Please Scroll Down to See Forums Below almost-pro
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Anyone have links to success stories or anything? My liver enzymes are quite high and I need them to come back down to normal range in 3-4 weeks for more bloodwork.
does milk thistle really work?
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almost-pro
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dirty v, what dose did u take and for how long?
almost-pro
New member
dirty v, what dose did u take and for how long?
Two different literature reviews have determined that there is no evidence it works for anything but mushroom poisoning. And no where is there any proof it works for 17aa's.
You should consider Tyler Liver Detox which was made specifically for doctors who have patients on 17aa's, as well as other liver ailments, and has phase one and phase two liver detox factors.
You should consider Tyler Liver Detox which was made specifically for doctors who have patients on 17aa's, as well as other liver ailments, and has phase one and phase two liver detox factors.
almost-pro
New member
ulter... is there any proof it lowers liver enzymes?
almost-pro said:
I have proof that milk thistle worked for me. Before and after liver values. My doctor remarked at the improvement given the amount of time between test. I took Tyler once from the AF store. The are probably the best protection supplement out that right now.
almost-pro said:
Yes there is. The ingredients are all listed as phase one and phase two liver detox factors in several articles.
The main ingredient Glucarate is patented by Ohio State University and has been clinically proven by the University in order to receive the patent. You can look it up.
I am not saying it's not a good component, I am saying it won't protect you while on 17aa's. Which I assume we're talking about here.
United States Patent 4,845,123
Walaszek , et al. July 4, 1989
Inventors: Walaszek; Zbigniew (Columbus, OH); Hanausek-Walaszek; Malgorzata (Columbus, OH); Webb; Thomas E. (Columbus, OH); Minton; John P. (Columbus, OH)
Assignee: The Ohio State University (Columbus, OH)
Appl. No.: 762339
Filed: August 5, 1985
Current U.S. Class: 514/473; 514/470; 514/574
Intern'l Class: A61K 031/19
Field of Search: 424/10 514/470,473,574
References Cited [Referenced By]
--------------------------------------------------------------------------------
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3928583 Dec., 1975 Furuno et al. 424/180.
Foreign Patent Documents
1066885 Apr., 1967 GB.
Other References
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Levvy, Biochem. J., 52:464-470 (1951).
Boyland et al, Invest. Urol., 2:439-445 (1965).
Bradley, J. Urol., 88:626-628 (1962).
Iida et al, Jpn J. Pharmacol., 15:88-90 (1965).
Miyakawa et al, Invest. Urol., 10:256-261 (1973).
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Boyland et al, Brit. J. Urol., 36:563-569 (1964).
Katayama, Jpn. J. Urol., 63:951-971 (1972).
Walaszek et al, Carcinogenesis, 5:767-772 (1984).
Zedeck et al, Eds., Inhibition of Tumor Induction and Development, Plenum Press, New York, Ch. 9:219 (1981).
Willett et al, N. Eng. J. Med., 310:430-434 (1984).
Walaszek et al, AACR Abstracts, vol. 35, No. 507 (1984).
American
Am J Med. 2002 Oct 15;113(6):506-15.
Milk thistle for the treatment of liver disease: a systematic review and meta-analysis.
Jacobs BP, Dennehy C, Ramirez G, Sapp J, Lawrence VA.
Department of Medicine, University of California, San Francisco 94143, USA. [email protected]
PURPOSE: Milk thistle, an herbal compound, is the dietary supplement taken most frequently by patients with chronic liver disease. We performed a systematic review of the literature to determine the efficacy and safety of this herb for the treatment of liver disease. METHODS: We searched English and non-English reports through July 1999 using thirteen databases and reference lists, and contacting manufacturers and technical experts. Reviewers independently screened all reports to identify randomized placebo-controlled trials that evaluated milk thistle for the treatment of liver disease. Outcomes of primary interest included mortality, histological findings on liver biopsy specimens, serum aminotransferase and albumin levels, and prothrombin times. RESULTS: Fourteen trials met inclusion criteria. Four trials reported outcomes for mortality among 433 participants. The overall summary odds ratio for mortality in the milk thistle group compared with placebo was 0.8 (95% confidence interval [CI]: 0.5 to 1.5; P = 0.6). Three trials assessed histology on liver biopsy; study quality was inversely associated with the likelihood of histological benefit for milk thistle compared with placebo. There were no differences in serum alanine aminotransferase, aspartate aminotransferase, or albumin levels, or prothrombin times, among participants assigned to milk thistle compared with those assigned to placebo. The only statistically significant difference was a greater reduction in alanine aminotransferase levels among patients with chronic liver disease assigned to milk thistle (-9 IU/L, 95% CI: -18 to -1 IU/L; P = 0.05), but this reduction was of negligible clinical importance and no longer statistically significant after limiting analyses to studies of longer duration or of higher quality. The frequency of adverse effects was low and, in clinical trials, indistinguishable from placebo. CONCLUSION: Treatment with milk thistle appears to be safe and well tolerated. We found no reduction in mortality, in improvements in histology at liver biopsy, or in biochemical markers of liver function among patients with chronic liver disease. Data are too limited to exclude a substantial benefit or harm of milk thistle on mortality, and also to support recommending this herbal compound for the treatment of liver disease.
Swiss
Drugs. 2001;61(14):2035-63.
The use of silymarin in the treatment of liver diseases.
Saller R, Meier R, Brignoli R.
Abteilung Naturheilkunde, University Hospital Zurich, Switzerland.
The high prevalence of liver diseases such as chronic hepatitis and cirrhosis underscores the need for efficient and cost-effective treatments. The potential benefit of silymarin (extracted from the seeds of Silybum marianum or milk thistle) in the treatment of liver diseases remains a controversial issue. Therefore, the objective of this review is to assess the clinical efficacy and safety of silymarin by application of systematic approach. 525 references were found in the databases, of which 84 papers were retained for closer examination and 36 were deemed suitable for detailed analysis. Silymarin has metabolic and cell-regulating effects at concentrations found in clinical conditions, namely carrier-mediated regulation of cell membrane permeability, inhibition of the 5-lipoxygenase pathway, scavenging of reactive oxygen species (ROS) of the R-OH type and action on DNA-expression, for example, via suppression of nuclear factor (NF)-kappaB. Pooled data from case record studies involving 452 patients with Amanita phalloides poisoning show a highly significant difference in mortality in favour of silibinin [the main isomer contained in silymarin] (mortality 9.8% vs 18.3% with standard treatment; p < 0.01). The available trials in patients with toxic (e.g. solvents) or iatrogenic (e.g. antispychotic or tacrine) liver diseases, which are mostly outdated and underpowered, do not enable any valid conclusions to be drawn on the value of silymarin.
