I take 1 mg of Folic acid daily. I also give myself an additional injection of Procrit once weekly to keep my red blood cells up for anemia. I still get tired.
my blood counts are not that bad.my energy level is around 20 % low as compared to my pre-tx level. Is 5 mg daily dosage somewhat on higher side? we don't want to add extra iron in our bodies.
I don't know if that is high,I'm going to ask my Dr next week if more would help me & see what she thinks of a higher dose for our bodies.
certainly some folic acid is condusive to health, but additional supplemental dosing may not be. Depends. Do you eat any from natural sources. If so, you may want to leave it at that. Only based on this one study, but done with rats whole livers are great for these studies since they behave almost identically to human livers, here's what was found:
Moderately High Folic Acid Supplementation Exacerbates Experimentally Induced Liver Fibrosis in Rats
Judit Marsillach*, Natàlia Ferré, Jordi Camps*,1, Francesc Riu*, Anna Rull* and Jorge Joven*
* Centre de Recerca Biomèdica, Hospital Universitari de Sant Joan, Institut de Recerca en Ciències de la Salut, Reus, Spain; Department of Clinical Biochemistry and Molecular Genetics, Hospital Clínic Universitari, Barcelona, Spain
To whom requests for reprints should be addressed at 1 Centre de Recerca Biomèdica, Hospital Universitari de Sant Joan, C. Sant Joan s/n, 43201 Reus, Catalunya, Spain. E-mail: ***@****
Under certain clinical circumstances, folic acid can have undesirable effects. We investigated the following: (i) the effects of moderately high folic acid supplementation on the course of liver impairment in CCl4-treated rats and (ii) the influence of folic acid supplements on the hepatic recovery following the interruption of the CCl4-induced toxic injury. Four experimental groups of rats were used: CCl4-treated rats (0.5 ml of CCl4 twice a week ip) fed standard chow for up to 12 weeks (Group A); treated rats fed chow supplemented with 25 mg/kg folic acid from weeks 6 to 12 (Group B); treated rats fed a standard diet but with CCl4 discontinued after 6 weeks to allow for tissue recovery over 4 weeks (Group C); rats as Group C but fed a diet supplemented with 25 mg/kg folic acid from weeks 6 to 10 (Group D). Liver and blood samples were obtained for biochemical, histological, and gene expression analyses. Animals that received the supplement had a higher content of collagen, activated stellate cells, and apoptotic parenchymal cells in biopsy tissue at weeks 8 and 10 of treatment and more extensive alterations in serum albumin and bilirubin concentrations (Group B vs. Group A). In some of the time periods analyzed, alterations were observed in the expression of genes related to apoptosis (B-cell leukemia/lymphoma 2, inhibitor of apoptosis 2) and to fibrosis (procollagen I, matrix metalloproteinase 7). In the recovery period (Groups C and D), folic acid administration was associated with increased hepatic inflammation and apoptosis and with a decrease in the tissue inhibitor of metalloproteinase-3 expression following 1 week of recovery. We conclude that folic acid administration aggravates the development of fibrosis in CCl4-treated rats. Follow-up studies are needed to determine whether folic acid treatment would be contraindicated in patients with chronic liver diseases.
So to avoid apoptosis, fibrosis etc I choose noy to supplement this vitamin.
Some may disagree with my rational but at stage 4 I didn't need more fibrosis and all the tx drugs can also do liver damage but here we have no choice, it treat with what you must of the disease will do even worse to you...but, so adding more things that might hurt it didn't make sense to me.
Niacin (vitamin B3) also has some concerns for a liver patient. It is usually amply supplied in most B-complexes but has been associated with liver damage.
Particularly true for those who drink any alcohol.
this was taken from medicine net.
Nicotinic acid (Niacin)
Niacin, like the stains, has been used to treat elevated blood cholesterol levels as well as elevated triglyceride levels. Also like the statins, niacin can damage the liver. It can cause mild transient elevations in blood levels of AST and ALT, jaundice, and, in rare instances, liver failure. Liver toxicity with niacin is dose-dependent; toxic doses usually exceed 2 grams per day. Patients with pre-existing liver diseases and those who drink alcohol regularly are at higher risk for developing niacin toxicity. The sustained-release preparations of niacin also are more likely to cause liver toxicity than the immediate-release preparations.
So the best advice is to get lots of fruits, veggies and things high in B vitamins without trying to overdose it. Also a healthy diet, with 3 bowel movements a day means the gut is kept in good shape, and when it is it makes some of its own B vitamin. Eat active yogurt to help promote this.
If you eat no greens, or fruit. then your nurse may be trying to improve you nutrition or trigyliserides but use only small doses and only if you do no drinking and are not in an advanced state of disease already, otherwise this can backfire on you.
My liver clinic does not revommend niacin for any of its patients, in fact they recommend against its use.
And taking too much Folic Acid is associated with an increase risk of prostate cancer....
1. Folic acid and Vit B12 are recommended by hepatologists for anemia during treatment because they are needed for red cell production.
2. Hep C is associated with reduced levels of B vitamins...and low serum B12 is a Tx negative.
(AASLD Nov 2008)
Vitamins B depletion, lower iron status and decreased antioxidative defense in patients with chronic hepatitis C treated by pegylated interferon alfa and ribavirin.
Lin CC, Yin MC, et al, Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung City, Taiwan, Republic of China.
Summary: In a study involving 152 healthy subjects and 109 patients infected with hepatitis C (HCV), treatment with pegylated interferon combined with ribavirin was found to decrease levels of vitamin B6, vitamin B1, vitamin B2 and iron. Infection with HCV was associated with reduced levels of vitamin B6 and folate, and the ************** further diminished B vitamin status, and was associated with a higher percentage of patients with insufficient iron status. Furthermore, HCV infection was associated with higher plasma levels of malondialdehyde and 8-isoprostane; ************** for HCV further exacerbated lipid oxidation. HCV infection was also associated with significantly lower vitamin C and glutathione levels; ************** was found to reduce alpha-tocopherol level and activity of glutathione peroxidase and superoxide dismutase. These results suggest that supplementation with B vitamins, iron, and vitamin C may be beneficial to patients with HCV, particularly those treated with pegylated interferon alfa and ribavirin. Additional research is warranted.
Serum B12 levels predict response to treatment with pegylated interferon and ribavirin in patients with chronic hepatitis C virus infection.
P. Rosenberg, K. Hagen, Gastroenterology and Hepatology, Karolinska University Hospital, Stockholm, SWEDEN;
BACKGROUND The current treatment regimen of hepatitis C infection (HCV) with pegylated interferon (pegIFN) and ribavirin (RVN) has greatly improved the outcome for patients, but still only about 50% are cured. The need for more effective treatment, as well as better tools to predict treatment outcome, is urgent. Cyanocobalamin (vitamin B12) is stored in hepatocytes, and essential in several biological processes. Studies have shown that B12 inhibits the translation of HCV RNA by interfering with the internal ribosome entry site. The clinical implication of B12 in the setting of antiviral treatment is unknown. AIM To evaluate the correlation between pretreatment B12 serum levels (s-B12) and end-of-treatment response (ETR) in patients with chronic HCV infection. METHODS 113 treatment naïve patients, undergoing treatment with peg-IFN α2a or 2b and RVN, at our clinic between the years 2000-2007 were identified. Serum samples were collected immediately before treatment start and stored at -70 degrees celcius awaiting analysis. S-B12 was analyzed according to routine methods. Baseline characteristics, including liver biopsy, and treatment response were collected from the medical records. Pre-treatment s-B12 levels were correlated to ETR using uni-variate analysis. The data was then further evaluated in a logistic regression model, including s-B12, genotype, viral load, fibrosis stage (Batts Ludwig), age, gender and any dose-reduction during treatment. RESULTS Of 113 patients, 99 (59 males and 40 females) completed treatment and had frozen baseline serum samples and medical records available. Mean s-B12 was 331 pmol/L in ETR and 260 pmol/L in non-responders (NR) (p=0.012). Median age at start of treatment was 49 years (range 27-81). In patients with s-B12 levels of ≤ 360 pmol/L, 23 (31.5%) were NR and 50 (68.5%) were ETR. In patients with s-B12 > 360 pmol/L, one (3.8%) was NR and 25 (96.2%) were ETR (p=0.0034). For further analysis, data on fibrosis stage and genotype was available in 89 patients. The results of the multi-variate analysis were as follows: Pre-treatment s-B12 > 360 pmol/L vs ≤ 360 pmol/L: OR 19.4 CI 1.8-208, p=0.013 Stage of fibrosis 3-4 vs 0-2: OR 0.26 CI 0.07-0.94, p=0.038 Genotype 2/3 vs 1/4/5: OR 10.1 CI 2.27-44.9, p=0.002 Dose reduction, age at treatment start and gender was not significantly correlated to ETR. CONCLUSIONS S-B12 > 360 pmol/L is significantly correlated to ETR in HCV patients treated with peg-IFN and RVN. This correlation is independent of previously known predictors of response. Our results suggest that B12 may be of importance for the suppression of viral replication during anti-viral treatment.
Besides that......Oxidative Stress causes low levels of Glutathione ....which causes low levels of SAMe....and SAMe is required for STAT1 methylation. In other words, low levels of glutathione and SAMe break JAK-Stat.....interferon signaling....which can cause interferon resistance (studies have shown that taking SAMe improves early response to Tx).
SAMe requires Vit B12, B6, and Folate as cofactors in this methylation (and a large % of the population have a genetic defect in the pathway needed to metabolize them).
That's why we included them in CS's Tx plan : )
Reduced expression of Jak-1 and Tyk-2 proteins leads to interferon resistance in hepatitis C virus replicon.
Hazari S, Taylor L, Haque S, Garry RF, Florman S, Luftig R, Regenstein F, Dash S.
Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, 1430 Tulane Avenue, New Orleans, USA.
BACKGROUND: Alpha interferon in combination with ribavirin is the standard therapy for hepatitis C virus infection. Unfortunately, a significant number of patients fail to eradicate their infection with this regimen. The mechanisms of IFN-resistance are unclear. The aim of this study was to determine the contribution of host cell factors to the mechanisms of interferon resistance using replicon cell lines. RESULTS: HCV replicons with high and low activation of the IFN-promoter were cultured for a prolonged period of time in the presence of interferon-alpha (IFN-alpha2b). Stable replicon cell lines with resistant phenotype were isolated and characterized by their ability to continue viral replication in the presence of IFN-alpha. Interferon resistant cell colonies developed only in replicons having lower activation of the IFN promoter and no resistant colonies arose from replicons that exhibit higher activation of the IFN promoter. Individual cell clones were isolated and nine IFN resistant cell lines were established. HCV RNA and protein levels in these cells were not altered by IFN- alpha2b. Reduced signaling and IFN-resistant phenotype was found in all Huh-7 cell lines even after eliminating HCV, suggesting that cellular factors are involved. Resistant phenotype in the replicons is not due to lack of interferon receptor expression. All the cell lines show defect in the JAK-STAT signaling and phosphorylation of STAT 1 and STAT 2 proteins were strongly inhibited due to reduced expression of Tyk2 and Jak-1 protein. CONCLUSION: This in vitro study provides evidence that altered expression of the Jak-Stat signaling proteins can cause IFN resistance using HCV replicon cell clones.
On the three areas that showed ****** in the Vit B study.....it's supposed to say "dr-ug Tx".
One last comment.....
The study you quoted on Folic Acid supplementation used 25 mg/kg of Folic Acid. If you used that amount on humans, it would be a huge dose. It seems to me the goal of the study was to see how much Folic Acid it would take to cause fibrosis....LOL
"Also like the statins, niacin can damage the liver."
Looks like some of the statins can also increase treatment response....
Intervirology. April 2009
An open pilot study exploring the efficacy of fluvastatin, pegylated interferon and ribavirin in patients with hepatitis C virus genotype 1b in high viral loads.
Sezaki H, Suzuki F, Akuta N, Yatsuji H, Hosaka T, Kobayashi M, Suzuki Y, Arase Y, Ikeda K, Miyakawa Y, Kumada H. Department of Hepatology, Toranomon Hospital, Tokyo, Japan.
OBJECTIVE: Response to pegylated (PEG) interferon (IFN) and ribavirin is achieved only in 40-50% of patients infected with hepatitis C virus (HCV) of genotype 1 in high viral loads, which needs to be improved. METHODS: In an open-label pilot study, fluvastatin (HMG-CoA reductase inhibitor), 20 mg daily, was given along with PEG-IFN/ribavirin to 21 patients with chronic hepatitis C. They were followed for HCV RNA in serum. RESULTS: During treatment for 48 weeks, HCV RNA was lost from serum in 93% of the patients. In the 15 patients who received 48-week therapy, a sustained virological response (SVR) with loss of HCV RNA 24 weeks after completion was achieved in 10 (67%), including 7 of the 9 (78%) male and 3 of the 6 (50%) female patients. In the remaining 6 patients who received 72-week therapy, SVR was gained in 4 (67%), including 1 of the 2 male and 3 of the 4 female patients aged 56, 58 and 62 years, respectively. CONCLUSION: Fluvastatin could be used safely to increase the response to PEG-IFN and ribavirin, especially in aged women who respond poorly to combined PEG-IFN/ribavirin.
regard folic and B3
you are right !
I didn't notice it said 25 mg...
now that I do I'm stymied.
They can't have been serious. It's got to be a typo right??
I mean, it's micrograms not milligrams normally dosed,
so 25 mg would be insane.
maybe we should write and clarify this? I can’t believe they’d do that, it would be ridiculous to call that moderate dosing…it has to be a typo.
my guess, and it's only based on what we know so far regarding the endocrine compromises that HCV exacerbates, is that the high ammonia and B deficiency both are related to a slower gut. Whether this is diet alone, or thyroid as well, or even medications (metformin etc.) causing a compromise in absorption rate...pain pills also for that matter...anything that slows the bowels really...these all do a lot of damage to both absorption AND the natural flora responsible for both production and absorption of said vitamins.
Ergo, if we could return the bowel to health, we would have the ideal method for assuring adequate nutrition.
However, I can see the point for most to supplement. Unless they can make all these changes a permanent part of their regime, deficiency would follow.
I’ve been eating live yogurt for 40 years so I’m not really too worried but most folks don’t do that I’ll bet. The really alive stuff is pretty potent and sour!
As to the genetic factor you mentioned, >>>>>>and a large % of the population have a genetic defect in the pathway needed to metabolize them.<<<<<
all they are saying is the signaling is off while treating, not whether this is a flaw from birth or a flaw brought on by the tx.
my guess would be the treatment causing these related genetic changes. Honestly I could feel my skin shriveling and shrinking on this tx...not to mention the dehydration that drives us half batty…both skin and eyeballs felt like I was in death valley all during tx..
Plus the Gomez-Romero study confirmed a 6 fold decrease in the midochondrial ratio with some PI’s and antivirals….which kinda confirms the drug themselves are causing major structural and signaling changes even if not AS pronounced as in the HIV arm of that study.
Back to B absorption,
If I'm remembering my info correctly, children absorb optimally and by that we mean they absorb about 15% of the nutrion taken in, so at our best we are not very efficient digesters. By adulthood that number is reduced to 10 or even 5%...even less in advanced diseases. Most of this loss is due to erosion of the intestine and the coatings created by years of junk foods, particularly white flour products that act like glues in the gut. The blocking and sluggishness changes the whole biology of digestion and the very high rates of intestinal disease in developed countries comparative to say Asia where fiber and unrefined foods still rule the day is ample proof of the truth of all this.
I think if someone has a sluggish bowel and/or bad diet and/or meds inhibiting movement then supplementation makes more sense.
I'm still eating greens and fiber galor, just choosing not to focus on the high folic content foods because to much could be as bad as too little, or at least I was...so shall we flip for who writes these guys?? I’m really curious now.
As to the statins, conundrums again, on the one hand, obviously we want things on board that might help our HCV to clear. Yet we have to be cautioned by where our liver is at, and by how statins work. Statins aren't friendly in later stage liver disease, for one reason the liver function slides and as this happens cholesterol can become too low. Even though normally the liver makes it's own cholesterol when enough isn't present, that only happens if the tissue is healthy. Once it reaches critical mass it can't keep up and of course kidney, pituitary and thyroid also play a role in cholesterol levels, and HCV lowers endocrine functions we know, ergo the statins may help one problem for some while creating two more. They are not a pantacea…it’s not like taking an aspirin. These drugs effect lipids at every level and lipids are essential to health.
Back when doing physical therapy I was more than a little put out by the statins because I saw so many patients on them improve their musculature and hydration when they discontinued them. Docs threw them at heart patients when they first came out (before they were even called statins I saw folks taking them)…and then rarely cared when they became too cramped up to even walk….sheesh…and These side effects are rarely shared with patients when they are prescribed, years ago they weren't even known of course, but now there is no excuse.
Also are people really aware these drugs work super differently in a sick liver. No is the answer. I went into an instant liver shut down from one drug this month...Cefuroxime (Vantin) but the statins can cause similar reactions in liver patients.
Here’s my biggest concern:
Honestly, I know the researchers hearts may be in the right place, but sometimes I wonder where there heads are at. I mean shouldn't there be some mention of what stage of liver disease they were testing on...and where they saw benefit vs. harm?
The fact that they are painting statins with this broad brush worries me both because of this and because if the tx drugs, (particularly the riba) are already interfering with lipids, and redistribution of adipose fat is already occuring (again Gomez-Romero ) then doesn't that really call into question how much of this is a good thing?
I don't know if you noticed it but last week they came out with a big bruhaha on the news about alpha lipoic acid not being good for us as originally thought...rolleyes. Every decade they reverse themselves. I was going to add it for BS control until I read the liver disease warnings…so none of these things are cure alls.
As a liver patient I think we need to weigh the metabolic effect on the liver first. It won’t make sense to destroy more liver trying to improve our hearts or pancreas or whatever.
Personally, weighing all the info, I was reticent to add any lipids to my regime because the purported benefit had to be weighed against both the rancidity factors and the knowledge that HCV virions protect themselves with lipids coating their outer shell, thus avoiding the chemo drugs. On the one hand, we can see that benefits have been observed, particularly where fibrosis is concerned…regarding PCC for instance, but does this help the virons survive is the unanswered question.
It would seem then, that less not more fats in the diets might aide SVR, and this would be the only reason why statins might make sense for some, less lipids equaling greater rates of SVR with statins….this would fit perfectly into my theory, that less lipids would reduce viron survival. So the real question becomes by what means do we get there?
If not by statin use than perhaps by a more vegetable oriented diet. One study I read recently suggested vegetarians had a higher rate of SVR but we need more confirmation to jump on that band wagon I think, because elimination of usable proteins has it’s own bad down side.
Yet as I said, at stage 4, with low cholesterol already statins hardly made sense for me, but for some it might have benefit, especially in early stage disease. Yet even there I would familiarize oneself with side effects and keep watch, and have monthly blood work if considering statins, wouldn't you?
My hepatology group from CPMC had me take a high dose of FA while also on Procrit to fight anemia. I'm a stage 4 liver patient.
I think a non-veggie eater would benefit from some FA. Some is essential.
However, after seeing that study I remember some older factoids.
Years ago Linus Pauling did a lot of research into Vitamin C, Folic acid, B3, B12, and a whole host of other natural cures. I remember back when he was using vitamin C to treat polio even, and with some success....heck they even did a "House episode" a while back with that very treatment. (many acidic things effect viruses...of course, they can also shut ones kidneys down if overdosed....)
However, one thing that came of his research was the fact that an overdosing of FA could cause B12 deficiency.
so overkill is Not good
scroll down to toxicity on above site
some doctors these days will prescribe 4000 or 5000 mcg for folks with anemia and at those doses it can cause big problems. Solving for one issue and causing another is never wisdom so knowing when to stop is an important concept.
I still can't belive those study numbers are right. When I first fought to get an RX for folic acid (30 yrs ago) 150mcg was a normal dose. The logic that 5mg (or 75 times the daily requirement) would be good for people escapes me. They can't be serious, who would write an Rx for that? Boy o boy. If you followed that logic we should all be given 75 times more oxygen....I mean if a little is good a lot would be better right....
nope, dead is more like it...now how's that for GOOFY ? : )
speaking of goofy, my hepatologist just doubled and double again and then once more my antibiotics....I finally put my foot down and said NO...not without a catheter draw...
and sure enough I didn't even have an infection...they were treating me for nothing but surface bacterium detected...sometimes sensitive tets can backfire especially for women...
but giving me 2 and 3x normal dosing...with a bad liver?? What are people thinkin'?
You think they know what they're doing...but then when you study it out you find out that's not true much of the time. If we don't do our own investigation it only to our own detrement.