proven from human trials:
minimum 3 -4 cups of coffe per day boost interferon response.
could you please post also the link-s to the trials results
could you please post also the link-s to the trials results
Never seen studies on hbv and coffee. Anyhow if coffee helps people with hcv theraphy then should be pretty much same for hbv.
"Anyhow if coffee helps people with hcv theraphy then should be pretty much same for hbv. " - I think that is a pretty bold statement that you are making. HCV is an RNA virus, its viral material always reside in the cytoplasm of the infected cell, unlike the cccDNA of hbv that resides inside the nucleus. Bear in mind, Interferon is always more effective against HCV, then HBV.
A recent news item in Nature Reviews Gastroenterology and Hepatology describes how caffeine affects liver fibrosis by inhibiting the adhesion and activation of hepatic stellate cells, which attenuates the progression of liver fibrosis.
Here is a human study re coffee intake and fibrosis. It is difficult to draw firm conclusions from these studies, however.
Liver Int. 2011 Aug;31(7):1047-53. doi: 10.1111/j.1478-3231.2011.02555.x. Epub 2011 May 31.
The effect of caffeine and alcohol consumption on liver fibrosis - a study of 1045 Asian hepatitis B patients using transient elastography.
Ong A, Wong VW, Wong GL, Chan HL.
Department of Medicine and Therapeutics and Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong SAR, China.
Role of caffeine consumption in chronic hepatitis B virus (HBV)-infected patients and the interaction with alcohol consumption is unclear.
This study aimed to investigate the relationship between caffeine and alcohol consumption and liver stiffness in chronic HBV-infected patients.
Chronic HBV-infected patients who underwent transient elastography examination in 2006-2008 were studied. Advanced fibrosis was defined as liver stiffness > 9 kPa for patients with normal alanine aminotransferase (ALT) or > 12 kPa for those with elevated ALT according to previous validation study. Caffeine and alcohol consumption was recorded using a standardized questionnaire. Excessive alcohol intake was defined as 30 g/day in men and 20 g/day in women.
The liver stiffness of 1045 patients who completed the questionnaire was 8.3 ± 6.2 kPa. Two hundred and sixteen (20.7%) patients had advanced fibrosis. Ninety-five (19.0%) patients who drank ≥ 1 cup of coffee had advanced fibrosis, compared with 121 (22.2%) patients who drank < 1 cup (P = 0.21). The amount of caffeine intake had positive correlation with the amount of alcohol intake (r(s) = 0.167, P < 0.001). Although 231 (22.1%) patients reported alcohol consumption, only 11 (1%) had excessive alcohol intake. The prevalence of advanced fibrosis among patients with mild to moderate alcohol intake (26, 18.8%) was comparable to that among non-drinkers (190, 21.0%) (P = 0.57).
Caffeine intake does not affect liver stiffness in chronic HBV-infected patients. Patients who drink coffee regularly tend to drink alcohol. Most chronic HBV-infected patients do not have excessive alcohol consumption. The prevalence of advanced fibrosis among mild to moderate alcohol drinkers was low in this population.
Association between vitamin D receptor, CCR5, TNF-a and TNF-b
gene polymorphisms and HBV infection and severity of liver disease
increasing of pegintf response with vit d levels on hcv (hbv trials never started, still pending but i think they ll never do)
Vitamin D supplementation improves response to antiviral treatment for recurrent hepatitis C
interesting data although about hcv, ridiculous doses 800iu daily used but still giving results, the study is old so still using the low doses at that time
also moderate sport can help.
"The prevalence of advanced fibrosis among patients with mild to moderate alcohol intake (26, 18.8%) was comparable to that among non-drinkers (190, 21.0%) (P = 0.57)" - this is a unsuspected conclusion.
Many thanks for the reference. The research is from Hong Kong, funny, Chinese are not known as heavy coffee drinkers and I think they may favor a milky type of coffee.
The item I refer to is as follow, it is a test-tube study, I think. I don't have access to the full article.
Nature Reviews Gastroenterology and Hepatology 10, 442 (August 2013) | doi:10.1038/nrgastro.2013.130
Liver: How caffeine affects liver fibrosis is revealed
A recent study has found that caffeine inhibits the adhesion and activation of hepatic stellate cells, which attenuates the progression of liver fibrosis. The researchers assessed cell migration and proliferation of LX-2 cells (an immortalized human hepatic stellate cell line) in vitro in the presence of different caffeine concentrations.
I think moderation is the key. What about supplements like selenium, zinc and calcium?
IMO, the key here is not to overdo. I have built my Vit D level from 48nmol/L to 129nmol/L before treatment. That's equivalent to 51.6ng/ml in this forum's scale. Australia use nmol/L measurement. So I have low Vit D level all my life until I started taking Vitamin D3 supplements 4 months ago.
Now my maintenance dose is about 5000iu per day.
no calcium and no diaries products, diaries are dangerous even without hbv unless sources are from animals in the wild and fed with no pesticiades or food not fresh or processed.they must have no antibiotics or ormones too....this is very difficult to find for those living in big cities so may be better to cut this complitely.
as to diaries on d3 supplements it is best to cut them, d3 will absorbed all calcium from other nutrients
your d3 is ok if you dont mean to use for therapeutic use, i mean boost your immune response towards hbv or boost intf response
What about supplements like selenium, zinc and calcium?
in heptech for cirrhosis doses are:
sel 400mcg daily
zinc 30mg daily
be sure sources are natural because the synthetic ones are toxic at certain levls while the natural ones are much better and less toxic in case of overdo
test for mutation may be a add on test before interferon.
Published on Friday, 04 May 2012 00:00
Written by Liz Highleyman
Chronic hepatitis B patients who do not have 2 common HBV mutations are more likely to achieve undetectable viral load and HBsAg loss when treated with pegylated interferon, according to study findings presented at the 47th International Liver Congress (EASL 2012) last month in Barcelona.
Hepatitis B virus (HBV) may carry variations in the "precore" and "core promoter" regions of its genome, which affect production of hepatitis B "e" antigen (HBeAg). Prior research has shown that these mutations are associated with more severe disease progression and poorer response to treatment compared with wild-type, or non-mutated, virus.
HBeAg loss in people who start out HBeAg positive is a measure of treatment success, along with undetectable HBV DNA viral load and hepatitis B surface antigen (HBsAg) loss; 1 study saw an HBeAg loss rate of 30% among patients treated with pegylated interferon. However, people who experience HBeAg loss still often have detectable HBV DNA and positive HBsAg, indicating that they are not cured.
Milan Sonneveld from Erasmus Medical Center in Rotterdam and colleagues performed a study to look at the relationship between the presence of precore/core promoter mutations and HBV DNA, HBeAg, and HBsAg persistence during interferon treatment.
The analysis included 214 HBeAg positive chronic hepatitis B patients treated with pegylated interferon alfa-2b (PegIntron); about half also received lamivudine (3TC; Epivir) for 52 weeks. Most (78%) were men, three-quarters were white, 19% were Asian, and the mean age was 34 years. Approximately one-third had HBV genotype A, 9% had genotype B, 14% had genotype C, and 40% had genotype D.
Participants were classified at baseline as having either only wild-type HBV or non-wild-type virus with detectable precore and/or core promoter mutations. Treatment response was evaluated 6 months after completion of therapy (week 78), with long-term follow-up at 3 years.
Precore and/or core promoter mutations were detected in 64% of patients, with frequencies varying substantially across different genotypes:
Genotype A: 69% wild-type, 7% precore, 24% core promoter, 0% both mutations;
Genotype B: 26%, 68%, 0%, and 5%, respectively;
Genotype C: 24%, 7%, 45%, and 24%, respectively;
Genotype D: 11%, 40%, 18%, and 32%, respectively.
At baseline, participants with only wild-type virus had significantly higher levels of HBV DNA (9.20 vs 8.86 log copies/mL), HBeAg (2.81 vs 2.33 log IU/mL), and HBsAg (4.53 vs 4.28 log IU/mL) than those with precore/core promoter mutations.
Participants with only wild-type HBV were significantly more likely than those with mutations to respond to treatment by all measures at 78 weeks:
Undetectable HBV DNA (<400 copies/mL): 20% vs 2%, respectively;
HBsAg loss: 18% vs 2%, respectively;
HBeAg loss: 42% vs 32%, respectively;
Combined response of HBeAg loss + HBV DNA < 10,000 copies/mL: 34% vs 11%, respectively.
After 3 years of follow-up, response rates were higher overall, and wild-type virus still predicted better response:
Undetectable HBV DNA: 78% vs 25%, respectively;
HBsAg loss: 61% vs 13%, respectively;
Sustained HBeAg loss: 87% vs 80% (no longer significant).
In a multivariate analysis, exclusively wild-type HBV at baseline was the strongest pre-treatment predictor of 78-week outcomes:
HBV DNA undetectability: odds ratio (OR) 7.93, or about 8-fold higher likelihood;
HBsAg clearance: OR 4.64, or nearly 5-fold higher;
Combined response: OR 2.90, or about triple likelihood.
Alanine aminotransferase (ALT) level had a minimal effect on treatment response among patients with wild-type virus compared with a nearly linear association for those with precore/core promoter mutations.
"Precore and core promoter mutants may be detected in a majority of HBeAg positive chronic hepatitis B patients," the investigators concluded. "Presence of mutants before [pegylated interferon treatment] is association with treatment failure."
"Patients with only wild-type virus have a high probability of virological response and HBsAg clearance through long-term follow-up," they continued. "Assessment of presence of mutants can help select patients with the highest probability of response [to pegylated interferon]."
During the question period, Sonneveld suggested that these findings may indicate that HBV with precore/core promoter mutations survive better in cells, and are perhaps less targeted by T-cells.
In a related study, Sonneveld's group also analyzed the relationship between precore/core promoter mutations and HBeAg levels and seroconversion in 138 HBeAg positive chronic hepatitis patients treated the nucleoside/nucleotide analogs lamivudine, adefovir (Hepsera), entecavir (Baraclude), and/or tenofovir (Viread).
They found that the presence of precore/core promoter mutations was associated with lower HBeAg levels and higher probability of HBeAg seroconversion. However, these mutations also predisposed patients to persistent HBV replication or HBeAg relapse after seroconversion, as was the case with pegylated interferon.
i think this applies to pegintf mono only, with the sequential treatment there were no differences about this, to note genotype D is all precore and bcp mutants, it is extremely rare to have hbeag positive after 15-20yo
surely it is for peg mono.not for sequential.
Look here for some ideas:
What I personally tried with success (I have chronic hep B, but I take no PEG):
Green coffee - works well, but it will lower Na (if one has that problem) and too much chlorogenic acid will block the VDR -> leading to more future problems (same for vit D3), according to mpkb.org
(HBsAG - coffee studies: http://www.medhelp.org/posts/Hepatitis-B/Chlorogenic-Acid/show/1947296
Coffee enemas (with green coffee) - works well (but be careful at the procedure in order not to hurt yourself)
phyllantus - works well, but lowers Na as well
Milk Thistle - works well, but it is high in oxalates, if one has problems.
If you want to supplement minerals, ionic form is the best way. I use labcatal (in Europe).
Also, Q10 seems to boost HB Antibodies production (http://www.ncbi.nlm.nih.gov/pubmed/10416052)
i m already using green coffee, but vdr needs to be fully activated hbv is blocking vdr already too much by nagalase secretion
where are the studies about green coffee and vdr?are they reliable?if so i ll stop it
from this discussion and study links, chlorogenic acid is an agonist of vdr receptor, if so green coffee is very ok and make sense with the weak pegintf boost effect
studies are too mixed between antagonist vdr....we should find a very high quality study on coffee and vdr because all human trials give good results on coffee and liver and the glucose lowering effect is also beneficial to the immune system, but the vdr block is not.....
we should find a human study with chlorogenic acid and vdr activation, one thing is certain vdr inhibition is immune suppressive
during interferron platelates count falls too much and reason to reduce dosing, is it marker of interferron or immune effect or its just a side effect of no use.
platlets fall is immune system working....it needs platlets in the liver to fix immune system cells there and keep them out of general blood flow
it is a method our body uses to keep the immune system concentrated in the liver