Squashing Hepatitis C with no interferon-ribavarin

Hi,

I am a 32 year Hep C survivor. I found and tried a new combo of drugs and supplements that reduced my count from over 500K to 11K in a very short time.

I posted the whole nine yards on Blogger ******* under this lnk    http://******************.********.com/

Not sure if links are allowed.

And no, I am not selling anything. I just want to try and help anyone who is looking for an alternative. Everything I am taking you can easily obtain yourself.

I hope this helps some of you.

[Trinity4]

See no value to it.  Reducing the viral load doesn't  stop the virus from attacking the liver but good luck with that anyway.

[nygirl7]

I'm sorry but 500k is really the same thing as 11k.
There is no cure for this disease without interferon and ribavirin and viral load has absolutely nothing at all to do with liver damage.  Plus, it goes up and down all of the time.

Have you had a biopsy to determine how much liver damage you have? What stage of the disease you have progressed to?  Please do not assume because the VL is down that you dont need to monitor and follow up on these things, you do.

[James10500]

Help people do what ? You have hepc and you still have hepc.  The goal is to get rid of the virus which you have not done.  

[meakea]

Unfortunately, some people still equate viral load numbers with how much harm Hep C is causing and that's simply not the case.

[Susan_1a_CC]

Thanks for the sentiment but the fact is there is no relationship between viral load and the amount of liver damage that may be taking place.  It's sort of like having a little bit of feces in a brownie vs. just a little - I don't want any of it!

[nygirl7]

Bwah that was the best anology I've ever heard about this disease.
You really are good that was great!

[James10500]

ROFLMAO

[evangelin]

If the viral load doesn't matter one bit, why does Joe's P.A. order a viral load for every appt. now?  They used to only want to know the viral load during TX but they have changed this practice.  I assume they have a good reason because this is  St. Louis  university and they conduct many trials and are very in touch with the latest.. It must matter to some extent or what would be the point?  
I still like to have information and weigh it's value for myself. I totally understand the need to keep people that need to TX from getting bad information but I still maintain that the gigantic pool of non responders should be aloud to freely exchange information that might prove helpful to them.  Some of us will still be unsuccessful even with the P.I.'s.  Others might not even be able to get a chance with a P.I. because of finances or other health problems.  I would like to see these posts  handled in a more fair and balanced manner so that people that may have something of value to share won't be too intimidated to bring it up.  For true non responders, improvement might be your only realistic goal in the foreseeable future.  I'm not saying to let the snake oil salesman run rampant, just don't shoot down everyone that breathes the word "alternative." If plan A is impossible we best be searching for a plan B. (Some of us need  a C,D,E and F too)
Ev

[Trinity4]

No one was shooting down alternatives evangelin.   Our comments pertained to the relationship between viral load and liver damage and the fact remains there is none.  Viral load has no bearing on the progression of fibrosis.  That is true fact stated many times in peer reviewed studies.

Why don't you ask your husband's medical team why they regularly track Joe's viral load?
Maybe then you can tell share their view with us.

Trinity

[nygirl7]

Perhaps his doctors just aren't that up to date on the whole viral load issue because this is not a subjective thing and it has been proven to be true. Like liver enzymes not always being indicative of the inflammation going on.  I had a low low viral load and yet I was stage 3 when diagnosed......there has to be validity to it as this is quite common.

One of the smart guys will know the links I am sure.

[James10500]

VL tracking is done to measure effectiveness of tx.  As I am sure you know.  But to say you survived Hep C as the op did and still have a VL of 11k unfortunately isn't true.  

Alternative treatments for Hep C simply don't exist.  Alternative treatments to help liver function yes, to kill all the little SOBs no.  

I've read posts by people who claim to be in the medical profession who've tried herbs, veterinary treatments, only to beat Hep C with SOC.

Why people think they can fool around with "alternative" treatments for Hep C I do not know. I wonder if people with Ebola Virus, or Yellow fever, are as gullible as heppers.

[Bali05]

I would rather start tx with 11k than 500k

[evangelin]

My inquiring mind would still like to know what this person is using.  I have pm'd them and hopefully I will hear back .  It may be nothing but I still want the information.
Several people have contacted me off line to tell me they have been using Hepatitis Technologies products and are having the same good results that Joe has. It doesn't change your viral load but it has a really good chance of giving you a more functional liver and protects from more damage.  They don't want to deal with any scorn or persecution so they won't tell about it on Medhelp...what a shame.  I don't enjoy the conflict either but my heart hurts  for the non-responders.
The problem with some of the natural products that can lower viral load is that they can also increase inflammation which could lead to more fibrosis/scarring..  For those who respond marginally, starting with a lower viral load could have some benefit.  I too would prefer for Joe to start with the lower number  but not at the cost of more damage.
I know someone who has had a similar drop by using the blueberry leaf  extract purchased from a person that most of us don't trust...me included.  He is the only one that carries the variety described in the study showing a viral reduction.  This person knows there is some risk to using this but  they relapsed after Tx and are hoping to start with a lower starting number next time.  I didn't decide to buy  the blueberry product ,as of yet,but I'm still  glad to know about it and will watch this persons progress.  
I wouldn't want this to go on and on like some of the threads debating this issue have, because I am needing to spend my time elsewhere right now.  I won't argue for the freedom of discussion every time I see a post I don't like. I just revisit it from time to time because it still bothers me.
Back to work,
Ev

[meakea]

Bali...you have a point that I totally agree with.  Getting the viral load to a lower point before starting treatment would be a good thing.  

[murariji]

Well said Evangelin. This is a forum for Hep C which should include discussion about living with it as well as curing it. As long as that distinction is made where is the harm? Many people believe 'religiously' that SOC is the only solution. It is a belief based on research of other people's research and publications, and their own experience. At best, all that can be said is that INF/Riba sometimes works, about 50% of the time. That is not exactly a text book 'cure'. What if Juices/Supplements/Positive thinking/ Eskimo pee, also sometimes work. Even if it is only 1% of the time it would help thousands get cured.
I agree it is correct to point out that still having the virus means you are not 'cured', but I don't agree that without annihilating every last virion you can't have a happy healthy life, and as mikesimon brought to light, a little poop in the cookie may not be all bad. Understandably anyone who has slogged through weeks and weeks of tx, or is going through it now doesn't want to hear that it's not necessary and that the right diet solves everything, but the responses to anyone making significant progress coping with the disease outside of SOC are pretty muted. I wouldn't be bold enough to post my improvement anywhere but my journal, and I have received only kind words here.
It is just a gut feeling I have, that perhaps those who have reached, or are well on the way to SVR miss.

[merryBe]

Sheesh medhelp, I fail to see the point of censorship.

Even if someone brings in an idea we don't agree with, since when are we such children that we cannot correct, instruct, debunk, or even, gasp, explore a new idea.

The verdict on alternatives curing is in, they don't, but the verdict at least for HIV people is that viral reduction equals longer life. 30 years is the average time from HIV to full blown AIDS now, whereas it used to be less than 5 years from being diagnosed.  This is all due to keeping the VL very low.

Obviously adjuncts have so far proved incapable of cure, but which of you who have not been able to REACH a cure using SOC would not gladly trade a viral load of 2 million for 10 thousand??

It's not JUST about inflammation, although that's somewhat true, but the virus also changes the way we metabolize, the whole lipid process is thrown off, as is the whole endocrine process, and God only knows what else.
I've been saying 50% of us have endocrine dysfunction, many have metabolic syndrome, thanks to this virus and provided the studies...and lately the stuff I've been reading on lipids is equally frightening...not just what happens to your belly fat and the hump on the back of your neck, but all the other parts of the body that are starved for enough lipids because this virus somehow reroutes them to storage. It goes on and on.

I just wish sometimes we could carry on conversations without the brain police deciding for us what is worthy of discussion.

LAst time I looked the average age in here was 60, not 6!!!

One reason I don't come in here as much anymore is because of the censorship.
I suppose this post will be censored for me saying this.

[Trinity4]

"I just wish sometimes we could carry on conversations without the brain police deciding for us what is worthy of discussion.:

Good luck with that one, it ain't never gonna happen. :)

Just to caveat on what has been said.  The thread is not about using Hepatitis Technologies, juices, co-existing with the virus, positive thinking for good karma and a happy and healthy life.  The OP distinctly said he lowered his viral load from 500k to 11k in a short period of time so what's his point?  He's got a low viral load, big whoop.  No mention of not wanting to treat or not being able to treat.  Fact remains he still has hepc but I guess it's whatever blows your boxers up.  The only defensiveness I see are from those who have gotten the impression this thread is about something else other than a low viral load.

Trinity

[FlGuy]

I think the name "hepcsurvivor" is a little presumptuous for someone who has hepc.

[murariji]

Hi Trinity, glad you are back.
Surely at some level the viral load is relevant. Maybe not 11k, but 1k? 100? 10?
If the liver becomes damaged due to the virus why is a lower viral load irrelevant?
Does it mean that damage done by a viral load of say 5,000 is already maximum damage, and anything higher than that is overkill?
And if there is a proven formula for reducing the viral load, apart from SOC, why does it stop short of total genocide of all the little boogers?
With much respect,
Murari

[Trinity4]

The relevance applies when treating or starting treatment with a low viral load which is <400,000 IU/mL.  I would love to see any study you can provide that shows the correlation between viral load and liver health.  I've yet to see anything from the AALSD, Clinical Care Options, Medscape or the likes that showed any correlation between viral load and liver damage.  We would know by now if there was a true connection.  The virus replicates and is going to attack the liver in the same manner whether there are millions, thousands or hundreds.  Reducing the viral load is not going to stop the attack on the liver because that it what it is designed to do and it's existance depends on it.  

Trinity

Trinity  

[Aaron57]

I'd much rather have 10 virons attacking my liver over time rather than 10 million , if I had a choice ...
And much rather at the time of starting Tx ,

Start Tx with a low VL , as this factor has been "proven" to be one of the "best" indicators of achieving SVR ..

Obviously, this is not true for all folks ... like NYgirl ,who continually says "low VL at the start of Tx is not import , that " 500k is really the same thing as 11k " , 500k = 5.69 log , 11K = 4.4 log ... that was unfortunately her experience ... but,  definitely this is not true for the majority of us infected .

For the majority of patients  , a low VL load < 400K at the start of Tx is a very very important predictor in achieving SVR , that has been continually proven over time with patients and CT's.

I'm not sure how anybody at this stage of research and trying to figure out what really is going on with  HCV , can discount  damage caused by this virus , by saying things such as

"We would know by now if there was a true connection... The virus replicates and is going to attack the liver in the same manner whether there are millions, thousands or hundreds"

Where is the data to support this statement ? ? ? None of these correlations have been proven or disproved at this time . The reality is the scientist and doctors just don't know..... yet

The only "thing" we know at this stage of research of this virus ... for 1a - is that there is maybe a 50% chance of attaining SVR , maybe ....  & that this virus damages our liver over time.

New info is being discovered every day ... not like several years ago .. thank the powers that be ! ! !

Any other presumption or conclusion at this time is only to assume ...... break down the word assume into 3 sections and what do you have ***/u/me ....

[Cory255]

" The lower the pre-treatment viral load, the more likely it is that a person will respond to current HCV therapies. "

http://hepatitiscnewdrugresearch.com/hcv-viral-load-test.html

[Cory255]

" A correlation between HCV viral load and disease progression has not been shown. "

http://hepatitiscnewdrugresearch.com/hcv-viral-load-test.html

[Trinity4]

http://www.webmd.com/hepatitis/c-hcv-viral-load

"With HCV, viral burden in hepatitis C does not necessarily predict the natural history of clinical disease. And therefore, patients need to understand that we use that measurement to help us guide therapy and response to therapy. We use it in conjunction with other types of laboratory data -- liver enzymes, liver biopsies sometimes, and viral genotype. Taken all together, these tests give us a snapshot of what is going on. But viral load numbers do not predict disease."

"Unlike HIV, HCV viral copies do not directly affect a patient's prognosis and how fast disease is progressing in the liver. Remember, we are measuring blood levels, not what is happening in liver cells. HIV viral load does have a lot to do with quicker progression to AIDS. But HCV viral load does not tell you how fast hepatitis is progressing."

[James10500]

Thanks for the links, my bookmarks HCV continue to grow.  All the better for sharing with others.

[Aaron57]

You said "I've yet to see anything from the AALSD, Clinical Care Options, Medscape or the likes that showed any correlation between viral load and liver damage."

"We would know by now if there was a true connection."

That is exactly the point  , there is no scientific data .... how would we know ?

Webmd  link you gave - Is 2 doctors opinions ... not scientifically validated data. If we read further down the link you gave , one of those doc goes on to say " I cannot say there is a cure" .... another "can of worms" ...

Too much is still not known , too many areas have not been studied about this virus. As we all know, it takes big $$ over many years and thousands of subjects, for the scientific data to say the impact is 100% like this or 100% like that ....

To give your opinion , ya we all have those , to say.... we would already know ? Data please ... not doctors opinions .

[Trinity4]

Ok Aaron, you'd like me to provide data.  To date, I can give you a multitude of links to studies and abstracts saying viral load plays no role in fibrosis progression.  Can you provide a link that says it has been proven low viral slows the progression of fibrosis?  You are a proponent of the hemopurifier that is supposed to lower the viral load yes?  Certainly you have data from that to support a lower viral load slows down fibrosis,  

I'm not going to argue the point any longer.  All I can say is I believe what all the renowned hepatologists and studies throughout the world have indicated so far.  VIRAL LOAD HAS NO BEARING ON FIBROSIS PROGRESSION......Prove me wrong, show me something, conclusive and I will gladly change my viewpoint.

Trinity    

[Trish77]

From Cory's link:

http://www.hivandhepatitis.com/hep_c/news/2011/0201_2011_a.html

"Elevated serum HCV RNA level was associated with an increased risk of cerebrovascular death, suggesting that individuals with an active HCV infection may trigger a stronger inflammation response by host-virus interaction leading to atherothrombosis," they continued. "Whether patients with persistent HCV infection had increased circulating levels of inflammation markers such as C-reactive protein or endothelial progenitor cells may provide insights on the mechanisms of HCV infection and cerebrovascular disease."

Since we know that HCV contributes to a number of extra-hepatic illnesses, we know that viral load causes damage.  Does elevated viral load cause more damage? Has there been enough targeted study to know?  This article Cory posted indicated that elevated viral load has an impact on this at least, it's not a stretch to think it may cause other issues as well, however it remains to be substantiated.   I think it's more reasonable to say there have been insufficient studies on it to conclude one way or the other rather than simply deciding there is or isn't harm and propogating that, with insufficient data to back that up.

Perhaps there is other data similar to what Cory has posted and reasons why experienced doctors are monitoring viral load on patients with HCV.

[child24angel]

Please, someone please, enlighten me.

Then why did my son pass away? if  some say
the viral load is so significant.  Wouldn't that  serve as a marker
to determine how damaged the liver is/was?

Low viral load.....I'm saying 2 mil....and steady.
They only did viral load  during TX...three times non-responder.
Then on maintenance therapy.  Viral load still at 2 mil.

All the while the liver was being damaged

They never used the viral load to determine liver damage, not once.
They used various labs, and MELD when the liver was
decompensated.   Two biopsies only. 1st one showed 1-2
next one, five years later 3-4...

I was informed time and time again the viral load has no bearing
on the amount of liver damage.

They used the viral load during tx only.
I can't believe the viral load is a predictor of liver damage.
I just can't.

[Trish77]

I haven't seen a single comment from anyone in this thread that says they believe that viral load equates with level of liver damage.  The first poster mentioned bringing down viral load but did not state why this is important to her/him, the next poster made the tie-in to liver damage.  

Subsequent comments were speculating on the possibility that viral load can potentially cause some damage in general and also the speculation that there is more to be known on whether it contributes to fibrosis - one person's opinion that they'd like to see more data and other people saying they are sufficiently satisfied there is no connection.  I don't see any issue with those opinions.  I have not seen anybody firmly stating there is a connection but rather stating firmly there is none.

Subsequent comments are related to the concept that the impact of viral load in general needs further exploration.

I haven't seen anyone in this thread saying that viral load is a predictor of liver damage.  I think you can relax on that score.

[Bali05]

very often with a spike in viral load we also see ALTs go up indicating more ongoing
cell damage.When on tx we usually see big improvement of ALTs with the rapid drop of
viral load even when still detectable.
Viral load has no meaning for over time accumulated liver damage (scarring)
since viral load can vary greatly during that process.

I think we can all agree the less copies of virus to be found the better with the ultimate
goal to be and stay UND forever.

[child24angel]

Thanks for letting me know I can relax on that score.

What I'm saying is........

Viral load does not indicate how much damage is
being done to the liver.  It does not indicate the progression
of fibrosis or cirrhosis as I tried to explain above.

Have a good day and try to relax

[evangelin]

I've always been influenced in my thinking on this subject because back when Joe was sick and getting sicker, he had a very high viral load in the hundreds of millions.  I don't often see people post those really high numbers but that is where Joe started.  Since using HR's supplements, it has so far, never been that high again but we were approximately 3 years and 2 failed TX down the road before we found HR's supplements. His viral load has been staying in the 1 millions.  I know this is only data from 1 person and it is also a person with cirrhosis but that is our experience and I can just share it for what it is worth. Joe isn't as sick as when we first began by any apparent sign. I don't want to be argumentative at all.  I just want to share information peacefully.  Maybe Joe's case is just a fluke. He still has cirrhosis, but he is stable and feeling decent most days.

I promised myself not to stay on here all day because my laundry room is getting scary.  I need to put all my attention to knocking out a few laundry virons today :>)
Best regards,
Ev

[Bill1954]

There may be some hepatic protection involved with large reductions in viral load; the HALT-C study was large and considered very comprehensive and provided excellent statistical weight. From hivandhepatitis.com:

http://www.hivandhepatitis.com/2008icr/easl/docs/042908_d.html
~~~~~~~~~~~~~
“Conclusion

Based on these findings, the HALT-C investigators concluded that, "A significant decline in clinical outcomes was observed in patients with chronic HCV and advanced fibrosis or cirrhosis who achieved a profound decline in HCV RNA (> 4 log and/or undetectable with subsequent breakthrough or relapse) with full-dose [pegylated interferon] and ribavirin whether or not they remained on maintenance therapy."

"Whether additional clinical benefit can be derived when profound HCV RNA suppression is maintained with [pegylated interferon] remains unproven," they added.””
~~~~~~~~~~~~~
Relevance:

The original poster stated a reduction in viral load from 500,000 to 11,000; this translates as a log1.65 difference. To fit the criteria discussed in the HALT-C trial further viral suppression to 50 IU/ML would be required.

-Bill

[GSDgirl]

hey!!!!!  I might nor be average, far from it BUT I am 49 not 60ish.  Just had to get that in there.

Yea, I know that there are a lot younger than me but I am not old.

[merryBe]

gsgirl, go girl, that's brevity we all can use!! too bad it's not 29, but I still fee that way don't you??  (until I look in the mirror ; )  ).

all....ok, come let us reason together someone once said.

medicine knows a lot more about this virus than it did 17 years ago when they first identified it.

we know that certain virus's are more virulant in smaller numbers, they kill in days.
we know hcv isn't that way, but we also know that the immune system has to stay in high gear for years, the more the virons, the more the macrophages, interlukins etc must be made. Why do you think the spleen gets enlarged over time?

Here's whats operative, I'll use numbers mentioned on this thread,
lets say a person has a VL of 2 mil. that's roughley 300,000 virons per drop of blood; vs. say a person with 15k pr ml.  or roughly 3,000 per drop of blood.

Now each viron does a variety of things, it changes the way fats and proteins are metabolized, it has a cascading effect therfore on all glandular functions, it basically farms your cells, yes, it breeds in the liver, it tried to hop inside every lipid particle as they mature (become harder) and hitch a ride in the bloodstream....do whatever damage they do there and then return to the liver to breed again.
Think of them as fish, swimming in the oceans and them going upstream to spawn again.

Now, I don't understand all they do, medicine has made strides but there are literally dozens and dozens of chemical processes that these virons are known to disrupt or utilize to their advantage in order to survive.  They remind me a little of salmon, knowing how to return to the same spawning ground (the liver), and a little of beavers, who know when an where to damn a stream the better to survive.

My point however, is that if every viron does a certain amount of damage, then having 3,000 virons per drop of blood would surely give one a better chance than having 300,000 per drop.  It only stands to reason.

It's hard to even get my mind around what that VL means, I mean, what happens to the blood cells, the red, the white, the platelets...how can they survive as well crowded in with 350,000 enemies in a single drop of blood?
I'm not saying it's the only factor, we know the inflammation is key and doesn't seem related to VL...SEEM being the key word.  

However, the possiblity exists that concurrently there is more destruction of blood cells, more compensation that both the liver and the immune system, and hence the glands as well as all other organs must do to keep up with higher VL.
It remains to be seen why the spleen enlarges, why the pituitary stops secreting growth hormone, why the other glands begin to fail, why the adipose tissue is redistrubuted...all these things could be protective, or they could be that the strain is wearing everything out.
Everything.

I just don't think it's as cut and dry as saying VL has nothing to do with anything.

As I said, HIV is a good example of the opposite being true. There you see that lowering the viral load had extended the average life span from 5 years to 30 years beyond diagnosis. The antiviral therapies are responsible for that gain.
Meaning that HIV, also a retrovirus and the closest one to hcv in terms of attributes, is survivable when VL is kept low.

Could we talk??  Can we at least see this as a possibility??

I'm not saying this to defend the poster of this thread, I'm saying it, because to me it makes sense.

mb

[Trinity4]

Not everyone experiences gland failure, cirrhosis, enlarged spleens, digestive problems, fatigue, brain damage, brain fog and so on and so forth.  I had no extra-hepatic manifestations except for PCT.  Had I not developed that I would have never known I had HCV.  Healthy as a horse with HCV well over 40 years.  However, my liver didn't fair so well and I didn't help it by adding alcohol.

HIV and HCV are worlds apart as far viral load goes.  It's been shown that those who are coinfected have a tendency for faster fibrosis progression.  How many times have we seen people post they've had HCV for 40 years with a long established viral load in the millions but biopsy showed very little fibrosis?  We've also seen people post they've had HCV for 40 years with a long established low viral load but biopsy showed extensive liver damage.

To date, I have to believe that the experts know what they are talking about when it comes to the correlation between viral load and liver damage.  We can speculate all day long but the bottom line is until new guidelines are set regarding low viral load and less liver damage I must side with the medical data currently available.

Trinity

[Trinity4]

Just a few - many more out there

http://www.wjgnet.com/1007-9327/10/2409.pdf

http://www.hepcprimer.com/biopsy/inf-3.html

http://digestive.niddk.nih.gov/ddiseases/pubs/chronichepc/

[merryBe]

as first glance I'd agree, medical data, yada yada, however then I recall things like less than .01% of the general populace with pituitary deficiancy, and 40% of the hcv populace..

reminds me of why even medical knowledge must be taken with grains of salt...so much specialization leads to short-sightedness. Reminds me sometimes of the blind men walking around the elephant.
it also reminds me that the scientific bosses, our doctors, don't always know everything.

Remember the joke about the brain and the ashhole?  The bosy BODY started having a debate within it's members one day, the blood said it should be boss because it nourished and brought air to all, the heart said I should be boss, because without him the blood goes no where...the legs said they should be boss because without them the body went nowhere, everyone had its turn, the brain of course had its say, and succintly and scientifically proved why it needed to be boss as it had all the knowledge and gave all the commands..on and on it went....finally....the ashhole said it had something to say and they all laughed and told it to shut up, who even cares what he thinks or does.  So he did, he shut up good and tight...
the next thing you know, the blood was polluted the heart started skipping beats, the legs got wobbly the brain made no sense at all...the mouth was all gibberish without any legs to stand on....which only goes to prove you don't have to be the brains to be the boss, just an ashhole!!

mb

[James10500]

The virus was first identified in 1994 ?  Huh didn't know.

In the mid 1970s, Harvey J. Alter, Chief of the Infectious Disease Section in the Department of Transfusion Medicine at the National Institutes of Health, and his research team demonstrated how most posttransfusion hepatitis cases were not due to hepatitis A or B viruses. Despite this discovery, international research efforts to identify the virus, initially called non-A, non-B hepatitis (NANBH), failed for the next decade. In 1987, Michael Houghton, Qui-Lim Choo, and George Kuo at Chiron Corporation, collaborating with Dr. D.W. Bradley from CDC, used a novel molecular cloning approach to identify the unknown organism and develop a diagnostic test.[61] In 1988, the virus was confirmed by Alter by verifying its presence in a panel of NANBH specimens. In April 1989, the discovery of the virus, renamed hepatitis C virus (HCV), was published in two articles in the journal Science.[62][63] The discovery led to significant improvements in diagnosis and improved antiviral treatment.[61]

[portann]

Hi Trin,

I hope and guess you're doing great, given your strength and determination.

I wish you well with all my might and rapid success on your next tx. Yay, STAT-C's!

I saw your input tonight about high and low viral load and wanted to point out this very recent and interesting study (2010):

http://jco.ascopubs.org/content/28/30/4587.abstract

"Conclusion Elevated serum levels of HCV RNA and ALT and HCV genotype 1 infection are independent risk predictors of hepatocellular carcinoma. These findings have strong implications for the management of chronic HCV."

Surprising, given the commonly held views we've shared about this...something I'd like to hear from others (such as willing) about in terms of its relevance and/or credibility.

Regards and good night,

Susan (the real portann)

[Trish77]

Frankly, new information comes to light every day.  I don't think it's a worthless endeavour at all for someone to decide to bring down their viral load, particularly if they have undergone treatment and it has been unsuccessful.  It is far too unknown what influence the viral load DOES have on so many other organisms in the body.  Not enough studies, not enough data for a virus that is relatively new and so much studies yet to be done and new information coming out all the time.  What we know today is far different than what was known five years ago and so on.  Any information people have should be welcome here without it turning into a game of King of the Hill.  I'm finding it interesting to read posts such as Cory's and Bill's and Susan/Portann's and other things.  Like so many other topics, some new information might make people a little uncomfortable at first and be a bit unnerving but far better to be open to new information and adjust approach where necessary to successfully tackle this thing.

[Trinity4]

Speaking for myself, I am not playing a game of "King of the Hill" nor am I unnerved or uncomfortable with new information.  I welcome any data whether it proves or disproves the correlation between viral load and liver health.

I base the informaton I post regarding no correlation between viral load and fibrosis progression on what has been studied, investigated and documented over the last 20 years. This is not to say that the current information is absolute and that it's inconceivable to think that a low viral load plays a role in slowing down the progression of fibrosis. When and if new information arises that negates what has been studied and peer reviewed I will concede my views are incorrect but until those facts are available and wide spread I once again say I stand by the current established data.

Trinity    

[portann]

This is from 2009 and gives a brief overview of some of the the studies out there:

[...While there are many studies regarding the correlation of liver damage with serum HCV-RNA titer, ALT level, and HCV genotypes, the conclusions are quite different. Adinolfi and colleagues held that serum HCV-RNA titer was correlated to the severity of liver damage, which could be accelerated by high HCV load and fat degeneration,6 while Zechini and colleagues suggested the serum ALT level, especially the AST level, was associated with liver damage.7 Puoti and colleagues argued the severity of liver damage and the clinical features had no correlations with HCV load, ALT level, and HCV genotype.8–,10...]

http://labmed.ascpjournals.org/content/40/3/167.full

Whatever the conclusions of this study, it acknowledges in its introduction that there is disagreement among scientists.

[merryBe]

james, well yes it was called non-a, non b earlier..which meant they had no idea what it was.  NOn-a non-b is just polite double speak for we are doctors but have no idea what virus this is. It wasn't until we identified it that we can really call it hcv.

they weren't able to identify AND prove by testing for the virus and its genotype until 91-92.

portann,
well that was my point exactly, that there's so much more than meets the eye.
now we add carcinoma as a result of high alt, well makes sense, high alt means more oxidation...more good news...rolleyes
gee, how about this, remember when they showed ants farming aphids for sugars?? yes the ants keep colonies of aphids and such the juices out of them, while leaving them alive...well it turns out these virons do the same, they suc.k out our juices, they farm our lipids and wait for them to harden so they can wear these raincoats out into the bloodstream before returning to their new home, another liver cell.
They also try to change the membrane permeability between liver cells, and when successful they can move from cell to cell without going for that swim....these are some smart little buggers. The more I learn about them, the more I know that very little is not effected in some way shape or form by all their mischief.

Trin and Trish,
I'm just relieved to see we are all willing to think outside the box sometimes. It's in our own interest to be as aware as we can, and also the more that is learned about how this disease behaves, the more doctors find the connections, the more they fear worldwide infection, the more chance of a cure. Its bad enough there are over a billion people with hepatitis, and still the word epidemic is never used.
Don't you wonder though why in all the annals of American medicine not one doctor has ever published a retraction when it is finally proven that his work was in error???

I just think its short sighted to think VL doesn't matter when it does effect all kinds of things, including cell death, meaning alt elevation, which isn't good for myriad reason.

Nobody is trying for king of the hill here, I think we've all made valid points.
But I'm reminded that I was told for years by a doctor that my elevated liver enzymes were no big deal, when in fact they are a big deal, and I had a serious disease.
Many in here have experienced the same.
Which means that sometimes the medical community is wrong, sometimes they don't know all the facts, sometimes it takes them years and years to see correlations.

One reason I think the research concerning VL vs. imflammation is flawed is because they fail to take into account 2 important sub groups. One group is hemophilia, when one has this the immune system is more compromised and hcv can take a worse toll, the other group is half the human race, women. Men and women to be more precise.
SHow me a study which showed the decine of women vs. the decline of men that proves VL has no bearing on health.

Why this is important is because womens organs are smaller than mens, smaller livers by 1/3, but smaller everything generally speaking. That means that we have less ability to recover from the onslaught than men do....and yet what study distinguishes between us?
I'd be curious as to the average lifespan of women vs. men at any given VL. Maybe that would tell a different tale, and one worthy of note perhaps.

[Aaron57]

X 2 , Trish77 - new info comes to light every day ...

This is why folks should not state conclusively, over what is still unknown .. to presume old research data is 100% complete and 100% accurate is ... just not right .. in my opinion, nothing dealing with this virus is 100% confirmed ... except trying to rid our bodies of it ,  takes time , $$ & luck .....

Trin , one link you provided had 90 patients .. not much to go on and not dated .. one other NDDIC pretty generic and not dated ...

Thank you & posted by Portann :

http://jco.ascopubs.org/content/28/30/4587 ,

This one is current 2010 & 925 subjects followed over thousands of person years ... I'll look for some others I have , but this is quite a detailed long term study ...

Results: Fifty-five participants newly developed hepatocellular carcinoma during 8,476 person-years of follow-up, giving an incidence rate of 648.9 per 100,000 person-years. The cumulative hepatocellular carcinoma risk increased from 1.1% for HCV RNA seronegative status to 6.4% for low HCV RNA levels and to 14.7% for high HCV RNA levels (P < .001). The cumulative risk also increased with elevated serum ALT levels from 1.7% for persistently ≤ 15 U/L to 4.2% for ever more than 15 U/L but never more than 45 U/L and to 13.8% for ALT ever ≥ 45 U/L (P < .001). Having HCV genotype 1 was associated with a higher cumulative hepatocellular carcinoma risk (12.6%) than not having HCV genotype 1 (4.5%; P < .001).

Conclusion Elevated serum levels of HCV RNA and ALT and HCV genotype 1 infection are independent risk predictors of hepatocellular carcinoma. These findings have strong implications for the management of chronic HCV.

If you want to bash on the HP , by all means go ahead .. this dialysis type medical device has just now entered into it's ... first ... CT's 2 months ago , and there is no results or data yet ... if .... if ...  it works and stands up to the CT criteria over time and trials ...  reduction of VL before starting TX .... without another drug ... or,  controlling VL in non responders & relapsers, that is the intent of the device and the company making it .
I like the idea ... and has been the focal point of my support of furthering it's studies since our earlier ... discussions ...
Do you agree that starting Tx with a low VL improves the chances of attaining SVR ?

It's good to see you keep an open mind ...

[Trish77]

The Op didn't say anything at all about fibrosis in his post.  Only that he's a 32 year survivor of Hep C and was pleased to bring his viral load down.  No mention on if he has ever tried treatment at all or anything, is a relapser or non-responder and regardless if that is the case, fact remains his post was in reference to bringing down viral load, period.  You chose to focus narrowly on fibrosis in that regard, fair enough.  However, as subsequent posts have shown, there is some merit or at least worthy discussion to the impact of viral load in the big picture on much more than fibrosis alone when it comes to management of HCV.  With regards to fibrosis - good thing you are keeping an open mind as I'm sure many are interested in being able to discuss the issues unfettered and unmolested for having divergent points of view.  Some, as you know, have a particular stake in being able to do that, being forced to manage with their HCV rather than be rid of it, at least for the time being.

[Trinity4]

"Do you agree that starting Tx with a low VL improves the chances of attaining SVR?"

If you read my early posts it's quite apparent that I do agree.  The OP did not state his intentions for lowering his viral load.  The topic of his post was squashing hepc with no interferon or ribavirin.  I do not know if his meaning implies he intends to treat and has lowered his viral load for optimal results or if he intends to maintain a low viral in hopes fibrosis progression will slow.  Least I assume for as you so eloquently stated above, any presumption or conclusion at this point would only be to assume so between assuming and brains with an ******* I better damn well have my facts straight. :)

Irrespective of what the OP's intentions were this thread has certainly produced some thought provoking dialogue without the intervention of the thought police who many times decide for us what our actual intentions are.  

Trinity

[Aaron57]

Ya Trin , his post is not that clear ... , but it did start ...
Thought provoking and sharing of information as well as helpful open minded dialog ..... that has led to more info available to us ..... that is what these forums are all about (to me) ... and i would venture to say, his post has created a successful one that is interesting reading for many members, even if we have strayed, if only a bit, from the original intent ... as at the center of the subject is VL,  ... and VL is so important to all of us ....... well maybe not to all , that would be those who already have their minds made up it's not important relative to liver health  .....

My hope is that over time , as there is much more data available that has been produced over time and scientific studies being conducted nowadays compared to yesterday on long term effects of this virus , we will know the answers to this and the other many unanswered questions about the effects of this virus...

"All I can say is I believe what all the renowned hepatologists and studies throughout the world have indicated so far.  VIRAL LOAD HAS NO BEARING ON FIBROSIS PROGRESSION......Prove me wrong, show me something, conclusive and I will gladly change my viewpoint."

Not an attack , just curious .. any change in your viewpoint Trin ?

Thankfully we have gotten this far without any "thought police" intervention , let's hope we can continue without any censoring !

[murariji]

Well I for one have enjoyed the discussion, now if Goofydad could just put it all into language I understand, that would be the cherry on the top.

[Trish77]

" now if Goofydad could just put it all into language I understand, that would be the cherry on the top."

Now you're just baiting him........ ;->

[Trinity4]

My response was to the relevance of viral load.  I do not find that topic narrow given there was no other information provided.  Additionally, my viewpoint remains the same regarding viral load, nothing has changed.  I did not veer off topic, "molest or attack", make reference to King of the Hill, chastize or character assissin anyone for having a different opinion.  It's nice of you to "be glad for me" that I can keep an open mind but just so you know I manage quite nicely all by myself without hiding my intentions or making derogatory remarks.  If you're referring to past trangressions let's keep it in the past. This thread isn't about archaeology and digging up dem bones.  

Trinity

[James10500]

Merry you are wrong about the discovery date of Hep C.  Trying to tell people with hep c who have gone through treatment for hep c  that hep c was discovered 17 years ago is ridiculous.  I could post links all day to prove this.  My god, the FDA approved the first treatment for hep c in 1992.

[merryBe]

ok james, well maybe I'm remebering the dates wrong. It may be I was thinking of when the blood tests became available...I've seen that date of 92 hundreds of times, but it might be that they called it that before hand. Although I had 2 friends with it, and they were calling it non-a non-b all through the 80's. But you sound like you're sure, so I'll stand corrected. Peace.

I'm actually kind of relieved in a weird way to see the cancer data. I think my doc thought I was being anal by trying to get off EVERYthing they had me on during tx (about 5 extra drugs), but I was determined to get my alt down and keep in down..looks like that might have been wisdom after all.
.it also means some of what I've been saying, like nix the tylenol and the meds that are keeping the alt high is making more and more sense.
When you think about it, all ALT is doing is telling us how many liver cells are dying each day, and even though we are told that double or triple the normal cell death is only a slight elevation, I've always thought that made little sense.
I mean if we were losing our rods and cones in our eyes, or our heart muscle at 2 or 3 times a normal rate would they say that??  So it makes no sense to think that elevated enzymes couldn't be a bad thing. Had my GP thought so, maybe I'd have been tested for hcv before I got to stage 3/4, but that idiot didn't even think to test me.

[James10500]

Peace and good health to you !!!!

[Dee1956]

Just saw this post, like you I had elevated liver enzymes from the late 80's on.  I was tested for Hep C in the 90s and received 3 false negatives from two different labs so I understand what you are saying.  There are many mistakes made in the name of medicine.   At one time they said it was crazy to wash your hands before surgery and doctor who came up with it was ridiculed for it.
Germs?....what are those? :)

[mikesimon]

I believe that the PRIMARY cause of liver damage from HCV infection is caused by the immune response to the virus. That response often causes collateral damage to bystander cells - uninfected bystander cells - which is why there can be a significant damage with a low viral load as well as mild or no damage with a high load. I formerly was convinced that the virus itself is not cytopathic. I am no longer that certain.
I posted the following article in 2009.


HCV itself may be cytopathic
by mikesimon
, Feb 25, 2009 08:59AM
Genomic analysis reveals a potential role for cell cycle perturbation in HCV-mediated apoptosis of cultured hepatocytes.
Walters KA, Syder AJ, Lederer SL, Diamond DL, Paeper B, Rice CM, Katze MG.

Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington, United States of America.

The mechanisms of liver injury associated with chronic HCV infection, as well as the individual roles of both viral and host factors, are not clearly defined. However, it is becoming increasingly clear that direct cytopathic effects, in addition to immune-mediated processes, play an important role in liver injury. Gene expression profiling during multiple time-points of acute HCV infection of cultured Huh-7.5 cells was performed to gain insight into the cellular mechanism of HCV-associated cytopathic effect. Maximal induction of cell-death-related genes and appearance of activated caspase-3 in HCV-infected cells coincided with peak viral replication, suggesting a link between viral load and apoptosis. Gene ontology analysis revealed that many of the cell-death genes function to induce apoptosis in response to cell cycle arrest. Labeling of dividing cells in culture followed by flow cytometry also demonstrated the presence of significantly fewer cells in S-phase in HCV-infected relative to mock cultures, suggesting HCV infection is associated with delayed cell cycle progression. Regulation of numerous genes involved in anti-oxidative stress response and TGF-beta1 signaling suggest these as possible causes of delayed cell cycle progression. Significantly, a subset of cell-death genes regulated during in vitro HCV infection was similarly regulated specifically in liver tissue from a cohort of HCV-infected liver transplant patients with rapidly progressive fibrosis. Collectively, these data suggest that HCV mediates direct cytopathic effects through deregulation of the cell cycle and that this process may contribute to liver disease progression. This in vitro system could be utilized to further define the cellular mechanism of this perturbation.

http://tinyurl.com/dfvgd4

Mike