Before we talk about this amazing substance, let’s talk about what prompts its necessity in our research at all. Hepatoxicity, or liver toxicity, is often associated with administration of oral preparations/medications. This is especially so it seems when referring to research done using oral anabolics. Is the reason for this that they are “more toxic “than other oral preparations? Is it that they are taken more frequently? Or taken at higher dosages? Let’s look at that for a minute.
The Liver removes toxins from the blood. However we wish to look at it any oral medication is perceived to be a toxin by the research subject’s body- let’s use a rat for example. There are several ways to make a substance effective in spite of how efficient the liver is at removing the toxin from our research subject’s blood. One way is to simply dose the substance extremely high. So for example if an effective dose of acetaminophen (aka Tylenol) administered to rats would be 3mgs (purely hypothetical) the dosage could be as high as say 50mg. The liver would remove the majority of the acetaminophen, say all but the 3mg effective dose. While this is often demonstrated in over the counter preparations used in our research it is pretty inefficient and certainly not a cost effective way to overcome the livers extreme efficiency at removing toxins. Another way is to chemically alter the substance. This is what is most commonly exemplified in oral anabolics. It is referred to as methylation or 17 alpha akylation. It is the addition of a methyl group to the parent substance. The liver works to remove the methyl group, leaving the vast majority of the substance available and active in the research subjects system to do its job. It is an extremely effective delivery method and very effective at overcoming the livers efficiency at removing toxins. However it also causes the liver to work extremely hard, results in an elevation of liver enzymes, a decrease in the flow of bile, and has the potential to result in liver damage to various degrees.
This is where UDCA comes in. Now there are many herbal preparations out there than claim to do this and that for the liver in our research subjects, however, UDCA has solid science and documented research proving its efficacy at protecting as well as repairing the liver.
UDCA, or Ursodeoxycholic Acid, is proven to reduce elevated liver enzymes – the marker used in research subjects to measure liver duress, strain or impairment. Much of the damage caused to research test subjects when administering oral anabolics is due to the impairment of bile flow. Many of the salts in bile are actually toxic and cause liver cells death. UDCA increases the rate of bile flow, reducing the back up of these toxic bile salts, thus greatly reducing the cell damage or even death they may cause. UDCA is also proven to reduce cholesterol absorption.
All the things that we read about these herbal liver cleansing preparations claiming to do that have absolutely no solid research backing them up; UDCA really does and does effectively. If used when administering an oral anabolic to research subjects, it minimizes the adverse impact. If used post administration it reverses the adverse impacts. All in all, UDCA is a must have for our research when administering oral anabolics to research subjects. It truly is a proven, essential supplement for our research arsenal.
Check it out >> Ursodeoxycholic Acid (UDCA)
Refs:
*Lindor KD, Kowdley KV, Luketic VA et al. (September 2009). "High-dose ursodeoxycholic acid for the treatment of primary sclerosing cholangitis". Hepatology 50 (3): 808–14. doi:10.1002/hep.23082. . PMC 2758***. PMID 19585548
*Kotb MA (July 2008). "Review of historical cohort: ursodeoxycholic acid in extrahepatic biliary atresia". Journal of Pediatric Surgery 43 (7): 1321–7. doi:10.1016/j.jpedsurg.2007.11.043. PMID 18639689
*Jackson H, Solaymani-Dodaran M, Card TR, Aithal GP, Logan R, West J (October 2007). "Influence of ursodeoxycholic acid on the mortality and malignancy associated with primary biliary cirrhosis: a population-based cohort study". Hepatology 46 (4): 1131–7. doi:10.1002/hep.2179
*http://books.google.com/books?id=rHq...xicity&f=false
Ursodeoxycholic Acid (UDCA)
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