mojoey
Senior Member
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Reposted from my blog:
*Apologies on delay in live blood analysis videos. Having trouble uploading, but hopefully will remove tech dunce hat by end of day.
What a crazy 2-day stretch. Was on the amtrak for about half the time, taking in the aesthetically insane views of the bay area, Sacramento wildlife reserves, and Sierra mountains, while all the time wondering if there would ever be a day when these views would no longer be internalized as utterly lackluster. I remember there used to be a day when all these solo excursions made me feel deeply at the core--whether it be longing for someone to take it all in with me or a quality of the human spirit being laid out before my eyes--but these days I'm so focused on recovering that it's challenging for anything that's unrepresentative of progress to elicit an emotional ripple. Funny thing is: I don't mind it one bit. It takes a machine to be resourceful enough to find a way out of this illness, and I can honestly say I'm proud of myself for becoming one.
Peterson was practically glowing when he came into the room. "So we have some big news." Understatement of the year? He hashed over the details of the study, which I won't go over here. Instead, I'll report some of the (maybe) lesser-known aspects of it.
Peterson was very selective with his sample. He picked the patients that he thought were most likely to have the illness, and >90% of them were positive. The other sample sizes from around the country averaged out to something lke 60% positivity, so it's definitely possible 1) that XMRV isn't as ubiquitous as it seems, 2) detection methods aren't refined enough, 3) some of the patients in other sample sizes don't have CFIDS but rather have chronic fatigue.
He said I'm a very good candidate for XMRV because 1) it infects NK cells, 2) I have rnase-L abnormalities, 3) it's reactive with other viruses which I documented stealth infections of, and 4) it has a cortisol receptor, which is why my symptoms wax and wane so much due to stress.
We had a good laugh about Reeves and how I barely escaped falling into Reeves' group of "hypogonad males who complain about everything" with my normal hormonal levels.
Surprisingly, my only elevated cytokine is IL-8, which however is produced in the gut and correlates highly with my elevated coxsackie A and B titers. However, the IL-8 is also the cytokine that's most strongly associated with XMRV. Peterson's interpretation was that many of the drugs I took such as Zithromax, Mepron, Valtrex were either immunomodulatory or lowered my viruses without me knowing it. I nodded politely, but I only took all those drugs within a 3-month period back in summer '08. The next year of bug-killing was all photons and later, ozone.
I wanna take this opportunity to give a shout-out to the Bionic 880. I've never been more convinced that it is the most effective targeted antiviral, antibacterial, antifungal treatment I've ever tried. I don't think I give the machine and community of users that have helped guide my Bionic treatment the credit they deserve for getting me to this point of relative health compared to a year ago.
Back to XMRV: he's not sure if it's sexually transmitted, vector-transmitted, or maybe a human endogenous (HER) virus. I was really impressed that he was equally open to each option. He did say he doesn't believe it is highly contagious if sexually transmitted (most of us patients have had sexual partners, and the norm is that our partners do not develop CFIDS), and that the chances of vector transmission are slight (given that millions have it--although lyme patients would clearly disagree with this logic). I for one am really glad to hear he's open to the HER virus theory. These viruses are embedded in our embedded genome, yet the reason why some family members express them and some don't may have to do with the triggers which I'll talk about shortly. Peterson even waxed a bit about how some retrovirologists think that HER viruses may be advantageous to human genomes.
Another reason he thinks this virus is causative of CFS is because he took blood samples from 1984, inserted the virus into non-infected cell lines, and produced high viral loads. I think this is the fact that really impressed virologists involved in the study. However, he said we're relatively lucky to have a gammaretrovirus vs the lentivirus (HIV is a kind).
Ok so what does this mean for treatment? He thinks this study shows why Ampligen and other immune-modulating therapies caused relapse after patients got off the drugs: they didn't eradicate the virus. Ampligen has been proven to have some anti-infectious activity, but not nearly enough. He said if he were me, he would consider going on AZT, a reverse transcriptase inhibitor. He said some docs around the country are already trying this on CFIDS patients. His reads into patient personalities actually have a lot to do with his individual treatment recommendations. He knows I like to be aggressive with treatment (in fact most males in his practice do). As an allegory, he said that during the AZT trials for HIV patients, the patients that didn't wait for later-stage clinical trials to try the drug had better results. Hint hint.
As a bit of an aside, I'm really glad to have found a physician that fully understands the gender role discrepancies of the illness. He said he has found males in his practice to employ the same treatment tendencies as myself because he thinks it's much less socially acceptable to have this illness as a male than as a female. I rarely hear this discrepancy being mentioned in patient communities (probably because it's taboo for one patient to say to another my suffering is greater than yours), but I really agree with Peterson. He said 9 out of his first 12 Ampligen patients were male, and he believes the same guinea-pig aggression will be seen with AZT.
But this next part is very interesting for those that aren't convinced this virus is the end-all, be-all. I think I'm still hanging onto that bandwagon by a thread, especially after what Peterson told me next. I went back to what we talked about last time: the relation between immune dysfunction and autonomic nervous system dysfunction. Whereas last time, he seemed convinced that ANS dysfunction was secondary to immune dysfunction, this time around he didn't seem as steadfast. Because of the cortisol receptor business, he realizes that the ANS definitely has a part to play in triggering the retroviral activation as well as re-triggering it. Since I'm doing a therapy right now that focuses on restoring ANS and immune dysfunction at the same time, the following exchange was definitely the take-home of the appointment:
Me: "Since cortisol sets off XMRV, can the autonomic nervous system be the initial culprit? And let's say I take AZT and eradicate what virus is in my blood stream (btw we can never fully eradicate retroviruses based on medicine available now and maybe ever,) can't autonomic dysfunction reactivate it?"
Peterson: "Absolutely. In fact, the double-hit (#1 ANS dysfunction #2 viral trigger) theory is one of the leading ones among retrovirologists right now."
Holy bejeezus I got the ah-ha I was looking for... from a straight-edge allopathic physician.
Then for confirmation of what I thought he just implied:
Me: "Do you treat cases that aren't triggered by infections? Say physical or emotional trauma?
Peterson: "Of course, now that we know about the cortisol receptor."
This last question is one that several patients had wanted me to ask, and I think they'll be nothing short of ecstatic with that answer. The last time I saw Peterson, immune dysfunction seemed to be the holy grail. I can say with certainty that both the above lines and everything else between the lines during our visit now shows that to be merely prologue to Peterson's expanded view of the disease.
As for why this was my "ah-ha," I needed to know if there was a point to taking a toxic drug like AZT if the initial above-the-neck hit wasn't resolved. Now I know my intuition is right. Maybe the drug will have a place for me in the future. Maybe doing isopathic injections won't be enough to lower the viral loads, but that is a worry for later. Right now, even the signs from a purely drug-prescribing CFS physician are pointing me toward Sanum injections and possibly stem cells to regenerate the central nervous system.
*Apologies on delay in live blood analysis videos. Having trouble uploading, but hopefully will remove tech dunce hat by end of day.
What a crazy 2-day stretch. Was on the amtrak for about half the time, taking in the aesthetically insane views of the bay area, Sacramento wildlife reserves, and Sierra mountains, while all the time wondering if there would ever be a day when these views would no longer be internalized as utterly lackluster. I remember there used to be a day when all these solo excursions made me feel deeply at the core--whether it be longing for someone to take it all in with me or a quality of the human spirit being laid out before my eyes--but these days I'm so focused on recovering that it's challenging for anything that's unrepresentative of progress to elicit an emotional ripple. Funny thing is: I don't mind it one bit. It takes a machine to be resourceful enough to find a way out of this illness, and I can honestly say I'm proud of myself for becoming one.
Peterson was practically glowing when he came into the room. "So we have some big news." Understatement of the year? He hashed over the details of the study, which I won't go over here. Instead, I'll report some of the (maybe) lesser-known aspects of it.
Peterson was very selective with his sample. He picked the patients that he thought were most likely to have the illness, and >90% of them were positive. The other sample sizes from around the country averaged out to something lke 60% positivity, so it's definitely possible 1) that XMRV isn't as ubiquitous as it seems, 2) detection methods aren't refined enough, 3) some of the patients in other sample sizes don't have CFIDS but rather have chronic fatigue.
He said I'm a very good candidate for XMRV because 1) it infects NK cells, 2) I have rnase-L abnormalities, 3) it's reactive with other viruses which I documented stealth infections of, and 4) it has a cortisol receptor, which is why my symptoms wax and wane so much due to stress.
We had a good laugh about Reeves and how I barely escaped falling into Reeves' group of "hypogonad males who complain about everything" with my normal hormonal levels.
Surprisingly, my only elevated cytokine is IL-8, which however is produced in the gut and correlates highly with my elevated coxsackie A and B titers. However, the IL-8 is also the cytokine that's most strongly associated with XMRV. Peterson's interpretation was that many of the drugs I took such as Zithromax, Mepron, Valtrex were either immunomodulatory or lowered my viruses without me knowing it. I nodded politely, but I only took all those drugs within a 3-month period back in summer '08. The next year of bug-killing was all photons and later, ozone.
I wanna take this opportunity to give a shout-out to the Bionic 880. I've never been more convinced that it is the most effective targeted antiviral, antibacterial, antifungal treatment I've ever tried. I don't think I give the machine and community of users that have helped guide my Bionic treatment the credit they deserve for getting me to this point of relative health compared to a year ago.
Back to XMRV: he's not sure if it's sexually transmitted, vector-transmitted, or maybe a human endogenous (HER) virus. I was really impressed that he was equally open to each option. He did say he doesn't believe it is highly contagious if sexually transmitted (most of us patients have had sexual partners, and the norm is that our partners do not develop CFIDS), and that the chances of vector transmission are slight (given that millions have it--although lyme patients would clearly disagree with this logic). I for one am really glad to hear he's open to the HER virus theory. These viruses are embedded in our embedded genome, yet the reason why some family members express them and some don't may have to do with the triggers which I'll talk about shortly. Peterson even waxed a bit about how some retrovirologists think that HER viruses may be advantageous to human genomes.
Another reason he thinks this virus is causative of CFS is because he took blood samples from 1984, inserted the virus into non-infected cell lines, and produced high viral loads. I think this is the fact that really impressed virologists involved in the study. However, he said we're relatively lucky to have a gammaretrovirus vs the lentivirus (HIV is a kind).
Ok so what does this mean for treatment? He thinks this study shows why Ampligen and other immune-modulating therapies caused relapse after patients got off the drugs: they didn't eradicate the virus. Ampligen has been proven to have some anti-infectious activity, but not nearly enough. He said if he were me, he would consider going on AZT, a reverse transcriptase inhibitor. He said some docs around the country are already trying this on CFIDS patients. His reads into patient personalities actually have a lot to do with his individual treatment recommendations. He knows I like to be aggressive with treatment (in fact most males in his practice do). As an allegory, he said that during the AZT trials for HIV patients, the patients that didn't wait for later-stage clinical trials to try the drug had better results. Hint hint.
As a bit of an aside, I'm really glad to have found a physician that fully understands the gender role discrepancies of the illness. He said he has found males in his practice to employ the same treatment tendencies as myself because he thinks it's much less socially acceptable to have this illness as a male than as a female. I rarely hear this discrepancy being mentioned in patient communities (probably because it's taboo for one patient to say to another my suffering is greater than yours), but I really agree with Peterson. He said 9 out of his first 12 Ampligen patients were male, and he believes the same guinea-pig aggression will be seen with AZT.
But this next part is very interesting for those that aren't convinced this virus is the end-all, be-all. I think I'm still hanging onto that bandwagon by a thread, especially after what Peterson told me next. I went back to what we talked about last time: the relation between immune dysfunction and autonomic nervous system dysfunction. Whereas last time, he seemed convinced that ANS dysfunction was secondary to immune dysfunction, this time around he didn't seem as steadfast. Because of the cortisol receptor business, he realizes that the ANS definitely has a part to play in triggering the retroviral activation as well as re-triggering it. Since I'm doing a therapy right now that focuses on restoring ANS and immune dysfunction at the same time, the following exchange was definitely the take-home of the appointment:
Me: "Since cortisol sets off XMRV, can the autonomic nervous system be the initial culprit? And let's say I take AZT and eradicate what virus is in my blood stream (btw we can never fully eradicate retroviruses based on medicine available now and maybe ever,) can't autonomic dysfunction reactivate it?"
Peterson: "Absolutely. In fact, the double-hit (#1 ANS dysfunction #2 viral trigger) theory is one of the leading ones among retrovirologists right now."
Holy bejeezus I got the ah-ha I was looking for... from a straight-edge allopathic physician.
Then for confirmation of what I thought he just implied:
Me: "Do you treat cases that aren't triggered by infections? Say physical or emotional trauma?
Peterson: "Of course, now that we know about the cortisol receptor."
This last question is one that several patients had wanted me to ask, and I think they'll be nothing short of ecstatic with that answer. The last time I saw Peterson, immune dysfunction seemed to be the holy grail. I can say with certainty that both the above lines and everything else between the lines during our visit now shows that to be merely prologue to Peterson's expanded view of the disease.
As for why this was my "ah-ha," I needed to know if there was a point to taking a toxic drug like AZT if the initial above-the-neck hit wasn't resolved. Now I know my intuition is right. Maybe the drug will have a place for me in the future. Maybe doing isopathic injections won't be enough to lower the viral loads, but that is a worry for later. Right now, even the signs from a purely drug-prescribing CFS physician are pointing me toward Sanum injections and possibly stem cells to regenerate the central nervous system.
