nanonug
Senior Member
- Messages
- 1,709
- Location
- Virginia, USA
Well... Not really! At least not the part about life and liberty.
Some of you might have noticed that I went abruptly silent a few months ago. It wasn't because I died and it certainly wasn't because I caught crabs, which, as far as I know, I didn't. I simply needed some "me" time. That happens to brats like me, i.e., those who were raised without the benefit of siblings.
Much has happened and I believe I finally know what is the root cause of my lifelong misery.
I left Phoenix Rising at just about the time I was getting ready to be tested for Mast Cell Activation Syndrome. I found a wonderful Immunologist in Chantilly, Virginia, who was willing to follow Dr. Afrin's protocol. In particular, tests were ordered for serum tryptase, 24-hour urinary N-methyl-histamine and 24-hour urinary Prostaglandin D2. These tests were performed by Quest Diagnostics. The test results came back normal and instead of further pursuing the MCAS route, I decided to focus on a different thing as I felt that MCAS was an unlikely diagnostic. What both urinary tests showed me, however, was that I was peeing more than the container maximum of 3 liters.
I decided to focus my attention on the subject of diabetes insipidus. I found out that Labcorp was offering a very convenient blood test that measures both plasma vasopressin and plasma osmolality at the same time. Although this test required special preparation, at the time I decided to just get a preliminary picture of what was I going on. When I got the results back, one interesting fact became immediately apparent: although plasma osmolality was slightly elevated, there was absolutely no detectable vasopressin (it was below the lab's detection limit.) I then scheduled an appointment with an endocrinologist.
A few months earlier, the last Metametrix GI Effects test indicated some H. pylori in my digestive system so I convinced my GI doctor to prescribe me the common triple therapy consisting of omeprazole, amoxicillin and clarithromycin. I started taking that stuff and for the first four days didn't get any reaction. On the fifth day, however, and upon waking up, I felt more... alive! Not only that but I started working like a horse on steroids, something I hadn't been able to do for a long time. Because this experience with amoxicillin and clarithromycin had produced the same result a few years back, I concluded that coincidence it was not, that the antibiotics were indeed taking care of "something". Was it the H. pylori? I knew that H. pylori had been recently associated with certain neurological diseases, including Alzheimer's and Parkinson's. But I wasn't ready to jump to conclusions. Given the effects of the antibiotics, which for the second time had given me my life back, I scheduled an appointment with one certain infectious disease specialist.
The doctor, a specialist in infectious diseases, thought I might have Lyme disease. The appropriate tests were ordered but everything came back negative. Lyme disease it was not. The idiot cited "cost control" to stop testing at this point. I simply scheduled an appointment with a different infectious disease specialist.
Meanwhile, while waiting for the appointment with the endocrinologist, I found out via Wikipedia that nicotine has the power to stimulate the secretion of vasopression so I decided to give the nicotine patch a try. That was a great decision because it gave me an incredibly amount of energy. Shortly thereafter, I spoke to my psychiatrist about my little nicotine experiment and he gave a prescription for Adderall XR, thinking that I was simply taking advantage of the stimulating properties of nicotine. However, the Adderall XR made me feel like crap while the nicotine patch made me feel quite good. The nicotine was clearly doing something above and beyond the stimulating thing.
Fast forward a few weeks, my appointment with the endocrinologist was most interesting. The doctor, an Iraqi female unafraid to speak her mind, gave me a hard time due to my choice of not doing the required preparation for the osmolality test. I had no choice but to agree with her but pointed out that I was still supposed to have vasopressin for the measured osmolality. She was still not convinced, and suggested that the problem might be primary polydipsia instead. In any case, she ordered some additional blood tests which I did right there as by now I had been some 6 hours without eating or drinking anything. A follow up was scheduled and I am going to see her in the next couple of days. Just in case you are wondering, I did enjoy the vigorous exchange with the doctor. After all, it is not every day that you find a doctor that is willing to listen and challenge you at the same time. I confess to having what I can only describe as "fun". (Yes, I am weird like that!)
With egg on face, I decided to redo the same plasma vasopressin/osmolality test but this time with the appropriate preparation, i.e., a 12-hour fast including all fluids. For good measure, I also threw in urinary osmolality (first void) and CBC tests to get a more complete picture of my sorry state. The results that I got back confirmed the central diabetes insipidus hypothesis.
I finally saw the second infectious disease specialist and upon hearing my story, he was convinced my symptoms could all be explained by a case of chronic sinusitis gone bad. He put me on Augmentin (an amoxicillin and clavulanate combo) for 30 days. By day 15 things were as good as before which by now weren't really all that jolly. I am now just finishing the 30-day course without any effect and it is only logical to conclude that whatever effect I got was due to the clarithromycin.
The trees in my neighborhood started having sex. My misery started to increase in proportion to the amount of pollen in the air. I knew that it wouldn't take long for those terrible headaches to return. And return they did! Tried Claritin (loratadine) and got no effect. Switched to Allegra (fexofenadine) and the same non-effect I got. Finally, decided to try the zombiefying Benadryl and in a couple of hours my headaches were almost gone. Not only that, but I only took half the normal dosage. Now, the difference between Benadryl and the other non-drowsy antihistamines is that the latter don't cross the blood-brain barrier. This suggested to me that the screw up had to be in the central nervous system or thereabouts. Eventually I switched to Zyrtec (cetirizine) which still leaves me a little bit drowsy but not as much as Benadryl.
Started researching bugs susceptible to clarithromycin that not only inhabit the central nervous system but are also difficult to eradicate. I eventually focused on toxoplasma gondii. Ordered the relevant serological test and happily went to Labcorp. A couple of days later got an email telling me the results were available. Downloaded the PDF file with the result to my trusted Google Galaxy Nexus and anxiously waited for Android to open the document. Well, you guessed it, the result was positive, with absolute IgG more than four times the lab threshold! There was no doubt in my mind that I was infected with toxoplasma gondii.
I got the positive toxoplasmosis result just a week ago. But much learning I did since then. It appears that Toxoplasma gondii induces the astrocytes (in the brain) to produce an inordinate amount of a tryptophan metabolite known as kynurenic acid (KYNA). This KYNA acts as a negative allosteric modulator on the alpha7 nicotinic acetylcholine receptor. What this means is that this receptor becomes less, well, receptive to acetylcholine. But, so what? This receptor controls the release of glutamate into the synaptic space of glutamatergic neurons. But, again, so what? Well, glutamate is the main excitatory neurotransmitter in the brain. Without it, things start to slow to a crawl, resulting in a "sleepy" brain. On top of that, it seems that this same mechanism is at play in the hypothalamic-pituitary osmotic sensing and releasing of vasopressin. It also provides an explanation for why nicotine helped me - I was simply overwhelming the aforementioned alpha7 nicotinic acetylcholine receptor and inducing some level of glutamate release.
In the pipeline for the next few days I have two appointments, one with the endocrinologist and another with the infectious disease specialist. Meanwhile, I learned that galantamine, a drug and dietary supplement used in the treatment of Alzheimer's patients, also acts as a positive allosteric modulator of that mysterious alpha7 receptor. I am waiting for my online order to arrive.
(To be continued...)
Some of you might have noticed that I went abruptly silent a few months ago. It wasn't because I died and it certainly wasn't because I caught crabs, which, as far as I know, I didn't. I simply needed some "me" time. That happens to brats like me, i.e., those who were raised without the benefit of siblings.
Much has happened and I believe I finally know what is the root cause of my lifelong misery.
I left Phoenix Rising at just about the time I was getting ready to be tested for Mast Cell Activation Syndrome. I found a wonderful Immunologist in Chantilly, Virginia, who was willing to follow Dr. Afrin's protocol. In particular, tests were ordered for serum tryptase, 24-hour urinary N-methyl-histamine and 24-hour urinary Prostaglandin D2. These tests were performed by Quest Diagnostics. The test results came back normal and instead of further pursuing the MCAS route, I decided to focus on a different thing as I felt that MCAS was an unlikely diagnostic. What both urinary tests showed me, however, was that I was peeing more than the container maximum of 3 liters.
I decided to focus my attention on the subject of diabetes insipidus. I found out that Labcorp was offering a very convenient blood test that measures both plasma vasopressin and plasma osmolality at the same time. Although this test required special preparation, at the time I decided to just get a preliminary picture of what was I going on. When I got the results back, one interesting fact became immediately apparent: although plasma osmolality was slightly elevated, there was absolutely no detectable vasopressin (it was below the lab's detection limit.) I then scheduled an appointment with an endocrinologist.
A few months earlier, the last Metametrix GI Effects test indicated some H. pylori in my digestive system so I convinced my GI doctor to prescribe me the common triple therapy consisting of omeprazole, amoxicillin and clarithromycin. I started taking that stuff and for the first four days didn't get any reaction. On the fifth day, however, and upon waking up, I felt more... alive! Not only that but I started working like a horse on steroids, something I hadn't been able to do for a long time. Because this experience with amoxicillin and clarithromycin had produced the same result a few years back, I concluded that coincidence it was not, that the antibiotics were indeed taking care of "something". Was it the H. pylori? I knew that H. pylori had been recently associated with certain neurological diseases, including Alzheimer's and Parkinson's. But I wasn't ready to jump to conclusions. Given the effects of the antibiotics, which for the second time had given me my life back, I scheduled an appointment with one certain infectious disease specialist.
The doctor, a specialist in infectious diseases, thought I might have Lyme disease. The appropriate tests were ordered but everything came back negative. Lyme disease it was not. The idiot cited "cost control" to stop testing at this point. I simply scheduled an appointment with a different infectious disease specialist.
Meanwhile, while waiting for the appointment with the endocrinologist, I found out via Wikipedia that nicotine has the power to stimulate the secretion of vasopression so I decided to give the nicotine patch a try. That was a great decision because it gave me an incredibly amount of energy. Shortly thereafter, I spoke to my psychiatrist about my little nicotine experiment and he gave a prescription for Adderall XR, thinking that I was simply taking advantage of the stimulating properties of nicotine. However, the Adderall XR made me feel like crap while the nicotine patch made me feel quite good. The nicotine was clearly doing something above and beyond the stimulating thing.
Fast forward a few weeks, my appointment with the endocrinologist was most interesting. The doctor, an Iraqi female unafraid to speak her mind, gave me a hard time due to my choice of not doing the required preparation for the osmolality test. I had no choice but to agree with her but pointed out that I was still supposed to have vasopressin for the measured osmolality. She was still not convinced, and suggested that the problem might be primary polydipsia instead. In any case, she ordered some additional blood tests which I did right there as by now I had been some 6 hours without eating or drinking anything. A follow up was scheduled and I am going to see her in the next couple of days. Just in case you are wondering, I did enjoy the vigorous exchange with the doctor. After all, it is not every day that you find a doctor that is willing to listen and challenge you at the same time. I confess to having what I can only describe as "fun". (Yes, I am weird like that!)
With egg on face, I decided to redo the same plasma vasopressin/osmolality test but this time with the appropriate preparation, i.e., a 12-hour fast including all fluids. For good measure, I also threw in urinary osmolality (first void) and CBC tests to get a more complete picture of my sorry state. The results that I got back confirmed the central diabetes insipidus hypothesis.
I finally saw the second infectious disease specialist and upon hearing my story, he was convinced my symptoms could all be explained by a case of chronic sinusitis gone bad. He put me on Augmentin (an amoxicillin and clavulanate combo) for 30 days. By day 15 things were as good as before which by now weren't really all that jolly. I am now just finishing the 30-day course without any effect and it is only logical to conclude that whatever effect I got was due to the clarithromycin.
The trees in my neighborhood started having sex. My misery started to increase in proportion to the amount of pollen in the air. I knew that it wouldn't take long for those terrible headaches to return. And return they did! Tried Claritin (loratadine) and got no effect. Switched to Allegra (fexofenadine) and the same non-effect I got. Finally, decided to try the zombiefying Benadryl and in a couple of hours my headaches were almost gone. Not only that, but I only took half the normal dosage. Now, the difference between Benadryl and the other non-drowsy antihistamines is that the latter don't cross the blood-brain barrier. This suggested to me that the screw up had to be in the central nervous system or thereabouts. Eventually I switched to Zyrtec (cetirizine) which still leaves me a little bit drowsy but not as much as Benadryl.
Started researching bugs susceptible to clarithromycin that not only inhabit the central nervous system but are also difficult to eradicate. I eventually focused on toxoplasma gondii. Ordered the relevant serological test and happily went to Labcorp. A couple of days later got an email telling me the results were available. Downloaded the PDF file with the result to my trusted Google Galaxy Nexus and anxiously waited for Android to open the document. Well, you guessed it, the result was positive, with absolute IgG more than four times the lab threshold! There was no doubt in my mind that I was infected with toxoplasma gondii.
I got the positive toxoplasmosis result just a week ago. But much learning I did since then. It appears that Toxoplasma gondii induces the astrocytes (in the brain) to produce an inordinate amount of a tryptophan metabolite known as kynurenic acid (KYNA). This KYNA acts as a negative allosteric modulator on the alpha7 nicotinic acetylcholine receptor. What this means is that this receptor becomes less, well, receptive to acetylcholine. But, so what? This receptor controls the release of glutamate into the synaptic space of glutamatergic neurons. But, again, so what? Well, glutamate is the main excitatory neurotransmitter in the brain. Without it, things start to slow to a crawl, resulting in a "sleepy" brain. On top of that, it seems that this same mechanism is at play in the hypothalamic-pituitary osmotic sensing and releasing of vasopressin. It also provides an explanation for why nicotine helped me - I was simply overwhelming the aforementioned alpha7 nicotinic acetylcholine receptor and inducing some level of glutamate release.
In the pipeline for the next few days I have two appointments, one with the endocrinologist and another with the infectious disease specialist. Meanwhile, I learned that galantamine, a drug and dietary supplement used in the treatment of Alzheimer's patients, also acts as a positive allosteric modulator of that mysterious alpha7 receptor. I am waiting for my online order to arrive.
(To be continued...)