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One other question, as I feel a bit better having a forum full of people who understand me (since most people think I am just crazy and exaggerating this whole ordeal,)
Do any of you constantly feel as though you are in a dream like state? It's really hard for me to describe, but basically I feel like I am just in a constant daze/dream where I have no real emotion toward things, I am just watching the days pass by aimlessly and too tired to get anything done. A day comes, a day goes, and I sort of feel like I am in a dream almost.. really hard to describe and I wish I could be more clear as to what I mean, perhaps someone else has been through the same and can describe it more accurately than I can.
When spending 6 days in a hotel last week that is one thing that I noticed I didn't feel anymore.. the dream-like state. I felt like I was myself again (though still relatively tired, not AS tired as being here.)
Do any of you constantly feel as though you are in a dream like state? It's really hard for me to describe, but basically I feel like I am just in a constant daze/dream where I have no real emotion toward things, I am just watching the days pass by aimlessly and too tired to get anything done. A day comes, a day goes, and I sort of feel like I am in a dream almost.. really hard to describe and I wish I could be more clear as to what I mean, perhaps someone else has been through the same and can describe it more accurately than I can.
When spending 6 days in a hotel last week that is one thing that I noticed I didn't feel anymore.. the dream-like state. I felt like I was myself again (though still relatively tired, not AS tired as being here.)
mallen12132,
This is a very difficult road to navigate and my best advice is not to act with haste. If you move somewhere else without your belongings and you feel better than you should be cautious about bringing in items that might be contaminated.. But there have been a great many people who have gotten rid of all or most of their personal belongings and did not get better. Your money might be better spent on effective treatment (if that is what you need) rather than replecement of your personal belongings.
In my case we found a company that had a method to treat our whole house with an enzyme based product. We were out for a few days while they did this. It was expensive but far cheaper than the alternative. Follow up tests showed this to be effective. We have improved since then due to Dr. Brewer's protocol. We have a daughter who had moved out over four years ago but this did not improve her health.
I think it is important to remember that mycotoxins, mold spores and mold fragments will break down over time. Continued mold growth going forward is the main concern. If your new place is dry mold cannot grow there. If the humidity is above 50 per cent in any area then you need a dehumidifier. In high humidity mold can grow even if you can't see it.
If you store some of your belongings for a while it is important that they be stored in dry conditions.
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Soundthealarm21
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Derealization holy balls I hate that crap. I've lived with it for over 10 years now. The only time I feel like my oldself (awake) is when I'm on adderall. It's one of my worst symptoms. If it gets bad enough it leads to panic attacks, but I've got those well under control luckily.
Hi
I can't report any drastic changes from glutathione (I haven't really taken it long enough mainly because of the high price) but I have heard through the grapevine people have found that after some months of liposomal Glutathione their levels of urinary mycotoxins increased (hence it is likely to be involved somehow in pulling them out of cells so they can removed from the body).
NAC on the other hand I've been taking very consistently for about 9 months now at doses of between 1200-1800mg daily (in a combination with alpha lipoic acid and acetyl carnitine).
I will put my hand on a bible and swear that some long running health issues that have plagued me on-and-off for my whole life (unrelated to CFS) have completely disappeared. I've always suffered from occasional anxiety attacks and from obsessive compulsive behavior as well as having some destructive addictive tendencies as well.
Not really serious or life threatening though I basically learned to live with it by pushing them to the back of my mind and gradually adopting a strong christian outlook on life as well as staying busy and doing a lot of exercise because I didn't want to be stuck on pharmaceutical drugs but its something that always been there and when it hits it makes me feel very powerless & like I was never fully in control of my life.
However after using NAC, ALA & ALCAR for a while I started noticing that these things by-and-large disappeared even though my CFS remained and arguably my life was worse than ever by and large my mind has been much calmer.
I don't think it's a coincidence either because NAC is now recognised in the medical literature as possibly a breakthrough in treating/managing many & possibly all neurological and psychological disorders that have so far been very difficult to manage using conventional drugs.
Studies have looked into alzheimers, parkinsons, obsessive compulsive disorder, bipolar depression and NAC seems to be more effective in managing some of these conditions than any of the things the drug companies have spent decades trying to make and sell us. Even rat models have shown that that administration of NAC after stroke or trauma can rescue neurons from apoptosis likely by maintaining glutathione levels in the brain which prevents damage from reactive oxygen species and inflammation.
Personally (and this is my opinion) I think NAC is better than taking pure liposomal glutathione. Briefly this is where my thoughts are currently.
NAC is a derivative of the amino acid Cysteine. It is one of the 3 amino acids required to make the antioxidant glutathione and is the limiting precursor, i.e. Glutathione synthesis is limited by the availability of cysteine. NAC is a more effectively absorbed by the body than pure cysteine. NACs was actually first used to treat patients that overdosed on paracetamols. Basically paracetamol depletes the livers store of glutathione which is fine until the liver runs out of this antioxidant and liver failure and death follows. Large doses of NAC are given to overdose victims because it quickly restores the livers glutathione levels & detoxifies paracetamol. So it has been used at very high doses for decades with no dangerous side-effects.
It is used on long term by bodybuilders in particular heavy users of anabolic steroids to maintain liver function so it's use certainly predates any interest that the CFS community might have.
To summarise I prefer NAC over glutathione for these reasons
1) its cheaper
2) more studies exist on the role of glutathione in disease and disease management use NAC then liposomal glutathione.
3) NAC is a mucolytic agent and may help disrupt bacterial and fungal biofilms as well as thinning sticky mucous. Therefore it may enhance the effect of any antibiotic or antifungal drug you are taking (the problem here is that I can't find any consensus on whether oral NAC can reach the levels needed to attack biofilms or if it must be applied through a nasal spray).
It enhances immune function and 600mg twice daily has even been found to reduce your likelihood of catching a flu by about 50% so it does seem that oral NAC is doing something to prevent or blunt infection of the respiratory system.
4) by combining with glutamate to form glutathione it seems to have some extra function in the brain beyond just producing glutathione. I'm not smart enough to fully explain how this happens but it appears to be regulating or removing excess & unwanted glutamate which is overstimulating neurons that leads to apoptosis and inflammation which seems to be closely related to multiple neurological and psychological disorders.
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Forebearance
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mallen12132 said: [/QUOTE]Well in this instance would I ever be able to be around them if I put them in storage? I mean, if I can never wear the clothes again then it is best to just get rid of them, and ultimately if that is what I have to do then so be it. If that means getting my health back then it is the least of my concerns, I just wanted to find out the general consensus before I went around throwing things away just because. I have a new mattress that I will be sleeping on and won't sleep on/near anything that was part of the moldy house. That is basically what I was planning, thank you a ton for the information. I suppose worst case, if my stuff keeps me sick, then I could get rid of it afterwards? Or would the mycotoxins be all throughout the house at that point causing me to need to move yet again?[/QUOTE]
It's hard for me to give advice, since I did the extreme mold avoidance route. I put half my things in storage and got rid of the rest of them. Erik, the extreme mold avoidance guru, reported that most of his possessions had denatured and didn't bother him any more after sitting in a dry hot storage unit for five years. So I looked at it like: "What would be worth paying to store for five years?" and saved those things. In my climate it turned out that climate-controlled storage was a better option. If this treatment works on you, maybe you wouldn't have to keep your things in storage for that long.
I'd say it's safer to start with no old possessions in your new house.
It's hard for me to give advice, since I did the extreme mold avoidance route. I put half my things in storage and got rid of the rest of them. Erik, the extreme mold avoidance guru, reported that most of his possessions had denatured and didn't bother him any more after sitting in a dry hot storage unit for five years. So I looked at it like: "What would be worth paying to store for five years?" and saved those things. In my climate it turned out that climate-controlled storage was a better option. If this treatment works on you, maybe you wouldn't have to keep your things in storage for that long.
I'd say it's safer to start with no old possessions in your new house.
Ok status update on my end.
So I went to see an ENT recently, he was reasonably supportive of the mold theory and CFS. So he had me do a sinus ct scan and also a nasal swab and a sample of the morning sinus backflush to a lab.
The CT showed no evidence of funal hyphae and I haven't heard a positive on the growth of fungi in the swab/sinus fluid yet (but this can take a while).
Sinus structure was normal (i.e. no blockages or abnormally shaped bone cavities that could contribute to disease) but there was mucosal thickening suggesting sinus infection.
What they did find was a heavy growth of Staphylococcus aureus. The ENT couldn't say if the heavy presence of staph would cause systemic symptoms or CFS but that it certainly causes sinusistis/rhinitis and that its presence was significant.
I was given 4 courses of cephalexin to which it is sensitive and it certainly has made a huge difference so far. I'm about 2/3 through and it's not just my nose/sinuses that feel better but I just feel a lot more energetic and stronger all round. Some weird symptoms I had seem to be alleviated. For instance brain fog is much less, memory seems better & it is easier to communicate to people, I don't seem to get static shocks any more and it feels like I can breath much more easily. Orthostatic hypotension also seems to have alleviated.
Sleep is still a mess though and I still get the sense of a heaviness behind my eyes so I'm not convinced the antiobiotics will be able to clear the infection completely (as the Staph is likely to be in biofilms).
But I think I can say that Staphylococcus was contributing to systemic inflammation beyond localized infection in the sinuses. I have made an observation in the past that a large dose of antihistamines had a temporary effect in alleviating fatigue so it may be possible that Staph toxins aggravates mast cells in the mucosal tissues and that is could be contributing to mast cell activation.
In fact Staphylococcus does produce superantigens which is the cause of toxic shock (a form of lethal inflammation). It appears that Staphylococcus has been linked to CFS before in some veterinarian studies - although it doesn't seem like it has received much attention, judging by the lack of citations these 2 papers have received.
http://www.ncbi.nlm.nih.gov/pubmed/11561958
http://www.ncbi.nlm.nih.gov/pubmed/15129582
There has been a lot of immunological studies on CFS but I don't know if that is in regard to Staph antigens - Not being an immunologist myself I can really answer this but I did find this paper here below that could shed some light on the subject. All in all I think Staph could be something that is causing immune system fatigue and systemic inflammation and is something best eliminated from the sinuses if its presence is found.
The thing is that one third of humans carry Staph so when/why/how does it go from something that is harmless like a benign tumor into an aggressive and invasive pathogen?
Going back to Mold the reason why nothing may have shown up is that possibly any fungal colonization in the sinuses may have been destroyed by the mold protocol I have used for the last 3 months and maybe the Staph is a co-factor that needs to be treated separately. But then I only got a trichothecene result that was just on the detection level (although I understand that can be normal - the test isn't directly quantitative ). I will see my CFS doctor soon and I will get another mycotoxin test arranged and I'll see if he can give me an anti-Staph protocol as I'm certain the staph causes disease in biofilms and I'm not sure how effectively the antibiotics will clear that out.
Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.
Chowdhary VR1, Tilahun AY, Clark CR, Grande JP, Rajagopalan G.
Abstract
Chronic nasal and skin colonization with superantigen (SAg)-producing Staphylococcus aureus is well documented in humans. Given that trans-mucosal and trans-cutaneous absorption of SAgs can occur, we determined whether chronic exposure to small amounts of SAg per se could activate autoreactive CD4(+) and CD8(+) T cells and precipitate any autoimmune disease without further external autoantigenic stimulation. Because HLA class II molecules present SAg more efficiently than do mouse MHC class II molecules, HLA-DQ8 transgenic mice were implanted s.c. with mini-osmotic pumps capable of continuously delivering the SAg, staphylococcal enterotoxin B (total of 10 μg/mouse), or PBS over 4 wk. Chronic exposure to staphylococcal enterotoxin B resulted in a multisystem autoimmune inflammatory disease with features similar to systemic lupus erythematosus. The disease was characterized by mononuclear cell infiltration of lungs, liver, and kidneys, accompanied by the production of anti-nuclear Abs and deposition of immune complexes in the renal glomeruli. The inflammatory infiltrates in various organs predominantly consisted of CD4(+) T cells bearing TCR Vβ8. The extent of immunopathology was markedly reduced in mice lacking CD4(+) T cells and CD28, indicating that the disease is CD4(+) T cell mediated and CD28 dependent. The absence of disease in STAT4-deficient, as well as IFN-γ-deficient, HLA-DQ8 mice suggested the pathogenic role of Th1-type cytokines, IL-12 and IFN-γ. In conclusion, our study suggests that chronic exposure to extremely small amounts of bacterial SAg could be an etiological factor for systemic lupus erythematosus.
Human studies have shown that S. aureus carriage is associated with certain autoimmune diseases such as granulamatosis with polyangiitis, multiple sclerosis and rheumatoid arthritis through their SAg (22–26). However, to date no direct experimental evidence exists to date to prove that staphylococcal SAg (SSAg) by themselves (without the use of exogenous antigens) are capable of inducing any spontaneous autoimmune disease. Conventional laboratory mice will not be suitable for such investigation because SSAg bind weakly to mouse MHC class II molecules. However, it is well established that SSAg bind more efficiently to human MHC (HLA) class II molecules (27). Therefore, we and others have shown that transgenic mice expressing HLA class II molecules such as, HLA-DQ6, -DQ8 or -DR3, mount a strong immune response to SSAg and are excellent tools to study the immunopathogenesis of diseases caused by SAg (15, 28–35). As several additional knockout mice are available on the HLA-DQ8 background (15), using HLA-DQ8 transgenic mouse model, we explored whether chronic exposure to extremely small non-lethal amounts of staphylococcal SAg by itself can precipitate any autoimmune disease without immunization with any autoantigens.
So I went to see an ENT recently, he was reasonably supportive of the mold theory and CFS. So he had me do a sinus ct scan and also a nasal swab and a sample of the morning sinus backflush to a lab.
The CT showed no evidence of funal hyphae and I haven't heard a positive on the growth of fungi in the swab/sinus fluid yet (but this can take a while).
Sinus structure was normal (i.e. no blockages or abnormally shaped bone cavities that could contribute to disease) but there was mucosal thickening suggesting sinus infection.
What they did find was a heavy growth of Staphylococcus aureus. The ENT couldn't say if the heavy presence of staph would cause systemic symptoms or CFS but that it certainly causes sinusistis/rhinitis and that its presence was significant.
I was given 4 courses of cephalexin to which it is sensitive and it certainly has made a huge difference so far. I'm about 2/3 through and it's not just my nose/sinuses that feel better but I just feel a lot more energetic and stronger all round. Some weird symptoms I had seem to be alleviated. For instance brain fog is much less, memory seems better & it is easier to communicate to people, I don't seem to get static shocks any more and it feels like I can breath much more easily. Orthostatic hypotension also seems to have alleviated.
Sleep is still a mess though and I still get the sense of a heaviness behind my eyes so I'm not convinced the antiobiotics will be able to clear the infection completely (as the Staph is likely to be in biofilms).
But I think I can say that Staphylococcus was contributing to systemic inflammation beyond localized infection in the sinuses. I have made an observation in the past that a large dose of antihistamines had a temporary effect in alleviating fatigue so it may be possible that Staph toxins aggravates mast cells in the mucosal tissues and that is could be contributing to mast cell activation.
In fact Staphylococcus does produce superantigens which is the cause of toxic shock (a form of lethal inflammation). It appears that Staphylococcus has been linked to CFS before in some veterinarian studies - although it doesn't seem like it has received much attention, judging by the lack of citations these 2 papers have received.
http://www.ncbi.nlm.nih.gov/pubmed/11561958
http://www.ncbi.nlm.nih.gov/pubmed/15129582
There has been a lot of immunological studies on CFS but I don't know if that is in regard to Staph antigens - Not being an immunologist myself I can really answer this but I did find this paper here below that could shed some light on the subject. All in all I think Staph could be something that is causing immune system fatigue and systemic inflammation and is something best eliminated from the sinuses if its presence is found.
The thing is that one third of humans carry Staph so when/why/how does it go from something that is harmless like a benign tumor into an aggressive and invasive pathogen?
Going back to Mold the reason why nothing may have shown up is that possibly any fungal colonization in the sinuses may have been destroyed by the mold protocol I have used for the last 3 months and maybe the Staph is a co-factor that needs to be treated separately. But then I only got a trichothecene result that was just on the detection level (although I understand that can be normal - the test isn't directly quantitative ). I will see my CFS doctor soon and I will get another mycotoxin test arranged and I'll see if he can give me an anti-Staph protocol as I'm certain the staph causes disease in biofilms and I'm not sure how effectively the antibiotics will clear that out.
Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.
Chowdhary VR1, Tilahun AY, Clark CR, Grande JP, Rajagopalan G.
Abstract
Chronic nasal and skin colonization with superantigen (SAg)-producing Staphylococcus aureus is well documented in humans. Given that trans-mucosal and trans-cutaneous absorption of SAgs can occur, we determined whether chronic exposure to small amounts of SAg per se could activate autoreactive CD4(+) and CD8(+) T cells and precipitate any autoimmune disease without further external autoantigenic stimulation. Because HLA class II molecules present SAg more efficiently than do mouse MHC class II molecules, HLA-DQ8 transgenic mice were implanted s.c. with mini-osmotic pumps capable of continuously delivering the SAg, staphylococcal enterotoxin B (total of 10 μg/mouse), or PBS over 4 wk. Chronic exposure to staphylococcal enterotoxin B resulted in a multisystem autoimmune inflammatory disease with features similar to systemic lupus erythematosus. The disease was characterized by mononuclear cell infiltration of lungs, liver, and kidneys, accompanied by the production of anti-nuclear Abs and deposition of immune complexes in the renal glomeruli. The inflammatory infiltrates in various organs predominantly consisted of CD4(+) T cells bearing TCR Vβ8. The extent of immunopathology was markedly reduced in mice lacking CD4(+) T cells and CD28, indicating that the disease is CD4(+) T cell mediated and CD28 dependent. The absence of disease in STAT4-deficient, as well as IFN-γ-deficient, HLA-DQ8 mice suggested the pathogenic role of Th1-type cytokines, IL-12 and IFN-γ. In conclusion, our study suggests that chronic exposure to extremely small amounts of bacterial SAg could be an etiological factor for systemic lupus erythematosus.
Human studies have shown that S. aureus carriage is associated with certain autoimmune diseases such as granulamatosis with polyangiitis, multiple sclerosis and rheumatoid arthritis through their SAg (22–26). However, to date no direct experimental evidence exists to date to prove that staphylococcal SAg (SSAg) by themselves (without the use of exogenous antigens) are capable of inducing any spontaneous autoimmune disease. Conventional laboratory mice will not be suitable for such investigation because SSAg bind weakly to mouse MHC class II molecules. However, it is well established that SSAg bind more efficiently to human MHC (HLA) class II molecules (27). Therefore, we and others have shown that transgenic mice expressing HLA class II molecules such as, HLA-DQ6, -DQ8 or -DR3, mount a strong immune response to SSAg and are excellent tools to study the immunopathogenesis of diseases caused by SAg (15, 28–35). As several additional knockout mice are available on the HLA-DQ8 background (15), using HLA-DQ8 transgenic mouse model, we explored whether chronic exposure to extremely small non-lethal amounts of staphylococcal SAg by itself can precipitate any autoimmune disease without immunization with any autoantigens.
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knackers323
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Well my symptoms have pretty closely aligned with CFS/ME symptoms in general.
Post-exertional malaise, brain fog, cognitive & memory problems, IBS, cold, heat, light & exercise intolerance, sleep disturbance (night owl tendencies), orthostatic intolerance, frequent need to urinate, weakness & mild general muscle pain, lack of appetite, alcohol intolerance, chemical and mold sensitivity, waking up with a strong hangover sensation or the 'kicked in the head' feeling & needing to sleep most of the day to avoid feeling worse.
There has been sinus/nasal symptoms for some time and arguably I would say on and off for years. The problem here is that I was diagnosed with allergies years ago and that basically blinded me to the possibility of chronic sinusitis/rhinitis as a cause or contributor to disease.
I assumed that any time I felt stuffy in the nose it was either a common cold (which would pass in a few days) or it was allergies so nothing could really be done about it & it wasn't related to systemic health. I only really started paying attention to the sinuses recently because I was frustrated with the supposed 'lack of progress' from the anti-mold protocol I was on - I was convinced that the antifungals weren't strong enough so I went to see the ENT for an independent test to see if they could directly find the fungal species - I didn't expect Staph to come up as a significant result.
The antihistamines I tried was polaramine but it had to be a reasonably high dosing and the the effect was very temporary and not always that noticeable. I'm only making an assumption that sinus infections could be aggravating mast cells and causing more inflammation hence anti-histamines may have some effect in temporarily calming the immune system. But I don't have any proof of this - its just a theory.
Are you using the antibiotic with the nasatouch? My doc gave me levoxaquin because it attacks strep and staph. He was pretty adamant that if we needed to attack the bacteria in the biofilm or it wouldn't break down. Haven't started yet. I've been waiting to see how the ampho and cheating px go before adding in anything else. I may start tomorrow as I've been on the protocol a little over a week with no major adverse effects. Not sure if/when a herx is going to hit. Sounds crazy but I've been waiting for the herx for a sign this is killing something off!
I was thinking I read somewhere that brewer doesn't swab for mold colonization because he thinks it is too deep in the sinuses to find. But I may have made that up. I read way too much of this stuff! I could probably benefit from a scan to make sure my nasal structure has no blockages just to make sure this stuff is actually going so where and not just falling back out of my nose. I do know that gray and shoe swabbed my nose about 7 years ago and I don't recall them finding anything.
Glad you found one of your culprits and are feeling better!!
I'm not using nasatouch - I don't even know what that is. The ENT I saw was a fairly orthodox specialist which is basically prescribe an antibiotic and good luck! - he did acknowledge biofilms but I didn't press the subject as I assume it's not something that conventional medicine has incorporated into standard treatment protocols. But he did say for heavy staph growth to also throw away your old pillows, bed sheets etc and wash your body with chlorohexidine to minimise risk of recontaminating yourself after antibiotic use. He went to on to say that sinusitis can continue to reoccur within families (i.e. close physical contact results in the family recontaminating themselves).
But to go further (i.e. attack the biofilms) I need to consult with my CFS doctor who I will see hopefully soon. The other possibility is maybe there's other pathogen that is being affected besides Staph- Bartonella maybe? I dunno... hopefully my CFS doc can explain this.
I'm still a little puzzled about how something like Staph that could make me so systemically ill yet cause no fever or traditional symptoms associated with bacterial infection. I always assumed that when you sick from a bacterial infection you get sick with a fever and you either get better (fever disappears) or you go into toxic shock and need ER help or you die. Obviously there are many forms of bacterial infection and the symptoms can be insidious - no wonder they call them stealth infections. At least some doctors are recognising this.
You should get a sinus ct scan done regardless. The ENT fella did explain that not everyone with sinusitis (that is sinus infections) present with noticeable symptoms and he said that he's seen patients with fungal balls in their sinus and they had no symptoms whatsoever - they were only picked up on a ct scan by accident. The CT scan is a very cheap, easy, uninvasive thing to do, it will give you some useful information even if its just to tell you that your sinus plumbing is healthy. He did say though that fungal hyphae deposit minerals around their colonies which you can observe through ct scan - they show up as little dots against the background.
It would have been good if the researchers of this mycotoxin detection study gave their patients nasal/sinus ct scans just to give some additional data to backup their theory. Fungal infections in the sinuses is something that orthodox medicine has recognised so it would be good if we had this additional information - at least to clarify any confusion.
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"here was mucosal thickening suggesting sinus infection."
Yes that is what showed in my CT scans way back furing and after my mold exposure. I used to get chronic sinus infections as well and I would feel tons of fatigue, laying on the couch all day. I remember one time it last a long time, and they finally tested a swab and prescribed me a third antibiotic based on it, and the next day I felt like I had a new life!
@redaxe, the nasotouch is the atomizer that ASL pharmacy makes, for the amphoB, etc. Brewer has hypothsized that staph might be complicating the colonization and biofilms, which is why a lot of patients are doing a round of atomized mupericin to kill off the staph. My new doctor just prescribed it for me.
Yes that is what showed in my CT scans way back furing and after my mold exposure. I used to get chronic sinus infections as well and I would feel tons of fatigue, laying on the couch all day. I remember one time it last a long time, and they finally tested a swab and prescribed me a third antibiotic based on it, and the next day I felt like I had a new life!
@redaxe, the nasotouch is the atomizer that ASL pharmacy makes, for the amphoB, etc. Brewer has hypothsized that staph might be complicating the colonization and biofilms, which is why a lot of patients are doing a round of atomized mupericin to kill off the staph. My new doctor just prescribed it for me.
Put your clothes in storage for now. That could be in plastic boxes in someone's basement, or in actual storage but be aware they use pesticides in storage places. In a few months you can think about it again. You don't know whether you have extremely toxic molds in your house, nor how sensitive you really are.
soulfeast
Senior Member
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Just finished treatment for pseudomonas aeruginosa using nasotouch and atomized cipro with chelating agent. My inflammation levels are very much down. I am not sure if it's treatment of pseudomonas aeruginosa or mast cell stabilizer having more effect since I understand it can take up to 6 months to have full effect.
We have had layers of bacteria,it seems.. culture/PCR, treat, culture/PCR again, treat..
I agree regarding mast cells. Thanks for sharing!
We have had layers of bacteria,it seems.. culture/PCR, treat, culture/PCR again, treat..
I agree regarding mast cells. Thanks for sharing!
Skii I did have die off/herxing but it was tolerable mainly bloody nose, congestion, headache, tired.The BEG spray sometimes stung but again it was tolerable.
I was also doing ampho b at the same time but had to drop that until after the BEG /rifampin protocol - it was too much on my sinus- could not handle the congestion.
Now I am back on doing the ampho B regimen every other day half dose and it seems I can handle it this time - fingers crossed!
I am really happy the vertigo has abated that was quite bothersome.
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