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Bill Sardi
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Posted December 12, 2013: by Bill Sardi
Hepatitis C is ineffectively and agonizingly treated with interferon injections. An oral medication for Hep C has just been approved by the FDA. But this viral monster can continue its attack on the liver until a liver transplant is needed.
The medical literature clearly points to vitamins and herbal supplements are being effective against HEP C. Doctors ignore this evidence.
Recently someone sent an e-mail inquiring which dietary supplements a person might take, based upon published studies, to combat HEP C. Here is how I responded, with abstracts of scientific reports posted below.
Dosages not indicated means follow recommendation on package.
©2013 Bill Sardi, Knowledge of Health, Inc.
References to all of the above are provided below:
Hepatology. 2009 Dec; 50(6):1756-64.
Gonzalez O, Fontanes V, Raychaudhuri S, Loo R, Loo J, Arumugaswami V, Sun R, Dasgupta A, French SW.
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA 90095-1732, USA.
The hepatitis C viral (HCV) genome is translated through an internal ribosome entry site (IRES) as a single polyprotein precursor that is subsequently cleaved into individual mature viral proteins. Nonstructural protein 5A (NS5A) is one of these proteins that has been implicated in regulation of viral genome replication, translation from the viral IRES and viral packaging. We sought to identify cellular proteins that interact with NS5A and determine whether these interactions may play a role in viral production. Mass spectrometric analysis of coimmunoprecipitated NS5A complexes from cell extracts identified heat shock proteins (HSPs) 40 and 70. We confirmed an NS5A/HSP interaction by confocal microscopy demonstrating colocalization of NS5A with HSP40 and with HSP70. Western analysis of coimmunoprecipitated NS5A complexes further confirmed interaction of HSP40 and HSP70 with NS5A. A transient transfection, luciferase-based, tissue culture IRES assay demonstrated NS5A augmentation of HCV IRES-mediated translation, and small interfering RNA (siRNA)-mediated knockdown of HSP70 reduced this augmentation. Treatment with an inhibitor of HSP synthesis, Quercetin, markedly reduced baseline IRES activity and its augmentation by NS5A. HSP70 knockdown also modestly reduced viral protein accumulation, whereas HSP40 and HSP70 knockdown both reduced infectious viral particle production in an HCV cell culture system using the J6/JFH virus fused to the Renilla luciferase reporter. Treatment with Quercetin reduced infectious particle production at nontoxic concentrations. The marked inhibition of virus production by Quercetin may partially be related to reduction of HSP40 and HSP70 and their potential involvement in IRES translation, as well as viral morphogenesis or secretion.
Quercetin may allow for dissection of the viral life cycle and has potential therapeutic use to reduce virus production with low associated toxicity.
PMID: 19839005
Liver Int. 2005 Jun; 25(3):613-21.
Bruck R, Aeed H, Brazovsky E, Noor T, Hershkoviz R.
Department of Gastroenterology, The E. Wolfson Medical Center, Holon, Israel. rafib@tasmc.health.gov.il
Allicin, the immunologically active component of garlic, has been found to affect oxidative stress and immune response in several experimental systems. In the present study, we examined the ability of allicin to prevent immune-mediated, concanavalin A (Con A)-induced liver damage in mice.
Mice were pretreated with allicin for 7 days before their inoculation with Con A (15 mg/kg). The serum levels of liver enzymes and liver histology were examined 24 h after Con A administration. The effect of Con A and allicin on serum levels of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB) activation in the liver were examined 2 h after Con A administration, in a separate group of rats, and the effect of allicin on Con A-induced expression of inducible nitric oxide synthase (iNOS) was determined by western blot analysis 24 h after Con A injection.
The histopathologic damage in the mouse livers, and the Con A-induced increase of aminotransferases and TNF-alpha were markedly inhibited in the mice pretreated with allicin before Con A injection (P < 0.01). NF-kappaB binding activity to the nucleus, which increased 2 h after Con A administration, was attenuated by allicin. The expression of iNOS protein which was induced following Con A administration was significantly attenuated by allicin. In vitro studies showed that allicin inhibited TNF-alpha-mediated T cell adhesion to extracellular matrix components and to endothelial cells. Allicin also inhibited TNF-alpha-mediated intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression on human vascular endothelial cells.
This study demonstrates that immune-mediated liver damage in mice can be prevented by allicin, probably because of its immunomodulatory effects on T cells and adhesion molecules and inhibition of NF-kappaB activation.
PMID: 15910499
Hepatology. 2013 Mar;57(3):925-33. doi: 10.1002/hep.26186. Epub 2013 Feb 7.
Bitetto D, Bortolotti N, Falleti E, Vescovo S, Fabris C, Fattovich G, Cussigh A, Cmet S, Fornasiere E, Ceriani E, Pirisi M, Toniutto P.
Department of Medical Sciences Experimental and Clinical, Medical Liver Transplantation Unit, Internal Medicine, University of Udine, Italy.
Recent data suggest that vitamin A modulates the expression of type I interferon receptor enhancing the antireplication effect of interferon-α onhepatitis C virus (HCV). This study aimed to investigate the prevalence of vitamin A deficiency among patients with chronic HCV infection and to assess whether vitamin A deficiency could be associated with unresponsiveness to interferon-based antiviral therapy. The analysis included 199 consecutive treatment-naïve chronic HCV patients in whom pretreatment serum vitamin A and 25-OH vitamin D were measured; 119 healthy blood donors were used as controls. Median (interquartile range) serum vitamin A in HCV-positive patients was significantly lower than in controls: 256 ng/mL (128-440) versus 742 (624-942, P<0.0001). Overall sustained viral response was achieved in 122/199 patients, 46/109 infected by difficult to treat HCV genotypes. In these latter, 39/104 (37.5%) were nonresponders. At multivariate analysis, nonresponse to antiviral therapy was predicted by carriage of interleukin (IL)-28B T/* genotypes, baseline serum levels of γGT>60 IU/mL, of HCV RNA>600,000 IU/mL, of vitamin A≤100 ng/mL, and a cumulative dose of ribavirin≤80%. Seventeen patients (9.0%) had both serum levels of vitamin A≤100 ng/mL and of vitamin D≤20 ng/mL; the presence of a combined vitamin A and D deficiency was found to be a strong independent predictor of nonresponse to antiviral therapy. Conclusion: A high percentage of patients with chronic HCV infection have serum vitamin A deficiency. This condition is associated with nonresponse to antiviral therapy.
Copyright © 2012 American Association for the Study of Liver Diseases.
PMID: 23213086
J Clin Biochem Nutr. 2012 Nov;51(3):178-84.
Matsumura H, Nirei K, Nakamura H, Arakawa Y, Higuchi T, Hayashi J, Yamagami H, Matsuoka S, Ogawa M, Nakajima N, Tanaka N, Moriyama M.
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1, Oyaguchi Kamimachi, Itabashiku, Tokyo 173-8610, Japan.
We administered zinc supplementation therapy over three years to patients with chronic hepatitis C and reported and that the aspartate aminotransferase (AST) and alanine aminotaransferase (ALT) levels decreased, and platelet counts increased, significantly in the group with increased serum zinc concentrations. We are continuing this treatment to clarify the long-term consequences and report here the changes in serumzinc concentrations over seven years and compare the cumulative incidence of hepatocellular carcinoma (HCC). We administered polaprezinc to 32 patients, randomly selected for zinc therapy (treatment group), while another 30 formed the control group. We measured the serum zinc and albumin concentrations and conducted a prospective study to determine long-term outcomes. The changes and rates of change of serum zinc concentrations after seven years were 76.7 ± 18.2 µg/dl and +0.302 ± 0.30% in the treatment group and 56.7 ± 12.4 µg/dl and +0.033 ± 0.21% in the control group and had increased significantly (p = 0.0002, p = 0.0036). Progression of liver disease seemed to vary, depending on serum albumin concentrations. In the group with baseline serum albumin concentrations of 4.0 g/dl or more, the change and rate of change of serum zinc concentrations increased significantly, and the cumulative incidence of HCC tended to decrease, in the treated group. According to multivariate analysis, the factors that contribute to a reduction in the incidence of HCC are zinc therapy (risk ratio: 0.113, 95% CI: 0.015-0.870, p = 0.0362), and platelet counts (0.766, 0.594-0.989, 0.0409). Zinc supplementation therapy seems to improve liver pathology and reduce the incidence of HCC.
chronic hepatitis C, cumulative incidence of HCC, serum zinc concentrations, zinc supplementation therapy
PMID: 23170044
Lipids. 2008 Apr;43(4):325-33.
Kawashima A, Tsukamoto I, Koyabu T, Murakami Y, Kawakami T, Kakibuchi N, Takaguchi K, Kita K, Okita M.
Department of Natural Science and Ecological Awareness, Graduate School of Humanities and Sciences, Nara Women’s University, Kitauoyanishimachi, Nara 630-8506, Japan. faa_kawashima@cc.nara-wu.ac.jp
Eicosapentaenoic acid (EPA) (1.8 g/day) was administered to 12 chronic hepatitis C patients receiving combination therapy of pegylated interferon (PEG-IFN) alpha-2b and ribavirin for 48 weeks (EPA group). Twelve patients were not administered EPA (control group). All patients also received vitamin E and C (300, 600 mg/day, respectively) during the therapy. Serum alanine aminotransferase improved to a normal level in 8 of 12 patients from the EPA group and 6 of 12 patients from the control group after 12 weeks. Lymphocyte counts decreased significantly after 8 weeks in the control group, but not the EPA group. T-helper (Th) 1 decreased after 4 weeks in the control group, but not in the EPA group (two-way ANOVA; P < 0.05). Th1/Th2 ratios were elevated in 9 of 12 patients in the EPA group, and 3 out of 12 in the control group (P < 0.05) after 8 weeks. After 12 weeks, the arachidonic acid/EPA molar ratio of erythrocyte membrane phospholipid correlated negatively with the leukocyte count (n = 24, r = -0.439, P < 0.05) and the neutrophil count (n = 24, r = -0.671, P < 0.02). The hemoglobin level improved after 48 weeks compared with 24 weeks in only the EPA group. These findings suggest that EPA supplementation may be useful in therapy for chronic hepatitis C.
PMID: 18320252
Expert Rev Anti Infect Ther. 2012 Nov;10(11):1273-7.
Gastroenterology/Division, Duke Clinical Research Institute Hepatology/Gastroenterology Research, Duke University, Durham, NC 27708, USA. hans.tillmann@duke.edu
Evaluation of: Rocco A, Compare D, Coccoli P et al. Vitamin B12 supplementation improves rates of sustained viral response in patients chronically infected with hepatitis C virus. Gut doi:10.1136/gutjnl-2012-302344 (Epub ahead of print) (2012). Vitamin B12 was first mentioned to have a role in HCV treatment approximately a decade ago, but it has not been well translated into clinical medicine. Recently, however, a randomized trial has reported significantly better response at all time-points during therapy with pegylated interferon plus ribavirin, if such therapy was combined withvitamin B12. This correlates with reports on vitamin B12 being able to inhibit HCV in vitro and a report that vitamin B12 levels were related to treatment response. If further validated, vitamin B12 is another vitamin reported to be beneficial for HCV therapy. Vitamin D had repeatedly been reported to be associated with response to HCV therapy. It will be interesting to see whether vitamins such as B12 and D will remain relevant in the light of direct antivirals.
PMID: 23241183
J Viral Hepat. 2013 Jul;20(7):486-93.
Petta S, Grimaudo S, Marco VD, Scazzone C, Macaluso FS, Cammà C, Cabibi D, Pipitone R, Craxì A.
Cattedra di Gastroenterologia, DiBiMIS, University of Palermo, Palermo, Italy. petsa@inwind.it
Lower 25-hydroxyvitamin D [25(OH)D] serum levels have been associated with the severity of liver fibrosis in genotype 1 chronic hepatitis C patients (G1CHC). In addition, a recent genome-wide study identified genetic variants (rs12785878, near dehydrocholesterol reductase, DHCR7; rs10741657, near CYP2R1; and rs7041, near vitamin D-binding protein, GC) affecting 25(OH)D serum levels in healthy populations. We aimed to assess the association between vitamin D serum levels and its genetic determinants, with the severity of liver fibrosis. Two hundred and sixty patients with biopsy-proven G1CHC were consecutively evaluated. The 25(OH)D serum levels were measured by high-pressure liquid chromatography. All patients were genotyped for DHCR7 rs12785878, CYP2R1 rs10741657 and GC rs7041 single nucleotide polymorphisms. DHCR7 GG genotype (P = 0.003) and the severity of fibrosis (P = 0.03) were independent factors associated with lower 25(OH)D serum levels in multiple linear regression analysis. Interestingly, 53.8% (7/13) of patients with DHCR7 GG genotype had severe liver fibrosis, compared to 27.1% (67/247) of those with DHCR7 TT/TG genotype (P = 0.03). By multivariate logistic regression analysis, severe fibrosis was independently associated with older age (OR, 1.056; 95% CI, 1.023-1.089, P = 0.001), low cholesterol (OR, 0.984; 95% CI, 0.974-0.994, P = 0.002), high triglycerides (OR, 1.008; 95% CI, 1.002-1.015, P = 0.01), low 25(OH)D (OR, 0.958; 95% CI, 0.919-0.999, P = 0.04), DHCR7 GG genotype (OR, 4.222; 95% CI, 1.106-16.120; P = 0.03), moderate-severe steatosis (OR, 2.588; 95% CI, 1.355-4.943; P = 0.004) and moderate-severe necroinflammatory activity (grading) (OR, 2.437; 95% CI, 1.307-4.763; P = 0.001). No associations were found between liver fibrosis and both CYP2R1 and GC genotypes. In patients with G1CHC, GG homozygosis for DHCR7 gene and lower 25(OH)D levels are independently associated with the severity of liver fibrosis.
PMID: 23730842
Dig Dis Sci. 2002 Mar;47(3):543-8.
Lévy S, Hervé C, Delacoux E, Erlinger S.
Department of Hepatology and INSERM U-481 and Hôpital Beaujon, Clichy, France.
Thiamine deficiency is a common feature in chronic alcoholic patients, and its pathophysiology remains poorly understood. Until now, thiaminedeficiency has been considered to be mainly the result of alcoholism irrespective of the underlying liver disease. The aims of the study were to compare the prevalence of thiamine deficiency in alcohol- and hepatitis C virus-(HCV-) related cirrhosis and in patients with chronic hepatitis Cwithout cirrhosis. Forty patients with alcoholic cirrhosis (group A), 48 patients with HCV-related cirrhosis (group B), and 59 patients with chronichepatitis C without cirrhosis (group C) were included prospectively. Thiamine status was evaluated by concomitant determination of erythrocyte transketolase activity, thiamine diphosphate (TDP) effect, and direct measurement of erythrocyte thiamine and its phosphate esters by HPLC.Thiamine was mainly present in erythrocytes in its diphosphorylated form. Prevalence of thiamine deficiency and levels of TDP in thiamine-deficient patients were similar in patients of group A (alcoholic cirrhosis) and of group B (viral C cirrhosis). None of the patients with chronic hepatitis (group C) was deficient. Thiamine deficiency was not correlated with the severity of the liver disease or disease activity. No impairment of thiaminephosphorylation was found in the three groups. conclusion, alcoholic or HCV-related cirrhotics have the same range of thiamine deficiency, while no patient without cirrhosis has thiamine deficiency, and impaired phosphorylation does not account for the deficiency observed in cirrhotics. We suggest that thiamine should be given to patients with cirrhosis irrespective of its cause.
PMID: 11911339
Saudi J Gastroenterol. 2012 Mar-Apr;18(2):106-10
Khan MS, Dilawar S, Ali I, Rauf N.
Department of Biochemistry, Bannu Medical College, Khyber Pakhtunkhwa, Bannu, Pakistan. mshoaibkhan2003@yahoo.com
The compelling evidence reported that selenium is an essential trace mineral for human beings. Selenium plays a pivotal role in the restoration of immune functions. High rates of hepatitis B and C are present in Pakistan. Epidemiologic surveys demonstrated an inverse association between selenium (Se) level and regional cancer incidence, as well as viral infection. The present study was designed to evaluate the concentration of selenium in the serum of patients suffering from hepatitis B and C.
In this cross-sectional descriptive analytical study, serum selenium concentration of 150 patients suffering from hepatitis B and C, along with 26 healthy controls, was determined by atomic absorption spectrophotometer equipped with hydride generation system, model Analytic Jena (Vario III).
The mean and standard deviation of serum selenium concentration observed in male and female patients with hepatitis C were 101.60 ± 0.55 and 77.43 ± 0.47 μ g/L, respectively, whereas the mean and standard deviation of serum selenium concentration observed in male and female patients with hepatitis B were 107.58 ± 0.44 and 137.8 ± 0.36 μg/L. Analysis of t test showed significant difference between C and B (P<0.001) patients in serum selenium concentration, when compared with the control.
The obtained results indicate that serum selenium concentration of hepatitis B and C patients is less than serum seleniumconcentration of healthy individuals. However, serum selenium decline is relative to severity of disease. Based on findings of this study, it is proposed that selenium should be supplemented in such patients in order to optimize nutritional support and to get better treatment response.
PMID: 22421715
Monolaurin for Hepatitis C REFERENCE
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