Avatar universal

Squashing Hepatitis C with no interferon-ribavarin


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.
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Avatar universal
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.


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317787 tn?1473358451
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? :)
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1491755 tn?1333201362
Peace and good health to you !!!!
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233616 tn?1312787196
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.
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1491755 tn?1333201362
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.

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Avatar universal
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.  

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Avatar universal
" 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........ ;->
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1523804 tn?1316560909
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.
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1130586 tn?1316266292
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 !

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Avatar universal
"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.  

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Avatar universal
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.
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1130586 tn?1316266292
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 ...
Helpful - 0
233616 tn?1312787196
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.

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.
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Avatar universal
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...]


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

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Avatar universal
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.
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Avatar universal
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):


"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)

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1491755 tn?1333201362
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]
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233616 tn?1312787196
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!!

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Avatar universal
Just a few - many more out there



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Avatar universal
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.

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233616 tn?1312787196
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.

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.

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475300 tn?1312423126
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.
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87972 tn?1322661239
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:


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.””

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.

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