I have read many threads, but found no definitive answer to: after the hepC has been killed below detection, can drinking alchohol lower the immune system enough to reactivate the virus? I would like only research or statistical evidence please. Some claim absolutely not, others, like my own doctor, claim its possible. However hard I try, I have found no actual studies or research giving a final, up to date, conclusion (2012).
- answers about liver damage
- answers about general health advice regarding alchohol
- answers about the cases of severe medically caused immuno-suppresion, except as far as they may relate to the immuno response of alcohol specifically
Thank you for your specificity, as alot of the problem with determining an answer to this question is the endless off topic answers and common knowledge alchohol warnings.
Or do you meaning by below detection you are treating and the virus is suppress but you have a ways to go before finishing treatment?
If you are cured (SVR) then you have no virus left to multiple. The hepatitis C virus doesn't interact with alcohol. The virus finds an environment to replicate in (the liver) And replicates trillions of times a day. Either you are chronically infected or you are not.
"half-life of 3–5 h and a clearance and production rate of ∼1012 particles per day (Zeuzem et al., 1998⇓ ; Neumann et al., 1998"
Each virion only lives less than a day which is why the virus must replicate many times per day. Either the virus replicates or it dies. This is how the new antiviral drug work. They interfere with the virus's replication process.
The Department of Veterans Affairs
Active alcohol intake is considered a relative contraindication to interferon-based therapy.(12,13) This recommendation is based on the documented noncompliance of heavy drinkers with different medical therapies,(14) and the fact that the side effects of interferon therapy make it extremely difficult to comply with, even in patients without ongoing substance abuse.(15) Because abstinence prior to therapy is considered standard management, major trials of anti-hepatitis C therapy excluded active drinkers,(16,17) and did not evaluate alcohol history as a predictor variable in treatment response. As such, the effects of alcohol on HCV treatment response come only from much smaller studies.
Nearly all studies of the effect of alcohol on treatment responses have been with interferon monotherapy, and none has been blinded or randomized. Examples include two Japanese studies, one in which 16 of 53 patients were defined as heavy drinkers, and only 6% of all drinkers normalized their alanine aminotransferase (ALT) during treatment, compared with 30% of nondrinkers.(18) A second study found that ALT normalization segregated directly with alcohol intake, 53% in nondrinkers, 43% in those consuming 70 g/day.(19)
More recently, an Italian study (20) required abstinence from alcohol for 6 months prior to and during interferon monotherapy. Sustained virological response was significantly reduced in those with >75 g/day alcohol consumption prior to abstinence (9%), compared with nondrinkers (33%). In the only published study examining the role of alcohol on response in patients treated with interferon and ribavirin, a German group (21) treated 81 patients whose alcohol use histories were characterized prior to, during, and after interferon and ribavirin therapy. Twenty-one patients (26%) reported alcohol use while on therapy, 6 requiring inpatient treatment for detoxification. No significant differences were found, however, in therapeutic outcome and ALT levels after treatment based on alcohol consumption before or during combination therapy.
In summary, published studies mostly suggest a negative effect of alcohol on the response to hepatitis C therapy. However, these were all small, nonrandomized, unblinded studies, so basing firm conclusions on them is difficult. Moreover, none of the studies reported patient compliance with therapy. As such, it remains unknown whether observed response differences seen in drinkers actually reflect biological differences, or whether the heavy drinkers were merely less compliant with therapy."
SVR is a good thing. Studies have shown that with a six-month SVR (which means no detectable virus in your blood for six months after finishing treatment), relapse occurred in only 1-2% of patients. So, for every 100 people who finished treatment and attained SVR, the virus will return in only 2 of them. However, for these people, the virus never really left. The medicine was able to eliminate most of the virus (so much that medical tests couldn't detect it), but after treatment ended, for whatever reason the virus was able to continue replicating itself.
Patients with Ongoing Alcohol Use
in those who completed HCV therapy, SVR was similar in drinkers and nondrinkers . Thus, alcohol users should not be excluded from antiviral therapy but treatment adherence should be stressed
Patients with Ongoing Alcohol Use
Alcohol is an important cofactor in the progression of HCV disease to cirrhosis and HCC (43) . Thus, patients with hepatitis C should limit or abstain from alcohol consumption. Limited data suggest that heavy alcohol consumption of >80 g/day (approximately eight drinks or more per day) reduces HCV treatment response. It is unknown whether consuming less alcohol compromises HCV treatment response (44) . In patients with recent alcohol consumption, there were higher treatment discontinuation rates; however, in those who completed HCV therapy, SVR was similar in drinkers and nondrinkers (45) . Thus, alcohol users should not be excluded from antiviral therapy but treatment adherence should be stressed (9) .
RECOMMENDATIONS IN PATIENTS WITH ONGOING ALCOHOL USE
1. Patients should be encouraged to decrease consumption or to abstain (III).
2. Patients should be referred for behavioral intervention to reduce alcohol use (III).
3. Antiviral therapy should be offered to patients regardless of prior alcohol use who otherwise meet criteria for therapy (II-2).
4. Alcohol consumption should be discouraged during antiviral treatment, because alcohol reduces adherence and treatment response (III).
This is interesting. I think the onus is on your doctor to provide the science to support his claim. Or more specifically show how alcohol can impair antiviral and antibacterial immune response and thereby leaving a previously infected individual vulnerable to the reactivation of HCV
He would have to establish the virus is "killed" in a previously HCV infected individual; and,
Establish a direct link between alcohol and "reactivation" of the Hepatitis C virus to the exclusion of all other possibilities such as relapse, HCV-HIV coinfection, liver fibrosis progression HBV-related disorders, chemotherapy or other underlying haematological conditions.
Do you know of anyone of that relapsed after the 6mo post boceprivir tx? or are the stats you speak of here, are you referring to boceprivir tx? I have recently felt some liver pain, had another quant PCR done and just received a call to come in. Instead of making an appt to review results, going to go pick up results. I had other lab work done too, hopefully it's just my thyroid is still going crazy. Hope you're well and still as full of it as ever!!
Wow what a nice surprise to see your name show up again, as a matter of fact they did a follow up study on SVR results using boceprevir and the results were great. So you have no worries there.
HCV Protease Inhibitor Boceprevir Demonstrates Durable Sustained Response with No Late Relapse
Among the 290 patients who achieved SVR, no cases of late relapse were confirmed.
1 person was confirmed to have been re-infected with HCV based on genotype/subtype sequence
29 patients (5%) experienced serious adverse events during extended follow-up, similar to those previously described during initial follow-up.
Still full of it???... SURE
Interesting! : ) To answer you: I contracted the virus and was lucky enough to have fought it off on my own, so only antibodies were present. My doctor said the virus, "was still there, just at undetectable levels." She apparently is into the 'persistent viral theory' which seemed to make sense at the time, since I read a study about a few the severely immuno-suppressed getting it back; the researchers claimed it proved the virus was still present, but in small quantites. I'm not sure if this is outdated, or proven to be due to another reason, such as reinfection, instead of reactivation?
I would doubt if your doctor is a gastroenterologist or hepatologist as they appear to not know the basics of hepatitis C infection.
So if you have positive antibodies for hepatitis C and no viral load (HCV RNA) and did not treat your hepatitis C, your immune system fought off the virus when you where first exposed to it and you never were chronically infected. Since you were never chronically infected there is no virus to come back.
From the CDC -
What do the results of the two tests mean?
People who have a positive antibody test along with a negative RNA
test have had an infection that has been cleared. He or she is not
People who have a positive antibody test along with a positive RNA test
have an ongoing (chronic) Hepatitis C infection.
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