"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.
"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.
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.
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
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)
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
About chlorogenic acid and VDR, I did not find studies, I found some stuff related to the "Marshall Protocol". Here one can better understand: http://synergyhn.wordpress.com/cga/ .
CGA blocks the VDR (as well as Vit D) and makes one feel BETTER. Because it suppresses the immune system. It is the immune system activated that makes us feel sick (like, for ex, when one is on interferon).
There is also bacteria in our gut producing substances that block the VDR, bacteria, viruses as well. This is according to dr Marshall. According to others (maybe vits sellers?), vit D helps. Where is the truth, somwhere in the middle?
You are on vit D?...what is your 1,25D level? ...to see if dr Marshall's theory confirms in your case
I don't think studies should be trusted so much. I took a lot of supps in high doses and did more harm then good, that is why I think it is better NOT to take anything in high doses. and take whole foods if possbile instead of supps, the reason is the way those supps are manufactured, leaving residual stuff, heavy metalls, junk that we swallow with the pill.
But that is only my experience, maybe for others is different.
What I found very good for the liver/health are coffee enemas (I used green coffee). Those were used for cancer therapy (see ****** therapy). I don't think this way CGA and coffeine gets into the blood.
One needs to make sure he got the procedure right before starting, in order not to hurt his colon.
why are you so sure vit D activates the VDR? (in the case of people with chronic disease)
Like they say on the MP site, if Vit D would activate the VDR, your antimicrobial peptides ( produced after vdr activated) should be sky high (after taking very high vit D doses). Do you see high values for cathelicidin and other stuff (rezulting from vdr activation) in your lab results?
I don't think you do, because in this case you would have already cured hep B.
If you don't, vit D dose not activate VDR, or the VDRs are blocked (which should be the case with chronic disease)...but then I see no point in taking high d3 dosage, when the real problem is unblocking the vit d receptors. You just create more problems.
what you are saying is wrong there is gcmaf, vitd and oleic acid to attach to vdr and there is nagalase and vit d kept ultralow by viruses, but it is useless to discuss we are already doing it and seeing what hbsag does
no need of hypothesis or talk like this we are doing it directly and checking the results good or bad and they are good for now
I am wondering if the ALT is high after IFN, what's a good supplement to take? Currently after 4 weeks, (2 shots on 180mcg and 2 shots on 90mcg), my neutrophils are slightly going up from 0.36 to 0.48 and 0.80. ALT has elevate from pre-treatment of 40-50 to 131.
Can you advise why it's not good to take calcium supplement? I am currently cutting down on dairy food.
alt must stay elevated that s a very good sing, it is immune system killing infected cells if both hbsag and hbvdna are going down
there is no way to lower hbsag without killing infected cells and have elevated alt, although 131 is still low alt it is a good sign
i d not take anything else but vitamin d, 4 cup of coffee or green coffee as these increased pegintf response on human trials
don t worrry about neutrophils, they need to go down and also plats, it means they are going and stopping inside the liver where the infection is and where they re needed.as long as they are not less than 0.5 and plts less than 25K what you have to look at is hbsag only
OK, just came back from an appointment with the nurse. Still on 90mcg for 4 weeks now and looks like the 5th for tomorrow. The reason for the reduction was the low counts in certain blood and neutrophils. Bone marrow suppression was their concern.
ALT has stabilized from 131 to 109 in one week. Likewise AST has drop to the 70's. Neutrophils decreased from 0.80 to 0.77.
It's only been 6 injections so far. Also, the nurse said with my small frame, 90mcg can be sustained. I guess it does make sense. ALT elevated from the 40's is also a good sign. The pain right now.......the weekly blood test.
All in all, I guess this is like a blind treatment as I have no clue to the pre-HbsAg level and the ongoing numbers. Just the viral load at week 12. All I can do is eat, pray, love.
Currently taking once every other day, zinc 25mg, selenium 200mcg, Vit D 5000iu and Mega B complex. Eating healthy as always (just started this Feb, better late than never).
what is your serum level of vitd25oh?if less than 100ng/ml it is better to go for 10.000iu daily with no milk, no butter and no cheese diet (no to everything which has calcium), use biotech d3 plus possibly
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