Why Every Athlete SHOULD Use TUDCA Part 1

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TUDCA
TUDCA

You guys have heard me talk and briefly touch on TUDCA in previous articles but after a high amount of demand for more information on this ingredient, I felt compelled to give it a full amount of my time and efforts because it seems people are still somewhat undecided as to whether this supplement would benefit them. In reality, I believe EVERYONE, especially if your an athlete, SHOULD BE SUPPLEMENTING WITH TUDCA YEAR ROUND. The only thing I feel needs to be undulated is the dosage…but we’ll get more into that later. Lets start off with the basics to make sure we’re all understanding of this molecule, its pharmacokinetics and dynamics, its benefits, as well as practical application. TUDCA (AKA Tauroursodeoxycholic Acid) is a water soluble bile acid that is very well known for having the ability to counteract the toxicity of normal bile acids that can cause a host of damaging effects to your body (especially on the liver.) Normal bile salts will reach our intestines -> become metabolized into UDCA -> then are bound to a taurine molecule (forming TUDCA.) TUDCA seems much more effective at raising bile concentrations of UDCA than UDCA alone because that taurine molecule which enhances overall bioavailability (1.)

Now that we all have that understanding of the basics of what TUDCA is, lets move into the portion that you actually care about…what does TUDCA possess thats so beneficial to athletes. TUDCA has been shown to help with overall healthy functioning of the liver and has numerous beneficial interactions with glucose metabolism, fat mass, and skeletal muscle. Larghi et al states “results from animal studies and preliminary data from pilot studies in patients with primary biliary cirrhosis suggest that tauroursodeoxycholic acid has metabolic properties that may favour its long-term use as an alternative to ursodeoxycholic acid for patients with chronic cholestatic liver diseases. No direct comparison of tauroursodeoxycholic and ursodeoxycholic acids have yet been carried out in primary biliary cirrhosis. The effects of ursodeoxycholic and tauroursodeoxycholic acids were compared in 23 patients with primary biliary cirrhosis according to a crossover design. Both drugs were administered at the daily dose of 500 mg. in a randomly assigned sequence for two 6-month periods separated by a 3-month wash-out period. Serum liver enzymes related to cholestasis and cytolysis consistently improved, as compared to baseline values, during the administration of both ursodeoxycholic and tauro-ursodeoxycholic acids, but no significant difference between these two bile acids was found. Both treatments were well tolerated and no patient complained of side effects. In the short-term, tauro-ursodeoxycholic acid appears to be safe and at least as effective as ursodeoxycholic acid for the treatment of primary biliary cirrhosis” (2.) An even more interesting study entitled “Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study” (3) actually looked at dosages of 500, 1000, and 1500 mugs of TUDCA over a 6 month period. They performed a dose-response study on 24 patients with primary biliary cirrhosis who were randomly assigned to receive 500, 1000, or 1500 mg daily of tauroursodeoxycholic acid for six months. Biliary enrichment with ursodeoxycholic acid ranged from 15% to 48% and was not related with the dose. Serum liver enzyme levels decreased significantly after the first month of treatment with all the three doses. No significant difference among the three doses was found, although further reduction over time occurred with 1000 and 1500mg daily. Plasma total and HDL cholesterol significantly decreased in patients administered the two higher doses. Diarrhea was the only side effect. In conclusion, a dose of about 10mg/kg body wt/day of tauroursodeoxycholic acid should be used for long-term studies in patients with primary biliary cirrhosis. It is very clear that TUDCA supplementation aids in overall healthy liver functioning by lowering cholesterol levels, lowering liver enzymes, and improving/restoring normal function.

References

  1. Metabolism of orally administered tauroursodeoxycholic acid in patients with primary biliary cirrhosis. K D Setchell, C M Rodrigues, M Podda, A Crosignani. Gut. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8675100)
  2. Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study. A. Larghi, A. Crosignani, P. M. Battezzati, G. De Valle, M. Allocca, P. Invernizzi, M. Zuin, M. Podda. Aliment Pharmacol Ther. 1997 (https://www.ncbi.nlm.nih.gov/pubmed/9146783)
  3. Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study. A. Crosignani, P. M. Battezzati, K. D. Setchell, P. Invernizzi, G. Covini, M. Zuin, M. Podda. Dig Dis Sci. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8674405)
  4. Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women. Marleen Kars, Ling Yang, Margaret F. Gregor, B. Selma Mohammed, Terri A. Pietka, Brian N. Finck, Bruce W. Patterson, Jay D. Horton, Bettina Mittendorfer, Gökhan S. Hotamisligil, Samuel Klein. Diabetes. 2010 (https://www.ncbi.nlm.nih.gov/pubmed/20522594)
  5. Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes. Umut Özcan, Erkan Yilmaz, Lale Özcan, Masato Furuhashi, Eric Vaillancourt, Ross O. Smith, Cem Z. Görgün, Gökhan S. Hotamisligil. Science. Author manuscript; available in PMC 2016 Feb 4.. Published in final edited form as: Science. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16931765)
  6. Glucose-induced beta cell dysfunction in vivo in rats: link between oxidative stress and endoplasmic reticulum stress. C. Tang, K. Koulajian, I. Schuiki, L. Zhang, T. Desai, A. Ivovic, P. Wang, C. Robson-Doucette, M. B. Wheeler, B. Minassian, et al. Diabetologia. 2012 (https://www.ncbi.nlm.nih.gov/pubmed/22396011)
  7. Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation. Mitsuhiro Watanabe, Sander M. Houten, Chikage Mataki, Marcelo A. Christoffolete, Brian W. Kim, Hiroyuki Sato, Nadia Messaddeq, John W. Harney, Osamu Ezaki, Tatsuhiko Kodama, et al. Nature. 2006 (https://www.ncbi.nlm.nih.gov/pubmed/16400329)
  8. Differences in the metabolism and disposition of ursodeoxycholic acid and of its taurine-conjugated species in patients with primary biliary cirrhosis. P. Invernizzi, K. D. Setchell, A. Crosignani, P. M. Battezzati, A. Larghi, N. C. O’Connell, M. Podda. Hepatology. 1999 (https://www.ncbi.nlm.nih.gov/pubmed/9918905)
  9. Does tauroursodeoxycholic acid (TUDCA) treatment increase hepatocyte proliferation in patients with chronic liver disease? C. Panella, E. Ierardi, M. F. De Marco, M. Barone, F. W. Guglielmi, L. Polimeno, A. Francavilla. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8541578)
  10. TUDCA and UDCA are incorporated into hepatocyte membranes: different sites, but similar effects. U. Leuschner, S. Guldutuna, S. Bhatti, A. Elze, M. Imhof, T. You, G. Zimmer. Ital J Gastroenterol. 1995 (https://www.ncbi.nlm.nih.gov/pubmed/8563010)
  11. Effects of prolonged glucose infusion on insulin secretion, clearance, and action in normal subjects. G. Boden, J. Ruiz, C. J. Kim, X. Chen. Am J Physiol. 1996 (https://www.ncbi.nlm.nih.gov/pubmed/8779946)

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