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Il28b testing update
the profile has just changed and it's good for us, but requires understanding as it just got more complex.
I will try to explain and then give you the study.
We have long chains of encoding within our DNA. Each strand within that long chain has a combo of the basic proteins. When we speak of the alleles within a group, it is these pieces of data we referrence.
the patient only need know that how these proteins are encoded within your cells determines how strongly your body may be able to fight this virus.
Past threads have discusses the first test that became available as a genetic predictor.
Now labcorp (through Arup) is making available 2 single nucleotide polymorphisms rather than 1.
what that means is that we will know the Interleukin program within 2 of our gene programs, and have a better predictor of outcome.
Now here's where it gets tricky.
the original test some members already got showed a 2-3 fold increase in SVr with the right genes.
this test is known as the IL28b rs12979860
with this test the best combo to have is C/C, followed by C/T, and by TT being the worst.
Now they have moved up the chain to test one more set of alleles, and this test is call the IL28b rs8099917.
with this group T/T is the most favorable outcome, followed by G/T followed by GG being the worst.
now you see where confusion could come in. TT is least favorable with the test for one grouping, and most favorable with the group next door!!
here's the study:
http://www.natap.org/2010/HCV/050310_09.htm
now I just happened to have had this testing done and my results arrived today.
to my surprise I was CC on the rs 12979860 and TT on the rs 8099917
it doesn't get any better than that.
this means that I should be able to clear with a PI added especially if I keep my IR down and get my Dietary restrictions in place.
It also means my diet had a great deal to do with why I didn't clear because I was extremely compliant on tx and my genes helped, so I should have cleared, except for being stage 3/4 which also may have lowered my chances.
I will try to explain and then give you the study.
We have long chains of encoding within our DNA. Each strand within that long chain has a combo of the basic proteins. When we speak of the alleles within a group, it is these pieces of data we referrence.
the patient only need know that how these proteins are encoded within your cells determines how strongly your body may be able to fight this virus.
Past threads have discusses the first test that became available as a genetic predictor.
Now labcorp (through Arup) is making available 2 single nucleotide polymorphisms rather than 1.
what that means is that we will know the Interleukin program within 2 of our gene programs, and have a better predictor of outcome.
Now here's where it gets tricky.
the original test some members already got showed a 2-3 fold increase in SVr with the right genes.
this test is known as the IL28b rs12979860
with this test the best combo to have is C/C, followed by C/T, and by TT being the worst.
Now they have moved up the chain to test one more set of alleles, and this test is call the IL28b rs8099917.
with this group T/T is the most favorable outcome, followed by G/T followed by GG being the worst.
now you see where confusion could come in. TT is least favorable with the test for one grouping, and most favorable with the group next door!!
here's the study:
http://www.natap.org/2010/HCV/050310_09.htm
now I just happened to have had this testing done and my results arrived today.
to my surprise I was CC on the rs 12979860 and TT on the rs 8099917
it doesn't get any better than that.
this means that I should be able to clear with a PI added especially if I keep my IR down and get my Dietary restrictions in place.
It also means my diet had a great deal to do with why I didn't clear because I was extremely compliant on tx and my genes helped, so I should have cleared, except for being stage 3/4 which also may have lowered my chances.
I appreciate your observation but you are looking at one aspect only in my opinion.
The first method was to determine if higher doses made a difference as an induction and they didn't. You may recall there was more than one study about that idea, and they all proved punching hard early on does not work.
Reading on to the other methods and tests, and look James I know what the study says...in fact I read Infergen studys until my brain glazed over and developed a hard lipid shell...I choose this one to show both the frailty but the possibility.
the sides listed are the same sides we see with peg when weight based INF is not given.
All you would have to do is go back and read the sides that thin people who were being overdosed in here all had to know the truth of that, but look at it from the other side, we all drank the koolaide, we all took the peg knowing those sides were possible.
the point made later in the study was that lower doses might do a similar job. That even though this study failed at highest doses, and even though dosage and SVR are related, that 20-37% have SVR'd in former studys (not at such high doses) and that what this really shows is that they may be missing the forest for the trees.
My reasoning was, lets say we went to a different model that hasn't been tried, Say one where we break up the INF into a dose given 3 times a day, not the highest or the lowest either, but given 3 times, knowing the way the drug clears, and knowing that it's just like a lot of things that need dosing more often to work well. If something makes you sick at 24 mg, it doesn't mean you couldn't tolerate it at 18, or 16...or a lower number more often.
I'm on a drug like that now, and all the docs say I should be on between 30 and 60 mg per day with my condition, but I manage to get by on 15 mg because I space out small doses more often and in so doing I eliminate all the side effects for the most part and am doing better on 15 mg than I was on the higher doses they told me I must take.
my point here is, spread out correctly some medications can become as effective, and more problem free, at lower doses provided the dose is adjusted for it's half life correctly.
The first method was to determine if higher doses made a difference as an induction and they didn't. You may recall there was more than one study about that idea, and they all proved punching hard early on does not work.
Reading on to the other methods and tests, and look James I know what the study says...in fact I read Infergen studys until my brain glazed over and developed a hard lipid shell...I choose this one to show both the frailty but the possibility.
the sides listed are the same sides we see with peg when weight based INF is not given.
All you would have to do is go back and read the sides that thin people who were being overdosed in here all had to know the truth of that, but look at it from the other side, we all drank the koolaide, we all took the peg knowing those sides were possible.
the point made later in the study was that lower doses might do a similar job. That even though this study failed at highest doses, and even though dosage and SVR are related, that 20-37% have SVR'd in former studys (not at such high doses) and that what this really shows is that they may be missing the forest for the trees.
My reasoning was, lets say we went to a different model that hasn't been tried, Say one where we break up the INF into a dose given 3 times a day, not the highest or the lowest either, but given 3 times, knowing the way the drug clears, and knowing that it's just like a lot of things that need dosing more often to work well. If something makes you sick at 24 mg, it doesn't mean you couldn't tolerate it at 18, or 16...or a lower number more often.
I'm on a drug like that now, and all the docs say I should be on between 30 and 60 mg per day with my condition, but I manage to get by on 15 mg because I space out small doses more often and in so doing I eliminate all the side effects for the most part and am doing better on 15 mg than I was on the higher doses they told me I must take.
my point here is, spread out correctly some medications can become as effective, and more problem free, at lower doses provided the dose is adjusted for it's half life correctly.
Mer
So basically it's saying SVR isn't really durable and we need that constant influx of IFN in our bodies OR we lose SVR? The point of interferon is not to take it over and over to whack the virus and kill it BUT to train our own immune systems to do it right? So we do HAVE interferon it's just a matter of training it. If you do it 3x a day you are only relying on some concept that it "kills" the virus. It does NOT. WE DO.
What happens when a dope addict stops taking heroin, oxy. dilaudid? Their body goes into WITHDRAWL and tries to fight that. It does not work out p3acefully.
So if I get a flu or cancer and my body needs the *IFN to treat that I will after 4 years lose my 'systemic virologic response' and thus need more IFN to keep dosing myself to keep everything at bay?
I dont think so. Supposition is not fact. Please stop trying to pretend this is scientific. it flies in the face of EVERYTYHing we know to be true.
Otherwise - we are all dead. Take your pick.
So basically it's saying SVR isn't really durable and we need that constant influx of IFN in our bodies OR we lose SVR? The point of interferon is not to take it over and over to whack the virus and kill it BUT to train our own immune systems to do it right? So we do HAVE interferon it's just a matter of training it. If you do it 3x a day you are only relying on some concept that it "kills" the virus. It does NOT. WE DO.
What happens when a dope addict stops taking heroin, oxy. dilaudid? Their body goes into WITHDRAWL and tries to fight that. It does not work out p3acefully.
So if I get a flu or cancer and my body needs the *IFN to treat that I will after 4 years lose my 'systemic virologic response' and thus need more IFN to keep dosing myself to keep everything at bay?
I dont think so. Supposition is not fact. Please stop trying to pretend this is scientific. it flies in the face of EVERYTYHing we know to be true.
Otherwise - we are all dead. Take your pick.
half life means the time it takes to get to half the original plasma level. I know it's not an exact correlary but if we start giving the math formulae we will lose everyone.
bottom line is INF clears very quickly, half life is considered a standard for indicators of clearance,not just plasma levels, and ergo it's why docs choose one drug over another.
Particularly SSRI's benzo's, things where a short half life creats a yo-yo effect and all kinds of commensurate symptoms of low levels.
INF build very quickly when we have a virus, and clears quick as well..that's why sometimes you feel like you are getting sick...as INF goes up...then you are fine the next day...INF fell off when the body destroyed all the virus.
We invented peg not just because it provided a fix for the short half life, it also eliminated the patients who hate shots postponing their shots and sabotaging their tx.
It doesn't mean however that consensus INF didn't work better...CIFN...gee, why did they name it consensus...could that be a clue??
The truth is that you will achieve a more level amount with 3 shots a day than 2 if you choose to go the CINF route, and, it might be that the stats of 20-37% for relaspe groups could go higher were they to do that.
After all this virus makes millions of new copies everyday, it therefore means the drugs used need to be and remain at steady state. With the riba this is a problem in the beginning due to slow absorption rate, but once it reaches steady state it's anything but.
With INF there's no perfect world regardless of type. The 7th day fall off is real, or with daily injections same thing. The question becomes how to best overcome those issues.
bottom line is INF clears very quickly, half life is considered a standard for indicators of clearance,not just plasma levels, and ergo it's why docs choose one drug over another.
Particularly SSRI's benzo's, things where a short half life creats a yo-yo effect and all kinds of commensurate symptoms of low levels.
INF build very quickly when we have a virus, and clears quick as well..that's why sometimes you feel like you are getting sick...as INF goes up...then you are fine the next day...INF fell off when the body destroyed all the virus.
We invented peg not just because it provided a fix for the short half life, it also eliminated the patients who hate shots postponing their shots and sabotaging their tx.
It doesn't mean however that consensus INF didn't work better...CIFN...gee, why did they name it consensus...could that be a clue??
The truth is that you will achieve a more level amount with 3 shots a day than 2 if you choose to go the CINF route, and, it might be that the stats of 20-37% for relaspe groups could go higher were they to do that.
After all this virus makes millions of new copies everyday, it therefore means the drugs used need to be and remain at steady state. With the riba this is a problem in the beginning due to slow absorption rate, but once it reaches steady state it's anything but.
With INF there's no perfect world regardless of type. The 7th day fall off is real, or with daily injections same thing. The question becomes how to best overcome those issues.
Merry,
That's not what the study says. How do you arrive at the conclusion. Everyone in the study had a VL at 24 weeks, only one person #11 went UND at week 20 but then by week 24 had a VL again. The study was a total failure. All you have to do is look a figure 1.
Take care and good luck.
That's not what the study says. How do you arrive at the conclusion. Everyone in the study had a VL at 24 weeks, only one person #11 went UND at week 20 but then by week 24 had a VL again. The study was a total failure. All you have to do is look a figure 1.
Take care and good luck.
You keep saying the inf lasts 8 hours and that is just not true with a half life of 4 hours.
FIGUY-exactly, and that why when I said on the thread trying to disprove Lindahl's discovery about amantadine that treating for half the normal time, and with every other day shots was ludicrous. I don't really care that it was a small study, the idea that you could have gotten every patient to SVR in any group, even if very small (which is how many phase 1 studies are...20 patients is not uncommon), to get to 100% was highly unusual, and it warranted a serious follow up study, which no one ever did. They just tailored the follow up to fail.
But then, I'm remembering that when billions are at stake the tobacco companys had no problem finding dozens of doctors to say tobacco was safe.
JAMES, read the whole study, sometimes if we don't read through a whole document we can miss the point....the end stats were great AND that was for non-responders...people thought impossible to cure,
and not only that, but the stats when they dialed it back were good too
meaning you don't have to stay at the high dose, just punch it hard to start with.
This goes along with a LOT of what is now thought and discussed about that initial window of critical time and the need to overwhelm the virus so it can't adapt.
Honestly, where have you ever seen 50% of non-responder clear...other than with this approach.
My point is that I think they would have even better results with an 8 vs a 12 hour regime, because the INF only lasts 8 hours, so why even give the viron any time without INF in the system. Take the same daily dose, divide it in 3, and then you aren't leaving the patient with 8 hours in every 24 with almost no INF.
If they were to try that they might get better results even at lower dose.
You can't rule something ineffective that cures half a populace formerly non-responsive.
You can say we need to tweak it to not get sides as bad, but to dismiss it is foolhardy.
Look at all the other chemos, folks hug toilets for weeks, lose their hair and much much more, and no one says well its ineffective!! Not when the end result is folks are living WITHOUT the cancer!! So why conclude that with hcv? It does not compute.
mb
But then, I'm remembering that when billions are at stake the tobacco companys had no problem finding dozens of doctors to say tobacco was safe.
JAMES, read the whole study, sometimes if we don't read through a whole document we can miss the point....the end stats were great AND that was for non-responders...people thought impossible to cure,
and not only that, but the stats when they dialed it back were good too
meaning you don't have to stay at the high dose, just punch it hard to start with.
This goes along with a LOT of what is now thought and discussed about that initial window of critical time and the need to overwhelm the virus so it can't adapt.
Honestly, where have you ever seen 50% of non-responder clear...other than with this approach.
My point is that I think they would have even better results with an 8 vs a 12 hour regime, because the INF only lasts 8 hours, so why even give the viron any time without INF in the system. Take the same daily dose, divide it in 3, and then you aren't leaving the patient with 8 hours in every 24 with almost no INF.
If they were to try that they might get better results even at lower dose.
You can't rule something ineffective that cures half a populace formerly non-responsive.
You can say we need to tweak it to not get sides as bad, but to dismiss it is foolhardy.
Look at all the other chemos, folks hug toilets for weeks, lose their hair and much much more, and no one says well its ineffective!! Not when the end result is folks are living WITHOUT the cancer!! So why conclude that with hcv? It does not compute.
mb
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